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The Cardiovascular Institute of the Greater Los Angeles in Encino, is recognized throughout the Los Angeles for its commitment to excellence in patient care. While we’re known for our experience and ability to take care of the most complex cardiovascular problems, we are equally focused on prevention and early detection.

Dr. Ben-Zur recommends  that you read this regarding atherosclerosis.

Overview
Atherosclerosis is a condition in which fatty material collects along the walls of arteries. This fatty material thickens, hardens (forms calcium deposits), and may eventually block the arteries.
Atherosclerosis is a type of arteriosclerosis. The two terms are often used to mean the same thing.

Symptoms
Symptoms usually do not occur until blood flow becomes restricted or blocked.

Causes

Atherosclerosis is a common disorder of the arteries. It occurs when fat, cholesterol, and other substances build up in the walls of arteries and form hard structures called plaques.
Eventually, the plaques can make the artery narrow and less flexible, making it harder for blood to flow. If the coronary arteries become narrow, blood flow to the heart can slow down or stop. This can cause chest pain (stable angina), shortness of breath, heart attack, and other symptoms.
Pieces of plaque can break off and move through the bloodstream (embolization). This is a common cause of heart attack and stroke. Blood clots can also form around a tear (fissure) in the plaque. Clots block blood flow. If the clot moves into an artery in the heart, lungs, or brain, it can cause a stroke, heart attack, or pulmonary embolism.
Risk factors for atherosclerosis include:

  • • Diabetes
  • • Heavy alcohol use
  • • High blood pressure
  • • High blood cholesterol levels
  • • High-fat diet
  • • Increasing age
  • • Obesity
  • • Personal or family history of heart disease
  • • Smoking

Atherosclerosis can affect many different organ systems, including the heart, lungs, brain, intestines, kidneys, and limbs (extremities).

Treatment
To help prevent atherosclerosis or its complications (such as heart disease and stroke), make the following lifestyle changes:

  • • Avoid fatty foods. Eat well-balanced meals that are low in fat and cholesterol. Include several daily servings of fruits and vegetables. Adding fish to your diet at least twice a week may be helpful. However, do not eat fried fish.
  • • Do not drink more than one or two alcoholic drinks a day.
  • • Exercise regularly for 30 minutes a day if you are not overweight, and for 60 – 90 minutes a day if you are overweight.

Get your blood presure checked every 1 – 2 years, especially if high blood pressure runs in your family. Have your blood pressure checked more often if you have high blood pressure, heart disease, or you have had a stroke. Talk to your doctor.

  • • Everyone should keep their blood pressure below 140/90 mmHg
  • • If you have diabetes or have had a stroke or heart attack, your blood pressure should probably be less than 130/80 mm/Hg. Ask your doctor what your blood pressure should be.

Have your cholesterol checked and treated if it is high.

  • • Adults should have their cholesterol checked every 5 years. If you are being treated for high cholesterol, you will need to have it checked more often.
  • • All adults should keep their LDL (“bad”) cholesterol levels below 130-160 mg/dL.
  • • If you have diabetes, heart disease, or hardening of the arteries somewhere else in your body, your LDL cholesterol should be lower than 100 mg/dL.
  • • Few medications have been found to clear up plaque. Statins and other cholesterol-lowering drugs can help prevent more plaque from forming.

Your doctor may suggest taking aspirin or another drug called clopidogrel (Plavix) to help prevent blood clots from forming in your arteries. These medicines are called antiplatelet drugs. DO NOT take aspirin without first talking to your doctor.
Talk to your doctor about the safety of hormone replacement therapy for menopause.
Guidelines no longer recommend vitamins E or C, antioxidants, or folic acid to prevent heart disease.
A number of surgeries are performed to help prevent the complications of atherosclerosis. Some of these are:

  • • Angioplasty and stent – heart – discharge
  • • Angioplasty and stent placement – peripheral arteries
  • • Abdominal aortic aneurysm repair – open
  • • Coronary artery bypass surgery
  • • Carotid artery surgery
  • • Minimally invasive heart surgery

Tests & diagnosis 
A health care provider will perform a physical exam and listen to the heart and lungs with a stethoscope. Atherosclerosis can create a whooshing or blowing sound (“bruit”) over an artery.
Tests that may be used to diagnose atherosclerosis or its complications include:

  • • Ankle/brachial index (ABI)
  • • Aortic arteriography
  • • Arteriography
  • • Cardiac stress testing
  • • Carotid duplex
  • • CT scan
  • • Doppler study
  • • Extremity arteriography
  • • Intravascular ultrasound (IVUS)
  • • Magnetic resonance arteriography (MRA)
  • • Mesenteric arteriography
  • • Pulmonary angiography
  • • Renal arteriography

Prognosis 
Everyone starts to develop some amount of atherosclerosis as they grow older. In some people, the condition can cause complications such as a heart attack or stroke.
Complications

  • • Coronary heart disease
  • • Damage to organs (such as the kidneys, brain, liver, and intestines)
  • • Heart attack
  • • Stroke
  • • Too little blood to the legs and feet
  • • Transient ischemic attack (TIA)

When to contact a doctor 
Call for an appointment with your health care provider if you are at risk for atherosclerosis, especially if you have symptoms.
Talk to your doctor before starting a new exercise plan, especially if you have been diagnosed with coronary heart disease or you have ever had a heart attack

  • • This information is for you only.
  • • Always follow your healthcare provider’s instructions for taking medicines or other changes.
  • • Ask your provider about nonprescription medicines and supplements before you take them.

c@American Accreditation HealthCare Commission


The Cardiovascular Institute of the Greater Los Angeles has been treating patients in Los Angeles for more then 10 years. It was founded by Dr. Uri Ben-Zur, M.D., F.A.C.C. and the institute emphasizes innovation and research and state of the art treatments for cardiovascular disease by participation in clinical research studies to insure that the most appropriate and current treatments are available. We serve Beverly Hills, Brentwood, Westwood, and Hollywood including Culver City

Dr. Ben-Zur recommends that you read this information about Atherosclerosis.

Definition
Arteries are blood vessels that carry oxygen and nutrients from your heart to the rest of your body. Healthy arteries are flexible, strong and elastic. Over time, however, too much pressure in your arteries can make the walls thick and stiff — sometimes restricting blood flow to your organs and tissues. This process is called arteriosclerosis, or hardening of the arteries. 

Atherosclerosis is a specific type of arteriosclerosis, but the terms are often used interchangeably. Atherosclerosis refers to the buildup of fats in and on your artery walls (plaques), which can restrict blood flow. These plaques can also burst, causing a blood clot. Although atherosclerosis is often considered a heart problem, it can affect arteries anywhere in your body. Atherosclerosis is a preventable and treatable condition. 

Symptoms
Atherosclerosis develops gradually. There are usually no atherosclerosis symptoms until an artery is so narrowed or clogged that it can’t supply adequate blood to your organs and tissues. Sometimes a blood clot completely obstructs blood flow, or even breaks apart and causes blood clots that can trigger a heart attack or stroke.

Atherosclerosis symptoms depend on which arteries are affected. For example:

  • If you have atherosclerosis in your heart arteries, you may have symptoms similar to those of a heart attack, such as chest pain (angina).
  • If you have atherosclerosis in the arteries leading to your brain, you may have symptoms such as sudden numbness or weakness in your arms or legs, difficulty speaking or slurred speech, or drooping muscles in your face.
  • If you have atherosclerosis in the arteries in your arms and legs, you may have symptoms of peripheral arterial disease, such as leg pain when walking (intermittent claudication).

Sometimes atherosclerosis causes erectile dysfunction in men.

When to see a doctor
If you think you have atherosclerosis — or risk factors for hardening of the arteries — talk to your doctor. Also pay attention to early symptoms of inadequate blood flow, such as chest pain (angina), leg pain or numbness. Early diagnosis and treatment can stop atherosclerosis from worsening and prevent a medical emergency.

Causes
Atherosclerosis is a slow, progressive disease that may begin as early as childhood. Although the exact cause is unknown, researchers suspect that atherosclerosis starts with damage or injury to the inner layer of an artery. The damage may be caused by:

  • • High blood pressure
  • • High cholesterol
  • • An irritant, such as nicotine
  • • Certain diseases, such as diabetes

Once the inner wall of an artery is damaged, blood cells called platelets often clump at the injury site to try to repair the artery, leading to inflammation. Over time, fatty deposits (plaques) made of cholesterol and other cellular waste products also accumulate at the injury and harden, narrowing your arteries. The organs and tissues connected to the blocked arteries then don’t receive enough blood to function properly.
Eventually pieces of the fatty deposits may rupture and enter your bloodstream. This can cause a blood clot to form and damage your organs, such as in a heart attack. A blood clot can also travel to other parts of your body and partially or totally block blood flow to another organ.

Risk factors
Hardening of the arteries occurs over time. In addition to simply getting older, factors that increase the risk of atherosclerosis include:

  • • High blood pressure
  • • High cholesterol
  • • Diabetes
  • • Obesity
  • • Smoking
  • • A family history of aneurysm or early heart disease

Complications
The complications of atherosclerosis depend on the location of the blocked arteries. For example:

  • Coronary artery disease. When atherosclerosis narrows the arteries close to your heart, you may develop coronary artery disease, which can cause chest pain (angina) or a heart attack.
  • Carotid artery disease. When atherosclerosis narrows the arteries close to your brain, you may develop carotid artery disease, which can cause a transient ischemic attack (TIA) or stroke.
  • Peripheral artery disease. When atherosclerosis narrows the arteries in your arms or legs, you may develop circulation problems in your arms and legs called peripheral arterial disease. This can make you less sensitive to heat and cold, increasing your risk of burns or frostbite. In rare cases, poor circulation in your arms or legs can cause tissue death (gangrene).
  • Aneurysms. Atherosclerosis can also cause aneurysms, a serious complication that can occur anywhere in your body. An aneurysm is a bulge in the wall of your artery. Pain and throbbing in the area of an aneurysm is a common symptom. If an aneurysm bursts, you may face life-threatening internal bleeding. Although this is usually a sudden, catastrophic event, a slow leak is possible. If a blood clot within an aneurysm dislodges, it may obstruct an artery at some distant point

Preparing for your appointment
Your doctor will first perform a physical exam if you think you have atherosclerosis. You’ll have your blood pressure checked to see if you have high blood pressure, a common sign of atherosclerosis. Your doctor may also listen to the blood flowing through your arteries using a stethoscope to see if there are any abnormalities.
One of the most common tests doctors perform when checking for atherosclerosis is a blood test to check your cholesterol level and blood sugar. You’ll need to go without eating or drinking anything but water for nine to 12 hours before your blood test. Your doctor should tell you ahead of time if this test will be performed during your visit.
If your doctor thinks you have atherosclerosis, you may need more tests to confirm the diagnosis. 

Tests and diagnosis
Your doctor may find signs of narrowed, enlarged or hardened arteries during a physical exam. These include:

  • • A weak or absent pulse below the narrowed area of your artery
  • • Decreased blood pressure in an affected limb
  • • Whooshing sounds (bruits) over your arteries, heard with a stethoscope
  • • Signs of a pulsating bulge (aneurysm) in your abdomen or behind your knee
  • • Evidence of poor wound healing in the area where your blood flow is restricted

Depending on the results of the physical exam, your doctor may suggest one or more diagnostic tests, including:

  • Blood tests. Lab tests can detect increased levels of cholesterol and blood sugar that may increase the risk of atherosclerosis.
  • Doppler ultrasound. Your doctor may use a special ultrasound device (Doppler ultrasound) to measure your blood pressure at various points along your arm or leg. These measurements can help your doctor gauge the degree of any blockages, as well as the speed of blood flow in your arteries.
  • Ankle-brachial index. This test can tell if you have atherosclerosis in the arteries in your legs and feet. Your doctor may compare the blood pressure in your ankle with the blood pressure in your arm. This is known as the ankle-brachial index. An abnormal difference may indicate peripheral vascular disease, which is usually caused by atherosclerosis.
  • Electrocardiogram (ECG). An electrocardiogram records electrical signals as they travel through your heart. An ECG can often reveal evidence of a previous heart attack or one that’s in progress. If your signs and symptoms occur most often during exercise, your doctor may ask you to walk on a treadmill or ride a stationary bike during an ECG.
  • Angiogram. To better view blood flow through your heart, brain, arms or legs, your doctor may inject a special dye into your arteries before an X-ray. This is known as an angiogram. The dye outlines narrow spots and blockages on the X-ray images.
  • Other imaging tests. Your doctor may use ultrasound, a computerized tomography (CT) scan or a magnetic resonance angiogram (MRA) to study your arteries. These tests can often show hardening and narrowing of large arteries, as well as aneurysms and calcium deposits in the artery walls.

Treatments and drugs
Lifestyle changes, such as eating a healthy diet and exercising, are often the first line of defense in treating atherosclerosis. But sometimes, medication or surgical procedures may be recommended as well.
Various drugs can slow — or sometimes even reverse — the effects of atherosclerosis. Here are some common choices:

  • Cholesterol medications. Aggressively lowering your low-density lipoprotein (LDL) cholesterol, the “bad” cholesterol, can slow, stop or even reverse the buildup of fatty deposits in your arteries. Boosting your high-density lipoprotein (HDL) cholesterol, the “good” cholesterol, may help, too. Your doctor can choose from a range of cholesterol medications, including drugs known as statins and fibrates.
  • Anti-platelet medications. Your doctor may prescribe anti-platelet medications, such as aspirin, to reduce the likelihood that platelets will clump in narrowed arteries, form a blood clot and cause further blockage.
  • Anticoagulants. An anticoagulant, such as heparin or warfarin (Coumadin), can help thin your blood to prevent clots from forming.
  • Blood pressure medications. Medications to control blood pressure — such as beta blockers, angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers — can help slow the progression of atherosclerosis.
  • Other medications. Your doctor may suggest certain medications to control specific risk factors for atherosclerosis, such as diabetes. Sometimes medications to treat symptoms of atherosclerosis, such as leg pain during exercise, are prescribed.

Sometimes more aggressive treatment is needed. If you have severe symptoms or a blockage that threatens muscle or skin tissue survival, you may be a candidate for one of the following surgical procedures:

  • Angioplasty. In this procedure, your doctor inserts a long, thin tube (catheter) into the blocked or narrowed part of your artery. A wire with a deflated balloon is passed through the catheter to the narrowed area. The balloon is then inflated, compressing the deposits against your artery walls. A mesh tube (stent) is usually left in the artery to help keep the artery open. Angioplasty may also be done with laser technology.
  • Endarterectomy. In some cases, fatty deposits must be surgically removed from the walls of a narrowed artery. When the procedure is done on arteries in the neck (the carotid arteries), it’s known as carotid endarterectomy.
  • Thrombolytic therapy. If you have an artery that’s blocked by a blood clot, your doctor may insert a clot-dissolving drug into your artery at the point of the clot to break it up.
  • Bypass surgery. Your doctor may create a graft bypass using a vessel from another part of your body or a tube made of synthetic fabric. This allows blood to flow around the blocked

Lifestyle and home remedies
Lifestyle changes can help you prevent or slow the progression of atherosclerosis.

  • Stop smoking. Smoking damages your arteries. If you smoke, quitting is the best way to halt the progression of atherosclerosis and reduce your risk of complications.
  • Exercise most days of the week. Regular exercise can condition your muscles to use oxygen more efficiently. Physical activity can also improve circulation and promote development of new blood vessels that form a natural bypass around obstructions (collateral vessels). Ideally, you should exercise 30 to 60 minutes most days of the week. If you can’t fit it all in one session, try breaking it up into 10-minute intervals. You can take the stairs instead of the elevator, walk around the block during your lunch hour, or do some sit-ups or push-ups while watching television.
  • Eat healthy foods. A heart-healthy diet based on fruits, vegetables and whole grains – and low in saturated fat, cholesterol and sodium — can help you control your weight, blood pressure and cholesterol. Try substituting whole-grain bread in place of white bread, grabbing an apple, banana or carrot sticks as a snack, and reading nutrition labels to control the amount of salt and fat you eat.
  • Manage stress. Reduce stress as much as possible. Practice healthy techniques for managing stress, such as muscle relaxation and deep breathing.

If you have high cholesterol, high blood pressure, diabetes or another chronic disease, work with your doctor to manage the condition and promote overall health.

Prevention
The same healthy lifestyle changes recommended to treat atherosclerosis also help prevent it. You’ve heard it before — stop smoking, eat healthy foods, exercise regularly, maintain a healthy weight, drink less alcohol. Just remember to make changes one step at a time, and keep in mind what lifestyle changes are manageable for you in the long run. 

Remember this article is for your information only. Dr. Ben-Zur recommends consulting your physician prior to making any changes in your diet, exercise or medical program.

By Mayo Clinic staff

Atherosclerosis is a condition in which fatty material collects along the walls of arteries. This fatty material thickens, hardens (forms calcium deposits), and may eventually block the arteries.
Atherosclerosis is a type of arteriosclerosis. The two terms are often used to mean the same thing

Causes

Atherosclerosis is a common disorder of the arteries. It occurs when fat, cholesterol, and other substances build up in the walls of arteries and form hard structures called plaques.
Eventually, the plaques can make the artery narrow and less flexible, making it harder for blood to flow. If the coronary arteries become narrow, blood flow to the heart can slow down or stop. This can cause chest pain (stable angina), shortness of breath, heart attack, and other symptoms.
Pieces of plaque can break off and move through the bloodstream (embolization). This is a common cause of heart attack and stroke. Blood clots can also form around a tear (fissure) in the plaque. Clots block blood flow. If the clot moves into an artery in the heart, lungs, or brain, it can cause a stroke, heart attack, or pulmonary embolism.
Risk factors for atherosclerosis include:

  • • Diabetes
  • • Heavy alcohol use
  • • High blood pressure
  • • High blood cholesterol levels
  • • High-fat diet
  • • Increasing age
  • • Obesity
  • • Personal or family history of heart disease
  • • Smoking

Atherosclerosis can affect many different organ systems, including the heart, lungs, brain, intestines, kidneys, and limbs (extremities).

Symptoms

Symptoms usually do not occur until blood flow becomes restricted or blocked.

Exams and Tests

A health care provider will perform a physical exam and listen to the heart and lungs with a stethoscope. Atherosclerosis can create a whooshing or blowing sound (“bruit”) over an artery.
Tests that may be used to diagnose atherosclerosis or its complications include:

  • • Ankle/brachial index (ABI)
  • • Aortic arteriography
  • • Arteriography
  • • Cardiac stress testing
  • • Carotid duplex
  • • CT scan
  • • Doppler study
  • • Extremity arteriography
  • • Intravascular ultrasound (IVUS)
  • • Magnetic resonance arteriography (MRA)
  • • Mesenteric arteriography
  • • Pulmonary angiography
  • • Renal arteriography
Treatment

To help prevent atherosclerosis or its complications (such as heart disease and stroke), make the following lifestyle changes:

  • • Avoid fatty foods. Eat well-balanced meals that are low in fat and cholesterol. Include several daily servings of fruits and vegetables. Adding fish to your diet at least twice a week may be helpful. However, do not eat fried fish.
  • • Do not drink more than one or two alcoholic drinks a day.
  • • Exercise regularly for 30 minutes a day if you are not overweight, and for 60 – 90 minutes a day if you are overweight.

Get your blood presure checked every 1 – 2 years, especially if high blood pressure runs in your family. Have your blood pressure checked more often if you have high blood pressure, heart disease, or you have had a stroke. Talk to your doctor.

  • • Everyone should keep their blood pressure below 140/90 mmHg
  • • If you have diabetes or have had a stroke or heart attack, your blood pressure should probably be less than 130/80 mm/Hg. Ask your doctor what your blood pressure should be.

Have your cholesterol checked and treated if it is high.

  • • Adults should have their cholesterol checked every 5 years. If you are being treated for high cholesterol, you will need to have it checked more often.
  • • All adults should keep their LDL (“bad”) cholesterol levels below 130-160 mg/dL.
  • • If you have diabetes, heart disease, or hardening of the arteries somewhere else in your body, your LDL cholesterol should be lower than 100 mg/dL.
  • • Few medications have been found to clear up plaque. Statins and other cholesterol-lowering drugs can help prevent more plaque from forming.

Your doctor may suggest taking aspirin or another drug called clopidogrel (Plavix) to help prevent blood clots from forming in your arteries. These medicines are called antiplatelet drugs. DO NOT take aspirin without first talking to your doctor.
Talk to your doctor about the safety of hormone replacement therapy for menopause.
Guidelines no longer recommend vitamins E or C, antioxidants, or folic acid to prevent heart disease.
A number of surgeries are performed to help prevent the complications of atherosclerosis. Some of these are:

  • • Angioplasty and stent – heart – discharge
  • • Angioplasty and stent placement – peripheral arteries
  • • Abdominal aortic aneurysm repair – open
  • • Coronary artery bypass surgery
  • • Carotid artery surgery
  • • Minimally invasive heart surgery
Outlook (Prognosis)

Everyone starts to develop some amount of atherosclerosis as they grow older. In some people, the condition can cause complications such as a heart attack or stroke.

Possible Complications
  • • Coronary heart disease
  • • Damage to organs (such as the kidneys, brain, liver, and intestines)
  • • Heart attack
  • • Stroke
  • • Too little blood to the legs and feet
  • • Transient ischemic attack (TIA)
When to Contact a Medical Professional

Call for an appointment with your health care provider if you are at risk for atherosclerosis, especially if you have symptoms.
Talk to your doctor before starting a new exercise plan, especially if you have been diagnosed with coronary heart disease or you have ever had a heart attack.

Alternative Names

Arteriosclerosis; Hardening of the arteries; Plaque buildup – arteries

**

This article is for your information only.  Always consult your physician prior to making any changes in your diet, exercise or medical program.

References

Goldstein LB. Prevention and management of stroke. In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap 58.
Fuster V. Atherosclerosis, thrombosis, and vascular biology. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap 69.
Mosca L, Banka CL, Benjamin EJ, et al. Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women: 2007 Update. Circulation. 2007; 115: 1481-1501

What Is Atherosclerosis?
Atherosclerosis — hardening and narrowing of the arteries — gets a lot of bad press, with good reason. This progressive process silently and slowly blocks arteries, putting blood flow at risk.

Atherosclerosis is the usual cause of heart attacks, strokes, and peripheral vascular disease — what together are called “cardiovascular disease.” Cardiovascular disease is the No. 1 killer in America, with more than 900,000 deaths last year.

How does atherosclerosis develop? Who gets it, and why? Atherosclerosis is a mouthful, but it doesn’t need to be a mystery. This deadly process is preventable and treatable. Read on, and get to know your enemy.

Atherosclerosis: How It Happens
Arteries are blood vessels that carry blood from the heart throughout the body. They’re lined by a thin layer of cells called the endothelium. The endothelium works to keep the inside of arteries toned and smooth, which keeps blood flowing.

“Atherosclerosis starts when high blood pressure, smoking, or high cholesterol damage the endothelium,” says Richard Stein, MD, national spokesperson for the American Heart Association. “At that point, cholesterol plaque formation begins.”

Cholesterol invasion. Bad cholesterol, or LDL, crosses damaged endothelium. The cholesterol enters the wall of the artery.
Plaque formation. Your white blood cells stream in to digest the LDL cholesterol. Over years, the accumulating mess of cholesterol and cells becomes a plaque in the wall of the artery.

“It’s a jumble of lipids, or cholesterol, cells, and debris, and it creates a bump on the artery wall,” explains Stein. As the process of atherosclerosis continues, “the bump gets bigger.” A big enough bump can create a blockage.

Atherosclerosis tends to happen throughout the body. “So if you have plaque in your heart, you’re at a higher risk for stroke, and vice versa,” says Stein.
Atherosclerosis usually causes no symptoms until middle or older age. Once narrowings become severe, they choke off blood flow and can cause pain. Blockages can also suddenly rupture, causing blood to clot inside an artery.
Atherosclerosis: Plaque Attacks
Plaques from atherosclerosis can behave in different ways.

  • • They can stay within the artery wall. There, the plaque grows to a certain size and stops. “Because they don’t block blood flow, these plaques may never cause any symptoms,” says Stein. 
  • • They can grow in a slow, controlled way into the path of blood flow. Eventually, they cause significant blockages. Pain on exertion (in the chest or legs) is the usual symptom. 
  • • The worst-case scenario: plaques can suddenly rupture, allowing blood to clot inside an artery. In the brain, this causes a stroke; in the heart, a heart attack.

The plaques of atherosclerosis cause the three main kinds of cardiovascular disease:

  • Coronary artery disease: Stable plaques in the heart’s arteries cause angina (chest pain on exertion). Sudden plaque rupture and clotting causes heart muscle to die. This is a heart attack, or myocardial infarction. 
  • Cerebrovascular disease: Ruptured plaques in the brain’s arteries causes strokes, with the potential for permanent brain damage. Temporary blockages in an artery can also cause transient ischemic attacks (TIAs), which are warning signs of stroke; however, there is no brain injury.
  • Peripheral artery disease: Narrowing in the arteries of the legs caused by plaque. Peripheral artery disease causes poor circulation. This causes pain on walking and poor wound healing. Severe disease may lead to amputations.

Atherosclerosis: Who Gets It?
It might be easier to ask, who doesn’t get atherosclerosis?
Atherosclerosis starts early. In autopsies of young American soldiers killed in action in the Korean and Vietnam wars, half to three-quarters had early forms of atherosclerosis.
And what about today, with our salads and StairMasters? A 2001 study of 262 apparently healthy people’s hearts may surprise you:

  • • 51.9% had some atherosclerosis
  • • Atherosclerosis was present in 85% of those older than 50
  • • 17% of teenagers had atherosclerosis

No one had symptoms, and very few had narrowings in any arteries. This was very early disease, detectable only by special tests.
If you are 40 and generally healthy, you have about a 50% chance of developing serious atherosclerosis in your lifetime. The risk goes up as you get older. The majority of adults older than 60 have some atherosclerosis but often do not have noticeable symptoms.
There is good news. Rates of death from atherosclerosis have fallen by 25% since 30 years ago. This is thanks to both improved treatments and better lifestyles.
Between heart attacks, strokes, and peripheral vascular disease, though, atherosclerosis still causes more than 900,000 deaths in the U.S. each year.  Diseases caused by atherosclerosis are the most common cause of death in the U.S.
Atherosclerosis: How to Prevent It
Atherosclerosis is progressive, but it’s also preventable. For example, nine risk factors are to blame for up to 90% of all heart attacks:

  • • Smoking
  • • High cholesterol
  • • High blood pressure
  • • Diabetes
  • • Abdominal obesity (“spare tire”)
  • • Stress
  • • Not eating fruits and vegetables
  • • Excess alcohol intake (more than one drink for women, one or two drinks for men, per day)
  • • Not exercising regularly

You may notice all of these have something in common: You can do something about them! Experts agree that reducing your risk factors leads to a lower risk of cardiovascular disease.
For people at moderate or higher risk — those who’ve had a heart attack or stroke, or who suffer angina — taking a baby aspirin a day can be important. Aspirin helps prevent clots from forming. Ask your doctor before starting daily aspirin, as it can have side effects.
Atherosclerosis: Treatment
Once a blockage is there, it’s generally there to stay. With medication and lifestyle changes, though, plaques may slow or stop growing. They may even shrink slightly with aggressive treatment.

  • Lifestyle changes: Reducing the lifestyle risk factors that lead to atherosclerosis will slow or stop the process. That means a healthy diet, exercise, and no smoking. These lifestyle changes won’t remove blockages, but they’re proven to lower the risk of heart attacks and strokes.
  • Medicines:Taking medication for high cholesterol and high blood pressure will slow and perhaps even halt the progression of atherosclerosis, as well as lower your risk of heart attacks and stroke.  

Using invasive techniques, physicians can also open up blockages from atherosclerosis, or go around them:

  • Angiography and stenting: Cardiac catheterization with angiography of the coronary arteries is the most common angiography procedure performed. Using a thin tube inserted into an artery in the leg or arm, doctors can access diseased arteries. Blockages are visible on a live X-ray screen. Angioplasty (catheters with balloon tips) and stenting can often open up a blocked artery. 
  • Bypass surgery: Surgeons “harvest” a healthy blood vessel (often from the leg or chest). They use the healthy vessel to bypass a segment blocked by atherosclerosis.

These procedures involve a risk of complications. They are usually saved for people with significant symptoms or limitations caused by atherosclerosis.
** Remember this article is for your information only. Dr. Ben-Zur recommends consulting your physician prior to making any changes in your diet, exercise or medical program.

© 2007 WebMD, Inc. All rights reserved.

Atherosclerosis (ath-er-o-skler-O-sis) is a disease in which plaque (plak) builds up on the insides of your arteries.  Arteries are blood vessels that carry oxygen-rich blood to your heart and other parts of your body.
Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood.  Over time, plaque hardens and narrows your arteries.  The flow of oxygen-rich blood to your organs and other parts of your body is reduced.  This can lead to serious problems, including heart attack, stroke, or even death.

What Causes Atherosclerosis?

The exact cause of atherosclerosis isn’t known. However, studies show that atherosclerosis is a slow, complex disease that may start in childhood. It develops faster as you age.
Atherosclerosis may start when certain factors damage the inner layers of the arteries. These factors include:

  • • Smoking
  • • High amounts of certain fats and cholesterol in the blood
  • • High blood pressure
  • • High amounts of sugar in the blood due to insulin resistance or diabetes

When damage occurs, your body starts a healing process. Fatty tissues release compounds that promote this process. This healing causes plaque to build up where the arteries are damaged. 
Over time, the plaque may crack. Blood cells called platelets (PLATE-lets) clump together to form blood clots where the cracks are. This narrows the arteries more and worsens angina (chest pain) or causes a heart attack.

Who Is At Risk for Atherosclerosis?

Coronary artery disease (atherosclerosis of the coronary arteries) is the leading cause of death in the United States. 
The exact cause of atherosclerosis isn’t known. However, certain traits, conditions, or habits may raise your chance of developing it. These conditions are known as risk factors. Your chances of developing atherosclerosis increase with the number of risk factors you have. 
You can control most risk factors and help prevent or delay atherosclerosis. Other risk factors can’t be controlled.

Major Risk Factors
  • Unhealthy blood cholesterol levels. This includes high LDL cholesterol (sometimes called bad cholesterol) and low HDL cholesterol (sometimes called good cholesterol).
  • High blood pressure. Blood pressure is considered high if it stays at or above 140/90 mmHg over a period of time.
  • • Smoking. This can damage and tighten blood vessels, raise cholesterol levels, and raise blood pressure. Smoking also doesn’t allow enough oxygen to reach the body’s tissues.
  • Insulin resistance. This condition occurs when the body can’t use its own insulin properly. Insulin is a hormone that helps move blood sugar into cells where it’s used.
  • Diabetes. This is a disease in which the body’s blood sugar level is high because the body doesn’t make enough insulin or doesn’t use its insulin properly.
  • Overweight or obesity. Overweight is having extra body weight from muscle, bone, fat, and/or water. Obesity is having a high amount of extra body fat.
  • Lack of physical activity. Lack of activity can worsen other risk factors for atherosclerosis.
  • Age. As you get older, your risk for atherosclerosis increases. Genetic or lifestyle factors cause plaque to build in your arteries as you age. By the time you’re middle-aged or older, enough plaque has built up to cause signs or symptoms.
    • • In men, the risk increases after age 45.
    • • In women, the risk increases after age 55.
  • Family history of early heart disease. Your risk for atherosclerosis increases if your father or a brother was diagnosed with heart disease before 55 years of age, or if your mother or a sister was diagnosed with heart disease before 65 years of age.

Although age and a family history of early heart disease are risk factors, it doesn’t mean that you will develop atherosclerosis if you have one or both. 
Making lifestyle changes and/or taking medicines to treat other risk factors can often lessen genetic influences and prevent atherosclerosis from developing, even in older adults.

Emerging Risk Factors

Scientists continue to study other possible risk factors for atherosclerosis.
High levels of a protein called C-reactive protein (CRP) in the blood may raise the risk for atherosclerosis and heart attack. High levels of CRP are proof of inflammation in the body. Inflammation is the body’s response to injury or infection. Damage to the arteries’ inner walls seems to trigger inflammation and help plaque grow. 
People with low CRP levels may get atherosclerosis at a slower rate than people with high CRP levels. Research is under way to find out whether reducing inflammation and lowering CRP levels also can reduce the risk of atherosclerosis.
High levels of fats called triglycerides in the blood also may raise the risk of atherosclerosis, particularly in women.

Other Factors That Affect Atherosclerosis

Other risk factors also may raise your risk for developing atherosclerosis. These include:

  • • Sleep apnea. Sleep apnea is a disorder in which your breathing stops or gets very shallow while you’re sleeping. Untreated sleep apnea can raise your chances of having high blood pressure, diabetes, and even a heart attack or stroke.
  • • Stress. Research shows that the most commonly reported “trigger” for a heart attack is an emotionally upsetting event—particularly one involving anger.
  • • Alcohol. Heavy drinking can damage the heart muscle and worsen other risk factors for atherosclerosis. Men should have no more than two drinks containing alcohol a day. Women should have no more than one drink containing alcohol a day.
What Are the Signs and Symptoms of Atherosclerosis?

Atherosclerosis usually doesn’t cause signs and symptoms until it severely narrows or totally blocks an artery. Many people don’t know they have the disease until they have a medical emergency, such as a heart attack or stroke.
Some people may have other signs and symptoms of the disease. These depend on which arteries are severely narrowed or blocked.
The coronary arteries supply oxygen-rich blood to your heart. When plaque narrows or blocks these arteries (a condition called coronary artery disease, or CAD), a common symptom is angina (AN-ji-na or an-JI-na).
Angina is chest pain or discomfort that occurs when your heart muscle doesn’t get enough oxygen-rich blood. Angina may feel like pressure or a squeezing pain in your chest. You also may feel it in your shoulders, arms, neck, jaw, or back. 
This pain tends to get worse with activity and go away when you rest. Emotional stress also can trigger the pain.
Other symptoms of CAD are shortness of breath and arrhythmias (irregular heartbeats). 
The carotid arteries supply oxygen-rich blood to your brain. When plaque narrows or blocks these arteries (a condition called carotid artery disease), you may have symptoms of a stroke. These symptoms include sudden numbness, weakness, and dizziness.
Plaque also can build up in the major arteries that supply oxygen-rich blood to the legs, arms, and pelvis (a condition called peripheral arterial disease). When these arteries are narrowed or blocked, it can lead to numbness, pain, and sometimes dangerous infections.

How Is Atherosclerosis Diagnosed?

Your doctor will diagnose atherosclerosis based on:

  • • Your medical and family histories
  • • Your risk factors
  • • The results of a physical exam and diagnostic tests
Specialists Involved

If you have atherosclerosis, a doctor, internist, or general practitioner may handle your care. Your doctor may send you to other health care specialists if you need expert care. These specialists may include:

  • • A cardiologist (a doctor who specializes in treating people with heart problems). You may see a cardiologist if you have coronary artery disease (CAD).
  • • A vascular specialist (a doctor who specializes in treating people with blood vessel problems). You may see a vascular specialist if you have peripheral arterial disease (PAD).
  • • A neurologist (a doctor who specializes in treating people with disorders of the nervous system). You may see a neurologist if you’ve had a stroke due to carotid artery disease.
Physical Exam

During the physical exam, your doctor may listen to your arteries for an abnormal whooshing sound called a bruit (broo-E). Your doctor can hear a bruit when placing a stethoscope over an affected artery. A bruit may indicate poor blood flow due to plaque.
Your doctor also may check to see whether any of your pulses (for example, in the leg or foot) are weak or absent. A weak or absent pulse can be a sign of a blocked artery.

Diagnostic Tests and Procedures

Your doctor may order one or more tests to diagnose atherosclerosis. These tests also can help your doctor learn the extent of your disease and plan the best treatment.

Blood Tests

Blood tests check the levels of certain fats, cholesterol, sugar, and proteins in your blood. Abnormal levels may show that you have risk factors for atherosclerosis.

EKG (Electrocardiogram)

An EKG is a simple test that detects and records the electrical activity of your heart. An EKG shows how fast your heart is beating and whether it has a regular rhythm. It also shows the strength and timing of electrical signals as they pass through each part of your heart. 
Certain electrical patterns that the EKG detects can suggest whether CAD is likely. An EKG also can show signs of a previous or current heart attack.

Chest X Ray

A chest x ray takes a picture of the organs and structures inside the chest, including your heart, lungs, and blood vessels. 
A chest x ray can reveal signs of heart failure.

Ankle/Brachial Index

This test compares the blood pressure in your ankle with the blood pressure in your arm to see how well your blood is flowing. This test can help diagnose PAD.

Echocardiography

This test uses sound waves to create a moving picture of your heart. Echocardiography provides information about the size and shape of your heart and how well your heart chambers and valves are working. 
The test also can identify areas of poor blood flow to the heart, areas of heart muscle that aren’t contracting normally, and previous injury to the heart muscle caused by poor blood flow.

Computed Tomography Scan

A computed tomography, or CT, scan creates computer-generated images of the heart, brain, or other areas of the body. The test can often show hardening and narrowing of large arteries.

Stress Testing

During stress testing, you exercise to make your heart work hard and beat fast while heart tests are performed. If you can’t exercise, you’re given medicine to speed up your heart rate. 
When your heart is beating fast and working hard, it needs more blood and oxygen. Arteries narrowed by plaque can’t supply enough oxygen-rich blood to meet your heart’s needs. A stress test can show possible signs of CAD, such as:

  • • Abnormal changes in your heart rate or blood pressure
  • • Symptoms such as shortness of breath or chest pain
  • • Abnormal changes in your heart rhythm or your heart’s electrical activity

During the stress test, if you can’t exercise for as long as what’s considered normal for someone your age, it may be a sign that not enough blood is flowing to your heart. But other factors besides CAD can prevent you from exercising long enough (for example, lung diseases, anemia, or poor general fitness). 
Some stress tests use a radioactive dye, sound waves, positron emission tomography (PET), or cardiac magnetic resonance imaging (MRI) to take pictures of your heart when it’s working hard and when it’s at rest. 
These imaging stress tests can show how well blood is flowing in the different parts of your heart. They also can show how well your heart pumps blood when it beats.

Angiography

Angiography (an-jee-OG-ra-fee) is a test that uses dye and special x rays to show the insides of your arteries. This test can show whether plaque is blocking your arteries and how severe the plaque is. 
A thin, flexible tube called a catheter is put into a blood vessel in your arm, groin (upper thigh), or neck. A dye that can be seen on x ray is then injected into the arteries. By looking at the x-ray picture, your doctor can see the flow of blood through your arteries.

How Is Atherosclerosis Treated?

Treatments for atherosclerosis may include lifestyle changes, medicines, and medical procedures or surgery.

Goals of Treatment

The goals of treatment are to:

  • • Relieve symptoms
  • • Reduce risk factors in an effort to slow, stop, or reverse the buildup of plaque
  • • Lower the risk of blood clots forming
  • • Widen or bypass clogged arteries
  • • Prevent diseases related to atherosclerosis
Lifestyle Changes

Making lifestyle changes can often help prevent or treat atherosclerosis. For some people, these changes may be the only treatment needed.

  • • Follow a healthy eating plan to prevent or reduce high blood pressure and high blood cholesterol and to maintain a healthy weight.
  • • Increase your physical activity. Check with your doctor first to find out how much and what kinds of activity are safe for you.
  • • Lose weight, if you’re overweight or obese.
  • • Quit smoking, if you smoke. Avoid exposure to secondhand smoke.
  • • Reduce stress.
Follow a Healthy Eating Plan

Recommend healthy eating, physical activity, and controlling your weight. 
Therapeutic Lifestyle Changes (TLC). Your doctor may recommend TLC if you have high cholesterol. TLC is a three-part program that includes a healthy diet, physical activity, and weight management. 
With the TLC diet, less than 7 percent of your daily calories should come from saturated fat. This kind of fat is mainly found in meat and poultry, including dairy products. No more than 25 to 35 percent of your daily calories should come from all fats, including saturated, trans, monounsaturated, and polyunsaturated fats. 
You also should have less than 200 mg a day of cholesterol. The amounts of cholesterol and the different kinds of fat in prepared foods can be found on the Nutrition Facts label.
Foods high in soluble fiber also are part of a healthy eating plan. They help block the digestive track from absorbing cholesterol. These foods include:

  • • Whole grain cereals such as oatmeal and oat bran
  • • Fruits such as apples, bananas, oranges, pears, and prunes
  • • Legumes such as kidney beans, lentils, chick peas, black-eyed peas, and lima beans

A diet high in fruits and vegetables can increase important cholesterol-lowering compounds in your diet. These compounds, called plant stanols or sterols, work like soluble fiber. 
Fish are an important part of a heart healthy diet. They’re a good source of omega-3 fatty acids, which may help protect the heart from blood clots and inflammation and reduce the risk for heart attack. Try to have about two fish meals every week. Fish high in omega-3 fats are salmon, tuna (canned or fresh), and mackerel.
You also should try to limit the amount of sodium (salt) that you eat. This means choosing low-sodium and low-salt foods and “no added salt” foods and seasonings at the table or when cooking. The Nutrition Facts label on food packaging shows the amount of sodium in the item.
Try to limit drinks with alcohol. Too much alcohol will raise your blood pressure and triglyceride level. (Triglycerides are a type of fat found in the blood.) Alcohol also adds extra calories, which will cause weight gain. Men should have no more than two drinks containing alcohol a day. Women should have no more than one drink containing alcohol a day.

Dietary Approaches to Stop Hypertension (DASH) eating plan. Your doctor may recommend the DASH eating plan if you have high blood pressure. The DASH eating plan focuses on fruits, vegetables, whole grains, and other foods that are heart healthy and lower in salt/sodium. 
This eating plan is low in fat and cholesterol. It also focuses on fat-free or low-fat milk and dairy products, fish, poultry, and nuts. The DASH eating plan is reduced in red meats (including lean red meat), sweets, added sugars, and sugar-containing beverages. It’s rich in nutrients, protein, and fiber.
The DASH eating plan is a good heart healthy eating plan, even for those who don’t have high blood pressure.

Increase Physical Activity

Regular physical activity can lower many atherosclerosis risk factors, including LDL (“bad”) cholesterol, high blood pressure, and excess weight. Physical activity also can lower your risk for diabetes and raise your levels of HDL cholesterol (the “good” cholesterol that helps prevent atherosclerosis).
Check with your doctor about how much and what kinds of physical activity are safe for you. Unless your doctor tells you otherwise, try to get at least 30 minutes of moderate-intensity activity on most or all days of the week. You can do the activity all at once or break it up into shorter periods of at least 10 minutes each. 
Moderate-intensity activities include brisk walking, dancing, bowling, bicycling, gardening, and housecleaning. 
More intense activities, such as jogging, swimming, and various sports, also may be appropriate for shorter periods.

Maintain a Healthy Weight

Maintaining a healthy weight can decrease your risk factors for atherosclerosis. A general goal to aim for is a body mass index (BMI) of less than 25. 
BMI measures your weight in relation to your height and gives an estimate of your total body fat. 
A BMI between 25 and 29 is considered overweight. A BMI of 30 or more is considered obese. A BMI of less than 25 is the goal for preventing and treating atherosclerosis. Your doctor or other health care provider can help you determine an appropriate goal for you.

Quit Smoking

If you smoke or use tobacco, quit. Smoking can damage and tighten blood vessels and raise your risk for atherosclerosis. 
The U.S. Department of Health and Human Services has information on how to quit smoking.

Reduce Stress

Research shows that the most commonly reported “trigger” for a heart attack is an emotionally upsetting event—particularly one involving anger. Also, some of the ways people cope with stress, such as drinking, smoking, or overeating, aren’t heart healthy. 
Physical activity can help relieve stress and reduce other atherosclerosis risk factors. Many people also find that meditation or relaxation therapy helps them reduce stress.

Medicines

To help slow or reverse atherosclerosis, your doctor may prescribe medicines to help lower your cholesterol or blood pressure or prevent blood clots from forming. 
For successful treatment, take all medicines as your doctor prescribes.

Medical Procedures and Surgery

If you have severe atherosclerosis, your doctor may recommend one of several procedures or surgeries.
Angioplasty is a procedure to open blocked or narrowed coronary (heart) arteries. Angioplasty can improve blood flow to the heart, relieve chest pain, and possibly prevent a heart attack. Sometimes a small mesh tube called a stent is placed in the artery to keep it open after the procedure.
Coronary artery bypass grafting (CABG) is a type of surgery. In CABG, arteries or veins from other areas in your body are used to bypass (that is, go around) your narrowed coronary arteries. CABG can improve blood flow to your heart, relieve chest pain, and possibly prevent a heart attack. 
Bypass grafting also can be used for leg arteries. In this surgery, a healthy blood vessel is used to bypass a narrowed or blocked blood vessel in one of your legs. The healthy blood vessel redirects blood around the artery, improving blood flow to the leg.
Carotid artery surgery removes plaque buildup from the carotid arteries in the neck. This opens the arteries and improves blood flow to the brain. Carotid artery surgery can help prevent a stroke.

How Can Atherosclerosis Be Prevented or Delayed?

Taking action to control your risk factors can help prevent or delay atherosclerosis and its related diseases. Your chance of developing atherosclerosis goes up with the number of risk factors you have. 
Making lifestyle changes and taking prescribed medicines are important steps. 
Know your family history of health problems related to atherosclerosis. If you or someone in your family has this disease, be sure to tell your doctor. Also, let your doctor know if you smoke.

Living With Atherosclerosis

Improved treatments have reduced deaths from atherosclerosis-related diseases. These treatments also have improved the quality of life for people with these diseases. 
You may be able to prevent or delay atherosclerosis and the problems it can cause, mainly by maintaining a healthy lifestyle. This, along with ongoing medical care, can help you avoid the problems of atherosclerosis and live a long, healthy life. 
Research continues look for ways to improve the health of people who have atherosclerosis or may get it. The goals of research are to:

  • • Find more effective medicines
  • • Identify people at greatest risk earlier
  • • Find out how well alternative treatments work
Ongoing Health Care Needs

If you have atherosclerosis, work closely with your doctor and other health care providers to avoid serious problems, like heart attack and stroke. 
Talk to your doctor about how often you should schedule office visits or blood tests. Be sure to let your doctor know if you develop new symptoms or if your symptoms worsen.

Support Groups

Community resources are available to help you learn more about atherosclerosis. Contact your local public health departments, hospitals, and local chapters of national health organizations to learn more about available resources in your area.
Talk about your lifestyle changes with your spouse, family, or friends—whoever can provide support or needs to understand why you’re changing your habits. They may be able to help you make lifestyle changes, like helping you plan healthier meals. 
Because atherosclerosis tends to run in families, your lifestyle changes may help many of your family members too.

Key Points
  • • Atherosclerosis is a disease in which plaque builds up on the insides of your arteries.
  • • Over time, plaque hardens and narrows your arteries. The flow of oxygen-rich blood to your organs and other parts of your body is reduced. This can lead to serious problems, including heart attack, stroke, or even death.
  • • Atherosclerosis can affect any artery in the body.
    • • Coronary artery disease (CAD) occurs when plaque builds up in the coronary (heart) arteries. CAD is a leading cause of death in the United States.
    • • Carotid artery disease happens when plaque builds up in the carotid arteries (the arteries that supply blood and oxygen to your brain).
    • • Peripheral arterial disease (PAD) occurs when plaque builds up in the major arteries of the legs, arms, and pelvis. 

  • • The exact cause of atherosclerosis isn’t known. It may start when certain factors damage the inner layers of arteries. When damage occurs, your body starts a healing process. This healing causes plaque to build up where the arteries are damaged. Over time, the plaque may crack and causes blood clots to form in the arteries. This can worsen angina (chest pain) or cause a heart attack.
  • • Many factors raise your risk for atherosclerosis. Major risk factors include unhealthy cholesterol levels, high blood pressure, smoking, insulin resistance, diabetes, overweight or obesity, lack of physical activity, age, and a family history of early heart disease.
  • • Atherosclerosis usually doesn’t cause signs and symptoms until it severely narrows or totally blocks an artery. Many people don’t know they have the disease until they have a medical emergency, such as a heart attack or stroke. Other signs and symptoms depend on which arteries are narrowed or blocked.
  • • Your doctor will diagnose atherosclerosis based on your medical and family histories, your risk factors, and the results of a physical exam and diagnostic tests.
  • • Treatments for atherosclerosis may include lifestyle changes, medicines, and medical procedures and surgery. Lifestyle changes include following a healthy eating plan, increasing physical activity, maintaining a healthy weight, quitting smoking, and reducing stress.
  • • Taking steps to control your risk factors can help prevent or delay atherosclerosis and its related diseases. These steps include making lifestyle changes and/or taking medicines as prescribed by your doctor.
  • • Improved treatments have helped reduce deaths from atherosclerosis-related diseases. However, the number of people diagnosed with atherosclerosis remains high.
  • • If you’ve been diagnosed with atherosclerosis, you can control the disease with lifestyle changes and/or medicines. See your doctor regularly, and call him or her if you develop any new symptoms or your symptoms worsen.

This article is for your information only.  Always consult your physician prior to making any changes in your diet, exercise or medical program.

Atherosclerosis is a disease of large and medium-sized muscular arteries and is characterized by endothelial dysfunction, vascular inflammation, and the buildup of lipids, cholesterol, calcium, and cellular debris within the intima of the vessel wall. This buildup results in plaque formation, vascular remodeling, acute and chronic luminal obstruction, abnormalities of blood flow, and diminished oxygen supply to target organs.

Pathophysiology
A complex and incompletely understood interaction exists between the critical cellular elements of the atherosclerotic lesion. These cellular elements are endothelial cells, smooth muscle cells, platelets, and leucocytes. Vasomotor function, the thrombogenicity of the blood vessel wall, the state of activation of the coagulation cascade, the fibrinolytic system, smooth muscle cell migration and proliferation, and cellular inflammation are complex and interrelated biological processes that contribute to atherogenesis and the clinical manifestations of atherosclerosis. 

The mechanisms of atherogenesis remain uncertain. The “response-to-injury” theory is most widely accepted. Endothelial injury causes vascular inflammation and a fibroproliferative response ensues. Probable causes of endothelial injury include oxidized low-density lipoprotein (LDL) cholesterol; infectious agents; toxins, including the byproducts of cigarette smoking; hyperglycemia; and hyperhomocystinemia. Circulating monocytes infiltrate the intima of the vessel wall, and these tissue macrophages act as scavenger cells, taking up LDL cholesterol and forming the characteristic foam cell of early atherosclerosis. These activated macrophages produce numerous factors that are injurious to the endothelium.

Elevated serum levels of LDL cholesterol overwhelm the antioxidant properties of the healthy endothelium and result in abnormal endothelial metabolism of this lipid moiety. Oxidized LDL is capable of a wide range of toxic effects and cell/vessel wall dysfunctions that are characteristically and consistently associated with the development of atherosclerosis. These dysfunctions include impaired endothelium-dependent dilation and paradoxical vasoconstriction. These dysfunctions are the result of direct inactivation of nitric oxide by the excess production of free radicals, reduced transcription of nitric oxide synthase messenger RNA (mRNA), and posttranscriptional destabilization of mRNA.

The decrease in the availability of nitric oxide also is associated with increased platelet adhesion, increased plasminogen activator inhibitor, decreased plasminogen activator, increased tissue factor, decreased thrombomodulin, and alterations in heparan sulfate proteoglycans. The consequences include a procoagulant milieu and enhanced platelet thrombus formation. Furthermore, oxidized LDL activates inflammatory processes at the level of gene transcription by up-regulation of nuclear factor kappa-B, expression of adhesion molecules, and recruitment of monocytes/macrophages.

The lesions of atherosclerosis do not occur in a random fashion. Hemodynamic factors interact with the activated vascular endothelium. Fluid shear stresses generated by blood flow influence the phenotype of the endothelial cells by modulation of gene expression and regulation of the activity of flow-sensitive proteins. Atherosclerotic plaques characteristically occur in regions of branching and marked curvature at areas of geometric irregularity and where blood undergoes sudden changes in velocity and direction of flow. Decreased shear stress and turbulence may promote atherogenesis at these important sites within the coronary arteries, the major branches of the thoracic and abdominal aorta, and the large conduit vessels of the lower extremities.
The earliest pathologic lesion of atherosclerosis is the fatty streak. The fatty streak is observed in the aorta and coronary arteries of most individuals by age 20 years. The fatty streak is the result of focal accumulation of serum lipoproteins within the intima of the vessel wall. Microscopy reveals lipid-laden macrophages, T lymphocytes, and smooth muscle cells in varying proportions.

The fatty streak may progress to form a fibrous plaque, the result of progressive lipid accumulation and the migration and proliferation of smooth muscle cells. Platelet-derived growth factor, insulinlike growth factor, transforming growth factors alpha and beta, thrombin, and angiotensin II are potent mitogens that are produced by activated platelets, macrophages, and dysfunctional endothelial cells that characterize early atherogenesis, vascular inflammation, and platelet-rich thrombosis at sites of endothelial disruption. The relative deficiency of endothelium-derived nitric oxide further potentiates this proliferative stage of plaque maturation.

These smooth muscle cells are responsible for the deposition of extracellular connective tissue matrix and form a fibrous cap that overlies a core of lipid-laden foam cells, extracellular lipid, and necrotic cellular debris. Growth of the fibrous plaque results in vascular remodeling, progressive luminal narrowing, blood-flow abnormalities, and compromised oxygen supply to the target organ. Human coronary arteries enlarge in response to plaque formation, and luminal stenosis may only occur once the plaque occupies greater than 40% of the area bounded by the internal elastic lamina. Developing atherosclerotic plaques acquire their own microvascular network called vasa vasorum, which are prone to hemorrhage and contribute to progression of atherosclerosis Denudation of the overlying endothelium or rupture of the protective fibrous cap may result in exposure of the thrombogenic contents of the core of the plaque to the circulating blood. This exposure constitutes an advanced or complicated lesion. The plaque rupture occurs due to weakening of the fibrous cap. Inflammatory cells localize to the shoulder region of the vulnerable plaque. T lymphocytes elaborate interferon gamma, an important cytokine that impairs vascular smooth muscle cell proliferation and collagen synthesis. Furthermore, activated macrophages produce matrix metalloproteinases that degrade collagen. These mechanisms explain the predisposition to plaque rupture and highlight the role of inflammation in the genesis of the complications of the fibrous atheromatous plaque. A plaque rupture may result in thrombus formation, partial or complete occlusion of the blood vessel, and progression of the atherosclerotic lesion due to organization of the thrombus and incorporation within the plaque.

Mortality/Morbidity
Atherosclerosis is the leading cause of death in the developed world, and atherosclerosis is predicted to be the leading cause of death in the developing world within the first quarter of the next century.

  • • Atherosclerosis is responsible for more than half of the yearly mortality in the United States, and more than 500,000 people die annually of myocardial infarction alone. This rate of mortality costs the country more than $100 billion a year. More than 50 million people in the United States are candidates for some form of dietary and/or drug treatment to modify their lipid profile.
  • • An encouraging decrease in mortality due to coronary heart disease in the developed world has occurred. Unfortunately, this decrease has not occurred in the developing world, and an exponential increase in tobacco habituation and the adoption of a Western diet high in saturated fats likely predicts the continued increase in death and disability due to coronary heart disease.

Sex
Atherosclerosis is more common among men than women. The higher prevalence of atherosclerosis in men is thought to be due to the protective effects of the female sex hormones. This sex effect is absent after menopause in women. The incidence of coronary heart disease among women parallels that of men, but women demonstrate an approximately 10-year chronological delay in the onset of clinical manifestations.

Age
Most cases of atherosclerotic vascular disease become clinically apparent in patients aged 40-70 years.
Clinical
The symptoms of atherosclerosis are highly variable. Patients with mild atherosclerosis may present with clinically important symptoms and signs of disease and myocardial infarction, or sudden cardiac death may be the first symptom of coronary heart disease. However, many patients with anatomically advanced disease may have no symptoms and experience no functional impairment. Initially thought to be a chronic, slowly progressive, degenerative disease, it is now apparent that atherosclerosis is a disease with periods of activity and quiescence. Although a systemic disease, atherosclerosis manifests in a focal manner and affects different organ systems in different patients for reasons that remain unclear.

  • • Progressive luminal narrowing of an artery due to expansion of a fibrous plaque results in impairment of flow once more than 50-70% of the lumen diameter is obstructed. This impairment in flow results in symptoms of inadequate blood supply to the target organ in the event of increased metabolic activity and oxygen demand. Stable angina pectoris, intermittent claudication, and mesenteric angina are examples of the clinical consequences of this mismatch.
  • • Rupture of a plaque or denudation of the endothelium overlying a fibrous plaque may result in exposure of the highly thrombogenic subendothelium and lipid core. This exposure may result in thrombus formation, which may partially or completely occlude flow in the involved artery. Unstable angina pectoris, myocardial infarction, transient ischemic attack, and stroke are examples of the clinical sequelae of partial or complete acute occlusion of an artery. Atheroembolism is a distinct clinical entity that may occur spontaneously or as a complication of aortic surgery, angiography, or thrombolytic therapy in patients with advanced and diffuse atherosclerosis.
  • • Angina pectoris is characterized by retrosternal chest discomfort that typically radiates to the left arm and may be associated with dyspnea. Angina pectoris is exacerbated by exertion and relieved by rest or nitrate therapy. Unstable angina pectoris describes a pattern of increasing frequency or intensity of episodes of angina pectoris and includes pain at rest. A prolonged episode of angina pectoris that may be associated with diaphoresis is suggestive of myocardial infarction.
  • • Stroke, reversible ischemic neurological deficit, and transient ischemic attack are a range of manifestations of impairment of vascular supply to the central nervous system and are characterized by the sudden onset of a focal neurological deficit of variable duration, respectively.
  • • Peripheral vascular disease typically manifests as intermittent claudication, impotence, and nonhealing ulceration and infection of the extremities. Intermittent claudication describes calf, thigh, or buttock pain that is exacerbated by exercise and relieved by rest. Intermittent claudication may be accompanied by pallor of the extremity and paresthesias.
  • • Visceral ischemia may be occult or symptomatic prior to symptoms and signs of target organ failure.
  • • Mesenteric angina is characterized by epigastric or periumbilical postprandial pain and may be associated with hematemesis, hematochezia, melena, diarrhea, nutritional deficiencies, and weight loss.
  • • Abdominal aortic aneurysm typically is asymptomatic prior to the dramatic and often fatal symptoms and signs of rupture, although patients may describe a pulsatile abdominal mass.
  • • Atheroembolism may present with symptoms of digital necrosis, gastrointestinal bleeding, myocardial infarction, retinal ischemia, cerebral infarction, and renal failure.

Physical
The physical signs of atherosclerosis provide objective evidence of extracellular lipid deposition, stenosis or dilatation of large muscular arteries, or target organ ischemia or infarction.

  • • Hyperlipidemia – Xanthelasma, tendon xanthomata
  • • Coronary artery disease – Fourth heart sound, tachycardia, hypotension, hypertension
  • • Cerebrovascular disease – Diminished carotid pulses, carotid artery bruits, focal neurological deficits
  • • Peripheral vascular disease – Decreased peripheral pulses, peripheral arterial bruits, pallor, peripheral cyanosis, gangrene, ulceration
  • • Abdominal aortic aneurysm – Pulsatile abdominal mass, peripheral embolism, circulatory collapse
  • • Atheroembolism – Livedo reticularis, gangrene, cyanosis, ulceration (The presence of pedal pulses in the setting of peripheral ischemia suggests microvascular disease and includes cholesterol embolization.)

Causes
A number of large epidemiological studies in North America and Europe have identified numerous risk factors for the development and progression of atherosclerosis. The risk factors can be divided into modifiable and nonmodifiable risk factors and include hyperlipidemia, hypertension, cigarette habituation, diabetes mellitus, age, and sex. More recently, a number of novel risk factors have been identified that add to the predictive value of the established risk factors and may prove to be a target for future medical interventions.

  • • Hyperlipidemia: Hyperlipidemia is an established risk factor for atherosclerosis. Convincing evidence that lowering serum cholesterol reduces the risk of subsequent coronary heart disease events and overall mortality exists.
  • • Hypertension
    • • Hypertension is a risk factor for the development of atherosclerosis, atherosclerotic cardiovascular disease, and stroke. The mechanism by which hypertension causes these effects is not known, and some uncertainty exists as to what the primary and secondary factors are in a typically multifactorial syndrome. These factors may include hyperlipidemia, hypertension, diabetes mellitus, obesity, and physical inactivity.
    • • Hypertension is associated with morphologic alterations of the arterial intima and functional alterations of the endothelium that are similar to the changes observed in hypercholesterolemia and established atherosclerosis. Endothelial dysfunction is a feature of hypertension, hyperlipidemia, and atherosclerosis and is known to represent and contribute to the procoagulant, proinflammatory, and proliferative components of atherogenesis. Hypertension has been shown, in both epidemiologic and experimental studies, to accelerate atherosclerotic vascular disease and increase the incidence of clinical complications.
  • • Diabetes mellitus: An important risk factor for hyperlipidemia and atherosclerosis and commonly associated with hypertension, abnormalities of coagulation, platelet adhesion and aggregation, increased oxidative stress, and functional and anatomic abnormalities of the endothelium and endothelial vasomotion.
  • • Cigarette habituation: A major and modifiable risk factor for atherosclerosis and is associated with an increased relative risk of dying from vascular disease. The mechanisms are complex and likely multifactorial and result in endothelial dysfunction and a relatively hypercoagulable state. This increased relative risk rapidly and significantly is reduced with smoking cessation. The relative risk is reduced to the extent that the incidence of coronary heart disease in people who have recently quit smoking is similar to that of people who have not smoked for at least 2 years. It should also be mentioned that air polution in recent years has gained increasing recognition as a contributing modifiable risk factor in the urban communities. The mechanism is thought to be through the participation of combusion derived nanoparticles acting through proinflamatory or alternatively direct cardiac toxic pathways.
  • • Novel risk factors: The established risk factors noted above successfully predict future cardiac events in about 50-60% of patients. In recent years, a concerted effort to identify and validate new markers of future risk of the clinical consequences of atherosclerosis has been made.
    • • C-reactive protein: Baseline C-reactive protein (CRP) levels add to the predictive value of lipid parameters in determining the risk of first myocardial infarction in apparently healthy men and women without a history of coronary heart disease. Baseline CRP levels also were found to be predictive of symptomatic peripheral vascular disease in a cohort of healthy men. CRP reflects systemic inflammation, and these results support the hypothesis that chronic inflammation may play a role in the pathogenesis and progression of atherosclerosis. Standardization of the CRP assay is required before this test may be clinically useful, and whether this is a truly modifiable risk factor remains unclear. Some early evidence exists that risk factor modification, particularly the use of aspirin and the hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, may reduce plaque inflammation.
    • • Homocysteine: Homozygous hyperhomocystinemia is associated with extensive atherosclerosis at an early age. The inherited enzymatic abnormalities of homocysteine metabolism that result in such abnormal levels of the amino acid fortunately are very rare. However, approximately 5-7% of the general population have mild elevations of plasma homocysteine, and recent evidence has confirmed that mild hyperhomocystinemia is an independent risk factor for atherosclerosis. Of the risk for coronary artery disease in the general population, 10% has been estimated as being attributable to homocysteine. Atherogenesis due to hyperhomocystinemia likely is due to oxidative damage to the endothelium followed by platelet activation and thrombus formation. Treatment options for an elevated plasma homocysteine level include folic acid and, possibly, vitamin B-6. A number of clinical trials that will assess the efficacy of this intervention are underway.
    • • Fibrinogen: Fibrinogen may be elevated in association with risk factors for atherosclerosis, including smoking, age, and diet; however, recent evidence suggests that elevated levels of fibrinogen are a strong independent predictor of future cardiovascular events in apparently healthy patients and patients with a prior history of cardiovascular disease. This association may be as strong as the established association between hypercholesterolemia and coronary heart disease.
    • • Lipoprotein (a): Numerous studies have linked elevated plasma levels of lipoprotein (a), an LDL-like moiety that circulates in the blood attached to apolipoprotein (a), with the development of coronary artery disease. This complex shares structural domains with the fibrinolytic enzyme plasminogen and may render the molecule prothrombotic. The LDL-like moiety is susceptible to oxidation and may be particularly atherogenic. However, the results of prospective studies have been discordant and have not proven the relationship between elevated plasma levels of lipoprotein (a) and coronary artery disease inconclusively. Niacin is known to reduce plasma levels of lipoprotein (a), although whether this truly is a modifiable risk factor remains unclear.

Laboratory Studies

  • • Lipid profile: Elevated LDL cholesterol is a risk factor for atherosclerotic vascular disease. High triglycerides are associated with low high-density lipoprotein (HDL) cholesterol and are a probable risk factor for vascular disease.
  • • Blood glucose and hemoglobin A1c: Routine measurement of blood glucose and hemoglobulin A1c is appropriate in patients with diabetes mellitus. Measuring any number of parameters that may reflect inflammation, coagulation, fibrinolytic status, and platelet aggregability is possible. These measurements may prove to be valuable, but, at this time, how these measurements affect clinical decision-making is unclear, and including them in routine clinical practice is premature.

Imaging Studies

  • • Ultrasonography aids in evaluating brachial artery reactivity and carotid artery intima-media thickness, which are measures of vessel wall function and anatomy, respectively. These evaluations remain research techniques at this time but hold promise as reliable noninvasive, and therefore repeatable, measures of disease and surrogate end-points for the evaluation of therapeutic interventions.
    • • Brachial artery reactivity: The loss of endothelium-dependent vasodilation is a feature of even the early stages of atherosclerosis. The availability of high-resolution ultrasonographic systems makes the visualization and measurement of small peripheral conduit vessels, such as the human brachial artery, possible. Flow-mediated dilation of the brachial artery has been pioneered as a means of evaluating the health and integrity of the endothelium. The healthy endothelium dilates in response to an increase in blood flow, whereas vessels affected by atherosclerosis do not dilate and may paradoxically constrict.
    • • Carotid artery intima-media thickness: B-mode ultrasonography of the common and internal carotid arteries is a noninvasive measure of arterial wall anatomy that may be performed repeatedly and reliably in asymptomatic individuals. The combined thickness of the intima and media of the carotid artery is associated with the prevalence of cardiovascular risk factors and disease and an increased risk of myocardial infarction and stroke. This association is at least as strong as the associations observed with traditional risk factors.

Other Tests
Coronary Angiography  
Coronary angiography, was the first available vivo assessment of the coronary arteries consisting of injection of an iodinated contrast agent through a catheter placed at the ostium of the coronaries. The contrast agent is then visualized through x-ray fluoroscopic examination of the heart. One of the limitations of coronary angiography is that only the vessel space occupied by blood is visualized. The actual extent of atherosclerotic plaque volume in the wall cannot be assessed with this technique.

Intravascular ultrasound (IVUS) 
Intravascular ultrasound (IVUS) has long been considered the “gold standard” for the study of the anatomy of the vessel wall and is a catheter-based examination that provides images of the thickness and the acoustic density of the vessel wall. It can depict the presence of atherosclerotic plaques not visible with contrast coronary angiography and may reveal signs of recent disruption.

Computed Tomography  
Multidetector computed tomography (MDCT) technology can allow for excellent visualization of the coronary arteries but relatively high radiation dose is one of the limitations of this approach. However, newer generations of CT scanners may be able to reduce the required radiation exposure to make this technology more promising for screening asymptomatic patients.

Magnetic Resonance Imaging  
 
MRI can be used to noninvasively gain information about blood vessel wall structure and characterize plaque composition.

Scintigraphic Techniques  
 
Nuclear perfusion imaging is performed with the use of single-photon emission computed tomography (SPECT) or positron emission tomography (PET) which relies on administration of radionuclide isotope that is accumulated by the targeted tissue.

Medical Care
The prevention and treatment of atherosclerosis requires control of the known modifiable risk factors for this disease. This includes the medical treatment of hypertension, hyperlipidemia, diabetes mellitus, and cigarette habituation.

  • • Hypertension
    • • Hypertension is a risk factor for the development of atherosclerosis, atherosclerotic cardiovascular disease, and stroke. The mechanism by which hypertension causes these effects is not known, and some uncertainty exists as to what the primary and secondary factors are in a typically multifactorial syndrome. These factors may include hyperlipidemia, hypertension, diabetes mellitus, obesity, and physical inactivity.
    • • Dietary and pharmacological treatment of hypertension is associated with a decreased incidence of stroke and, to a lesser degree, atherosclerotic cardiovascular disease.
  • • Hyperlipidemia
    • • Convincing evidence that lowering serum cholesterol reduces the risk of subsequent coronary heart disease events and overall mortality exists.
    • • The HMG-CoA reductase inhibitors inhibit the rate-limiting step of cholesterol synthesis in the liver. HMG-CoA reductase inhibitors are effective in lowering the serum total cholesterol, LDL cholesterol, and triglyceride levels and in raising the serum HDL cholesterol level, and they have a low incidence of adverse effects, the most common being hepatotoxicity and myopathy.
    • • The success of the HMG-CoA reductase inhibitors in reducing circulating lipid levels and improving the clinical and anatomic course of atherosclerosis has focused attention on the management of hyperlipidemia. In addition, an important role remains for other hypolipidemic agents that may be of particular benefit for patients with refractory LDL hypercholesterolemia, hypertriglyceridemia, low HDL cholesterol, and elevated lipoprotein (a).
  • • Secondary prevention of coronary artery disease
    • • The Scandinavian Simvastatin Survival Study (4S) examined the effects of simvastatin on mortality in 4444 patients with established coronary heart disease and elevated total serum cholesterol. A statistically significant 29% reduction in the overall mortality rate (8.2% versus 11.5%) and a 42% reduction in the cardiac mortality rate (5% versus 8.5%) occurred after an average of 5.4 years of follow-up.
    • • The Cholesterol and Recurrent Events (CARE) study examined the effects of pravastatin on mortality rates and cardiac events in 1159 patients with established coronary heart disease and serum cholesterol concentrations that are within the reference range or are mildly elevated. A statistically significant 24% reduction in the incidence of fatal coronary heart disease or nonfatal myocardial infarction (9.9% versus 12.9%) occurred after an average of 5 years of follow-up. A lower total mortality rate (8.6% versus 9.4%) and coronary heart disease mortality rate (4.6% versus 5.7%) occurred in patients receiving pravastatin, although the results were not statistically significant.
    • • The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) trial examined the effects of 40 mg of pravastatin on the incidence of coronary events over a period of 6.1 years in 9014 patients with known coronary heart disease and a broad range of initial cholesterol levels. The following relative risk reductions occurred: 24% for death from coronary heart disease (P <0.001), 22% for the overall mortality rate (P <0.001), 29% for all cardiovascular outcomes (P <0.001), and 19% for stroke (P = 0.048). The effects were similar for all predefined subgroups.
  • • Primary prevention of coronary artery disease
    • • The West of Scotland Coronary Prevention Study (WOSCOPS) examined the effects of pravastatin on the incidence of nonfatal myocardial infarction and coronary mortality rates in 6595 men with moderate hypercholesterolemia and no prior history of coronary heart disease. A statistically significant 29% reduction in nonfatal myocardial infarction (4.6% versus 6.5%) and a 30% reduction in death from all cardiovascular causes (1.6% versus 2.3%) occurred after an average of 4.9 years of follow-up.
    • • The Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) examined the effects of lovastatin on the incidence of a first major coronary event in 5608 men and 997 women with average total cholesterol and LDL cholesterol and below-average HDL cholesterol levels. A statistically significant 37% reduction in the incidence of the first major coronary event (4% versus 6.8%) occurred after an average of 5.2 years.
  • • Therapy with lipid-lowering agents should be a component of multiple risk factor intervention and only is indicated as an adjunct to diet therapy when the response to a diet restricted in saturated fat and cholesterol has been inadequate. The NCEP guidelines recommend aggressive lipid-lowering therapy for patients at high risk for coronary heart disease. More than 50 million individuals in the United States are candidates for some form of dietary and/or pharmacological intervention to modify their lipid profile. Pharmacoeconomic studies of implementation of the NCEP guidelines confirm the cost-effectiveness of primary and secondary prevention. Evidence exists that physicians are poorly compliant with these guidelines.
  • • For patients with diabetes mellitus, strict control of comorbid risk factors is especially important, and ample evidence exists that this reduces the incidence of the clinical complications of microvascular and macrovascular disease.
    • • Cholesterol lowering with the HMG-CoA reductase inhibitors has yielded important reductions in coronary heart disease events in patients with diabetes mellitus.
    • • The benefit of strict glycemic control in the prevention of macrovascular disease has been difficult to confirm, although this intuitively is beneficial and is known to retard the progression of microvascular disease.
  • • Cigarette habituation: The risks of cigarette smoking are reduced rapidly and significantly with smoking cessation. The relative risk is so significant that the incidence of coronary heart disease in people who have recently quit smoking is similar to that of people who have not smoked within 2 years.

Diet

  • • The primary treatment of LDL hypercholesterolemia is dietary and includes restriction of caloric intake, saturated fats, and cholesterol. The NCEP and the American Heart Association (AHA) made specific recommendations for dietary therapy for coronary heart disease prevention. The recommended daily intake of nutrients is described by the step I and step II diets and is appropriately tailored to the level of coronary heart disease risk.
  • • Moderate alcohol intake is associated with a reduced incidence of coronary heart disease events. The mechanism(s) of this benefit is not well understood. Heavy alcohol intake probably is associated with an increased incidence of coronary heart disease events, as well as cardiomyopathy and arrhythmia and obviously should be discouraged.
  • • Sinha et al concluded that high intakes of red or processed meat were associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality. The baseline population was a cohort of half a million people aged 50-71 years from the National Institutes of Health-AARP (formerly known as the American Association of Retired Persons) Diet and Health Study.51

Activity
Physical inactivity is a minor modifiable risk factor for coronary heart disease, and regular exercise has been shown to reduce the risk of coronary heart disease in a number of observational epidemiological studies. The mechanisms for this apparent benefit may include an increase in HDL cholesterol and a decrease in body weight, insulin resistance, and blood pressure. The optimal intensity and duration of exercise is not known; however, 20-30 minutes of aerobic exercise of mild-to-moderate intensity (including walking) 3 times per week probably is appropriate.

Medication
Prevention and treatment of atherosclerosis requires risk factor control, including the medical treatment of hypertension, diabetes mellitus, and cigarette habituation.

Advances in the understanding of the vascular biology of atherosclerosis raises the possibility of novel therapies that may address more directly the various aspects of endothelial dysfunction and the role of endothelial dysfunction in atherogenesis. Potential cellular targets include vascular smooth muscle cells, monocyte/macrophage cell lines, platelets, and endothelial cells. Evidence exists that antiplatelet agents, antioxidant therapies, amino acid supplementation, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers may prove to prevent or slow the progression of the disease.

Combination therapy in the future may allow for even greater achievement of greater LDL-C lowering with associated cardiovascular benefit. However, one such drug Vytorin which combines a new class of lipid lowering drug Ezetimibe (decreases small intestinal absorption of cholesterol) with Simvastatin, has shown no incremental benefit on cardiovascular morbidity and mortality over and above that demonstrated for simvastatin alone.

HMG-CoA reductase inhibitors
These agents are competitive inhibitors of 3-hydroxy-3-methyl Co-A reductase, an enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis, resulting in up-regulation of LDL receptors in response to the decrease in intracellular cholesterol. The HMG-CoA reductase inhibitors are indicated for the secondary prevention of cardiovascular events and for the treatment of hypercholesterolemia and mixed dyslipidemia. 
A number of HMG-CoA reductase inhibitors are indicated for patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments. However, these agents may be less effective in patients with rare homozygous familial hypercholesterolemia, possibly because these patients are lacking functional LDL receptors, making it more likely to raise serum transaminases.

  • • The prognosis of atherosclerosis depends on a number of factors, including systemic burden of disease, the vascular bed(s) involved, and the degree of flow limitation. Wide variability exists, and clinicians appreciate that many patients with critical limitation of flow to vital organs may survive many years, despite a heavy burden of disease. Conversely, myocardial infarction or sudden cardiac death may be the first clinical manifestation of atherosclerotic cardiovascular disease in a patient who is otherwise asymptomatic with minimal luminal stenosis and a light burden of disease.
  • • Much of this phenotypic variability is likely to be determined by the relative stability of the vascular plaque burden. Plaque rupture and exposure of the thrombogenic lipid core are critical events in the expression of this disease process and determine the prognosis. The ability to determine and quantify risk and prognosis in patients with atherosclerosis is limited by the inability to objectively measure plaque stability and other predictors of clinical events.
  • • The most effective and probably the most cost-efficient means of reducing the burden of disease secondary to atherosclerosis in the general population is primary prevention. The role of diet and exercise in the prevention of atherosclerotic cardiovascular disease has been well established. Education of the general population regarding healthy dietary habits and regular exercise will reduce the prevalence of multiple coronary heart disease risk factors. Medical therapies aimed at improving blood pressure control and various lipid parameters are appropriate for the prevention of first coronary heart disease events, if these risk factors are refractory to lifestyle interventions.
  • • This information is for you only.
  • • Always follow your healthcare provider’s instructions for taking medicines. Do not miss any doses, do not take less medicine, and do not stop taking medicine without talking to your provider first. It can be dangerous to suddenly stop taking blood pressure medicine. Also, do not increase your dosage of any medicine without first talking with your provider.
  • • Ask your healthcare provider or pharmacist for information about the drugs you are taking.
  • • Ask your provider about nonprescription medicines and supplements before you take them.

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Atherosclerosis is a condition in which patchy deposits of fatty material (atheromas or atherosclerotic plaques) develop in the walls of medium-sized and large arteries, leading to reduced or blocked blood flow.

  • • Atherosclerosis is caused by repeated injury to the walls of arteries.
  • • Many factors contribute to this injury, including high blood pressure, tobacco smoke, diabetes and high levels of cholesterol in the blood.
  • • Often, the first symptom is pain or cramps at times when blood flow cannot keep up with the tissues‘ need for oxygen.
  • • To prevent atherosclerosis, people need to stop using tobacco, improve their diet, exercise regularly, and maintain control of their blood pressure and diabetes.
  • • If atherosclerosis causes complications, such as a heart attack or stroke, these are treated.

In the United States and most other developed countries, atherosclerosis is the leading cause of illness and death. Estimates for 2005 in the United States alone are that about 16 million people have atherosclerotic heart disease and 5.8 million have stroke. Cardiovascular disease, primarily coronary and cerebrovascular atherosclerosis, caused almost 870,000 deaths in 2005—almost twice as many as cancer caused and 9 times as many as injuries caused. This year an estimated 1.2 million Americans will have a new or recurrent heart attack. Despite significant medical advances, heart attacks due to coronary artery disease (atherosclerosis that affects the arteries supplying blood to the heart and strokes (due to atherosclerosis that affects the arteries to the brain are responsible for more deaths than all other causes combined.

Atherosclerosis can affect the medium-sized and large arteries of the brain, heart, kidneys, other vital organs, and legs. It is the most important and most common type of arteriosclerosis, a general term for several diseases in which the wall of an artery becomes thicker and less elastic Causes. The development of atherosclerosis is complicated, but the primary event seems to be repeated, subtle injury to the artery‘s wall through various mechanisms. These mechanisms include physical stresses from turbulent blood flow (such as occurs where arteries branch, particularly in people who have high blood pressure) and inflammatory stresses involving the immune system, certain infections, or chemical abnormalities in the bloodstream (high cholesterol, diabetes). The infections may be due to bacteria (Chlamydia pneumoniae or Helicobacter pylori) or to viruses (cytomegalovirus and others).

Atherosclerosis begins when the injured arterial wall creates chemical signals that cause certain types of white blood cells (monocytes and T cells) to attach to the wall of the artery. These cells move into the wall of the artery. There, they are transformed into foam cells, which collect cholesterol and other fatty materials, and trigger growth of smooth muscle cells in the artery wall. In time, these fat-laden foam cells accumulate. They form patchy deposits (atheromas, also called plaques) covered with a fibrous cap in the lining of the artery wall. With time, calcium accumulates in the plaques. Plaques may be scattered throughout medium-sized and large arteries, but they usually form where the arteries branch
How Atherosclerosis Develops

The wall of an artery is composed of several layers. The lining or inner layer (endothelium) is usually smooth and unbroken. Atherosclerosis begins when the lining is injured or diseased. Then certain white blood cells called monocytes and T cells are activated and move out of the bloodstream and through the lining of an artery into the artery’s wall. Inside the lining, they are transformed into foam cells, which are cells that collect fatty materials, mainly cholesterol. In time, smooth muscle cells move from the middle layer into the lining of the artery’s wall and multiply there. Connective and elastic tissue materials also accumulate there, as may cell debris, cholesterol crystals, and calcium. This accumulation of fat-laden cells, smooth muscle cells, and other materials forms a patchy deposit called an atheroma or atherosclerotic plaque. As they grow, some plaques thicken the artery’s wall and bulge into the channel of the artery. These plaques may narrow or block an artery, reducing or stopping blood flow. Other plaques do not block the artery very much but may split open, triggering a blood clot that suddenly blocks the artery

Plaques can grow into the opening (lumen) of the artery, gradually causing it to narrow. When atherosclerosis narrows an artery, tissues supplied by the artery may not receive enough blood and oxygen. Plaques also can grow into the wall of the artery, where they do not block blood flow. Both kinds of plaques can split open (rupture), exposing the material within to the bloodstream. This material triggers blood clot formation. These blood clots can suddenly block all blood flow through the artery, which is the main cause of a heart attack or stroke. Sometimes these blood clots break off, travel through the bloodstream, and block an artery elsewhere in the body. Similarly, pieces of the plaque can break off and travel through the bloodstream and block an artery elsewhere.

Risk Factors
Risk factors for atherosclerosis include tobacco use, high levels of cholesterol in the blood, high blood pressure, diabetes, obesity, physical inactivity, and diet. Dietary factors include low daily consumption of fruits and vegetables and other than moderate alcohol consumption (that is, none or too much). These risk factors can usually be modified. Risk factors that cannot be modified include having a family history of early atherosclerosis (that is, having a close relative who developed the disease at a young age), advancing age, and male sex. Men have a higher risk than women, although women who have coronary artery disease are more likely to die than men who have the disease.

Smoking: One of the most important modifiable risk factors is smoking. (Using other forms of tobacco, such as snuff and chewing tobacco, also increases risk.) A smoker‘s risk of developing coronary artery disease is directly related to the amount of tobacco smoked daily. The risk of a heart attack is increased threefold in men and sixfold in women who smoked 20 or more cigarettes per day compared with nonsmokers. In people who already have a high risk of heart disease, tobacco use is particularly dangerous.

Tobacco use decreases the level of high-density lipoprotein (HDL) cholesterol—the “good” cholesterol—and increases the level of low-density lipoprotein (LDL) cholesterol—the “bad” cholesterol. Smoking increases the level of carbon monoxide in the blood, which may increase the risk of injury to the lining of the artery‘s wall. Tobacco use causes arteries already narrowed by atherosclerosis to constrict, further decreasing the amount of blood reaching the tissues. In addition, tobacco use increases the blood‘s tendency to clot (by making platelets stickier), so that it increases the risk of peripheral arterial disease 
People who quit using tobacco have only half the risk of those who continue to use tobacco—regardless of how long they smoked before quitting. Quitting also decreases the risk of death after coronary artery bypass surgery or a heart attack and the risk of illness and death in people who have peripheral arterial disease. The benefits of quitting tobacco use begin immediately and increase with time.

Secondhand smoke (smoke breathed in from someone else‘s smoking) appears to increase risk also. It should be avoided.
Cholesterol Levels: A high level of LDL cholesterol level is another important modifiable risk factor. A diet that is high in saturated fats causes LDL cholesterol levels to increase in susceptible people. Cholesterol levels also increase as people age and are normally higher in men than in women, although levels increase in women after menopause. Several hereditary disorders result in high levels of cholesterol or other fats. People with these hereditary disorders can have extremely high levels of cholesterol and (if untreated) die of coronary artery disease at an early age.

Lowering high LDL cholesterol levels through the use of drugs called statins can significantly reduce the risk of heart attacks, strokes, and death.
Not all types of cholesterol increase the risk of atherosclerosis. A high level of HDL (good) cholesterol decreases the risk of atherosclerosis, and a low level increases the risk.

The desired level of total cholesterol, which includes LDL and HDL cholesterol and triglycerides, is 140 to 200 mg/dL (3.6 to 5.2 mmol/L). Risk of a heart attack more than doubles when the total cholesterol level approaches 300 mg/dL (7.8 mmol/L). The risk is decreased when the LDL cholesterol level is below 130 mg/dL (3.4 mmol/L), and the HDL cholesterol level is above 40 mg/dL (1 mmol/L). In high-risk people, such as those who have diabetes or who already have atherosclerotic heart disease, heart attacks, stroke, or bypass surgery, LDL cholesterol should be below 70 mg/dL (1.8 mmol/L) However, the percentage of HDL cholesterol in relation to total cholesterol is a more reliable measure of risk than is the total or LDL cholesterol level. HDL cholesterol should account for more than 25% of total cholesterol. High triglyceride levels are often associated with low HDL cholesterol levels. However, evidence suggests that high triglyceride levels alone may also increase the risk of atherosclerosis.

High Blood Pressure: Uncontrolled high diastolic or systolic blood pressure is a risk factor for heart attack and stroke, which are caused by atherosclerosis. The risk of cardiovascular disease starts increasing when blood pressure levels are above 110/75 mm Hg. Reducing high blood pressure clearly lowers risk. Doctors usually try to achieve a blood pressure of less than 140/90 mm Hg, and often less than 130/80 mm Hg in those with diabetes or kidney disease.

Diabetes Mellitus: People who have type 1 diabetes  tend to develop disease that affects small arteries, such as those in the eyes, nerves, and kidneys, leading to vision loss, nerve damage, and kidney failure. Some people with type 1 diabetes and most people with type 2 diabetes tend to develop atherosclerosis in large arteries. These people also tend to develop atherosclerosis at an earlier age and more extensively than do people who do not have diabetes. The risk of developing atherosclerosis is 2 to 6 times higher for people with diabetes, particularly women. Women who have diabetes, unlike those who do not, are not protected from atherosclerosis before menopause. People who have diabetes have the same risk of death as someone who has had a prior heart attack, and doctors usually try to help these people keep other risk factors (such as high cholesterol levels and high blood pressure) under careful control.

Obesity: Obesity, particularly abdominal (truncal) obesity, increases the risk of coronary artery disease (atherosclerosis of the arteries that supply blood to the heart). Abdominal obesity increases the risk of other risk factors for atherosclerosis: high blood pressure, type 2 diabetes, and high cholesterol levels. Losing weight reduces the risk of all these disorders.

Physical Inactivity: Physical inactivity appears to increase the risk of developing coronary artery disease, and much evidence suggests that regular exercise even to a moderate degree reduces this risk and decreases mortality. Exercise can also help modify other risk factors for atherosclerosis—by lowering blood pressure and cholesterol levels and by helping with weight loss and decreasing insulin resistance.

Diet: There is substantial evidence that regular vegetable and fruit consumption can decrease coronary artery disease risk. It is unclear whether fruits and vegetables appear beneficial due to the substances (phytochemicals) they contain, or whether people who eat a lot of fruits and vegetables also eat less saturated fat and are more likely to take fiber and vitamins. However, phytochemicals called flavonoids (in red and purple grapes, red wine, black teas, and dark beers) appear especially protective. High concentrations in red wine may help explain why the French have a relatively low incidence of coronary artery disease, even though they use more tobacco and consume more fat than Americans do. But no studies prove that eating flavonoid-rich foods or using supplements instead of foods prevents atherosclerosis. Increased fiber content in certain vegetables may decrease total cholesterol and may decrease blood glucose and insulin levels. However, excessive fiber interferes with the absorption of certain minerals and vitamins. In general, foods rich in phytochemicals and vitamins are also rich in fiber.

Fat is an essential part of the diet. The notion that eating less fat is important to a healthy diet is only partly true because the type of fat also matters. The main types of fats are

  • • Saturated and trans fats
  • • Unsaturated fats (polyunsaturated and monounsaturated)
  • • Fats may be soft (or liquid) or firm at room temperature. Soft fats, such as oils and some margarines, tend to be higher in polyunsaturated and monounsaturated fats. Hard fats, such as butter and shortening, tend to be higher in saturated and trans fats. Saturated and trans fats are more likely to cause atherosclerosis. Thus, whenever possible, people should limit the amount of saturated and trans fats in their diet and choose foods with monounsaturated or polyunsaturated fats instead. Saturated and trans fats are found in red meat, many fast food and junk food items, full-fat dairy products (such as cheese, butter, and cream), and hard (stick) margarines. Monounsaturated fats are found in canola and olive oil, soft margarines with no trans fat, nuts, and olives. Polyunsaturated fats are found in nuts, seeds, oils, and mayonnaise. Two types of polyunsaturated fats—omega-3 and omega-6 fats—are essential to a healthy diet. Omega-3 fats are found in fatty fish such as salmon, omega-3 eggs, canola oil, and walnuts. Omega-6 fats are found in some nuts and seeds and in safflower, sunflower, and corn oils.

Alcohol Intake: People who drink a moderate amount of alcohol seem to have a lower risk of coronary artery disease than do people who drink too much or do not drink at all. Alcohol increases the level of good cholesterol, HDL, and it also decreases the risk of blood clots and inflammation and helps protect the body from the by-products of cell activity. However, more than moderate alcohol consumption > 14 drinks per week for men and > 9 drinks per week for women) can cause significant health problems and increase the risk of death.

High Blood Levels of Homocysteine (Hyperhomocysteinemia): People who have very high levels of homocysteine (an amino acid) in their blood, usually because of a hereditary disorder, have an increased risk of coronary artery disease, usually at a young age. High levels of homocysteine may directly injure the lining of arteries, making the formation of plaques more likely. High homocysteine levels may also promote the formation of blood clots. However, giving people drugs that lower homocysteine levels does not seem to reduce risk of death.

Symptoms
Symptoms depend on where the affected artery is located and whether it is gradually narrowed or suddenly blocked. With narrowing, atherosclerosis usually does not produce symptoms until the interior of an artery is narrowed by more than 70%. The first symptom of a narrowed artery may be pain or cramps at times when blood flow cannot keep up with the tissues’ need for oxygen. For instance, during exercise, a person may feel chest pain because the oxygen supply to the heart is inadequate. While walking, a person may feel leg cramps (intermittent claudication) because the oxygen supply to the leg muscles is inadequate. If the arteries supplying one or both kidneys become narrowed, kidney failure or dangerously high blood pressure can result.

If the arteries supplying the heart (coronary arteries) are blocked, a heart attack can result. Blockage in the arteries supplying the brain can cause a stroke. Blockage of the arteries in the legs can cause gangrene of a toe, foot, or leg.

Diagnosis
People who have symptoms that suggest a blocked artery have tests to look for the location and extent of the blockage. Different tests are used depending on what organ seems to be involved. People with atherosclerotic arteries in one organ often have atherosclerosis in other arteries. Therefore, when doctors find atherosclerotic blockage in one artery, for example in the leg, they usually do tests to look for blockage in other arteries, such as those in the heart. Doctors also test for certain risk factors in people who have an atherosclerotic blockage. For example, they measure the fasting levels of blood glucose, cholesterol, and triglycerides. Doctors usually also do these tests as part of the routine yearly examination in adults.

Some doctors recommend tests to look for atherosclerotic blockage in people who have no symptoms as part of a prevention strategy. Such tests include an electron beam computed tomography (CT) scan or magnetic resonance imaging (MRI) of the heart and ultrasound of the arteries in the neck (carotid arteries). Electron beam CT and MRI can detect hardened (calcified) plaque in the coronary arteries. Ultrasonography of the carotid arteries can detect thickening of the artery wall, which suggests atherosclerosis. However, many doctors think that these tests rarely change the advice they would give based on the person‘s other, more easily recognized, risk factors.

Prevention and Treatment
To help prevent atherosclerosis, people need to stop tobacco use, lower LDL cholesterol levels, lower blood pressure, lose weight, and exercise. People who have diabetes must maintain strict control of their blood sugar (glucose). People who are at high risk for atherosclerosis also may benefit from taking certain drugs. Helpful drugs include the statins (even if cholesterol levels are normal or only slightly high) and aspirin or other antiplatelet drugs.
When atherosclerosis becomes severe enough to cause complications, the complications themselves must be treated. Complications include angina, heart attack, abnormal heart rhythms, heart failure, kidney failure, stroke, and leg cramps (intermittent claudication) or gangrene.

# This article is for your information only.  Dr Ben-Zur recommends consulting your physician prior to making any changes in your diet, exercise or medical program.

Arteries are blood vessels that carry oxygen and nutrients from your heart to the rest of your body. Healthy arteries are flexible, strong and elastic. Over time, however, too much pressure in your arteries can make the walls thick and stiff — sometimes restricting blood flow to your organs and tissues. This process is called arteriosclerosis, or hardening of the arteries.

Atherosclerosis is a specific type of arteriosclerosis, but the terms are often used interchangeably. Atherosclerosis refers to the buildup of fats in and on your artery walls (plaques), which can restrict blood flow. These plaques can also burst, causing a blood clot. Although atherosclerosis is often considered a heart problem, it can affect arteries anywhere in your body. Atherosclerosis is a preventable and treatable condition. 
Atherosclerosis develops gradually. There are usually no atherosclerosis symptoms until an artery is so narrowed or clogged that it can’t supply adequate blood to your organs and tissues. Sometimes a blood clot completely obstructs blood flow, or even breaks apart and causes blood clots that can trigger a heart attack or stroke.

Atherosclerosis symptoms depend on which arteries are affected. For example:

  • If you have atherosclerosis in your heart arteries, you may have symptoms similar to those of a heart attack, such as chest pain (angina).
  • If you have atherosclerosis in the arteries leading to your brain, you may have symptoms such as sudden numbness or weakness in your arms or legs, difficulty speaking or slurred speech, or drooping muscles in your face.
  • If you have atherosclerosis in the arteries in your arms and legs, you may have symptoms of peripheral arterial disease, such as leg pain when walking (intermittent claudication).

Sometimes atherosclerosis causes erectile dysfunction in men.

When to see a doctor
If you think you have atherosclerosis — or risk factors for hardening of the arteries — talk to your doctor. Also pay attention to early symptoms of inadequate blood flow, such as chest pain (angina), leg pain or numbness. Early diagnosis and treatment can stop atherosclerosis from worsening and prevent a medical emergency.

Causes

Atherosclerosis is a slow, progressive disease that may begin as early as childhood. Although the exact cause is unknown, researchers suspect that atherosclerosis starts with damage or injury to the inner layer of an artery. The damage may be caused by:

  • • High blood pressure
  • • High cholesterol
  • • An irritant, such as nicotine
  • • Certain diseases, such as diabetes

Once the inner wall of an artery is damaged, blood cells called platelets often clump at the injury site to try to repair the artery, leading to inflammation. Over time, fatty deposits (plaques) made of cholesterol and other cellular waste products also accumulate at the injury and harden, narrowing your arteries. The organs and tissues connected to the blocked arteries then don’t receive enough blood to function properly.
Eventually pieces of the fatty deposits may rupture and enter your bloodstream. This can cause a blood clot to form and damage your organs, such as in a heart attack. A blood clot can also travel to other parts of your body and partially or totally block blood flow to another organ.

Risk Factors

Hardening of the arteries occurs over time. In addition to simply getting older, factors that increase the risk of atherosclerosis include:

  • • High blood pressure
  • • High cholesterol
  • • Diabetes
  • • Obesity
  • • Smoking
  • • A family history of aneurysm or early heart disease

Complications

The complications of atherosclerosis depend on the location of the blocked arteries. For example:

  • Coronary artery disease. When atherosclerosis narrows the arteries close to your heart, you may develop coronary artery disease, which can cause chest pain (angina) or a heart attack.
  • Carotid artery disease. When atherosclerosis narrows the arteries close to your brain, you may develop carotid artery disease, which can cause a transient ischemic attack (TIA) or stroke.
  • Peripheral artery disease. When atherosclerosis narrows the arteries in your arms or legs, you may develop circulation problems in your arms and legs called peripheral arterial disease. This can make you less sensitive to heat and cold, increasing your risk of burns or frostbite. In rare cases, poor circulation in your arms or legs can cause tissue death (gangrene).
  • Aneurysms. Atherosclerosis can also cause aneurysms, a serious complication that can occur anywhere in your body. An aneurysm is a bulge in the wall of your artery. Pain and throbbing in the area of an aneurysm is a common symptom. If an aneurysm bursts, you may face life-threatening internal bleeding. Although this is usually a sudden, catastrophic event, a slow leak is possible. If a blood clot within an aneurysm dislodges, it may obstruct an artery at some distant point.

Work up

Your doctor may find signs of narrowed, enlarged or hardened arteries during a physical exam. These include:

  • • A weak or absent pulse below the narrowed area of your artery
  • • Decreased blood pressure in an affected limb
  • • Whooshing sounds (bruits) over your arteries, heard with a stethoscope
  • • Signs of a pulsating bulge (aneurysm) in your abdomen or behind your knee
  • • Evidence of poor wound healing in the area where your blood flow is restricted

Depending on the results of the physical exam, your doctor may suggest one or more diagnostic tests, including:

  • Blood tests. Lab tests can detect increased levels of cholesterol and blood sugar that may increase the risk of atherosclerosis.
  • Doppler ultrasound. Your doctor may use a special ultrasound device (Doppler ultrasound) to measure your blood pressure at various points along your arm or leg. These measurements can help your doctor gauge the degree of any blockages, as well as the speed of blood flow in your arteries.
  • Ankle-brachial index. This test can tell if you have atherosclerosis in the arteries in your legs and feet. Your doctor may compare the blood pressure in your ankle with the blood pressure in your arm. This is known as the ankle-brachial index. An abnormal difference may indicate peripheral vascular disease, which is usually caused by atherosclerosis.
  • Electrocardiogram (ECG). An electrocardiogram records electrical signals as they travel through your heart. An ECG can often reveal evidence of a previous heart attack or one that’s in progress. If your signs and symptoms occur most often during exercise, your doctor may ask you to walk on a treadmill or ride a stationary bike during an ECG.
  • Angiogram. To better view blood flow through your heart, brain, arms or legs, your doctor may inject a special dye into your arteries before an X-ray. This is known as an angiogram. The dye outlines narrow spots and blockages on the X-ray images.
  • Other imaging tests. Your doctor may use ultrasound, a computerized tomography (CT) scan or a magnetic resonance angiogram (MRA) to study your arteries. These tests can often show hardening and narrowing of large arteries, as well as aneurysms and calcium deposits in the artery walls

Treatment

Lifestyle changes, such as eating a healthy diet and exercising, are often the first line of defense in treating atherosclerosis. But sometimes, medication or surgical procedures may be recommended as well.
Various drugs can slow — or sometimes even reverse — the effects of atherosclerosis. Here are some common choices:

  • Cholesterol medications. Aggressively lowering your low-density lipoprotein (LDL) cholesterol, the “bad” cholesterol, can slow, stop or even reverse the buildup of fatty deposits in your arteries. Boosting your high-density lipoprotein (HDL) cholesterol, the “good” cholesterol, may help, too. Your doctor can choose from a range of cholesterol medications, including drugs known as statins and fibrates.
  • Anti-platelet medications. Your doctor may prescribe anti-platelet medications, such as aspirin, to reduce the likelihood that platelets will clump in narrowed arteries, form a blood clot and cause further blockage.
  • Anticoagulants. An anticoagulant, such as heparin or warfarin (Coumadin), can help thin your blood to prevent clots from forming.
  • Blood pressure medications. Medications to control blood pressure — such as beta blockers, angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers — can help slow the progression of atherosclerosis.
  • Other medications. Your doctor may suggest certain medications to control specific risk factors for atherosclerosis, such as diabetes. Sometimes medications to treat symptoms of atherosclerosis, such as leg pain during exercise, are prescribed.

Sometimes more aggressive treatment is needed. If you have severe symptoms or a blockage that threatens muscle or skin tissue survival, you may be a candidate for one of the following surgical procedures:

  • Angioplasty. In this procedure, your doctor inserts a long, thin tube (catheter) into the blocked or narrowed part of your artery. A wire with a deflated balloon is passed through the catheter to the narrowed area. The balloon is then inflated, compressing the deposits against your artery walls. A mesh tube (stent) is usually left in the artery to help keep the artery open. Angioplasty may also be done with laser technology.
  • Endarterectomy. In some cases, fatty deposits must be surgically removed from the walls of a narrowed artery. When the procedure is done on arteries in the neck (the carotid arteries), it’s known as carotid endarterectomy.
  • Thrombolytic therapy. If you have an artery that’s blocked by a blood clot, your doctor may insert a clot-dissolving drug into your artery at the point of the clot to break it up.
  • Bypass surgery. Your doctor may create a graft bypass using a vessel from another part of your body or a tube made of synthetic fabric. This allows blood to flow around the blocked or narrowed artery.

Lifestyle modifications

Lifestyle changes can help you prevent or slow the progression of atherosclerosis.

  • Stop smoking. Smoking damages your arteries. If you smoke, quitting is the best way to halt the progression of atherosclerosis and reduce your risk of complications.
  • Exercise most days of the week. Regular exercise can condition your muscles to use oxygen more efficiently. Physical activity can also improve circulation and promote development of new blood vessels that form a natural bypass around obstructions (collateral vessels). Ideally, you should exercise 30 to 60 minutes most days of the week. If you can’t fit it all in one session, try breaking it up into 10-minute intervals. You can take the stairs instead of the elevator, walk around the block during your lunch hour, or do some sit-ups or push-ups while watching television.
  • Eat healthy foods. A heart-healthy diet based on fruits, vegetables and whole grains – and low in saturated fat, cholesterol and sodium — can help you control your weight, blood pressure and cholesterol. Try substituting whole-grain bread in place of white bread, grabbing an apple, banana or carrot sticks as a snack, and reading nutrition labels to control the amount of salt and fat you eat.
  • Manage stress. Reduce stress as much as possible. Practice healthy techniques for managing stress, such as muscle relaxation and deep breathing.

If you have high cholesterol, high blood pressure, diabetes or another chronic disease, work with your doctor to manage the condition and promote overall health.

This information is only for you. Always follow your healthcare provider’s instructions for taking medicines. Do not miss any doses, do not take less medicine, and do not stop taking medicine without talking to your provider first. It can be dangerous to suddenly stop taking blood pressure medicine. Also, do not increase your dosage of any medicine without first talking with your provider.

  • • Ask your healthcare provider or pharmacist for information about the drugs you are taking.
  • • Ask your provider about nonprescription medicines and supplements before you take them.

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Atherosclerosis is the accumulation of plaque inside blood vessels. It usually starts early in life and progresses slowly, but the rate of its progression varies considerably from person to person. Because plaque buildup can slow down or prevent blood flow almost anywhere in the body, atherosclerosis contributes to many diseases, most importantly heart attack and stroke. 
Atherosclerosis contributes to more mortality—half or more of all deaths—and serious morbidity in the Western world than any other disorder. The risk factors for atherosclerosis have been well studied, and significant public health efforts are directed toward lowering the incidence and severity of atherosclerosis.

  • Arteriosclerosis is a general term for hardening of the arteries. Atherosclerosis is a specific form of arteriosclerosis, and the most important, but the two terms are often used interchangeably. Two other types of arteriosclerosis that are different from atherosclerosis are recognized: arteriosclerosis obliterans and medial calcific arteriosclerosis.
  • • Hardening of the arteries
  • • Cardiovascular disease

The American Heart Association recognizes six stages of atherosclerotic lesion:

  • Type I lesions are present even in children, and are composed of isolated foam cells in the arterial wall.
  • Type II lesions are also known as fatty streak lesions and feature more foam cells.
  • Type III lesions feature pools of fatty material located outside the cells, and can be present in young adults.
  • Type IV lesions are called atheromas and have a core of cell-free lipid (fat).
  • Type V lesions are known as fibroatheromas and are surrounded by fibrous tissue and may also contain calcifications, which make the arteries remarkably hard and inflexible. These are present in older adults.
  • Type VI lesions are called complicated and include surface defects, blood clotting activity, and may result in formation of blood clots that can break off and be brought to other parts of the body by the blood stream

SIGNS & SYMPTOMS
Early atherosclerosis has no symptoms. In some cases, the first sign of atherosclerosis is a catastrophic event caused by a plaque in the artery breaks off and travels, or causes complete blockage of the blood supply to a vital organ. Other times, early diagnosis of atherosclerosis can be made based on symptoms in the organ(s) supplied by the affected blood vessels. Different diseases may develop depending on which arteries are affected.

  • Coronary artery disease: Atherosclerosis affecting the coronary arteries (the arteries that supply the heart) is a significant cause of heart attacks, and in some—but not all— cases can show up as a particular kind of chest pain, angina pectoris.
  • Carotid artery disease: The carotid arteries supply blood to the brain and are also susceptible to plaque formation. Atherosclerosis can lead to blockage of the carotid arteries and cause a stroke, heralded by the sudden loss of specific abilities, such as the ability to speak. Sometimes the turbulence of the blood rushing past the plaques can cause a sound called a bruit, which can be heard when a stethoscope is put over the carotids.
  • • Peripheral arterial disease occurs when plaque builds up in the major arteries that supply the legs, arms, and pelvis. Reduced blood flow can lead to numbness, pain, and sometimes dangerous infections.

CAUSES:
The exact causes of atherosclerosis are the subject of much active research, but the consensus is that damage to the cells lining the arteries, the endothelial cells, is the key event that causes the disease to begin and to get worse.

Blood vessels

The vessels most often affected by atherosclerosis are large arteries with fast, turbulent blood flow. Arteries bring oxygen-rich blood from the heart to the rest of the body. The wall of an artery is made up of several layers: the innermost endothelium, which is adjacent to the flowing blood; the middle layer called themedia; and the outermost adventitia. Importantly, monocytes (a type of inflammatory cell that travels in the bloodstream) are able to stick to and cross the endothelial layer, after which they take up residence in the blood vessel wall as macrophages.

Plaque

Plaque is a waxy aggregate of fatty substances, cholesterol, intact and dead cells, calcium precipitates, and proteins such as fibrin. In an atherosclerotic plaque, there are three components:

  • • Cells, including smooth muscle cells as well as macrophages that got there by migrating from the bloodstream
  • • Connective tissue components, including collagen
  • • Lipid (fat) deposits, both inside and outside of cells

Macrophages cause plaques to grow bigger when they ingest lipids that are circulating in the bloodstream, and cell debris that is sitting nearby in the plaque. When macrophages soak up lipids, they become foam cells. Foam cells can distort the inner surface of the blood vessel. As plaques grow, they can become detached from the blood vessel wall and attract platelets, which begins the process of blood clot formation. 

DIAGNOSIS
There are a number of ways to determine whether a person has risk factors for atherosclerosis, and to determine if he or she has atherosclerotic plaques.

  • • Blood tests check the levels of certain fats, cholesterol, sugar, and proteins in the blood. Abnormal levels may indicate an increased risk for atherosclerosis.
  • • Electrocardiograms, or EKGs, are simple tests that detect and record the heart’s electrical activity with electrodes placed at various places on the body. Certain electrical patterns that the EKG detects can suggest the presence of coronary artery disease (atherosclerosis in the heart), or show evidence of heart attacks in the past (or present).
  • • Ankle/brachial index refers to blood pressures measured in the ankles and compared to pressures in the arm. If significant peripheral arterial disease is impeding flow to the legs, the pressure in the ankles is expected to be much lower than that in the arms.
  • • Echocardiography uses sound waves to create a moving picture of the heart and provides information about the size, shape, and dynamics of the heart.
  • • Computed tomography scanning is a series of x-rays that are then combined into a creates computer-generated images of the heart, brain, or other areas of the body. The test can often show hardening and narrowing of large arteries.
  • • Angiography uses dye and special imaging equipment to visualize blood flow through the arteries. It can demonstrate plaque blocking arteries and how severe the plaque is.

Treatment options include no- or low-cost “lifestyle” changes, medication regimens, or surgical options to remove plaques or restore circulation to vulnerable organs.

Lifestyle changes

Making lifestyle changes can often help prevent or treat atherosclerosis. For some people, these changes may be the only treatment needed. The following can help decrease risk of atherosclerosis:

  • • Following a healthy eating plan to prevent or reduce high blood pressure and to maintain a normal weight
  • • Regular exercise
  • • Quitting smoking and avoiding exposure to secondhand smoke
  • • Stress reduction
Medication

Doctors have a wide range of drug choices for helping patients lower blood pressure and cholesterol levels, which in turn helps prevent atherosclerosis. Drugs for blood pressure management include beta blockers, ACE inhibitors, calcium channel blockers, and angiotensin-receptor blockers. Drugs for lowering cholesterol include statins. Aspirin also reduces the risk of dying from a second heart attack by reducing the ability of platelets to form blood clots, which are part of the atherosclerotic lesion.

Surgery

If an atherosclerotic lesion is blocking flow in one of the coronary arteries, the best option to treat it may be stenting, angioplasty, or bypass grafting. Vascular surgeons can also remove plaques surgically in a procedure called an endarterectomy, or destroy the plaque with high-intensity laser beams mounted on catheters (laser angioplasty).

Prevention 

Primary prevention

Primary prevention refers to preventing atherosclerosis before it starts. Since the disease is thought to begin in childhood, ways to prevent it must begin then. According to guidelines released in 2003 by the American Heart Association, atherosclerosis prevention in childhood includes giving the child a healthy diet, keeping weight within healthy ranges and monitoring blood pressure, preventing her exposure to secondhand smoke, and promoting plenty of activity. For children at higher risk owing to underlying health problems or a strong family history, the guidelines are more detailed and involve close monitoring of the child’s cholesterol and body mass index.[2] These guidelines are based on the best evidence available. For ethical and logistical reasons, there is never likely to be a research study in which some children get these healthy interventions and others do not.

Secondary and tertiary prevention

Secondary prevention refers to early diagnosis of a disease, and tertiary prevention refers to reducing the harmful effects of a disease once it has been diagnosed. Sometimes both these concepts are called secondary prevention. 
The strategies for secondary prevention of atherosclerosis are similar to those for primary prevention. They include watching one’s cholesterol and triglycerides (lipids), getting exercise, monitoring blood pressure, and in many cases taking medications such as statins or aspirin. For more information, visit the American Heart Association’s page on prevention.

Chances of Developing Atherosclerosis

Many risk factors have been identified, and they are usually classified as modifiable (something a person can change) or non-modifiable (something a person can’t change):

Modifiable risk factors
  • Smoking increases the chances of developing and dying from atherosclerosis.
  • High blood cholesterol, specifically at levels > 240 mg/dL, is a risk factor that can be modified by diet and medications.
  • • High triglycerides, at levels > 400 mg/dL, are another risk factor.
  • High blood pressure, of 140 over 90 or higher, makes the heart muscle work harder and also harms the arteries.
  • • Physical inactivity and obesity are highly correlated and increase the risk of atherosclerosis, even in the absence of other risk factors.
  • Diabetes, if uncontrolled, greatly increases the risk of death from atherosclerosis. Most diabetics die from heart attacks caused by atherosclerosis.
  • Sleep apnea is a disorder in which breathing stops or gets very shallow during sleep. Untreated sleep apnea raises the risk of high blood pressure, which is a risk factor for atherosclerosis.
  • Stress: Common “triggers” for a heart attack are an emotionally upsetting event or unaccustomed exercise.
  • Alcohol: Heavy drinking can damage the heart muscle and worsen other risk factors for atherosclerosis.
Non-modifiable risk factors
  • • Heredity, or what is inherited from one’s parents, contributes to the risk of atherosclerosis.
  • • Gender: Before age 60, men are at higher risk than women.
  • • Age: Risk is higher for men older than 45 and for women older than 55.
Related Problems

If the only problem atherosclerosis caused was plaques in vessels, it might not be as serious a disease. But the plaques themselves, because they can block blood flow or cause blood clots, lead to further problems. These include stroke, heart attack, and peripheral vascular disease.

Related disorders

Many people with atherosclerosis also have obesity, metabolic syndrome, diabetes, high blood pressure, and/or hyperlipidemia (abnormal cholesterol or triglycerides). These conditions are thought to contribute to the development of atherosclerosis. 
***Because atherosclerosis is so common and so deadly, and because it is thought to result from the complicated interaction of many factors, it is the topic of a great deal of research. Recent avenues of research include some of the following topics.

  • • Omega-3 fatty acids: Omega-3 fatty acids, which are found abundantly in wild fatty fish as well as flaxseed oil, are effective in the prevention and, possibly, the treatment of atherosclerosis.[5] Research is ongoing into who might benefit most from eating omega-3 fatty acid-rich foods.
  • • Vitamin E and other antioxidants: There is conflicting evidence available as to the usefulness of taking vitamin E supplements to prevent or treat atherosclerosis

# Remember this article is for your information only. Dr. Ben-Zur recommends consulting your physician prior to making any changes in your diet, exercise or medical program. 
Ref://

  1. • Stary HC, Chandler AB, Dinsmore RE, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation. Sep 1;92(5):1355-74.Abstract | Full Text
  2. • Kavey RE, Daniels SR, Lauer RM, Atkins DL, Hayman LL, Taubert K; American Heart Association. American Heart Association guidelines for primary prevention of atherosclerotic cardiovascular disease beginning in childhood. Circulation. 2003 Mar 25;107(11):1562-6. Full Text
  3. • Wolk R, Shamsuzzaman AS, Somers VK. Obesity, sleep apnea, and hypertension. Hypertension. 2003 Dec;42(6):1067-74. Epub 2003 Nov 10. Abstract |Full Text
  4. • Strike PC, Steptoe A. Behavioral and emotional triggers of acute coronary syndromes: a systematic review and critique. Psychosom Med. 2005 Mar-Apr;67(2):179-86. Abstract | Full Text
  5. •  von Schacky C. n-3 fatty acids and the prevention of coronary atherosclerosis. Am J Clin Nutr. 2000 Jan;71(1 Suppl):224S-7S. Abstract | Full Text
  6. • Harris A, Devaraj S, Jialal I. Oxidative stress, alpha-tocopherol therapy, and atherosclerosis. Curr Atheroscler Rep. 2002 Sep;4(5):373-80. Abstract
  7. • Blankenhorn DH, Hodis HN. Atherosclerosis–reversal with therapy. West J Med. 1993 Aug;159(2):172-9. Abstract | Full Text



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