Monthly Archives: August 2014


straight from the heart

These proverbs come from Dr. Uri Ben-Zur’s book, “Straight from the Heart.” Check out more  here!

1. Only you can prevent heart disease.

2. Don’t forget your diet and exercise.

3. Salt is a deadly weapon.

4. If you lose weight, you may not need any of the medications you are taking.

5. The first symptom of heart disease is often sudden death.

6. Call me first if you have any problem. The only time I will get upset is if you don’t call me when you are sick.

7. Bring your friends and family members, so that we can help a few more people.

8. If you don’t want to meet me in the emergency room, take a walk with me at the beach.

9. You must brush your arteries twice a day with diet and exercise

10. Eat egg whites, fish, and vegetables.


Vegan Taco Boats



• 4 medium zucchini (or substitute 4 medium yellow squash or one medium butternut squash), Cut in half lengthwise

• 1/2 small onion (chopped)

• 1/2 green bell pepper (chopped)

 • 1 avocado (optional)

• 1/2 cup salsa (homemade: put 1 medium tomato, 2 cloves of garlic, 1/2 tbsp of cilantro, 1/2 a lemon freshly squeezed, 1/4 cup of onion and 1/2 tsp jalapeño (optional) into a food processor)


• 15 oz can of salt-free tomato sauce (or substitute put 2 medium tomatoes in food processor)


• 15oz  of boiled garbanzo beans (or substitute black beans or pinto beans)

• 1/2 cup quinoa


• 1 tsp garlic powder
• 1 tsp cumin
• 1 tsp chili powder
• 1 tsp paprika
• 1/2 tsp oregano


• 1/4 cup of water

Cooking Directions:

• Zucchini, Alternative Yellow Squash: Bring a large pot of water to boiling (no need to add salt or oil), preheat oven to 400°F, halve the zucchini or yellow squash, take a spoon and hollow out the center of the zucchini or yellow squash (leaving a 1/4 inch thick shell on each side), chop the scooped out flesh and place it into a medium sauce pan, once the water is boiling place zucchini or yellow squash in the water for 1 minute. Then take a large baking pan, put the salsa in the bottom and place the zucchini or yellow squash on top inside facing up, add ingredients from sauce pan (see below), cover with foil and bake for 20 minutes.

• Alternative Butternut Squash: Preheat oven to 400°F, fill a large backing pan 1/2 way with water, halve the butternut squash, take a spoon to clean and throw out seeds, and place the halved butternut squash inside facing down in pan, cook until soft (30-45 minutes). Take the butternut squash  out of the oven, put halves on a plate, drain the water out of the pan, place 1/2 cup salsa on bottom of pan, place butternut squash into pan inside facing up, add ingredients from sauce pan (see below), cover with foil and bake for 20 minutes.

• In a medium sauce pan add all the spices, tomato sauce, water, beans, quinoa, onion, green pepper and if applicable flesh from zucchini or yellow squash. Cook on medium/ medium high for 10-15 minutes.

• Use a spoon, fill in the hollow zucchini or yellow squash or butternut squash.

Let it cool down and add avocado (optional) for both the zucchini and butternut squash


A special thanks to Melissa F. from Denver, Co for her contribution to our blog with this recipe!

Peripheral Artery Disease is a silent killer. The Western diet contributes to significant plaque buildup in your arteries which can eventually cause a stroke, heart attack, and death. Call Dr. Uri Ben-Zur to schedule an appointment and talk about ways we can partner for your vascular health. No one knows more about cardiology and peripheral artery disease than Dr. Ben-Zur. We look forward to meeting you and joining our family.

Peripheral vascular disease is a disease of the arteries of the body other than the arteries in the heart or the brain and affects about 8% of the population. The most common area of peripheral vascular disease occurs in the legs. Just as in atherosclerosis of the heart vessels leading to coronary artery disease, the arteries of the leg can become clogged with cholesterol and make it difficult for blood to travel to those tissues of the leg.


Image shows an artery of the leg clogged with plaque. This makes it difficult for blood to reach the lower leg.


Peripheral artery disease usually affects people over the age of 60. However, there are several risk factors:

  • Smoking
  • High Blood Pressure
  • Atherosclerosis
  • Diabetes
  • High Cholesterol
  • Age over 60
  • African American or Hispanic Race


Prevalence of PAD (%) by age group (years)




The most common symptom of PAD is called claudication. Claudication refers to pain in the leg upon exertion that goes away after rest. It is important to note however, that 40% of individuals with PAD do not experience any leg pain at all. Pain can also be found in the buttock, hip, or thigh upon exertion. Physical signs in the leg that may indicate peripheral arterial disease include muscle atrophy, hair loss, smooth shiny skin, skin that is cool to the touch especially if accompanied by pain while walking (which is relieved by stopping walking), decreased or absent pulses in the feet, non-healing ulcers or sores in the legs or feet, and cold or numb toes.

Preventing PAD

  • Physical activity and exercise are important for preventing PAD and for improving symptoms of PAD.
  • Avoid use of tobacco—smoking increases the risk of PAD by 2-6 times and it worsens the symptoms of PAD.
  • Control high blood pressure, cholesterol, and diabetes.
  • Supervised exercise training programs can improve and prolong walking distance in individuals with PAD.

Diagnosis and Treatment of PAD:

In patients with symptoms of PAD, the ankle-brachial index (ABI) is a non-invasive test that measures the blood pressure in the ankles and compares it with the blood pressure in the arms at rest and after exercise. Imaging tests such as ultrasound, magnetic resonance angiography (MRA), and computed tomographic (CT) angiography can provide additional information in diagnosing PAD.


  • Individuals with PAD are at risk for developing coronary artery disease and cerebrovascular disease, which could lead to a heart attack or stroke.5
  • Aspirin or other similar anti-platelet medications may prevent the development of serious complications from PAD and associated atherosclerosis.3,5
  • All efforts must be made to stop smoking.
  • Severe cases may require surgery to bypass blocked arteries.


References and further reading:


No one in Los Angeles has more experiences with pacemakers than Dr. Uri-Ben-Zur. If you feel faint or dizzy at all, please make an appointment to see us today at the Cardiovascular Institute of Greater Los Angeles.


Task Force of the American College of Cardiology indications for Pacemakers:

Guidelines for pacemakers have been established by a task force formed by the American College of Cardiology. There are two major reasons for permanent pacemaker insertion: patients with symptoms stemming from an arrhythmia and the location of the abnormality

Patients need to have symptoms correlated with an arrhythmia. For instance, a correlation between bradyarrhythmias with the symptoms of dizziness, syncope, shortness of breath and confusion must be established. In addition, the location of the abnormality needs to be considered. Pacemakers are indicated for individuals with conduction abnormalities at the AV node or below.

Class I — The following conditions represent severe conduction disease and are generally considered to be class I indications for pacing:

  • Complete (third-degree) AV block
  • Advanced second-degree AV block (block of two or more consecutive P waves)
  • Symptomatic Mobitz I or Mobitz II second-degree AV block
  • Mobitz II second-degree AV block with a widened QRS or chronic bifascicular block, regardless of symptoms
  • Exercise-induced second- or third-degree AV block (in the absence of myocardial ischemia)

Sinus bradycardia in which symptoms are clearly related to the bradycardia (usually in patients with a heart rate below 40 beats/min or frequent sinus pauses). (Sick Sinus Syndrome)

  • Symptomatic chronotropic incompetence.



Class II — Patients with less severe forms of acquired AV block may still benefit from pacemaker placement. In such patients, determinations are often based upon correlation of bradycardia with symptoms, exclusion of other causes of symptoms, and uncommonly based on results of electrophysiology (EP) testing.

Conditions in which pacemaker placement can be considered include the following:

  • Asymptomatic Mobitz II second-degree AV block with a narrow QRS interval; patients with associated symptoms or a widened QRS interval have a class I indication for pacemaker placement.
  • First-degree AV block when there is hemodynamic compromise because of effective AV dissociation secondary to a very long PR interval.
  • Bifascicular or trifascicular block associated with syncope that can be attributed to transient complete heart block, based upon the exclusion of other plausible causes of syncope, even if syncope isn’t correlated with AV block (specifically ventricular tachycardia)
  • Sinus bradycardia (heart rate <40 beats/min) in a patient with symptoms suggestive of bradycardia, but without a clearly demonstrated association between bradycardia and symptoms.
  • Sinus node dysfunction in a patient with unexplained syncope.
  • Chronic heart rates <40 beats/min while awake in a minimally symptomatic patient.
  • A less distinct group of patients with sinus bradycardia of lesser severity (heart rate >40 beats/min) who complain of dizziness or other symptoms that correlate with the slower rates.


  1. Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. Circulation 2008; 117:e350.
  2. Tracy CM, Epstein AE, Darbar D, et al. 2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. [corrected]. Circulation 2012; 126:1784.
  3. Vardas PE, Auricchio A, Blanc JJ, et al. Guidelines for cardiac pacing and cardiac resynchronization therapy. The Task Force for Cardiac Pacing and Cardiac Resynchronization Therapy of the European Society of Cardiology. Developed in collaboration with the European Heart Rhythm Association. Europace 2007; 9:959.
  4. Birnie D, Williams K, Guo A, et al. Reasons for escalating pacemaker implants. Am J Cardiol 2006; 98:93.
  5. Hayes DL, Barold SS, Camm AJ, Goldschlager NF. Evolving indications for permanent cardiac pacing: an appraisal of the 1998 American College of Cardiology/American Heart Association Guidelines. Am J Cardiol 1998; 82:1082.
  6. Recommendations for pacemaker prescription for symptomatic bradycardia. Report of a working party of the British Pacing and Electrophysiology Group. Br Heart J 1991; 66:185.
  7. Zeltser D, Justo D, Halkin A, et al. Drug-induced atrioventricular block: prognosis after discontinuation of the culprit drug. J Am Coll Cardiol 2004; 44:105.
  8. Scheinman MM, Peters RW, Suavé MJ, et al. Value of the H-Q interval in patients with bundle branch block and the role of prophylactic permanent pacing. Am J Cardiol 1982; 50:1316.
  9. Dhingra RC, Wyndham C, Bauernfeind R, et al. Significance of block distal to the His bundle induced by atrial pacing in patients with chronic bifascicular block. Circulation 1979; 60:1455.
  10. European Heart Rhythm Association, Heart Rhythm Society, Zipes DP, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol 2006; 48:e247.

Groh WJ. Arrhythmias in the muscular dystrophies. Heart Rhythm 2012; 9:1890.

What is an ICD?

An ICD (implantable cardioverter defibrillator) is an electronic device that is designed to monitor your heart rate and rhythm. If your heart beats with a very fast or very slow rate in an abnormal pattern, an electrical jolt is delivered to the heart muscle to restore normal rate and rhythm. The implantable device originated from the use of external defibrillators that shocks the heart with leads on the skin. 


Why is an ICD needed? 

Ventricular tachycardia or VT (incredibly fast heart beats) and ventricular fibrillation or VF (unproductive fluttering of the heart) are two life-threatening heart rhythms that cause the heart to beat very fast. These conditions can lead to sudden cardiac death (SCD) if not treated immediately.

If you have experienced at least one of these arrhythmias or your heart has other underlying risk factors for heart disease you are at a high risk having future occurrences of these arrhythmias that can lead to SCD. Your doctor will recommend ICD in order to prevent potential SCD.

Who needs an ICD? 

  • Had a prior episode of sudden cardiac arrest
  • Had a prior episode of ventricular fibrillation
  • Had at least one episode of ventricular tachycardia
  • Had a prior heart attack and have an increased risk for sudden cardiac arrest or sudden cardiac death
  • Have hypertrophic cardiomyopathy


Who is not a good candidate for an ICD?

  • Patients with ventricular tachyarrhythmias due to a completely reversible disorder in the absence of structural heart disease (eg, electrolyte imbalance, drugs, or trauma).
  • Patients who do not have a reasonable expectation of survival with an acceptable functional status for at least one year, even if they otherwise meet ICD implantation criteria.
  • Patients with incessant ventricular tachycardia (VT) or ventricular fibrillation (VF).
  • Patients with significant psychiatric illnesses that may be aggravated by device implantation or that may preclude systematic follow-up.
  • Patients with syncope without inducible ventricular tachyarrhythmias and without structural heart disease.



Cleveland Clinic – Implantable Cardioverter Defibrillator (Cleveland Clinic)

General principles of the implantable cardioverter-defibrillator (UptoDate) source=machineLearning&search=Implantable+Cardioverter+Defibrillator&selectedTitle=1%7E150&sectionRank=1&anchor=H2#H179461098

Hypertension: The silent killer

What is hypertension? Hypertension is high blood pressure. Blood pressure is the pressure of blood against the walls of the arteries. The higher the blood pressure, the harder it is for the heart to pump blood against such pressure. This fatigues the heart and causes it to become larger and more muscular in order to accommodate the increased work load and eventually fail over time. In addition, the arteries can become damaged from the increased pressure, rupture, and cause debilitating and often fatal strokes. Lastly, hypertension can cause organs in your body to become deprived of blood and lead to irrevocable damage to that organ and sometimes death. Hypertension is known as the silent killer because most people who have hypertension feel fine and have no symptoms at all. Yes, you could have severe hypertension for years and not even know it.  This is why it is critical to contact your physician and schedule at least two blood pressure readings to find out if you have hypertension and receive the appropriate treatment. Despite the fact that symptoms are not often present, there are a few symptoms to watch out for:

  • Headaches
  • Anxiety
  • Shortness of breath

What is your blood pressure? Here are examples of ideal and pathological blood pressures:

Normal blood pressure: systolic <120 mmHg and diastolic <80 mmHg

•Prehypertension: systolic 120 to 139 mmHg or diastolic 80 to 89 mmHg

•Stage 1 hypertension: systolic 140 to 159 mmHg or diastolic 90 to 99 mmHg

•Stage 2 hypertension: systolic ≥160 or diastolic ≥100 mmHg

•Isolated systolic hypertension: blood pressure of ≥140/<90 mmHg

•Isolated diastolic hypertension: blood pressure <140/≥90 mmHg

•Malignant hypertension: severe hypertension with retinal hemorrhages, exudates, or papilledema, with or without hypertensive encephalopathy

•Hypertensive urgency: severe hypertension (diastolic pressure >120 mmHg) in asymptomatic patients

•Definitions based upon ambulatory or home blood pressure measurements are somewhat different





Lowering Blood Pressure:

Medication may be necessary to help control your hypertension. I will discuss medical treatments later in this blog. However, here are a few things you can do to lower your blood pressure.

  1. Lower your salt intake. Salt increases blood pressure. Here is why: Salt is made of one sodium molecule and one chloride molecule. These molecules act as a magnet due to their different charges. Water has both a positive and a negative pole and has an attraction for the sodium in salt. Therefore, where sodium goes, water follows it like a magnet. When you eat salt, your body holds on to extra water and it enters the blood. This process increases your blood volume and more blood equals more blood pressure against the walls of your arteries.
  2. Exercise regularly. Of course it is important that you consult your physician before engaging in an exercise program to determine if you are healthy enough and do not already have dangerously high hypertension. Exercise increases blood pressure and can be a fatal cocktail with exercise. In addition, lifting weights and other static exercises can increase blood pressure. Your physician will advise you on the best strategy to lower your blood pressure. The American Heart Association recommends the following if your doctor deems fit:
  • For most healthy people, get the equivalent of at least 150 minutes (2 hours and 30 minutes) per week of moderate-intensity physical activity, such as brisk walking.
  • If you need to lower your blood pressure or cholesterol, aim for 40 minutes of moderate to vigorous physical activity 3 to 4 times per week.
  • You can incorporate your weekly physical activity with 30 minutes a day on at least 5 days a week.
  • Physical activity should be performed in episodes of at least 10 minutes, and preferably, it should be spread throughout the week.
  • Include flexibility and stretching exercises.
  • Include muscle strengthening activity at least 2 days each week.
  1. Lose fat weight. There is muscle and lean body weight and there is fat weight. Obesity increases blood pressure by a proposed set of complicated hormonal pathways. Losing weight has been proven to lower blood pressure. Eating less total calories per day and exercising will help to lose fat.
  2. Reduce alcohol consumption
  3. Avoid caffeine


What are some other causes of hypertension?

Sleep Apnea:

Sleep apnea is a disease in which an individual does not breathe adequately at night. This leads to a state of hypoxia (not enough oxygen). When the body does not ventilate adequately, carbon dioxide builds up in the body which is acidic. The body tries to balance the ph by absorbing a basic compound called bicarbonate (HCO3-). This takes place in the kidneys but in order to absorb bicarbonate, water must be accompanied with it (that’s just how it is, we didn’t invent kidneys). Remember how if we have more water in our body, it enters the blood stream and increases blood volume? More blood volume equals more blood pressure.  In addition, a hypercapnic (high levels of carbon dioxide) induce blood vessels to constrict. If the arteries have less area, then blood pressure increases. The same amount of blood has to travel through a smaller vessel (Pressure = Force/Area). Hypertension due to sleep apnea needs to be controlled with medication. Fixing sleep apnea with a CPAP does little to correct blood pressure.


Hyperaldostronism is a disease where the body secretes too much aldosterone. Aldosterone is a chemical that causes the reabsorption of sodium and water in the kidney. This increases blood volume, thus pressure.  Hyperaldostronsim causes the body to lose potassium. Therefore, specific medication that prevents further loss of potassium while ridding the body of sodium is necessary to control this problem. In some instances, surgery may be needed to correct the problem.

Cushings  Disease:

Cushing’s Disease is a disease in which the body produces too much cortisol. There is a difference between Cushing’s disease and Cushing’s syndrome. However, that is beyond the scope of this blog. For now just remember that cortisol increases blood pressure and is treated surgically.

Renal Artery Stenosis:

Renal Artery Stenosis occurs when the arteries that supply the kidneys have an area of stenosis unilaterally or bilaterally. Since all blood flows through the kidneys to be filtered, when the arteries become stenosed, the flow of blood is hindered and increases the blood pressure against the walls of the capillaries. Renal artery stenosis is usually suspected after numerous medial trials have failed.

Medication as cause:

There are a vast number of medications that can induce hypertension in an individual. Your physician will work with you on finding the right medication schedule in order to minimize hypertension and discuss strategies.


A growing number of people are taking compounds like testosterone, Human Growth Hormone, Insulin-like Growth Factor (IGF-1), and pre-workout supplements. These substances are extremely dangerous. Testosterone cause increased blood pressure and arterial tone, human growth factor can cause the heart to become more muscular and less effective at pumping blood-this is lethal, and pre-workouts contain substances that activate the sympathetic nervous system and cause arteries to constrict (which increases blood pressure). In addition, pre-workouts cause the heart to work even harder against higher pressures. Eventually, the heart will fatigue and fail prematurely.  Always be forthcoming with your physician about drugs and compounds that you are taking. Your physician has a confidentiality agreement with you and cannot disclose such activity. Your physician cares about you and just wants to be able to serve you better.


Medications that treat hypertension:

Thiazide diuretics- (water pills): Thiazide diuretics act on the kidney to excrete sodium. Remember, where sodium goes, water goes. These pills reduce water in the body thus, reduce blood volume and pressure.

Loop Diuretics- (furosemide, Lasix): Loop diuretics are powerful diuretics that block sodium, potassium, and chloride from entering the body in excess. Water is attracted to these molecules so blocking them also blocks water from entering the body and reduces blood volume and pressure.

Potassium sparing diuretics (spironolactone, triamterene): These diuretics block the aldosterone receptor and hold on to potassium. This drug is used in special cases such as hyperaldostronism and often sleep apnea.

ACE Inhibitors- (lisinopril, “prils”): These drugs block an enzyme that converts a series of compounds from causing an increase in water volume and constriction of the blood vessels. These medications are particularly useful in diabetics and have been shown to prevent diabetic damage to kidneys.

ARB’s (losartan, “sartans”): These drugs block a compound called angiotensin from binding to their receptors and causing vasoconstriction (constriction of the arteries).

Carbonic anyhydrase inhibitors: (acetazolamide): These drugs block carbonic anhydrase in the kidney and are used for mountain sickness but have a weak effect on total water loss so they are not commonly used.

Alpha 2 agonists (clonidine): Inhibits sympathetic outflow which causes vasodilation which widens the lumen of the artery thus decreasing pressure

Beta blockers (atenolol, “olol’s”): These drugs act in numerous ways which your physician can discuss. There are several varieties that work on different beta and also alpha receptors.

Calcium Channel blockers: These drugs have two subclasses and numerous effects. Please discuss these medications with your physician for more information.

Please join our blog! We want to hear from you and discuss your individual concerns and experiences. We welcome patients, students, and physicians.

What do you know about cholesterol?

Dyslipidemia (or high cholesterol) means that an individual has an overabundance of lipids (fats) in their bloodstream. This is important because high cholesterol levels are linked to an increase in cardiovascular disease and obesity. Cardiovascular disease associated with high cholesterol are due to atherosclerosis or hardening of the arteries that takes place when cholesterol is deposited into the lumen of arteries and begins to limit blood flow to organs of the body. The arteries become more and more occluded over time until the artery can no longer supply an organ with the blood that it needs. This can lead to heart attacks (myocardial infarctions) or even stroke or death.


Image shows as cholesterol plaque grows, it gets harder for blood to pass through.


It is important to contact your physician for regular visits to see if you are an at risk patient for high cholesterol. Patients that are in high risk groups should be screened regularly based on the American Heart Association and The American College of Cardiologists guidelines. Any person over the age of two years old who is in a at risk group should see their physician in order to make sure their cholesterol levels are within healthy levels.

Who is at risk? Major risk factors include:

  • Advancing age
  • High total cholesterol levels
  • High LDL
  • High triglyceride levels
  • Established coronary artery disease (CAD)
  • Family history of CAD
  • Presence of hypertension
  • Presence of diabetes mellitus
  • Smoking
  • Obesity
  • Family history
  • Elevated apo B
  • High C-reactive protein
  • Polycystic Ovarian Syndrome
  •  Hyperhomocysteinemia
  • hyperuricemia

Cholesterol is an essential fat that is used to make hormones and is integral in maintaining the integrity of cell membranes. The body makes cholesterol and it is also found in foods like:

  • Animal fats
  • Cheese
  • Egg yolks
  • Shell fish
  • Breast milk

Doctors use three different measures to determine lipid balance:

  1. LDL-Low Density Lipoprotein (bad cholesterol) the higher your LDL level, the higher your risk for cardiovascular disease and plaque formation.
  2. HDL-High Density Lipoprotein (good cholesterol) HDL removes bad cholesterol throughout your body and returns it to your liver so that it can be removed from your body. High HDL is protective and low HDL is linked to cardiovascular disease.
  3. Triglycerides-Fat in the blood. This is the fat that you eat mostly from plant oils and animal fats. Increased triglyceride levels increase the risk of cardiovascular disease by contributing to atherosclerotic plaque formation.

The American Heart Association and American College of Cardiology determine what healthy cholesterol levels are. The table demonstrates the general guidelines of the different types of cholesterols:



While lifestyle and dietary changes like exercise and healthy eating are paramount, medical treatment has been found to be very effective in controlling high cholesterol. Avoid foods like the ones mentioned earlier and exercise regularly if deemed fit by your physician. Some medical treatments available are as follows. Remember, your physician is the only person that can prescribe the correct drug and correct dosage for you based on your own individual blood work: Refer to the pathway below for statin drugs that act by blocking HMG-CoA


  • Statins– (atorvastatin, etc.): Statins act by competitively inhibiting HMG-CoA reductase, the first and key rate-limiting enzyme of the cholesterol biosynthetic pathway. Statins mimic the natural substrate molecule, HMG-CoA, and compete for binding to the HMGCR enzyme. This competition slows the rate of mevalonate production, the next molecule in the serial steps to produce cholesterol. Hence, in the presence of statins, the precursor HMG-CoA is not efficiently processed forward to produce mevalonate, blocking the pathway.
  • Fibrates-(Gemfibrozil): activators of the peroxisome proliferator-activated receptor-α (PPARα) in liver and muscle. In the liver this leads to increased β-oxidation of fatty acids (breakdown), thereby decreasing the liver’s secretion of triacylglycerol- and cholesterol-rich VLDLs, as well as increased clearance of chylomicron remnants, increased levels of HDLs and increased lipoprotein lipase activity which in turn promotes rapid VLDL turnover.
  • Niacin-Nicotinic acid:reduces the plasma levels of both VLDLs and LDLs by inhibiting liver VLDL secretion, as well as suppressing the flux of free fatty acid (FFA) release from adipose tissue by inhibiting lipolysis (fat breakdown). In addition, nicotinic administration strongly increases the circulating levels of HDLs. HOWEVER, do not use without contacting your physician first because niacin can cause flushing which can be extremely uncomfortable.
  • Resins-( Cholestyramine or colestipol):These compounds are non-absorbable resins that bind bile acids which are then not reabsorbed by the liver but excreted. The drop in hepatic reabsorption of bile acids releases a feedback inhibitory mechanism that had been inhibiting bile acid synthesis. As a result, a greater amount of cholesterol is converted to bile acids to maintain a steady level in circulation. Additionally, the synthesis of LDL receptors increases to allow increased cholesterol uptake for bile acid synthesis, and the overall effect is a reduction in plasma cholesterol. This treatment is ineffective in homozygous FH patients, since they are completely deficient in LDL receptors.
  • Ezetimibe: This drug is sold under the trade names Zetia® or Ezetrol® and is also combined with the statin drug simvastatin and sold as Vytorin® or Inegy®. Ezetimibe functions to reduce intestinal absorption of cholesterol, thus effecting a reduction in circulating cholesterol.

Latest Research from Up-To-Date:

Specific results from some of the trials of statins include:

●The Scandinavian Simvastatin Survival Study (4S) of patients with hyperlipidemia (baseline plasma total cholesterol levels between 212 and 309 mg/dL [5.5 and 8.0 mmol/L]) found that simvastatin therapy versus placebo for 5.4 years resulted in statistically significant reductions in total mortality (8 versus 12 percent), major coronary events (19 versus 28 percent), CHD deaths (42 percent reduction), revascularization procedures (CABG or coronary angioplasty, 37 percent reduction), and fatal plus nonfatal cerebrovascular events (2.7 versus 4.3 percent)

●The CARE trial treated patients with average cholesterol levels (mean serum total cholesterol concentration of 209 mg/dL [5.4 mmol/L]) with pravastatin (40 mg before sleep) or placebo [5]. At five years, benefits with pravastatin compared with placebo included significant reductions in the combined incidence of coronary death and nonfatal MI (10.2 versus 13.2 percent, p = 0.003), the need for revascularization (14.1 versus 18.8 percent, p<0.001), and the frequency of stroke (2.6 versus 3.8 percent, p = 0.03). The benefits were more apparent among women, older patients (above age 60), and pretreatment serum LDL-C above 125 mg/dL (3.2 mmol/L).

●More recently, the Heart Protection Study randomly assigned 20,536 subjects to simvastatin (40 mg/day) or placebo: 33 percent had baseline LDL-C <116 mg/dL (<3 mmol/L), 25 percent had a level of 116 to 135 mg/dL (3 to 3.5 mmol/L), and 42 percent had levels >135 mg/dL (>3.5 mmol/L) [13]. Entry criteria included a history of cardiovascular disease (coronary cerebrovascular or peripheral vascular disease), diabetes mellitus, or treated hypertension. Thus, most patients were treated for secondary prevention.

After an average follow-up of 5.5 years, there were significant reductions in all-cause mortality (12.9 versus 14.7 percent; relative risk reduction [RRR] 13 percent), deaths from heart disease or related blood vessel disease (7.6 versus 9.1 percent; RRR 17 percent), and major cardiovascular events (19.8 versus 25.2 percent; RRR 24 percent). The percent reduction in events was similar in the three tertiles of baseline LDL-C (the lowest being <116 mg/dL [<3 mmol/L]) and was also similar in those with a baseline LDL-C below 100 mg/dL (2.6 mmol/L).


When blood flow to the brain is momentarily dropped, a person can briefly lose consciousness and lose control over one’s posture. Syncope is physiologically related to abrupt decrease in blood pressure, heart rate, and blood volume and distribution. To correctly diagnose the cause of syncope your doctor will run a thorough review of your heart, blood circulations, and nervous system.



Prior to the actual syncopal episode certain symptoms also called premonitory symptoms manifest. Patients with past syncopal experience can recognize these symptoms and sit down or lie down with their feet up to anticipate and prevent passing out.


Syncopal symptoms

“dizziness, drowsiness, grogginess, light-headedness, “blacking out,” falling for no reason, feeling weak when standing

If you’ve experienced syncope with any of the above symptoms you should visit a doctor to find out any underlying medical conditions. Most patients with syncope can recover with proper treatment.


Types of syncope

(1) Vasovagal syncope

Vasovagal syncope is the most common type of syncope. When a you stand up a big portion of your blood moves below the diaphragm towards the lower part of your body due to gravity. With less blood returning to the heart, blood pressure is registered as reduced and the heart will compensate by raising the sympathetic response. The central nervous system will respond through vasovagal nerves to reduce this heightened “fight or flight” response by reducing the blood pressure (hypotension) and slowing the heart rate (bradycardia) which result in syncope.


(2) Situational syncope

Situational syncope is also a type of vasovagal syncope. The vasovagal response is triggered through particular kinds of situations related to physiological changes such as dehydration or hunger, intense emotions such as stress or fear, and use of substance such as alcohol or drugs. Some more extreme situations that cause panic attacks can cause you to hyperventilate (breathing too fast or too deeply that brings in too much oxygen expels carbon dioxide too quickly) can also lead to syncope. Other stimuli include forceful coughing, urinating (micturition syncope), and turning the neck or wearing a tight collar (carotid sinus hypersensitivity).

(3) Cardiac syncope

When there is an abnormality directly on the heart or blood vessel that prevents proper blood flow to the brain you can lose consciousness which is called cardiac syncope. You can have cardiac syncope when there are abnormal heart rhythm (arrhythmia), obstructed blood flow in the heart or blood vessels, valve disease, aortic stenosis, blood clot, or heart failure.

(4) Neurologic syncope

Neurological condition such as seizure, stroke, transient ischemic attack (TIA), and psychiatric symptoms can lead to loss of consciousness as well.

A good majority of the syncope cases ranging from 18 to 41 % depending on the clinical studies reported causes to be unknown. 

Evaluation of syncope patients

Initially a physician should identify presence of any life threatening causes and apply stabilizing management if necessary while finding a more thorough diagnoses and treatment plan. The emphasis should be doing a careful history taking and physical examination focusing on vital signs and the neurologic and cardiac examination. Concurrently any external or internal secondary injuries from fall should be identified especially in the head (i.e. subdural hematoma), wrist, or hip. 

After the initial evaluation additional tests are recommended.

  • Carotid sinus massage in patients >40 years old
  • Echocardiogram when there is previous known heart disease or data suggestive of structural heart disease or syncope secondary to cardiovascular cause.
  • Orthostatic challenge (lying to standing orthostatic test or head-up tilt testing) when syncope is related to the standing position or there is suspicion of a reflex mechanism.
  • Other less specific tests such as neurologic evaluation or blood tests are indicated only when there is suspicion of nonsyncopal transient loss of consciousness.


Treatment of syncope patients

Treatment is based upon addressing the underlying cause of syncope and prevention of recurrence.

  • Metabolic disorders — Low blood sugar (hypoglycemia) or low blood oxygen state (hypoxemia) have potential to cause syncope. Metabolic abnormalities, anemia, and hypovolemia can be effectively managed by specific therapy to correct these abnormalities.
  • Iatrogenic syncope — Iatrogenic syncope resulting from drug therapy is a preventable and treatable condition. It is especially common in elderly patients and those with coexisting chronic diseases, and diminished or blunted cardiovascular reflexes. In this setting, effective interventions include the elimination of the offending agent, substitution of an alternative agent, changing the dose, or altering the timing of drug administration.
  • Orthostatic hypotension — Identifying the underlying cause is crucial to appropriate treatment of orthostatic hypotension. Orthostatic hypotension associated with evidence of volume depletion should be treated with volume expansion and avoidance of precipitating factors (such as diuretic use). Orthostatic hypotension in the absence of volume depletion is most often due to an autonomic neuropathy or the administration of antidepressant drugs.
  • Cardiovascular disease with obstruction — Cardiac diseases that obstruct the outflow of blood generally require surgical correction or attenuation of the obstruction. As an example, aortic valve replacement for aortic stenosis will alleviate symptoms, prevent syncope, and prolong survival.Dynamic outflow obstruction resulting from hypertrophic cardiomyopathy is treated pharmacologically with beta blockers or calcium channel blockers. Refractory obstructive symptoms may be treated with nonpharmacologic methods such as septal myectomy or septal ablation. The cause of syncope in such patients may be due to undiagnosed ventricular arrhythmias that may increase the risk of death and may require therapy with an implantable cardioverter-defibrillator (ICD).
  • Implantable cardioverter-defibrillator therapy — ICD therapy is indicated in patients with who have syncope that is due to potentially life-threatening ventricular tachycardia that is otherwise not treatable. ICD therapy should also be considered for patients who have syncope due to an unknown cause but have underlying structural heart disease that places them at risk of sudden cardiac death.



  • Cleveland Clinic – Syncope (Cleveland Clinic)
  • Approach to the adult patient with syncope in the emergency department (UptoDate)
  • Evaluation of syncope in adults (UptoDate)
  • Management of the patient with syncope (UptoDate)


An understandable guide to chest pain and why it should not be ignored.


Image from:

When experiencing chest pain the first thing that comes to mind is heart attack. However, there are numerous causes of chest pain. In fact, as much as a quarter of the U.S. population experiences chest pain that is not related to the heart. Chest pain may also be caused by problems in your lungs, esophagus, muscles, ribs, vasculature, and even nerves. Although not every cause of chest pain is from the heart, some of the other sources of chest pain can be life-threatening as well. For this reason, it is very important to see your doctor immediately about any chest pain that you have experienced.



Angina and Heart Attack:

What is a heart attack? A heart attack is when the blood supply to the heart becomes compromised. The heart needs oxygen in order to pump oxygen-rich blood to your body so when an artery that supplies your heart becomes blocked (often from atherosclerosis), the heart is not getting the blood it needs to function properly. This is called ischemia-tissue that is deprived of oxygen. This can eventually lead to infarction, which is death of the heart tissue.Chest tightness or pressure that radiates down the left arm is the most common presentation. However, it is extremely important to note that not everyone experiences heart attacks the same way so it is critical to see your doctor for any chest pain.


Image shows dead or infarcted heart tissue after an occlusion due to an atherosclerotic plaque. Image courtesy of:


Risk factors for heart attack include:

  1. High cholesterol
  2. Hypertension
  3. Diabetes
  4. Genetic predisposition
  5. Smoking


This image shows normal heart vasculature on the left and the same heart with an occluded vessel on the right.


Image shows inside of an occluded vessel in the heart. This occlusion is the result of atherosclerotic plaque. This is known as coronary artery disease. The red blood cells are unable to get through the vessel resulting in a heart attack. Image from:



Medicine and often surgery are needed to re-establish blood flow to the heart. Your cardiologist will use a special balloon to open the area of stenosis or attach a nearby artery to the blocked artery to restore blood flow.



Pulmonary Embolism

A pulmonary embolism is a blood clot that usually forms in the legs that has reached the lungs and occluded a vessel inside of the lung. The occlusion inhibits blood from reaching the lung. Moreover, when the lung is compromised in this manner, the rest of the body can be deprived of oxygen-rich blood that it needs in order to function. This can result in permanent damage to the lung tissue, damage to other organs in your body, and low oxygen circulation in your blood. Chest pain and shortness of breath are commonly associated with this condition.






Image: A blood clot forming at the distal femur  (A) and a blood clot and lung vasculature (B). Images from:


Risk factors for a pulmonary embolus include:

  1. Prolonged sedentary state (long flights, being bedridden, sitting on couch).
  2. Recent surgery-especially hip surgery
  3. Birth control pill use
  4. Pregnancy
  5. Fractures
  6. Cancer

Image above shows a blood clot or pulmonary embolus trapped and occluding in the vein of the right lung. This occlusion can lead to ischemia (oxygen deprivation) and possible cell death.

Image above shows a blood clot or pulmonary embolus trapped and occluding a vein of the right lung. This occlusion can lead to ischemia (oxygen deprivation)of lung tissue and possible sudden death.  Image from:



Medicines known as blood thinners are used to treat pulmonary embolisms. Rarely, surgery may be indicated and a catheter will be placed into the vein in order to retrieve the clot or dissolve it on site. If necessary, a surgeon will put a filter into the femoral vein of the leg in order to catch any further clots.


Aortic Dissection:

The aorta is the biggest artery in the body.  It originates from the left ventricle and supplies virtually every part of the body with oxygenated blood.  A dissection is a tear of the innermost layer of tissue of the vessel.  This causes blood to flow into the middle layer of tissue and damages it causing it to become weak.  This is different from a ruptured aorta because there is not a hole in the vessel where blood can escape out.  Aortic dissection is often a surgical emergency that requires careful management. Aortic Dissection typically presents as a severe tearing pain that radiates to the back.

Image shows the two type A and one type B aortic dissection. In the DeBakey classification system, a type I dissection involves the entire aorta, while a type II dissection in­volves only the ascending aorta, and a type III dissection involves only the descending aorta. New staging systems that incorporate other aortic pathology have been devised, but are used primarily for research purposes.  Image from:

Image shows the two type A and one type B aortic dissection.In the DeBakey classification system, a type I dissection involves the entire aorta, while a type II dissection in­volves only the ascending aorta, and a type III dissection involves only the descending aorta. New staging systems that incorporate other aortic pathology have been devised, but are used primarily for research purposes.  Image from:


Image shows the tear in the aorta is between the tunica intima (closest to the vessel lumen) and the tunica media (which is the middle layer of the artery). The blood accumulates in between these two layers and will eventually grow larger and larger and eventually can rupture the aorta due to increasing pressure.  Image taken from:


Risk Factors for aortic dissection include:

  1. Hypertension
  2. Marfan Syndrome
  3. Ehlers-Danlos Syndrome
  4. Polycystic Kidney Disease
  5. Pregnancy
  6. Cocaine use


Treatment includes emergency surgery for type A and medical intervention for type B. For more information on Aortic Dissection, please see our blog page:



A very common cause of chest pain is GERD. GERD stands for gastroesophageal  Reflux Disease and is commonly known as heart burn. GERD occurs when stomach contents erupt through the esophagus. The pain from the stomach acid interacting with the lining of the esophagus can be confused with a heart attack.


Image shows the lower esophageal sphincter closed on the left and relaxed on the right allowing acid and stomach contents to travel upward through the esophagus. Image from:

Risk Factors:

  1. Obesity
  2. Smoking
  3. Pregnancy
  4. Diabetes
  5. Asthma
  6. Dry Mouth
  7. Wearing pants too tight in the waist
  8. Hiatal hernia
  9. Connective tissue disease like Scleroderma
  10. Drinking too much carbonated beverages
  11. Excessive use of ibuprofen


  1. Avoid risk factors if possible
  2. Antacids
  3. Histamine type II receptor antagonists (H2RA’s)
  4. Proton Pump Inhibitors
  5. Endoscopic treatments to strengthen the sphincter muscle
  6. Avoid spicy and fatty foods



A pneumothorax is commonly known as a collapsed lung. The lung is typically held against the chest wall by negative forces. However, due to trauma or spontaneous cause, the lung can become dislodged from the wall and collapse. Although typically seen in very tall and thin people, a pneumothorax can happen to anyone, especially in individuals with lung disease. A pneumothorax feels like a sudden sharp chest pain accompanied by a sudden shortness in breath.  Rarely, a tension pneumothorax can occur which is a medical emergency and must be treated immediately.


Image from:


Risk factors:

  1. Tall and think stature
  2. Asthma
  3. Any activity that may lead to trauma to the ribs
  4. Being male
  5. Smoking
  6. Being ages 20-40 years old
  7. Any lung disease-especially COPD
  8. Genetic  factors
  9. Mechanical ventilation
  10. A history of prior pneumothorax


Treatment Options:

A pneumothorax may go away on its own. However, if you have chest pain or think that you might have a pneumothorax, please see your doctor immediately or call 911. Typically, a physician will insert what is known as a chest tube into your pleural space. A pleural space is a small space between the lung and the chest wall that allows the lungs to move while breathing. The chest tube will be placed in the pleural space to decompress the area and restore negative pressure so that breathing and lung expansion return to normal. In rare cases where pneumothoraxes continue to occur, medical intervention may be needed to attach parts of the lung permanently to the chest wall to avoid further insults.

last pneumo

Image from:




Costochondritis refers to inflammation of sternum (breastbone) where the ribs attach. Most cases happen spontaneously with no explanation.  However, trauma, viral infection, heavy lifting, tumors, and arthritis can also cause these symptoms. Costochondritis presents with chest pain that typically hurts when a deep breath is taken. In addition, it also becomes tender when the sternum is touched on its sides.


Image shows the rib cartilage in blue that can become inflamed and feel like a heart attack. If you experience these symptoms, please see your doctor immediately or call 911.

Risk Factors:

Since most causes of this disease are unknown, the risk factors are unknown as well. It can be caused by heavy lifting so know your limitations.


  1. NSAID’s (Ibuprofen, Naproxen, etc.)
  2. Cortisol injection to affected area
  3. Bacterial causes should be treated with IV antibiotics and then followed by oral antibiotics for several weeks after.
  4. For costochondritis that does not resolve, surgery to remove the affected area may be warranted.


Pericarditis is typically caused by infection of the sac that surrounds the heart. This sac is called the pericardium, so when the sac becomes inflamed it is called pericarditis. Other causes for this inflammation are:

  • kidney failure
  • systemic lupus
  • cancer
  • heart attack
  • radiation
  • rheumatoid arthritis

The pain associated with pericarditis can cause shortness of breath and a sharp, intense pain that may radiate to the neck or arm. There may be pain in swallowing, coughing, and weakness and fatigue. A hallmark of this condition is that it is typically relieved when leaning forward and worsens while lying down. This condition can mimic many others so please consult your physician if you think you may have pericarditis. Pericarditis may present with nausea and even a fever and can lead to a more significant problem called cardiac tamponade. Cardiac tamponade is a condition in which the sac that surrounds the heart becomes so tight with fluid that it prevents blood flow from returning to the heart and requires surgery to drain this fluid.


Image from Nucleus Medical Media, Inc.

Risk Factors:

Risk factors include a weakened immune system or any of the reasons listed above.


  1. NSAID’s
  2. Corticosteroids
  3. Antibiotics for bacterial infection of the pericardium
  4. A pericardiocentisis may be needed to drain fluid from the pericardial sac


Always remember, it’s better to be safe than sorry. Always consult your physician if you have chest pain or dial 911.



Uri M. Ben-Zur, M.D., F.A.C.C. completed a residency in internal medicine and fellowships in interventional cardiology, clinical cardiology, and clinical electrophysiology.  He currently practices at the The Paulette Tashnek-Wagner Cardiovascular Institute of Greater Los Angeles located in Tarzana, CA.




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