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Monthly Archives: August 2014

Aortic Stenosis and Aortic Valve Replacement

Dr. Ben-Zur has been caring for and treating patients with aortic stenosis for over 20 years in the greater Los Angeles area. If you are experiencing any of these symptoms or just want to have a heart check-up, stop by Dr. Ben-Zur’s office today and join our family. We look forward to meeting you.

What is Aortic Stenosis?

Aortic  Stenosis occurs when  the aortic valve in the heart narrows and does not open fully. This can be caused either by a congenital condition, or by calcification of the valve.  Rheumatic fever (a condition caused by untreated strep throat infection) can also cause aortic stenosis. Symptoms can take a while to develop and may include: chest pain; fainting; feeling short of breath; feeling weak or overly tired, particularly with activity. Your Doctor may also tell you they noticed a heart murmur.

How is it Diagnosed?

Your Doctor will hear a heart murmur, and may than recommend an echocardiogram which shows moving pictures of your heart. Your Doctor will use that to determine how your heart is doing. Your Doctor may also require you to have other tests done.

What is the Treatment?

Aortic stenosis treatment depends on the severity of the condition and your symptoms. Treatment may include medications or surgery. If you do not have any symptoms you will see your Doctor regularly to check on your heart. If you do have symptoms, or tests show that the heart is not pumping well, you will need surgery.

What are Surgical Valve Replacement Indications?

The primary manifestations of severe aortic stenosis are: Chest pain; fainting; and heart failure. The median survival rate with onset of symptoms is 2 years, with a risk of sudden cardiac death. Therefore it is very important once it has been determined you require surgery to attend all appointments.  The aortic valve is replaced via a surgical procedure. The procedures done are Transcatheter Aortic Valve Replacement (TAVR) and Percutaneous Aortic Valvotomy. Percutaneous Aortic Valvotomy is used mainly in children and young adults. TAVR is primarily used in older adults and people deemed at high risk.

What Valves are Used?

There are two main types of valves used: Bioprosthetic and Mechanical. Both valves have similar survival benefits. Mechanical valves are used in younger patients because they are more durable, and there are studies that show bioprosthetic valves have a slight survival benefit in older patients. Mechanical valves will require life-long anticoagulation therapy, and are people that have them may be at a greater risk for bleeding.  If a person already has a mechanical valve in another position, or is already on lifelong anticoagulation therapy, it is recommended to receive a mechanical valve for Aortic valve replacement. Your Doctor can explain any questions or concerns you may have about Aortic Stenosis and its treatments.

References:

https://www.cardiosmart.org/Heart-Conditions/Aortic-Valve-Stenosis

http://www.heart.org/HEARTORG/Conditions/More/HeartValveProblemsandDisease/Problem-Aortic-Valve-Stenosis_UCM_450437_Article.jsp

good

“Polyunsaturated fats can have a beneficial effect on your heart when eaten in moderation and when used to replace saturated fat and trans fat in your diet.

What are polyunsaturated fats?

From a chemical standpoint, polyunsaturated fats are simply fat molecules that have one unsaturated carbon bond in the molecule, this is also called a double bond. Oils that contain polyunsaturated fats are typically liquid at room temperature but start to turn solid when chilled. Olive oil is an example of a type of oil that contains monounsaturated fats.

How do polyunsaturated fats affect my health?
Polyunsaturated fats can help reduce bad cholesterol levels in your blood which can lower your risk of heart disease and stroke. They also provide nutrients to help develop and maintain your body’s cells. Oils rich in polyunsaturated fats also contribute vitamin E to the diet, an antioxidant vitamin most Americans need more of.

Oils rich in polyunsaturated fats also provide essential fats that your body needs but can’t produce itself – such asomega-6 and omega-3 fatty acids. You must get essential fats through food. Omega-6 and omega-3 fatty acids are important for many functions in the body.

Are polyunsaturated fats better for me than saturated fats or trans fats?
Yes. While, all fats provide 9 calories per gram, monounsaturated fats and polyunsaturated fats can have a positive effect on your health, when eaten in moderation. The bad fats – saturated fats and trans fats – can negatively affect your health.

Which foods are high in polyunsaturated fats?
Most foods contain a combination of fats. Foods high in polyunsaturated fat include a number of plant-based oils, including:

  • soybean oil,
  • corn oil and
  • sunflower oil, as well as
  • fatty fish such as salmon, mackerel, herring and trout.

Other sources include some nuts and seeds such as walnuts and sunflower seeds, tofu and soybeans. The American Heart Association also recommends eating tofu and other forms of soybeans, canola, walnut and flaxseed, and their oils. These foods contain alpha-linolenic acid (ALA), another omega-3 fatty acid.

Are polyunsaturated fats lower in calories?

Polyunsaturated fats – like all fats – contain nine calories per gram.”

AHA Recommendation

For good health, the majority of the fats that you eat should be monounsaturated or polyunsaturated. Eat foods containing monounsaturated fats and/or polyunsaturated fats instead of foods that contain saturated fats and/or trans fats.

 

fats101

Fats 101:

“Does my body need fats?
Yes, it does. Dietary fats are essential to give your body energy and to support cell growth. They also help protect your organs and help keep your body warm. Fats help your body absorb some nutrients and produce important hormones, too. Your body definitely needs fat.

How many different fats are there?
There are four major dietary fats in the foods we eat: saturated fatstrans fatsmonounsaturated fats andpolyunsaturated fats. The four types have different chemical structures and physical properties. The bad fats, saturated and trans fats, tend to be more solid at room temperature (like a stick of butter), while monounsaturated and polyunsaturated fats tend to be more liquid (like liquid vegetable oil).

Fats can also have different effects on the cholesterol levels in your body. The bad fats, saturated fats and transfats raise bad cholesterol (LDL) levels in your blood. Monounsaturated fats and polyunsaturated fats can lower bad cholesterol levels and are beneficial when consumed as part of a healthy dietary pattern.

Do all fats have the same number of calories?
There are nine calories in every gram of fat, regardless of what type of fat it is. Fats are more energy-dense than carbohydrates and proteins, which provide four calories per gram. 

Consuming high levels of calories – regardless of the source – can lead to weight gain or being overweight. Consuming high levels of saturated or trans fats can also lead to heart disease and stroke. Health experts generally recommend replacing saturated fats and trans fats with monounsaturated fats and polyunsaturated fats – while still maintaining a nutritionally-adequate diet.

Are all foods labeled “trans fat-free” healthy foods?
Not necessarily. Foods labeled “0 trans fat” or cooked with “trans fat-free” oils may contain a lot of saturated fats, which raise your bad cholesterol levels. “Trans fat-free” foods may also be unhealthy in terms of their general nutrient content. For example, baked goods also tend to be high in added sugars and low in nutrients.

Can fats be part of a healthy diet?
Eating foods with fat is definitely part of a healthy diet. Just remember to choose foods that provide good fats (monounsaturated and polyunsaturated fats) and balance the amount of calories you eat from all foods with the amount of calories you burn. Aim to eat a dietary pattern that emphasizes intake of vegetables, fruits, and whole grains; includes low-fat dairy products, poultry, fish, legumes, non-tropical vegetable oils and nuts; and limits intake of sodium, sweets, sugar sweetened beverages and red meats. Doing so means that your diet will be low in both saturated fats and trans fats.

Does eating more healthfully mean giving up my favorite foods?
A healthy diet can include the foods you love. You don’t have to avoid these treats entirely, but you do need to eat less of foods that are low in nutrition and high in calories.”

 

References:

http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/HealthyEating/Fats-and-Oils_UCM_304495_Article.jsp

 

What is Atrial Fibrillation (AF or AFib)? 

 

Atrial fibrillation is the most common irregular heart rhythm that starts in the atria. The normal route of heart beating would start with an the SA node (sinus node sending out singular pulses of electrical stimulus at a time which flows through a predetermined route towards AV node next and dispersing to the ventricles. 

With Afib, SA node does not predominate as the singular starting point of the impulse. The atria has many different impulses rapidly fire simultaneously, causing a very fast, chaotic rhythm in the atria.

Normal Sinus Rhythm

Normal Sinus Rhythm

Atrial Fibrillation

Atrial Fibrillation

With such disorganized electrical impulse, atria cannot contract and/or squeeze blood effectively into the ventricle.

The many erratic atrial impulses converge on the AV node which a few of them pass of through and the ventricles contract irregularly, leading to a rapid and irregular heartbeat. The rate of impulses in the atria can range from 300 to 600 beats per minute.

 

Risk Factors

In developed countries hypertensive heart disease and coronary heart disease (CHD) are the most common underlying disorders. Rheumatic heart disease, although now uncommon in developed countries, is associated with a much higher incidence of AF. 

 

Diagnostic Tests 

Electrocardiogram (ECG)

afibrhythm

The modality of choice is EKG. A typical EKG for atrial fibrillation would exhibit “irregularly irregular rhythm.” There are no identifiable P waves, irregular RR intervals are irregular and the baseline EKG is a collection of numerous tiny and erratic spikes.

TREATMENT

Physicians must decide on optimal treatments for anticoagulation, rate control, and rhythm control.

(1) Prevention of systemic embolization

Every patient with AF should be evaluated for the need of antithrombotic therapy to prevent systemic embolization. This has traditionally been accomplished by the application of the CHADS2 risk score.

Modifications of this scoring system have resulted in the CHA2DS2-VASc score, which is now the recommended strategy for stroke risk assessment.

anticoagulation

Score Risk Anticoagulation Therapy Considerations
0 Low None or Aspirin Aspirin daily
1 Moderate Aspirin, Warfarin, or other oral anti-coagulant Aspirin daily or raise INR to 2.0-3.0, depending on patient preference
2 or greater Moderate or High Warfarin or other oral anti-coagulant Raise INR to 2.0-3.0, unless contraindicated

(Recommendations based on CHADS2 score)

Patients who may require antithrombotic therapy include those in whom cardioversion to sinus rhythm is being considered (regardless of the CHA2DS2-VASc score or method of cardioversion [electrical or pharmacologic]) and those who meet criteria for chronic anticoagulation. All patients whose risk of embolization exceeds the risk of bleeding are candidates for long-term antithrombotic therapy.

(2) Rate versus rhythm control

Majority of the AF patients quire the ventricular rate to be slowed down to a sinus rhythm. A rhythm control strategy uses either antiarrhythmic drug therapy, percutaneous catheter ablation, and/or a surgical procedure. Electrical cardioversion may be necessary prior to an attempt to maintain sinus rhythm.

Rate slowing drugs are generally started before rhythm control and continued in many patients who remain in sinus rhythm (in the event of return to AF).A rate control strategy generally uses drugs that slow conduction across the atrioventricular (AV) node, such as beta blockers, non-dihydropyridine calcium channel blockers, or digoxin.  

If you want to know more about your heart health, schedule an appointment with Dr. Uri Ben-Zur today and your friends at the Cardiac Institute of Greater Los Angeles where our patients ARE our family.

References 

Overview of atrial fibrillation (Overview of atrial fibrillation) http://www.uptodate.com/contents/overview-of-atrial-fibrillation?source=search_result&search=atrial+fibrillation&selectedTitle=1%7E150#H5
Atrial fibrillation (Wikipedia) http://en.wikipedia.org/wiki/Atrial_fibrillation
Cleveland Clinic – What is Atrial Fibrillation? (Cleveland Clinic) http://my.clevelandclinic.org/heart/atrial_fibrillation/afib.aspx#treated

Dr. Ben-Zur is a cardiologist and electrophysiologist who treats various heart conditions, including atrial fibrillation, a-fib, AF, arrhythmias, valvular disease, congestive heart failure, and many more. He services patients from Burbank, Sherman Oaks, Encino, Hollywood and beyond.

 

If you have had a family member suffer a stroke, you should make an appointment to see us today. With over 20 years of experience in treating the good people of Los Angeles, we are dedicated to your quest for a happy, healthy, and long life. Please call Dr. Uri Ben-Zur today to get the highest quality care in Southern California.

A stroke is an ischemic event. Ischemia means that a part of the body does not get enough oxygen because of a lack of blood flow. Ischemia is caused by either blockage of a blood vessel via thrombosis or arterial embolism, or by cerebral hypoperfusion (not enough blood flow).

Hemorrhagic stroke is caused by bleeding of blood vessels of the brain, either directly into the brain parenchyma or into the subarachnoid space surrounding brain tissue. As a result, the affected area of the brain cannot function normally, which might result in an inability to move one or more limbs on one side of the body, failure to understand or formulate speech, or a vision impairment of one side of the visual field.

A stroke is a medical emergency and can cause permanent neurological damage or death. Risk factors for stroke include old age, high blood pressure, previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, tobacco smoking and atrial fibrillation. High blood pressure is the most important modifiable risk factor of stroke. Cerebrovascular disease was the second leading cause of death worldwide in 2004.An ischemic stroke is occasionally treated in a hospital with thrombolysis (also known as a “clot buster”), and some hemorrhagic strokes benefit from neurosurgery. Treatment to recover any lost function is termed stroke rehabilitation, ideally in a stroke unit and involving health professions such as speech and language therapy, physical therapy and occupational therapy. Prevention of recurrence may involve the administration of antiplatelet drugs such as aspirin and dipyridamole, control and reduction of high blood pressure, and the use of statins. Selected patients may benefit from carotid endarterectomy and the use of anticoagulants.

 

Classification

Strokes can be classified into two major categories: ischemic and hemorrhagic. Ischemic strokes are caused by interruption of the blood supply, while hemorrhagic strokes result from the rupture of a blood vessel or an abnormal vascular structure. About 87% of strokes are ischemic, the rest are hemorrhagic. Some hemorrhages develop inside areas of ischemia (“hemorrhagic transformation”). It is unknown how many hemorrhagic strokes actually start as ischemic stroke.

 

Definition

In the 1970s the World Health Organization defined stroke as a “neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours,” although the word “stroke” is centuries old. This definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours.With the availability of treatments which can reduce stroke severity when given early, many now prefer alternative terminology, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary syndrome, respectively), to reflect the urgency of stroke symptoms and the need to act swiftly.

 

Ischemic

Main articles: Cerebral infarction and Brain ischemia

In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. There are four reasons why this might happen:

  • Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
  • Embolism
  • Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)
  • Venous thrombosis.
  • Abuser of stimulant drugs such as cocaine and methamphetamine are at a high risk for ischemic strokes.

Stroke without an obvious explanation is termed “cryptogenic” (of unknown origin); this constitutes 30-40% of all ischemic strokes.

 

Hemorrhagic

Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g., headache, previous head injury).

 

Signs and symptoms

Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases do not progress further. The symptoms depend on the area of the brain affected. The more extensive the area of brain affected, the more functions that are likely to be lost. Some forms of stroke can cause additional symptoms. For example, in intracranial hemorrhage, the affected area may compress other structures. Most forms of stroke are not associated with headache, apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral hemorrhage.

 

Early recognition

Various systems have been proposed to increase recognition of stroke. Different findings are able to predict the presence or absence of stroke to different degrees. Sudden-onset face weakness, arm drift (i.e., if a person, when asked to raise both arms, involuntarily lets one arm drift downward) and abnormal speech are the findings most likely to lead to the correct identification of a case of stroke increasing the likelihood by 5.5 when at least one of these is present). Similarly, when all three of these are absent, the likelihood of stroke is significantly decreased. While these findings are not perfect for diagnosing stroke, the fact that they can be evaluated relatively rapidly and easily make them very valuable in the acute setting.

 

Subtypes

If the area of the brain affected contains one of the three prominent central nervous system pathways—the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:

  • hemiplegia and muscle weakness of the face
  • numbness
  • reduction in sensory or vibratory sensation
  • initial flaccidity (limp muscles), replaced by spasticity (hyper-flexing muscles), hyperreflexia.

In most cases, the symptoms affect only one side of the body (unilateral). Depending on the part of the brain affected, the defect in the brain is usually on the opposite side of the body. However, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms, the presence of any one of these symptoms does not necessarily indicate a stroke.

In addition to the above CNS pathways, the brainstem gives rise to most of the twelve cranial nerves. A stroke affecting the brain stem and brain therefore can produce symptoms relating to deficits in these cranial nerves:

  • altered smell, taste, hearing, or vision (total or partial)
  • drooping of eyelid (ptosis) and weakness of ocular muscles
  • decreased reflexes: gag, swallow, pupil reactivity to light
  • decreased sensation and muscle weakness of the face
  • balance problems and nystagmus (twitching of the eye in response to straining them)
  • altered breathing and heart rate
  • weakness in sternocleidomastoid muscle with inability to turn head to one side
  • weakness in tongue (inability to protrude and/or move from side to side)

 

If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

  • aphasia (difficulty with verbal expression, auditory comprehension, reading and/or writing Broca’s or Wernicke’s area typically involved)
  • dysarthria (motor speech disorder resulting from neurological injury)
  • apraxia (altered voluntary movements)
  • visual field defect
  • memory deficits (involvement of temporal lobe)
  • hemineglect (involvement of parietal lobe-you can only see half of the visual field)
  • disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)
  • lack of insight of his or her, usually stroke-related, disability (patient is unaware they have a problem)

 

If the cerebellum is involved, the patient may have the following:

  • altered walking gait
  • altered movement coordination
  • vertigo and or disequilibrium

Associated symptoms

Loss of consciousness, headache, and vomiting usually occurs more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing the brain.

 

If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.

Causes

Thrombotic stroke

In thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke (see below) if the thrombus breaks off, at which point it is called an “embolus.” Two types of thrombosis can cause stroke:

  1. Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis. Diseases that may form thrombi in the large vessels include (in descending incidence): atherosclerosis, vasoconstriction (tightening of the artery), aortic, carotid or vertebral artery dissection, various inflammatory diseases of the blood vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy, Moyamoya disease and fibromuscular dysplasia.
  2. Small vessel disease involves the smaller arteries inside the brain: branches of the circle of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral and basilar artery.[26] Diseases that may form thrombi in the small vessels include (in descending incidence): lipohyalinosis (build-up of fatty hyaline matter in the blood vessel as a result of high blood pressure and aging) and fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts) and microatheroma (small atherosclerotic plaques).

Sickle-cell anemia, which can cause blood cells to clump up and block blood vessels, can also lead to stroke. A stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia.

Embolic stroke

An embolic stroke refers to the blockage of an artery by an arterial embolus (clot), a traveling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g., from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis).

Because an embolus arises from elsewhere, local therapy solves the problem only temporarily. Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms usually are maximal at start. Also, symptoms may be transient as the embolus is partially resorbed and moves to a different location or dissipates altogether.

Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree. In paradoxical embolism, a deep vein thrombosis embolizes through an atrial or ventricular septal defect in the heart into the brain.

 

Cerebral hypoperfusion (inadequate blood flow)

Cerebral hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to heart failure from cardiac arrest or arrhythmias (irregular beats), or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia (low blood oxygen content) may precipitate the hypoperfusion. Because the reduction in blood flow is global, all parts of the brain may be affected, especially “watershed” areas – border zone regions supplied by the major cerebral arteries. A watershed stroke refers to the condition when blood supply to these areas is compromised. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur.

 

 

Venous thrombosis

Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke.

 

Intracerebral hemorrhage

It generally occurs in small arteries or arterioles and is commonly due to hypertension, intracranial vascular malformations (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary haemorrhage has occurred. Other potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g., amphetamines or cocaine). The hematoma (clot) enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. A third of intracerebral bleed is into the brain’s ventricles. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or subarachnoid hemorrhage (which technically may also be classified as a type of stroke).

 

Silent stroke

A silent stroke is a stroke that does not have any outward symptoms, and the patients are typically unaware they have suffered a stroke. Despite not causing identifiable symptoms, a silent stroke still damages the brain, and places the patient at increased risk for both transient ischemic attack and major stroke in the future. Conversely, those who have suffered a major stroke are also at risk of having silent strokes. In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as MRI. Silent strokes are estimated to occur at five times the rate of symptomatic strokes. The risk of silent stroke increases with age, but may also affect younger adults and children, especially those with acute anemia.

 

Pathophysiology

Ischemic

Ischemic stroke occurs because of a loss of blood supply to part of the brain, initiating the ischemic cascade. Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds, and after approximately three hours will suffer irreversible injury possibly leading to death of the tissue, i.e., infarction. (This is why fibrinolytics such as alteplase are given only until three hours since the onset of the stroke.) Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atrial fibrillation, or in the carotid arteries, break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels. Since blood vessels in the brain are now occluded, the brain becomes low in energy, and thus it resorts into using anaerobic metabolism within the region of brain tissue affected by ischemia. Anaerobic metabolism produces less adenosine triphosphate (ATP) but releases a by-product called lactic acid. Lactic acid is an irritant which could potentially destroy cells since it is an acid and disrupts the normal acid-base balance in the brain. The ischemia area is referred to as the “ischemic penumbra”.

 

As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells’ proteins, lipids and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to apoptosis.[citation needed]

Ischemia also induces production of oxygen free radicals and other reactive oxygen species. These react with and damage a number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is particularly important. In fact, many antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the apoptosis cascade by means of redox signaling.

These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. However, brain tissue is especially vulnerable to ischemia since it has little respiratory reserve and is completely dependent on aerobic metabolism, unlike most other organs.

In addition to injurious effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that break down collagen, hyaluronic acid, and other elements of connective tissue. Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of the brain injury.

Hemorrhagic

Bleeding within the skull cavity can occur from various causes. Subdural and epidural bleeding mostly are the result of trauma.[38] Hemorrhagic strokes arise from bleeding within the brain parenchyma or intraventricular spaces, and are classified based on their underlying pathology. Some examples of hemorrhagic stroke are hypertensive hemorrhage, ruptured aneurysm, ruptured AV fistula, transformation of prior ischemic infarction, and drug induced bleeding.[39] They result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort and injure tissue. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature. Inflammation contributes to the secondary brain injury after hemorrhage.

 

Diagnosis

A CT showing early signs of a middle cerebral artery stroke with loss of definition of the gyri and grey white boundary

Stroke is diagnosed through several techniques: a neurological examination (such as the NIHSS), CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriography. The diagnosis of stroke itself is clinical, with assistance from the imaging techniques. Imaging techniques also assist in determining the subtypes and cause of stroke. There is yet no commonly used blood test for the stroke diagnosis itself, though blood tests may be of help in finding out the likely cause of stroke.

 

Physical examination

A physical examination, including taking a medical history of the symptoms and a neurological status, helps giving an evaluation of the location and severity of a stroke. It can give a standard score on e.g., the NIH stroke scale.

 

Imaging

For diagnosing ischemic stroke in the emergency setting:

CT scans (without contrast enhancements)

sensitivity= 16%

specificity= 96%

 

MRI scan

sensitivity= 83%

specificity= 98%

For diagnosing hemorrhagic stroke in the emergency setting:

 

CT scans (without contrast enhancements)

sensitivity= 89%

specificity= 100%

MRI scan

sensitivity= 81%

specificity= 100%

 

For the assessment of stable stroke, nuclear medicine scans SPECT and PET/CT may be helpful. SPECT documents cerebral blood flow and PET with FDG isotope the metabolic activity of the neurons.

 

Underlying cause

12-lead ECG of a patient with a stroke, showing large deeply inverted T-waves. Various ECG changes may occur in people with strokes and other brain disorders.

When a stroke has been diagnosed, various other studies may be performed to determine the underlying cause. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary, since the cause of stroke varies with age, comorbidity and the clinical presentation. Commonly used techniques include:

an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the precerebral arteries;

an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may spread to the brain vessels through the bloodstream);

a Holter monitor study to identify intermittent arrhythmias;

an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation);

blood tests to determine hypercholesterolemia, bleeding diathesis and some rarer causes such as homocysteinuria.

 

Prevention

Given the disease burden of strokes, prevention is an important public health concern. Primary prevention is less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year). Recent guidelines detail the evidence for primary prevention in stroke. In those who are otherwise healthy aspirin does not appear beneficial and thus is not recommended. In people who have had a myocardial infarction or those with a high cardiovascular it provides some protection against a first stroke.  In those who have previously had a stroke, treatment with medications such as aspirin, clopidogrel and dipyridamole be beneficial. The U.S. Preventive Services Task Force (USPSTF) recommends against screening for carotid artery stenosis in those without symptoms.

 

Risk factors

The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation (although magnitude of this effect is small: the evidence from the Medical Research Council trials is that 833 patients have to be treated for 1 year to prevent one stroke). Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking (active and passive), heavy alcohol consumption and drug use, lack of physical activity, obesity, processed red meat consumption[56] and unhealthy diet. Alcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (for example via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances). Drugs, most commonly amphetamines and cocaine, can induce stroke through intracranial vasculopathy and/or acute hypertension.

 

No high-quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation. Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use. Medication or drug therapy is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.

 

Blood pressure

Hypertension (high blood pressure) accounts for 35-50% of stroke risk. Blood pressure reduction of 10 mmHg systolic or 5 mmHg diastolic reduces the risk of stroke by ~40%. Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes. It is equally important in secondary prevention. Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy. The available evidence does not show large differences in stroke prevention between antihypertensive drugs —therefore, other factors such as protection against other forms of cardiovascular disease should be considered and cost.

Blood lipids

High cholesterol levels have been inconsistently associated with (ischemic) stroke. Statins have been shown to reduce the risk of stroke by about 15%. Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk, statins might exert their effect through mechanisms other than their lipid-lowering effects.

Diabetes mellitus

Diabetes mellitus increases the risk of stroke by 2 to 3 times. While intensive control of blood sugar has been shown to reduce microvascular complications such as nephropathy and retinopathy it has not been shown to reduce macrovascular complications such as stroke.

Anticoagulation drugs

Oral anticoagulants such as warfarin have been the mainstay of stroke prevention for over 50 years. However, several studies have shown that aspirin and antiplatelet drugs are highly effective in secondary prevention after a stroke or transient ischemic attack. Low doses of aspirin (for example 75–150 mg) are as effective as high doses but have fewer side effects; the lowest effective dose remains unknown. Thienopyridines (clopidogrel, ticlopidine) “might be slightly more effective” than aspirin and have a decreased risk of gastrointestinal bleeding, but they are more expensive.Their exact role remains controversial. Ticlopidine has more skin rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura. Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side effect. Low-dose aspirin is also effective for stroke prevention after sustaining a myocardial infarction.

Those with atrial fibrillation have a 5% a year risk of stroke, and this risk is higher in those with valvular atrial fibrillation. Depending on the stroke risk, anticoagulation with medications such as warfarin or aspirin is useful for prevention.[81] Except for in atrial fibrillation, oral anticoagulants are not advised for stroke prevention —any benefit is offset by bleeding risk.

 

In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke while increasing the risk of major bleeding. Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.

Surgery

Carotid endarterectomy or carotid angioplasty can be used to remove atherosclerotic narrowing (stenosis) of the carotid artery. There is evidence supporting this procedure in selected cases. Endarterectomy for a significant stenosis has been shown to be useful in the prevention of further strokes in those who have already had one. Carotid artery stenting has not been shown to be equally useful. Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients’ preferences. Surgery is most efficient when not delayed too long —the risk of recurrent stroke in a patient who has a 50% or greater stenosis is up to 20% after 5 years, but endarterectomy reduces this risk to around 5%. The number of procedures needed to cure one patient was 5 for early surgery (within two weeks after the initial stroke), but 125 if delayed longer than 12 weeks.

Screening for carotid artery narrowing has not been shown to be a useful screening test in the general population. Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke. To be beneficial, the complication rate of the surgery should be kept below 4%. Even then, for 100 surgeries, 5 patients will benefit by avoiding stroke, 3 will develop stroke despite surgery, 3 will develop stroke or die due to the surgery itself, and 89 will remain stroke-free but would also have done so without intervention.

Diet

Nutrition, specifically the Mediterranean-style diet, has the potential for decreasing the risk of having a stroke by more than half. It does not appear that lowering levels of homocysteine with folic acid affects the risk of stroke.

Women

A number of specific recommendations have been made for women including: taking aspirin after the 11th week of pregnancy if there is a history of previous chronic high blood pressure, blood pressure medications in pregnancy if the blood pressure is greater than 150 mmHg systolic or greater than 100 mmHg diastolic. In those who have previously had preeclampsia other risk factors should be treated more aggressively.

 

Previous stroke or TIA

Keeping blood pressure below 140/90 mmHg is recommended. Anticoagulation can prevent recurrent ischemic strokes. Among people with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%. However, a recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke. Stroke prevention treatment for atrial fibrillation is determined according to the CHADS/CHADS2 system. The most widely used anticoagulant to prevent thromboembolic stroke in patients with nonvalvular atrial fibrillation is the oral agent warfarin while a number of newer agents including dabigatran are alternatives which do not require prothrombin time monitoring.

Anticoagulants, when used following stroke, should not be stopped for dental procedures.

If studies show carotid stenosis, and the person has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after stroke.

 

Management

Ischemic stroke

Definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy).  Rapid cerebral blood flow restoration results in fewer brain cells dying, has been proved and quantified.

Tight control of blood sugars in the first few hours does not improve outcomes and may cause harm. High blood pressure is also not typically lowered as this has not been found to be helpful.

 

Thrombolysis

Thrombolysis with recombinant tissue plasminogen activator (rtPA) in acute ischemic stroke, when given before four and a half hours of symptom onset increases the risk of death in the short term but in the long-term improves the rate of independence; the change in long term mortality is not significant. Benefit is greater the earlier it is used, with a 10% benefit before 3 hours and a 5% benefit between 3 and 4.5 hours. When broken down by time to treatment it increases the chance of being alive and living independently by 9% in those treated within three hours, however the benefit for those treated between three and six hours is not significant. These benefits or lack of benefits occurred regardless of the age of the person treated. There is no reliable way to determine who will have an intracranial hemorrhage post treatment versus who will not.

 

Its use is endorsed by the American Heart Association and the American Academy of Neurology as the recommended treatment for acute stroke within three hours of onset of symptoms as long as there are not other contraindications (such as abnormal lab values, high blood pressure, or recent surgery). This position for tPA is based upon the findings of two studies by one group of investigators which showed that tPA improves the chances for a good neurological outcome. When administered within the first three hours thrombolysis improves functional outcome without affecting mortality. 6.4% of people with large strokes developed substantial brain hemorrhage as a complication from being given tPA thus part of the reason for increased short term mortality. Additionally, it is the position of the American Academy of Emergency Medicine that objective evidence regarding the efficacy, safety, and applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care. Intra-arterial fibrinolysis, where a catheter is passed up an artery into the brain and the medication is injected at the site of thrombosis, has been found to improve outcomes in people with acute ischemic stroke.

 

Hemicraniectomy

Large territory strokes can cause significant edema of the brain with secondary brain injury in surrounding tissue. This phenomenon is mainly encountered in strokes of the middle cerebral artery territory, and is also called “malignant cerebral infarction” because it carries a dismal prognosis. Relief of the pressure may be attempted with medication, but some require hemicraniectomy, the temporary surgical removal of the skull on one side of the head. This decreases the risk of death, although some more people survive with disability who would otherwise have died.

 

Hemorrhagic stroke

People with intracerebral hemorrhage require neurosurgical evaluation to detect and treat the cause of the bleeding, although many may not need surgery. Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse. People are monitored for changes in the level of consciousness, and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.

 

Stroke unit

Ideally, people who have had a stroke are admitted to a “stroke unit”, a ward or dedicated area in hospital staffed by nurses and therapists with experience in stroke treatment. It has been shown that people admitted to a stroke unit have a higher chance of surviving than those admitted elsewhere in hospital, even if they are being cared for by doctors without experience in stroke.

 

When an acute stroke is suspected by history and physical examination, the goal of early assessment is to determine the cause. Treatment varies according to the underlying cause of the stroke, thromboembolic (ischemic) or hemorrhagic.

 

 

 

Rehabilitation

Stroke rehabilitation is the process by which those with disabling strokes undergo treatment to help them return to normal life as much as possible by regaining and relearning the skills of everyday living. It also aims to help the survivor understand and adapt to difficulties, prevent secondary complications and educate family members to play a supporting role.

 

A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. These include physicians trained in rehabilitation medicine, clinical pharmacists, nursing staff, physiotherapists, occupational therapists, speech and language therapists, and orthotists. Some teams may also include psychologists and social workers, since at least one third of the people manifest post stroke depression. Validated instruments such as the Barthel scale may be used to assess the likelihood of a stroke patient being able to manage at home with or without support subsequent to discharge from hospital.

 

Good nursing care is fundamental in maintaining skin care, feeding, hydration, positioning, and monitoring vital signs such as temperature, pulse, and blood pressure. Stroke rehabilitation begins almost immediately.

 

For most people with stroke, physical therapy (PT), occupational therapy (OT) and speech-language pathology (SLP) are the cornerstones of the rehabilitation process. Often, assistive technology such as wheelchairs, walkers and canes may be beneficial. Many mobility problems can be improved by the use of ankle foot orthoses. PT and OT have overlapping areas of expertise, however PT focuses on joint range of motion and strength by performing exercises and re-learning functional tasks such as bed mobility, transferring, walking and other gross motor functions. Physiotherapists can also work with patients to improve awareness and use of the hemiplegic side. Rehabilitation involves working on the ability to produce strong movements or the ability to perform tasks using normal patterns. Emphasis is often concentrated on functional tasks and patient’s goals. One example physiotherapists employ to promote motor learning involves constraint-induced movement therapy. Through continuous practice the patient relearns to use and adapt the hemiplegic limb during functional activities to create lasting permanent changes. OT is involved in training to help relearn everyday activities known as the Activities of daily living (ADLs) such as eating, drinking, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for patients with the speech production disorders: dysarthria and apraxia of speech, aphasia, cognitive-communication impairments and/or dysphagia (problems with swallowing).

 

Patients may have particular problems, such as dysphagia, which can cause swallowed material to pass into the lungs and cause aspiration pneumonia. The condition may improve with time, but in the interim, a nasogastric tube may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still deemed unsafe, then a percutaneous endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely.

 

Treatment of spasticity related to stroke often involves early mobilizations, commonly performed by a physiotherapist, combined with elongation of spastic muscles and sustained stretching through various positionings. Gaining initial improvement in range of motion is often achieved through rhythmic rotational patterns associated with the affected limb. After full range has been achieved by the therapist, the limb should be positioned in the lengthened positions to prevent against further contractures, skin breakdown, and disuse of the limb with the use of splints or other tools to stabilize the joint.[23] Cold in the form of ice wraps or ice packs have been proven to briefly reduce spasticity by temporarily dampening neural firing rates. Electrical stimulation to the antagonist muscles or vibrations has also been used with some success.

 

Stroke rehabilitation should be started as quickly as possible and can last anywhere from a few days to over a year. Most return of function is seen in the first few months, and then improvement falls off with the “window” considered officially by U.S. state rehabilitation units and others to be closed after six months, with little chance of further improvement. However, patients have been known to continue to improve for years, regaining and strengthening abilities like writing, walking, running, and talking. Daily rehabilitation exercises should continue to be part of the stroke patient’s routine. Complete recovery is unusual but not impossible and most patients will improve to some extent: proper diet and exercise are known to help the brain to recover.

 

Some current and future therapy methods include the use of virtual reality and video games for rehabilitation. These forms of rehabilitation offer potential for motivating patients to perform specific therapy tasks that many other forms do not. Many clinics and hospitals are adopting the use of these off-the-shelf devices for exercise, social interaction and rehabilitation because they are affordable, accessible and can be used within the clinic and home.

 

Other novel non-invasive rehabilitation methods are currently being developed to augment physical therapy to improve motor function of stroke patients, such as transcranial magnetic stimulation (TMS) and transcranial direct-current stimulation (tDCS) and robotic therapies.

 

A stroke can also reduce people’s general fitness. Reduced fitness can reduce capacity for rehabilitation as well as general health. A systematic review found that there are inadequate long-term data about the effects of exercise and training on death, dependence and disability after a stroke. However, cardiorespiratory training added to walking programs in rehabilitation can improve speed, tolerance and independence during walking.

 

Prognosis

Disability affects 75% of stroke survivors enough to decrease their employability. Stroke can affect peoples’ physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion. Dysfunctions correspond to areas in the brain that have been damaged.

Some of the physical disabilities that can result from stroke include muscle weakness, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss, and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result.

Emotional problems resulting from stroke can result from direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy, and psychosis.

30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self-esteem, and withdrawal. Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.

Emotional lability, another consequence of stroke, causes the patient to switch quickly between emotional highs and lows and to express emotions inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to the patient’s actual emotions, a more severe form of emotional lability causes patients to laugh and cry pathologically, without regard to context or emotion. Some patients show the opposite of what they feel, for example crying when they are happy. Emotional lability occurs in about 20% of stroke patients.

 

Cognitive deficits resulting from stroke include perceptual disorders, Aphasia, dementia, and problems with attention and memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere.

Cognitive and psychological outcome after a stroke can be affected by the age at which the stroke happened, pre-stroke baseline intellectual functioning, psychiatric history and whether there is pre-existing brain pathology.

Up to 10% of people following a stroke develop seizures, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure.

 

Mechanical thrombectomy

MERCI Retriever L5.

Removal of the clot may be attempted in those where it occurs within a large blood vessel and may be an option for those who either are not eligible for or do not improve with intravenous thrombolytics. Significant complications occur in about 7%. As of October 2013, trials have not shown positive results.

 

Neuroprotection

Drugs that scavenge reactive oxygen species, inhibit apoptosis, or inhibit excitatory neurotransmitters have been shown experimentally to reduce tissue injury caused by ischemia. Agents that work in this way are referred to as being neuroprotective. Until recently, human clinical trials with neuroprotective agents have failed, with the probable exception of deep barbiturate coma. However, more recently NXY-059, the disulfonyl derivative of the radical-scavengin phenylbutylnitrone, is reported to be neuroprotective in stroke. This agent appears to work at the level of the blood vessel lining or endothelium. Unfortunately, after producing favorable results in one large-scale clinical trial, a second trial failed to show favorable results. Benefit of NXY-059 is questionable.

References:

http://en.wikipedia.org/wiki/Stroke

thai_peanut_empowered_noodle_bowl_recipe

Thai Peanut Empowered Noodle Bowl

Prep Time: 25 minutes

Cook Time: 5 minutes

Total Time: 30 minutes

Ingredients

For the Thai Peanut Sauce:
    • 1 large clove garlic
    • 2 tablespoons (30 mL) toasted sesame oil
    • 3 tablespoons (45 mL) natural smooth peanut butter or almond butter
    • 2 teaspoons (10 mL) grated fresh ginger (optional)
    • 3 tablespoons (45 mL) fresh lime juice, plus more as needed
    • 2 tablespoons plus 1 teaspoon (37 mL) low-sodium soy sauce (optional)
    • 1 to 2 teaspoons (5 to 10 mL) granulated sugar
For the Salad:
  • 4 ounces (115 g) gluten-free soba (buckwheat) noodles
  • Extra-virgin olive oil, for the noodles
  • 1 (16-ounce/454-g) bag frozen shelled edamame, thawed
  • 1 red bell pepper, diced
  • 1/2 seedless (English) cucumber, diced
  • 1 carrot, julienned
  • 4 green onions, chopped, plus more for serving
  • 1/4 cup (60 mL) fresh cilantro leaves, chopped
  • Sesame seeds, for serving

Instructions

Make the Thai Peanut Sauce:
    1. In a mini or regular food processor, combine the garlic, sesame oil, peanut butter, ginger (if using), lime juice, tamari, sugar (if using), and 2 to 3 tablespoons (30–45 mL) water. Process until combined.
Make the Salad:
  1. Cook the soba noodles according to the instructions on the package. Be sure not to overcook them—they should only take 5 to 9 minutes, depending on the brand. Drain the noodles and rinse them under cold water. Transfer the noodles to a large bowl and toss them with a drizzle of extra-virgin olive oil (this prevents the noodles from sticking together).
  2. Add the edamame, bell pepper, cucumber, carrot, green onions, and cilantro to the bowl with the noodles and toss until well combined.
  3. Pour your desired amount of the dressing over the salad and toss to coat. (Any leftover dressing will keep in an airtight container in the refrigerator for up to 1 week.)
  4. Portion the salad into 4 bowls and garnish each serving with a sprinkle of sesame seeds and some green onions. Serve any leftover dressing on the side.


Read more at http://ohmyveggies.com/thai-peanut-empowered-noodle-bowl-from-oh-she-glows/#r3Dkgq7jGzFwWQ1Q.99

Log in to the American Heart Association and register at this link: https://www.heart.org/gglRisk/main_en_US.html  to check your risk for a heart attack 🙂

 

Here is an example:

A male, 35 yearls old, 300lbs with a waist circumference over 40, LDL-180 Total Cholesterol-280, BP 130/90 has a 6% chance of having a heart attack in ten years.

 

That same male that eats vegetarian and loses weight to 174lbs, LDL-70, TC-280, BP-110/70, Total Cholesterol-140 drops their chance of heart attack to less than 1%.

This is for a man with low blood sugar and no family history of heart disease. HDL was input at 50. If you do not have recent blood work, please schedule an appointment with Dr. Ben-Zur or contact your physician.

 

The human body is a complex soup of chemicals called hormones, many of which originate in the brain and travel throughout the rest of the body exerting effects on many major organs. Human nature tells us that the brain and the heart are interconnected through our emotions, feelings, and behavior, and the “how” involves chemical messaging between the two. If we know that positive feelings such as love can have an impact on both, what about negative emotions like stress and sadness? New studies are suggesting that chemicals that cause mental health issues may also induce cardiovascular problems.

 

Depression

 

We may not want to admit it, but many of us are comfort-eaters. When things get us down we reach for something tasty and definitely less than healthy to lift our spirits. It’s something many of us are guilty of; unfortunately, it’s a tough habit to break. And it can be a real detriment to our health. Obesity and diet are huge risk factors for the heart, but it can be tough to reach for the doorknob rather than the fridge handle when you’re feeling sad. If that gloomy feeling sticks around for more than a few days, it may be a good idea to seek help from a health professional. In the meantime, reaching for healthier options such as fruits and vegetables as well as increasing your activity level may have the desired effect of making you feel better now and in the future. Making small, gradual changes is a great way to start on bigger goals and not nearly as intimidating to master.

 

Stress and Anxiety

When we feel stress, our bodies release hormones such as adrenaline (the so called fight-or-flight hormone) and cortisol. In an emergency setting, like a car accident or while public speaking, these chemicals make us perform better and react more quickly to the demands we face. Our hearts beat faster and harder and we may sometimes feel stronger than we really are. But experts are beginning to believe that over time with constant stress and the resulting constant release of these chemicals we may be doing damage to ourselves and our bodies. There is no study to firmly link stress and heart disease at this time, but that may change in the future. We know that chronic stress negatively impacts sleep hygiene and mood, and increases fatigue. When you are feeling stressed, take a step back and try to decide where the source of your stress is coming from. Is it your job, your boss? A family issue? A relationship? Determine if the stress is something that you can change or not, then take action. Do something for yourself to break the stress cycle. Take a few minutes out of your day to do something healthy that you may enjoy, for instance taking a walk, or playing with a pet is an active outlet for pent up feelings of stress. Exercise is a well known depression and stress fighter!

 

For more information:

http://www.heart.org/HEARTORG/GettingHealthy/StressManagement/HowDoesStressAffectYou/How-does-depression-affect-the-heart_UCM_460263_Article.jsp

http://www.heart.org/HEARTORG/GettingHealthy/StressManagement/HowDoesStressAffectYou/Mental-Health-and-Heart-Health_UCM_438853_Article.jsp

Maybe you or someone you know was recently diagnosed with paroxysmal atrial tachycardia (PAT), also known as paroxysmal supraventricular tachycardia (PSVT). The easiest way to demystify many seemingly complex medical conditions is to break them down into simpler parts, and it works to understand almost all conditions. Paroxysmal is medical jargon for sudden episode. The atrium is a region of your heart above the ventricle that is also involved with pumping blood, and tachycardia refers to a faster than normal heart beat. Put together you have a sudden burst of rapid beating in a portion of your heart.

Now that we have a better understanding what we are talking about, what causes this syndrome?

The heart is able to pump blood because of a pattern of electrical impulses that spread through the muscle causing it to contract, and in doing so moves blood through forward through the vascular system to the brain, kidneys, liver, skin, and other vital organs. The sinoatrial (SA) node found in the atrium normally acts as a pacemaker in the heart, initiating the signal which tells the rest of the heart muscle to squeeze.  Blood first enters the atria, which contract, pushing the blood to the ventricles. The ventricles contract shortly after they are filled by the atria and circulate blood throughout the body or the lungs, depending what side of the heart you are looking at. PAT/PSVT comes from an abnormal electrical signal in the atrium that causes the atria to contract more quickly and speeds up the heart rate. The signal may be too fast for the heart to properly fill with blood before pumping, and this can decrease the supply of blood to the whole body.

It sounds pretty scary, what are the symptoms?

Some people may not have any symptoms, others may notice:

-feeling lightheaded

-feeling dizzy

-feeling chest pain (also known as angina)

-feeling shortness of breath

-feeling rapid heartbeats or “palpitations”

-In rare cases patients may also lose consciousness or have cardiac arrest

 

How is it diagnosed?

Your doctor will ask you some questions and run some painless tests to look at the electrical conduction of your heart. Typically testing may start with an electrocardiogram (EKG/ECG) which consists of sticky pads which attach to your chest. You will not feel the electricity and most people report removing the sticky pads is the most uncomfortable part of the test. You may also have an ultrasound or other images taken of your heart or be asked to wear a monitor for a day to track the electrical signals in your heart over time.

How is it treated?

Your doctor will talk to you about your options, and many people don’t need treatment for the paroxysmal form of atrial tachycardia. The best things you can do to help yourself include:

Decreasing your coffee/caffeine intake

Decreasing your alcohol

Stop smoking

Improve your stress management skills

Get more sleep

 

Your doctor may also try techniques such as carotid sinus massage or have you perform a Valsalva maneuver to stop an episode of tachycardia; however these should be attempted by a doctor and should be supervised to minimize risks such as heart, brain, or lung injury.

 

Some people who have a persistent condition may need medications or a medical procedure called ablation which helps to slow the overactive pacemaker in the heart.

 

For more information:

http://www.heart.org/HEARTORG/Conditions/Arrhythmia/AboutArrhythmia/Tachycardia-Fast-Heart-Rate_UCM_302018_Article.jsp

Atrial_flutter34.svg

Have you ever felt dizzy or lightheaded? Come see the best in cardiology-Dr. Uri Ben-Zur and let us help you keep a heart-healthy life.

Atrial Flutter is an abnormal heart rhythm that occurs in the atria of the heart. When it first occurs, it is usually associated with a fast heart rate or tachycardia (beats over 100 per minute), and falls into the category of supra-ventricular tachycardias. While this rhythm occurs most often in individuals with cardiovascular disease (e.g. hypertension, coronary artery disease, and cardiomyopathy) and diabetes, it may occur spontaneously in people with otherwise normal hearts. It is typically not a stable rhythm, and frequently degenerates into atrial fibrillation. However, it does rarely persist for months to years.

A variety of other underlying conditions can predispose to the development of atrial flutter. These include:

  • Atrial flutter commonly occurs after initiation of an antiarrhythmic drug for the suppression of atrial fibrillation. It may occur in up to 15 percent of patients treated with flecainide or propafenone.
  • Any of the disorders that can cause atrial fibrillation, including thyrotoxicosis, obesity, obstructive sleep apnea, sick sinus syndrome, pericarditis, pulmonary disease, and pulmonary embolism.
  • Atrial flutter is a relatively uncommon complication of an acute myocardial infarction and is rarely, if ever, a manifestation of digitalis toxicity.
  • Atrial flutter can occur after cardiac surgery, both as a postoperative complication and as a late arrhythmia. The atrial flutter in these patients is re-entrant and may involve atypical isthmuses between natural barriers, atrial incisions, and scar, as well as the cavotricuspid isthmus, the site of involvement in typical atrial flutter
  • Some patients develop atypical left atrial flutter after atrial fibrillation ablation. These arrhythmias may be due to circuits created by scar from left atrial (LA) ablations, but are often amenable to ablation themselves. This issue is discussed in detail separately.

History and physical examination — Typical complaints include palpitations, fatigue, lightheadedness, and/or mild shortness of breath. Less common problems include significant dyspnea(shortness of breath), angina (chest pain mimicking heart attack), hypotension (low blood pressure), anxiety, presyncope  (lightheadedness), or infrequently, syncope (passing out). These symptoms are in large part attributable the rapid heart rate.

Electrocardiogram — For patients in atrial flutter at the time of the electrocardiogram (ECG), it generally shows an atrial rate of about 300 beats per minute (range 240 to 340). Typical P waves are absent, and the atrial activity is seen as a sawtooth pattern (also called F waves) in leads II, III, and aVF. There is typically 2:1 conduction across the atrioventricular (AV) node; as a result, the ventricular rate is usually one-half the flutter rate in the absence of AV node dysfunction. Even atrial to ventricular rate ratios (eg, 2:1 or 4:1 conduction) are much more common than odd ratios.

Echocardiogram — A transthoracic echocardiogram should be obtained in all patients with atrial flutter to evaluate the size of the right and left atria, the size and function of the right and left ventricles, and to detect possible pericardial or valvular heart disease or left ventricular hypertrophy.

DIAGNOSIS — The diagnosis of atrial flutter is almost always secured by the observation of a characteristic pattern on the electrocardiogram, which includes the presence of continuous, regular atrial electrical activity (depolarization and repolarization) at a characteristic rate of approximately 300 beats/min and a regular ventricular rate of about 150 beats/min in patients not taking atrioventricular (AV) nodal blockers. If there are sawtooth flutter waves in the leads II, III, and aVF, it is typical atrial flutter.

COMPLICATIONS — Serious complications of atrial flutter include myocardial ischemia, dizziness or syncope, heart failure (with either preserved or reduced left ventricular systolic function), or embolization of clot. Control of the ventricular rate or reversion to normal sinus rhythm will improve or prevent the first three; anticoagulation is frequently used to decrease the risk of embolization.

Classification-There are two types of atrial flutter, the common type I and rarer type II.[4] Most individuals with atrial flutter will manifest only one of these. Rarely someone may manifest both types; however, they can only manifest one type at a time.

Type I

  • Type I atrial flutter, counterclockwise rotation with 3:1 and 4:1 AV nodal block.
  • Type I atrial flutter, also known as common atrial flutter or typical atrial flutter, has an atrial rate of 240 to 340 beats/minute. However, this rate may be slowed by antiarrhythmic agents.
  • The reentrant loop circles the right atrium, passing through the cavo-tricuspid isthmus – a body of fibrous tissue in the lower atrium between the inferior vena cava, and the tricuspid valve. Type I flutter is further divided into two subtypes, known as counterclockwise atrial flutter and clockwise atrial flutter depending on the direction of current passing through the loop.
  • Counterclockwise atrial flutter (known as cephalad-directed atrial flutter) is more commonly seen. The flutter waves in this rhythm are inverted in ECG leads II, III, and aVF.
  • The re-entry loop cycles in the opposite direction in clockwise atrial flutter, thus the flutter waves are upright in II, III, and aVF.
  • Catheter ablation of the isthmus is a procedure usually available in the electrophysiology laboratory. Eliminating conduction through the isthmus prevents reentry, and if successful, prevents the recurrence of the atrial flutter.

 

Type II-

  • Type II flutter follows a significantly different re-entry pathway to type I flutter, and is typically faster, usually 340-440 beats/minute. Left atrial flutter is common after incomplete left atrial ablation procedures.

 

Management-In general, atrial flutter should be managed the same as atrial fibrillation. Because both rhythms can lead to the formation of thrombus in the atria, individuals with atrial flutter usually require some form of anticoagulation or anti-platelet agent. Both rhythms can be associated with dangerously fast heart rate and thus require medication for rate and or rhythm control. Additionally, there are some specific considerations particular to treatment of atrial flutter.

 

Cardioversion-Atrial flutter is considerably more sensitive to electrical direct-current cardioversion than atrial fibrillation, and usually requires a lower energy shock. 20-50J is commonly enough to revert to sinus rhythm. Conversely, it is relatively resistant to chemical cardioversion, and often deteriorates into atrial fibrillation prior to spontaneous return to sinus rhythm.

 

Ablation-Because of the reentrant nature of atrial flutter, it is often possible to ablate the circuit that causes atrial flutter. This is done in the electrophysiology lab by causing a ridge of scar tissue that crosses the path of the circuit that causes atrial flutter. Ablation of the isthmus, as discussed above, is a common treatment for typical atrial flutter.

 

References:

http://en.wikipedia.org/wiki/Atrial_flutter

http://www-uptodate-com.proxy.westernu.edu/contents/overview-of-atrial-flutter?source=search_result&search=atrial+flutter&selectedTitle=1~150


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