Heart Attack and Atherosclerosis Prevention Medical Author Revision: Dennis Lee, M.D., Daniel Kulick, M.D.
Medical Editor: William C. Shiel Jr., MD, FACP, FACR
Atherosclerosis and Heart Attack
Improving One's Cholesterol Profile
Anti-platelet, Anti-oxidant, Vitamins, and Ace Inhibitors
Introduction
Coronary artery disease is atherosclerosis (in lay terms, "hardening of the arteries") of the blood vessels that feed blood to the heart. Coronary artery disease leads to heart attacks and is the leading killer in the United States. The primary risk factors for coronary artery disease are diabetes, male gender, family history of coronary disease at an early age, smoking , elevated blood pressure (hypertension), high LDL cholesterol , and low HDL cholesterol. The control of diabetes and blood pressure has resulted in a small benefit in preventing heart attacks. On the other hand, stopping smoking has resulted in a significant reduction in heart attack risk. Additionally, the treatment of elevated cholesterol, particularly with the statin class of drugs such as pravastatin (Pravachol), lovastatin (Mevacor), and others, has significantly reduced the rate of death from heart disease.
However, these factors do not fully account for all of the risks for coronary disease since some patients without any of the above risk factors may develop heart attacks. In recent years, other risk factors that increase the risk for coronary artery disease have been identified. These include a high serum homocysteine level and certain subtypes of LDL cholesterol. Attention has focused on the treatment of those risk factors that can be improved. Following is a comprehensive review of causes and prevention of atherosclerosis and heart attacks.
What is atherosclerosis?
Atherosclerosis is a gradual process whereby hard cholesterol substances (plaques) are deposited in the walls of the arteries. Cholesterol plaques cause hardening of the artery walls and narrowing of the inner channel (lumen) of the artery. Arteries carry blood that is enriched with oxygen and nutrients to the vital organs such as the brain, heart, kidneys, and liver. Arteries also transport blood to other tissues such as the fingers, toes, nerves, bones, skin, and muscles. Healthy arteries can deliver an ample supply of blood to the organs and tissues. In contrast, arteries that are narrowed by atherosclerosis have difficulty delivering blood to the parts of the body they supply. For example, atherosclerosis of the arteries in the legs causes poor circulation in the lower extremities. Poor circulation in the lower extremities can lead to pain while walking or exercising, deficient wound healing, and/or leg ulcers. Atherosclerosis can also cause the complete blockage of an artery from a blood clot. Complete blockage of an artery interrupts oxygen supply, resulting in tissue injury or death. Thus, the blockage of an artery that furnishes blood to the brain can lead to stroke (death of brain tissue), and the blockage of the arteries to the heart can result in a heart attack (death of heart muscle), also called myocardial infarction, or MI.
What is coronary atherosclerosis?
Coronary atherosclerosis refers to the hardening and narrowing of the coronary arteries. Coronary arteries supply the blood that carries oxygen and nutrients to the heart muscle. When coronary arteries are narrowed or blocked by atherosclerosis, they cannot deliver an adequate amount of blood to the heart muscle. Disease caused by the lack of blood supply to heart muscle is called coronary artery disease. Coronary artery disease (CAD) includes heart attacks, sudden unexpected death, chest pain ( angina ), abnormal heart rhythms, and heart failure due to weakening of the heart muscle.
What is angina pectoris?
Angina pectoris is chest pain or pressure that occurs when the oxygen supply to the heart muscle cannot keep up with demand. Most commonly, the inadequate supply of oxygen is due to narrowing of the coronary arteries by atherosclerosis. When coronary arteries are narrowed by more than 50% to 70%, the arteries cannot increase the supply of blood to the heart muscle during exertion or other periods of high oxygen demand. An insufficient supply of oxygen to the heart muscle causes chest pain (angina). Chest pain that occurs with exercise or exertion is called exertional angina.
Exertional angina usually feels like a pressure, heaviness, squeezing, or aching across the chest. This pain may travel to the neck, jaw, arms, back, or even the teeth, and may be accompanied by shortness of breath, nausea, or a cold sweat. Exertional angina typically lasts from 1 to 15 minutes and is relieved by rest or by placing a nitroglycerin tablet under the tongue. Both resting and nitroglycerin decrease the heart muscle's demand for oxygen, thus relieving angina. Exertional angina may be the first warning sign of advanced coronary atherosclerosis.
Some individuals experience angina at rest. Angina at rest may be due to a spasm of the coronary arteries (a condition called Prinzmetal's angina). It can also indicate a critical narrowing of the coronary arteries since the heart is not receiving enough oxygen even at rest. Unlike a heart attack, there is no permanent muscle damage with brief angina episodes of either type.
What is a heart attack?
A heart attack (myocardial infarction) is the death of heart muscle due to the sudden and complete blockage of a coronary artery by a clot. A coronary artery blockage usually occurs in arteries that contain cholesterol plaques. A plaque can rupture and initiate the formation of a blood clot next to it. A blood clot can completely block blood flow through a coronary artery and deprive the heart muscle of needed nutrients and oxygen. The heart muscle then dies, which produces a heart attack. Click here to see some real life hearts that have been affected by heart attacks. 
The most common symptom of a heart attack is pain and pressure in the chest that is unrelieved by rest or nitroglycerin. The pain may not be in the chest, but may be felt only in one or both arms, the neck or jaw. Occasionally a heart attack may only manifest as sudden shortness of breath, or may be accompanied by nausea or a cold sweat. In some individuals, a heart attack may be "silent," which means the person does not experience chest pain or pressure and is unaware they are having a heart attack. In survivors of silent heart attacks, doctors can usually detect evidence of prior heart muscle damage by EKG and echocardiogram studies.
A heart attack can trigger the sudden onset of ventricular fibrillation. Ventricular fibrillation is a chaotic electrical rhythm of the heart that causes cardiac arrest (the heart stands still and ceases to pump blood). Ventricular fibrillation causes permanent brain damage and death unless a normal heartbeat can be restored within five minutes of its onset. Of the 1 million Americans who suffer heart attacks annually, approximately 400,000 of them die suddenly and unexpectedly from ventricular fibrillation before the victims can reach any medical assistance or the emergency room. For these people, the first sign of coronary heart disease is sudden unexpected death.
Unlike angina, a heart attack results in permanent damage of the heart muscle. After a heart attack, the damaged portion of the heart is left with a scar. If the amount of heart muscle damage and the area of scarring are small, the performance of the heart as a pump will not be significantly impaired. However, repeated heart attacks or a heart attack with extensive heart muscle damage can weaken the heart and cause heart failure. People with heart failure experience shortness of breath, tolerate exercise poorly, and lack vigor because their weakened heart muscle cannot pump enough blood to keep their bodies healthy and active.
Why is preventing coronary atherosclerosis important?
Coronary atherosclerosis is the major cause of heart attacks. Heart attacks are the major cause of sudden unexpected death among otherwise healthy adults in the prime of their lives. Heart attacks are also a significant cause of heart failure in this country. Heart failure considerably decreases the patient's longevity and quality of life. In dollar terms, coronary heart disease is costly. The total cost of coronary artery bypass surgery, coronary angioplasty and stenting, medications, and hospitalizations exceeds 50 billion dollars annually.
How common is coronary atherosclerosis?
More than 5 million Americans know they have coronary atherosclerosis. They are aware of their condition because they have either: 1) already suffered a heart attack; 2) are being treated with medications for angina pectoris; 3) have already undergone coronary artery bypass graft surgery to overcome coronary artery narrowing or blockage; 4) have already undergone coronary artery angioplasty with stent placement to alleviate coronary artery blockage; or 5) have had diagnostic tests that reveal the coronary artery disease. For every person who knows they have coronary heart disease, many more have atherosclerosis but are unaware of their condition. One or more of their coronary arteries may have already narrowed by more than 50%, but they have not yet developed angina or other symptoms of coronary heart disease. These individuals are at risk of suffering heart attacks, angina, and sudden death.
When does the coronary atherosclerosis process begin?
Although the coronary arteries are wide open at birth, the atherosclerosis process begins early in life. Between the ages of 10 and 20, "fatty streaks" are already being deposited on the inner lining of the coronary arteries. Over the years, some of these fatty streaks grow into larger cholesterol plaques that can protrude into the artery lumen and harden the artery walls. Many men and women between the ages of 20 and 30 typically are unaware that their coronary arteries are gradually accumulating cholesterol plaques. But by ages 40 to 50, many people have developed enough atherosclerosis to put them at risk for coronary heart disease.
Are atherosclerosis and heart attacks preventable?
Coronary atherosclerosis is both preventable and reversible. By adopting proper life style modifications and by taking medications, a person can: - Reduce or stop the formation of new cholesterol plaques on the artery walls;
- Reduce existing cholesterol plaques on the artery walls;
- Widen narrowed arteries; and
- Prevent the rupture of cholesterol plaques, which initiates blood clot formation.
Atherosclerosis prevention should start early, preferably during childhood and adolescence. Most scientists believe that preventing atherosclerosis is more effective than trying to reverse established blockages or getting rid of plaques in the arteries. Therefore, children and adolescents should be taught lifetime habits of regular exercise, avoidance of smoking, and good nutrition.
Have most people done enough to prevent atherosclerosis and heart attacks?
Unfortunately, many Americans have not taken adequate steps to prevent atherosclerosis. Reasons for this failure include: - Lack of awareness that they already have coronary atherosclerosis, and ignorance that coronary atherosclerosis and heart attacks are preventable;
- Lack of awareness of their blood cholesterol levels and profiles;
- Unwillingness or inability to quit cigarette smoking;
- High blood pressure or diabetes mellitus that are either undiagnosed or inadequately controlled;
- Lack of exercise, an excess of fat and cholesterol in their diet, and inability to lose excess weight; and
- Failure to take full advantage of medications that improve cholesterol profiles, usually out of fear of potential side effects.
What are the risk factors for coronary atherosclerosis and heart disease?
Well-known risk factors for coronary atherosclerosis and heart attacks are: - Elevated levels of LDL cholesterol (the "bad" cholesterol) in the blood;
- Family history of early coronary heart disease, including a heart attack or sudden death before age 55 in the father or other male first-degree relative, or before age 65 in the mother or other female first-degree relative;
- Cigarette smoking;
- Diabetes mellitus;
- High blood pressure; and
- Low levels of HDL (the "good" cholesterol) in the blood.
- Sedentary lifestyle
Less recognized but just as important risk factors for coronary atherosclerosis are: - A preponderance of small LDL cholesterol particles in the blood. LDL cholesterol particles come in different sizes. The size of a person's LDL cholesterol particles is predominantly genetically inherited. The smaller LDL cholesterol particles are far more dangerous in causing atherosclerosis than the larger particles. The smaller LDL particles can penetrate the wall of the arteries more easily than the larger LDL particles. A person with an abundance of small LDL cholesterol particles in the blood has a significantly higher risk of heart attack and coronary atherosclerosis than someone with larger LDL cholesterol particles in their blood.
- Abnormally elevated blood levels of Lipoprotein A, Lp(a). Lipoprotein A or Lp(a) is a LDL cholesterol particle that is linked chemically to a protein called apo(a). The level of Lp(a) in the blood is also genetically inherited. Men and women with elevated blood levels of Lp(a) have significantly higher rates of coronary atherosclerosis and heart attacks.
- Elevated homocysteine levels in the blood. Homocysteine is a metabolic by-product of animal protein. Tests are now available to measure homocysteine levels in the blood. Higher homocysteine levels in the blood are associated with atherosclerosis in coronary arteries and carotid arteries (arteries that supply blood to the brain).
- Chronic infection with certain viruses (such as CMV) and bacteria (such as chlamydia pneumonia ) may cause coronary artery inflammation that may aggravate atherosclerosis. This is a relatively new discovery, and is the topic of much ongoing research.
How can coronary atherosclerosis and heart attacks be prevented?
We can reduce our risks for atherosclerosis and heart attack by: - Controlling high blood pressure and diabetes mellitus
- Stopping cigarette smoking
- Exercising regularly
- Losing excess weight
- Lowering blood level of LDL cholesterol
- Increasing blood level of HDL cholesterol
- Lowering blood levels of Lp(a) cholesterol and triglyceride
- Increasing LDL cholesterol particle sizes
- Anti-platelet medications (such as low dose aspirin) to prevent blood clots
- Antibiotics to eradicate chronic infection
- Antioxidants to prevent blood vessel damage
- Folic acid and other B vitamins to decrease blood levels of homocysteine
- Ace inhibitors (such as ramipril , Altace) to prevent arthrosclerosis
What is cholesterol?
Cholesterol is a fatty substance (a lipid) that is an important part of the outer lining (membrane) of cells in the body of animals. Cholesterol is also found in the blood circulation of humans. The cholesterol in a person's blood originates from two major sources, dietary intake and liver production. Dietary cholesterol comes mainly from meat, poultry, fish, and dairy products. Organ meats, such as liver, are especially high in cholesterol content, while foods of plant origin contain no cholesterol. After a meal, cholesterol is absorbed by the intestines into the blood circulation and is then packaged inside a protein coat. This cholesterol-protein coat complex is called a chylomicron.
The liver is capable of removing cholesterol from the blood circulation as well as manufacturing cholesterol and secreting cholesterol into the blood circulation. After a meal, the liver removes chylomicrons from the blood circulation. In between meals, the liver manufactures and secretes cholesterol back into the blood circulation.
What is LDL and HDL cholesterol?
Cholesterol, like oil, cannot dissolve in the blood unless it is combined with special proteins called lipoproteins. (Without combining with lipoproteins, cholesterol in the blood will turn into a solid substance.) The cholesterol that is secreted by the liver into the blood is combined either with very low-density lipoproteins (VLDL) or high-density lipoproteins (HDL). VLDL cholesterol is then metabolized in the bloodstream to produce LDL cholesterol. The cholesterol combined with low-density lipoprotein is called LDL cholesterol, and the cholesterol combined with high-density lipoproteins is called HDL cholesterol.
How does cholesterol cause heart disease?
LDL cholesterol is called "bad" cholesterol, because elevated LDL cholesterol is associated with an increased risk of coronary heart disease. LDL lipoprotein deposits cholesterol on the artery walls, causing the formation of a hard, thick substance called cholesterol plaque. Over time, cholesterol plaque causes thickening of the artery walls and narrowing of the arteries, a process called atherosclerosis. Arteries that supply blood and oxygen to the heart muscles are called coronary arteries. When coronary arteries are narrowed by atherosclerosis, they are incapable of supplying enough blood and oxygen to the heart muscle during exertion. Lack of oxygen (ischemia) to the heart muscle causes chest pain, also formation of a blood clot in the artery can clause complete blockage of the artery, leading to death of heart muscle (heart attack). Atherosclerotic disease of coronary arteries (coronary heart disease) is the most common cause of death in the United States, accounting for about 600,000 deaths annually.
HDL is called the "good cholesterol" because HDL cholesterol particles prevent atherosclerosis by extracting cholesterol from the artery walls and disposing of them through the liver. Thus, high levels of LDL cholesterol and low levels of HDL cholesterol (high LDL/HDL ratios) are risk factors for atherosclerosis, while low levels of LDL cholesterol and high level of HDL cholesterol (low LDL/HDL ratios) are desirable.
What determines the level of LDL cholesterol in the blood?
The liver not only manufactures and secretes LDL cholesterol into the blood, it also removes LDL cholesterol from the blood. To remove LDL cholesterol from the blood, the liver relies on special proteins called LDL receptors that are normally present on the surface of liver cells. LDL receptors snatch LDL cholesterol particles from the blood and transport them inside the liver. A high number of active LDL receptors on the liver surfaces is associated with the rapid removal of LDL cholesterol from the blood and low blood LDL cholesterol levels. A deficiency of LDL receptors is associated with high LDL cholesterol blood levels.
Both heredity and diet have a significant influence on a patient's LDL, HDL and total cholesterol levels. For example, familial hypercholesterolemia (FH) is a common inherited disorder whose victims have a diminished number or nonexistent LDL receptors on the surface of liver cells. The resultant decreased activity of the LDL receptors limits the liver's ability to remove LDL cholesterol from blood. Thus, affected family members have abnormally high LDL cholesterol levels in the blood. They also tend to develop atherosclerosis and heart attacks during early adulthood.
Diets that are high in saturated fats and cholesterol decrease the LDL receptor activity in the liver, thereby raising the levels of LDL cholesterol in the blood. Fats are classified as saturated or unsaturated according to their chemical structure. Saturated fats are derived primarily from meat and dairy products and can raise blood cholesterol levels. Some vegetable oils made from coconut, palm, and cocoa are also high in saturated fats. On the other hand, most other vegetable oils are high in unsaturated fats. Unlike saturated fats, unsaturated fats do not raise blood cholesterol and can sometimes lower cholesterol. Olive and canola oil are high in monounsaturated fats, which may have a protective effect against coronary heart disease. Unfortunately, some vegetable oils are converted to saturated fats during a process called "hydrogenation" which can be required for food processing.
Does lowering LDL cholesterol prevent atherosclerosis and heart attacks?
Elevated LDL cholesterol is a major cause of atherosclerosis and heart attacks. Lowering LDL cholesterol by using medications, such as statins , along with low saturated fat and low cholesterol diets has been shown in numerous clinical trials to significantly reduce the risk of heart attacks and strokes in both men and women. Therefore, lowering LDL cholesterol is the first priority in preventing atherosclerosis and heart attacks.
The benefits of lowering LDL cholesterol include: - Reducing the formation of new cholesterol plaques;
- Eliminating existing plaques;
- Preventing rupture of existing plaques;
- Decreasing the risk of heart attacks; and
- Lowering the chance of strokes.
How low should LDL cholesterol be?
The National Cholesterol Education Program (NCEP) has issued In May 2001 desirable and undesirable levels of LDL cholesterol, total cholesterol, HDL cholesterol and triglyceride levels. They are:
LDL cholesterol (mg/dl)
<100 Optimal
100-129 Near or above optimal
130-159 Borderline high
160-189 High
> 190 Very high
Total cholesterol (mg/dl)
<200 Desirable
200-239 Borderline high
>240 High
HDL cholesterol (mg/dl)
<40 Low (undesirable)
>60 High (desirable)
Triglycerides (mg/dl)
<150 Normal
150-199 Borderline-high
200-499 High
>500 Very high
While NCEP expert panel designates LDL cholesterol of less than (<) 100 mg/dl as the optimal level, the panel is not recommending this level for all people. Instead, the target level (goal) of LDL cholesterol lowering is tailored to a person's risk of developing coronary heart disease (CHD). People with the highest CHD risks should have their LDL cholesterol lowered below 100 mg/dl, while people with lesser CHD risks will have higher LDL cholesterol target levels.
LDL cholesterol targets: - Individuals who already have CHD (such as prior heart attacks and bypass surgery), strokes, or diabetes mellitus should have LDL cholesterol target of < 100 mg/dl.
- Individuals who have no CHD or diabetes mellitus or prior strokes, but have 2 or more of the following risk factors (men over 45 and women over 55, cigarette smoking, high blood pressure, HDL cholesterol less than 40, and having first degree relatives with early onset of CHD) should have LDL cholesterol target of <130 mg/dl.
- Individuals with no CHD, no diabetes mellitus, and 0-1 risk factors should have LDL cholesterol target of <160mg/dl.
| Risk Category | LDL cholesterol Goal (mg/dl) | | Have CHD and/or diabetes,10-year risk >20% | <100 | | 2 or more risk factors,10-year risk <20% | <130 | | 0-1 risk factor , 10-year risk <10% | <160 |
Whether the NCEP LDL cholesterol treatment target levels are low enough is controversial. An increasing number of experts in treating blood lipid disorders believe that aggressively lowering LDL cholesterol below 80 further decreases atherosclerosis and heart attack rates. In order to achieve these levels, diet and exercise are insufficient and moderate to high doses of a statin drug also will be necessary on a long-term basis. However, the safety of moderate to high doses of statins over several decades is unknown. Thus, the decision to aggressively reduce the patient's LDL cholesterol level below the levels recommended by NCEP should be individualized after consultation with a doctor familiar with the treatment of lipid disorders.
How can LDL cholesterol levels be lowered?
In order to lower LDL cholesterol, the activity level of the LDL receptors must be increased. LDL receptor activities can be increased by diets that are low in cholesterol and saturated fats and by medications.
Lowering LDL cholesterol involves losing excess weight, exercising regularly, and following a diet that is low in saturated fat and cholesterol. Medications are prescribed when diet and exercise cannot reduce the LDL cholesterol to acceptable levels. The most effective and widely used medications to lower LDL cholesterol are called statins. Other medications used in lowering LDL cholesterol and in altering cholesterol profiles include nicotinic acid (niacin), fibrates such as gemfibrozil (Lopid), and resins such as cholestyramine (Questran).
Is lowering LDL cholesterol enough?
Unfortunately, the prevention and treatment of atherosclerosis are more complicated than just lowering LDL cholesterol levels. LDL cholesterol reduction is only half of the battle against atherosclerosis. Individuals who have normal or only mildly elevated LDL cholesterol levels can still develop atherosclerosis and heart attacks even in the absence of other risk factors such as cigarette smoking, high blood pressure, and diabetes mellitus. Additionally, successfully lowering elevated LDL cholesterol levels cannot always prevent atherosclerosis and heart attacks. In many clinical trials to lower LDL cholesterol, there were patients who adhered to their assigned diets, faithfully took their cholesterol-lowering medications, successfully lowered their LDL cholesterol to target levels, yet still suffered progressive atherosclerosis and heart attacks. It is clear that while lowering LDL cholesterol below NCEP target levels is an important step, there are other factors involved.
What are the other risk factors for heart attacks?
The other risk factors include: - Abnormally low HDL cholesterol levels.
- The size of the LDL cholesterol particles in the blood may be too small. Scientists have found that the size of LDL cholesterol particles in the blood is predominantly genetically inherited. People who have small and dense LDL cholesterol particles have a higher risk of developing atherosclerosis and heart attacks than those who have larger and more buoyant particles.
- Elevated Lp(a) cholesterol levels. The level of Lp(a) cholesterol is also predominantly genetically inherited. Individuals with elevated levels of Lp(a) cholesterol have a higher rate of atherosclerosis and risk of heart attacks.
- Elevated homocysteine levels.
What are LDL cholesterol particle size patterns A and B?
The LDL patterns A and B refer to the size of LDL cholesterol particles in the blood. Some doctors believe that small LDL cholesterol particles in the blood may pose a greater risk for developing atherosclerosis and heart attacks than the absolute level of LDL cholesterol in the blood. The size of LDL cholesterol particles is primarily inherited. A special blood test called polyacrylamide gradient gel electrophoresis can measure particle size and determine whether a person has blood cholesterol LDL pattern A or LDL pattern B.
Persons with LDL cholesterol pattern A have large, buoyant LDL cholesterol particles. Individuals with pattern A are more likely to have normal blood levels of LDL cholesterol, HDL cholesterol, and triglycerides. Pattern A is usually not associated with an increased likelihood of atherosclerosis.
Persons with LDL cholesterol pattern B have predominantly small and dense LDL cholesterol particles. Pattern B is frequently associated with low HDL cholesterol levels, elevated triglyceride levels, and the tendency to develop high blood sugar levels and type II diabetes mellitus. Individuals with pattern B are also more likely to develop high blood triglyceride levels after a fatty meal (postprandial hyperlipidemia). Pattern B is associated with accelerated atherosclerosis and a 3 to 5- fold increase in heart attack risk. Pattern B is believed to be the most important cause of atherosclerosis in people with normal or near normal total and LDL cholesterol levels.
Some scientists believe that the smaller LDL particles are more dangerous than the larger ones because they can more easily squeeze through the tiny gaps between the cells in the endothelium to reach inside the artery walls. The endothelium is a thin layer of cells which covers the inner wall of the arteries. The cells making up the endothelium have tiny gaps between them. Others postulate that the smaller LDL cholesterol particles are more easily oxidized. Oxidation of cholesterol is significant in the formation of cholesterol plaques.
How can LDL cholesterol size be enlarged?
Even though LDL cholesterol particle size is mainly genetically inherited, individuals who have small LDL particles (pattern B) can increase their particle size through diet, exercise, and medications.
Diets that are low in saturated fat and cholesterol, regular aerobic exercise, and loss of excess body fat have been determined to decrease the number of small LDL particles and increase the number of large LDL particles in the blood. In other words, lifestyle modifications can change pattern B to pattern A.
When lifestyle changes alone are unsuccessful, medications can be used. Even though the statin medications (discussed below) are effective in lowering the absolute levels of LDL cholesterol, they appear to have a limited effect on LDL cholesterol size pattern. Medications such as nicotinic acid (niacin) and gemfibrozil (Lopid) have been found effective in many instances in increasing the size of LDL cholesterol particles.
Why is HDL the good cholesterol?
HDL is the good cholesterol because it protects the arteries from the atherosclerosis process. HDL cholesterol extracts cholesterol particles from the artery walls and transports them to the liver to be disposed through the bile. It also interferes with the accumulation of cholesterol in the artery walls by the LDL cholesterol particles.
The risk of atherosclerosis and heart attacks in both men and is strongly related to HDL cholesterol levels. Low levels of HDL cholesterol are linked to a higher risk, whereas high HDL cholesterol levels are associated with a lower risk.
Very low and very high HDL cholesterol levels can run in families. Families with low HDL cholesterol levels have a higher incidence of heart attacks than the general population, while families with high HDL cholesterol levels tend to live longer with a lower frequency of heart attacks.
Like LDL cholesterol, life style factors and other conditions influence HDL cholesterol levels. HDL cholesterol levels are lower in persons who smoke cigarettes, eat a lot of sweets, are overweight and inactive, and in patients with type II diabetes mellitus.
HDL cholesterol is higher in people who are lean, exercise regularly, and do not smoke cigarettes. Estrogen increases a person's HDL cholesterol, which explains why women generally have higher HDL levels than men do.
For individuals with low HDL cholesterol levels, a high total or LDL cholesterol blood level further increases the incidence of atherosclerosis and heart attacks. Therefore, the combination of high levels of total and LDL cholesterol with low levels of HDL cholesterol is undesirable whereas the combination of low levels of total and LDL cholesterol and high levels of HDL cholesterol is favorable.
What are LDL/HDL and total/HDL ratios?
The total cholesterol to HDL cholesterol ratio (total chol/HDL) is a number that is helpful in estimating the risk of developing atherosclerosis. The number is obtained by dividing total cholesterol by HDL cholesterol. (High ratios indicate higher risks of heart attacks, low ratios indicate lower risk).
High total cholesterol and low HDL cholesterol increases the ratio and is undesirable. Conversely, high HDL cholesterol and low total cholesterol lowers the ratio and is desirable. An average ratio would be about 4.5. Ideally one should strive for rations of 2 or 3 (less than 4).
What are the treatment guidelines for low HDL cholesterol?
In clinical trials involving lowering LDL cholesterol, scientists also studied the effect of HDL cholesterol on atherosclerosis and heart attack rates. They found that even small increases in HDL cholesterol could reduce the frequency of heart attacks. For each 1 mg/dl increase in HDL cholesterol there is a 2 to 4% reduction in the risk of coronary heart disease. Although there are no formal NCEP target treatment levels of HDL cholesterol, HDL of <40 mg/dl is considered undesirable, and measures should be taken to increase it.
How can levels of HDL cholesterol be raised?
The first step in increasing HDL cholesterol levels (and decreasing LDL/HDL ratios) is life style modification. When life style modifications are insufficient, medications are used. In prescribing medications or medication combinations, doctors have to take into account medication side effects as well as presence or absence of other abnormalities in cholesterol profiles.
Regular aerobic exercise, loss of excess weight (fat), and cessation of smoking cigarettes will increase HDL cholesterol levels. Regular alcohol consumption (such as one drink a day) will also raise HDL cholesterol. However, there are different subclasses of HDL cholesterol which have varying degrees of effectiveness in preventing atherosclerosis. Alcohol is believed to increase the level of the less important subtype of HDL cholesterol. Because of other adverse health consequences of excessive alcohol consumption, alcohol is not recommended as a standard treatment for low HDL cholesterol.
Medications that are effective in increasing HDL cholesterol include nicotinic acid (niacin), gemfibrozil (Lopid), estrogen, and to a lesser extent, the statin drugs (discussed below). A newer medicine, fenofibrate (Tricor) has shown much promise in selectively increasing HDL levels and reducing serum triglycerides.
What is lipoprotein (a), Lp(a) cholesterol?
Lipoprotein (a), Lp(a), is a LDL cholesterol particle that is attached to a special protein called apo(a). In large part, a person's level of Lp(a) in the blood is genetically inherited. Elevated levels of Lp(a) (higher than 20 mg/dl to 30 mg/dl) in the blood are linked to a greater likelihood of atherosclerosis and heart attacks in both men and women. The risk is even more significant if the Lp(a) cholesterol elevation is accompanied by high LDL/HDL ratios.
Certain diseases are associated with elevated Lp(a) levels. Patients on chronic kidney dialysis and those with nephrotic syndromes (kidney diseases that cause leakage of blood proteins into the urine) tend to have high levels of Lp(a).
There are many theories as to how Lp(a) causes atherosclerosis although exactly how Lp(a) accumulates cholesterol plaques on the artery walls has not been well defined. Clinical trials that conclusively prove that lowering Lp(a) reduces atherosclerosis and the risk of heart attacks have not been conducted. Currently, there is no international standard for determining Lp(a) cholesterol levels, and commercial sources of Lp(a) testing may not have the same accuracy as research laboratories. Therefore, specifically measuring and treating elevated Lp(a) cholesterol levels are not widely performed in this country.
How can Lp(a) cholesterol levels be reduced?
Most lipid-lowering medications such as statins, Lopid, and cholestyramine have a limited effect in lowering Lp(a) cholesterol levels. Estrogen has been shown to lower Lp(a) cholesterol levels by approximately 20% in women with elevated Lp(a) cholesterol. Estrogen can also increase HDL cholesterol levels when given to postmenopausal women. Additionally, nicotinic acid (Niacin or Niaspan) in high doses has been found to be effective in lowering Lp(a) cholesterol levels by approximately 30%.
What are triglycerides, chylomicrons, and VLDL?
Triglyceride is a fatty substance that is composed of three fatty acids each of which is attached to a glycerol molecule. Like cholesterol, triglyceride in the blood either comes from the diet or the liver. Also, like cholesterol, triglyceride cannot dissolve and circulate in the blood without combining with a lipoprotein. Thus, after a meal, the triglyceride and cholesterol that are absorbed into the intestines are packaged into round particles called chylomicrons before they are released into the blood circulation.
A chylomicron is a collection of cholesterol and triglyceride that is surrounded by a lipoprotein outer coat. (Chylomicrons contain 90% triglyceride and 10% cholesterol.) There are special enzymes on the blood vessels that break up the triglyceride inside the chylomicrons, releasing fatty acids in the process. The fatty acids can either be used by the muscles as energy, or absorbed by fat cells where they are incorporated again into triglyceride that can be stored in the fat cells for future energy needs. The chylomicrons are then removed from the circulation by the liver.
The liver not only removes triglyceride and chylomicrons from the blood, it also synthesizes and packages triglyceride into VLDL (very low-density lipoprotein) particles and releases them back into the blood circulation. Therefore, before breakfast after an overnight fast, most of the triglyceride in the blood comes from the liver in the form of VLDL particles. Like chylomicrons, VLDL particles contain mostly triglyceride. Some of the VLDL particles lose triglyceride in the blood and become cholesterol-rich LDL particles.
Do high triglyceride levels cause atherosclerosis?
Whether elevated triglyceride levels in the blood lead to atherosclerosis and heart attacks is controversial. While most doctors now believe that an abnormally high triglyceride level is a risk factor for atherosclerosis, it is difficult to conclusively prove that raised triglyceride by itself can cause atherosclerosis. However, it is increasingly recognized that elevated triglyceride is often associated with other conditions that increase the risk of atherosclerosis including obesity , low levels of HDL- cholesterol, insulin resistance and poorly controlled diabetes mellitus, and small, dense LDL cholesterol particles.
What are the causes of elevated triglyceride levels?
In some people, abnormally high triglyceride levels (hypertriglyceridemia) are inherited. Examples of inherited hypertriglyceridemia disorders include mixed hypertriglyceridemia, familial hypertriglyceridemia, and familial dysbetalipoproteinemia.
Hypertrigleridemia can often be caused by non-genetic factors such as obesity, excessive alcohol intake, diabetes mellitus, kidney disease, and estrogen containing medications such as birth control pills.
How can elevated blood triglyceride levels be treated?
The first step in treating hypertriglyceridemia is a low fat diet with a limited amount of sweets, regular aerobic exercise, loss of excess weight, reduction of alcohol consumption, and stopping cigarette smoking. In patients with diabetes mellitus, meticulous control of elevated blood glucose is also important.
When medications are necessary, fibrates (such as Lopid), nicotinic acid, and statin medications can be used. Lopid not only decreases triglyceride levels but also increases HDL cholesterol levels and LDL cholesterol particle size. Nicotinic acid lowers triglyceride levels, increases HDL cholesterol levels and the size of LDL cholesterol particles, as well as lowers the levels of Lp (a) cholesterol. The statin drugs have been found effective in decreasing triglyceride as well as LDL cholesterol levels and, to a lesser extent, in elevating HDL cholesterol levels. A relatively new medicine, fenofibrate (Tricor) shows promise as an effective agent in lowering serum triglyceride levels, as well as raising the HDL, particularly in patients who have had suboptimal responses to Lopid. In some patients a combination of Lopid or Tricor with adjunctive statin therapy (see below) may be prescribed, while this combination is often effective in patients with complex lipid disorders, the potential for side effects may be increased, and such patients should be under strict medical supervision.
What are the statin drugs?
The statins are the most widely used medications today in lowering LDL cholesterol. Most of the clinical trials that showed heart attack reduction and improved longevity used one of the statins as the cholesterol lowering medication. Statins are well tolerated with low side effect rates when used long term. Statins not only lower blood LDL cholesterol levels, they also help increase HDL cholesterol levels. The statin medicines that are now on pharmacy shelves in the U.S. (putting the generic name first followed by the brand name in parentheses) are: - fluvastatin sodium (Lescol) made by Novartis
- atorvastatin calcium (Lipitor) made by Parke-Davis and Pfizer
- lovastatin (Mevacor) made by Merck
- pravastatin sodium (Pravachol) made by Bristol-Myers Squibb
- simvastatin (Zocor) made by Merck
The statins act by repressing or inhibiting an enzyme called HMG-CoA reductase. The role of this enzyme is the promotion of a chemical reaction early in the synthesis of cholesterol. By inhibiting HMG-CoA reductase, the statins hinder the production (synthesis) of cholesterol by the liver. Diminished synthesis of cholesterol in the liver in turn stimulates (increases) the activity of LDL receptors on the surface of liver cells. Increasing LDL receptor activity decreases LDL cholesterol levels in blood.
Studies have conclusively established that lowering LDL cholesterol with diet and statins reduces the risk of a second heart attack. The prevention of recurrent heart attacks in patients who have already suffered a heart attack is called secondary prevention.
Studies have also demonstrated that reducing LDL cholesterol with diet and statins reduces the risk of having the first heart attack. Prevention of heart attacks in those who have never had a heart attack is called primary prevention.
Studies have also confirmed that reducing LDL cholesterol benefits both men and women.
For more information regarding the side effects, precautions, and drug interactions of the various statins, please read the article on Statins, and visit the Medications Center.
What are the limitations of statins?
Statins are currently the most important class of medications in lowering LDL cholesterol, which is now the most important first step in preventing atherosclerosis and heart attacks. But statins are not the only answer. Other cholesterol-altering medications can also be important in the fight against atherosclerosis.
For example, in certain patients with familial hypercholesterolemia (FH), a statin alone may not be enough when LDL cholesterol levels are very high. A statin may need to be combined with another medication such as cholestyramine or nicotinic acid in order to lower the LDL cholesterol to acceptable levels.
Statins may also not be as effective as other medications in treating elevated Lp(a) cholesterol levels and in enlarging small LDL cholesterol particle sizes. For example, estrogen and niacin are more effective than statins in decreasing the blood Lp(a) cholesterol levels. Gemfibrozil and niacin are more effective than statins in raising blood HDL levels and in increasing the size of the LDL cholesterol particle. Diets rich in B vitamins or vitamin supplements, such as folic acid and vitamin B6, help lower blood homocysteine levels. Elevated homocysteine levels also aggravate atherosclerosis.
What is nicotinic acid?
Nicotinic acid (niacin) is a B vitamin. An average American diet contains 15-30 mg of niacin per day. However, in treating blood cholesterol and triglyceride disorders, high doses (1-3 grams a day) of nicotinic acid are necessary. Nicotinic acid increases HDL cholesterol, lowers LDL cholesterol, and improves the LDL/HDL ratio. Nicotinic acid also increases LDL cholesterol particle sizes while lowering Lp(a) cholesterol and triglyceride levels.
Nicotinic acid is most suited for individuals whose only problem is low HDL cholesterol. Nicotinic acid used alone can raise HDL cholesterol levels by 30% or more.
Nicotinic acid is not as effective as a statin in lowering LDL cholesterol levels. Therefore, when low HDL cholesterol is accompanied by high LDL cholesterol, most doctors use a statin to decrease the LDL cholesterol first. Statins can also modestly increase HDL cholesterol levels. If necessary, nicotinic acid can be added to a statin to further raise HDL cholesterol levels.
The most common side effect of nicotinic acid is a flushing sensation of the face and a general sense of itching, which occur about half an hour after taking the drug. Another side effect is upset stomach. These side effects can be partially alleviated by taking nicotinic acid with meals. Nicotinic acid comes in regular tablets or slow and sustained release capsules. The sustained release capsules release nicotinic acid from the stomach into the blood circulation more gradually than the regular tables. Therefore, the sustained release capsules such as Niaspan produce a lower incidence of upset stomach and skin flushing than the niacin tablets.
Another side effect is irritation of the liver with an abnormal elevation of liver enzymes in the blood. This liver irritation is usually reversible upon discontinuing nicotinic acid. Other side effects of nicotinic acid include aggravating blood sugar levels in patients with diabetes mellitus and precipitating painful arthritis attacks in patients with gout .
What is gemfibrozil (Lopid)?
Gemfibrozil (Lopid) is a fibric acid derivative that has been reported to raise HDL levels by about 15%. Gemfibrozil can also lower triglyceride levels and increase the size of LDL cholesterol particle sizes. Therefore, gemfibrozil is best suited for patients with elevated triglyceride levels, LDL cholesterol pattern B, and low HDL cholesterol.
Gemfibrozil is not as effective as the statins in lowering LDL cholesterol and is insufficient for this purpose when used alone. Therefore, medication combinations may be necessary in treating patients with high LDL cholesterol levels who also have other lipid abnormalities. Doctors generally avoid combining a statin drug with gemfibrozil because of concern over the added risk of muscle inflammation (myositis).
The side effects of gemfibrozil include nausea, stomach upset, and sometimes diarrhea . Like the statins and nicotinic acid, it can also cause liver irritation. The liver irritation is usually mild and reversible, but it occasionally can be severe enough to require stopping the drug. Gemfibrozil can cause gallstones when used over several years. The drug can also intensify the effectiveness of blood thinners such as Coumadin when both medications are used together. Thus, the dose of Coumadin should be adjusted to avoid over-thinning of the blood, which can lead to excessive bleeding.
What is Cholestyramine (Questran)?
Cholestyramine (Questran) and colestipol (Colestid) are sand-like materials which bind bile salts in the intestine and allow fat and cholesterol to be eliminated in the stool. Cholestyramine is a resin that increases LDL receptor activity and lowers LDL cholesterol. Cholestyramine has been used effectively in combination with gemfibrozil to help lower LDL cholesterol levels. With these drugs, cholesterol can be reduced by 20%, but triglyceride levels may increase. These drugs can have the side effects of bloating, nausea, indigestion, and constipation . They also interfere with the absorption of many other drugs from the stomach and intestine.
Who should undergo standard lipid profile testing?
It is recommended that every adult over 20 should have lipid panel tests (total cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride levels) every 5 years if LDL cholesterol is less than 130, and every 1-3 years if LDL cholesterol is borderline (between 130 and 160). This is particularly important for those with a family history of coronary artery disease. Once these cholesterol figures are known, the chance of developing heart disease can be determined in combination with the other risk factors that play a role in its development.
Who should undergo testing for LDL cholesterol particle size and Lp(a) cholesterol levels?
The scientific analysis for the determination of LDL size and Lp(a) is relatively new and is not standardized from laboratory to laboratory. Thus, results will vary to some degree between different laboratories. Also, because the use of any specific laboratory test is not widespread, the cost of testing remains expensive. (Lp(a) measurements cost approximately $100 and LDL size measurements about $200 - $300).
Because of the cost and the variability of testing, determination of these cholesterol components is not for everyone. Currently, persons who have been diagnosed with coronary artery disease whose risk factor profile would not otherwise predict coronary artery disease at the age at which it occurred, should be tested for these more specific cholesterol components. For example, if heart disease occurs at a young age without high LDL levels, high blood pressure, diabetes, or cigarette smoking, the physician and patient should then search for another risk factor such as small LDL size or elevated Lp(a).
Among persons without coronary heart disease, those with a family history of heart disease occurring early in life should be tested for these entities, which are predominantly determined by genetic inheritance. As the cost and accuracy of testing improves, the evaluation of these components should become more widespread.
What are platelet inhibitors?
A heart attack, or myocardial infarction, is the result of a blood clot that forms where a cholesterol plaque has accumulated in an artery to the heart (coronary artery). Blood clotting elements, called platelets, group together in the formation of a blood clot. This grouping (or aggregation) of platelets can be blocked, or inhibited, by aspirin. Therefore, aspirin can be used to prevent clot formation. For example, treatment with aspirin during a heart attack reduces mortality by 23%. Moreover, aspirin has a very important role in preventing a second heart attack or stroke (secondary prevention). In a patient with established blood vessel disease from cholesterol (atherosclerosis), aspirin reduces the risk of a heart attack, stroke, or death by 25%.
Recently, attention has been focused on other, more potent, inhibitors of platelets function. The benefits of these drugs in the prevention of a second heart attack (secondary prevention) have been found to be superior to those of aspirin. One of these drugs, ticlopidine (Ticlid), was shown to reduce the risk of stroke, heart attack, or vascular death by 30% as compared to aspirin in patients with recent stroke symptoms (The Canadian American Ticlopidine Study). In another study (Swedish Ticlopidine Multicenter Study), treatment with ticlopidine was associated with a 43% reduction in deaths from heart attack in patients who had not experienced a prior heart attack but who had symptoms of poor circulation. Ticlopidine's more common side effects include rash and diarrhea. In very rare cases, ticlopidine can cause a serious and potentially lethal reduction in the white blood count and platelet count. Clopidogrel (Plavix) is a medicine that is similar to ticlopidine but has demonstrated a much more favorable side effect and safety profile. Studies have also shown it to possibly be somewhat more effective than ticlopidine.
Ticlopidine and clopidogrel are also an excellent alternative to aspirin in patients who cannot take aspirin due to other conditions. Despite its increased cost relative to aspirin, clopidogrel may be a preferred prophylactic agent in many patients. Trials are now ongoing to determine if the combination of aspirin and clopidogrel provides more protective benefit than either agent alone.
Recent studies have reported a higher incidence of heart attacks in patients taking newer anti-inflammatory agents such as Celebrex and Vioxx. In these studies, the negative effects of these drugs were mitigated by the concomitant use of aspirin. For this reason, patients with risk factors for the development of coronary artery disease, or with known coronary artery disease, who are taking these medications should also take daily aspirin.
What are ACE inhibitors?
Angiotensin II is a naturally-produced chemical that helps the body to normally maintain blood pressure. Angiotensin II powerfully constricts the blood vessels and stimulates water and salt retention, which in turn causes a rise in blood pressure.
ACE (angiotensin converting enzyme) inhibitors are drugs that block, or inhibit, the formation of angiotensin II and are thus effective in lowering blood pressure. They have also been found to slow the progression of congestive heart failure and coronary artery disease and lower the mortality rate from these conditions. In a study of patients over a five year period, published in January, 2000, the ACE inhibitor, ramipril (Altace), was found to reduce mortality by 26%. Side effects of ACE inhibitors may include a dry cough, an increase in serum potassium, and kidney toxicity (predominantly in patients with some preexisting kidney insufficiency).
Another class of agents, ARB's (angiotensin receptor blockers) may share similar protective benefits with fewer side effects in some patients.
What about antioxidants?
Antioxidants are food supplements that have been promoted to prevent heart disease and stroke. An important early event in the development of a cholesterol plaque in atherosclerosis is the oxidative modification of LDL cholesterol (low density lipoprotein) particles in the blood and the subsequent interaction of this modified LDL with the wall of the coronary artery. This initiates the formation of the cholesterol plaque. Antioxidants that block the oxidative modification of LDL have been shown to slow the progression of atherosclerosis in animal experiments.
Examples of antioxidants include vitamin E and beta carotene. In humans, observational studies (studies that observe the frequency of related conditions) have found a relationship between the dietary intake of vitamin E and lower rates of heart attacks. Observational studies provide only circumstantial evidence, however, and credible evidence is obtained only by way of prospective, randomized trials with placebo (sugar pill) comparisons. In these studies, volunteers are monitored over time after agreeing to be randomly, and unknowingly, assigned to either the group receiving the study medication or the placebo. Several randomized trials that have been performed to date have yielded conflicting results on the benefits of antioxidant therapy. These results may possibly be due to the low doses of vitamin E used, the small number of patients in the study, or the limited duration of treatment. Recently, the Heart Outcomes Prevention Evaluation study used a high dose (400 IU per day) of vitamin E over a span of five years in patients with significant risk factors for heart disease or stroke. This study found no difference in the occurrence of heart attack or stroke in the group treated with vitamin E versus those given the placebo. This study demonstrated that antioxidant therapy does not have any benefit in persons who have or are at high risk for having atherosclerosis.
Folic acid, B vitamins, and homocysteine
Homocysteine is metabolized (chemically transformed) into methionine and cysteine with the help of the B vitamins; folic acid, B12, and B6 (pyridoxine). Therefore, insufficient amounts of these B vitamins in the body can theoretically hamper the metabolic breakdown of homocysteine, and hence increase its blood levels. High levels of homocysteine in the blood (hyperhomocysteinemia) can damage the inner surface of blood vessels, promote blood clotting, and accelerate atherosclerosis. The current state of knowledge regarding folic acid, homocysteine, and heart attacks is as follows: - The level of blood folate is an important determinant of the blood homocysteine level. Low blood folate levels are associated with high blood levels of homocysteine.
- Low blood folate is common among individuals who do not take multivitamins, but unusual among those who do.
- Taking folic acid supplements or eating folic acid fortified cereals can increase blood folate levels and decrease blood homocysteine levels.
- In a large population study involving women, those who had the highest consumption of folic acid (usually in the form of multivitamins) had fewer heart attacks than those who consumed the least amount of folic acid.
Even though current scientific evidence suggests that taking folic acid and vitamin B supplements to lower homocysteine levels should help prevent atherosclerosis and heart attacks, conclusive proof is still lacking because: - There are no conclusive studies (a prospective, randomized, placebo-controlled trial) demonstrating that increasing folic acid intake actually prevents atherosclerosis and heart attacks. (In this type of study, patients are evaluated over time and are randomly assigned to either a group taking the medication under study or a placebo. The results of this type of study are considered determinative.)
- There is no clinical study that demonstrates lowering blood levels of homocysteine actually prevents atherosclerosis and heart attacks.
There is also no official recommendation as to who should be tested for hyperhomocysteinemia. The optimal doses of the B vitamins, folic acid, B12, and B6, required to prevent and treat hyperhomocysteinemia are also uncertain. For folic acid, a daily dose of 0.8-1.0 mg is probably adequate.
How about exercise?
Studies of the effects of exercise in preventing heart attacks have yielded conflicting results. This is likely due to the fact that people who exercise regularly generally have healthier lifestyles and that many risk factors for heart disease can be influenced by exercise. Therefore, the specific role of exercise itself in heart attack prevention is difficult to isolate. For example, regular exercise has direct effects on weight control, blood pressure, diabetes, blood cholesterol, and smoking.
A recent study from Germany found that although exercise may not reverse the formation of cholesterol plaque, it does improve some of the chemical makeup of the blood vessels so that they can remain open more easily. Therefore, exercise seems to have a beneficial effect on the natural physiology of diseased coronary arteries.
What about other agents?
Hormone therapy (HT): In post-menopausal women, or women whose ovaries have been surgically removed, HRT with supplemental estrogens has been advocated. Its use is controversial, due to the balance of known benefits (e.g.: prevention of osteoporosis ) and risks (possible development of uterine or breast cancer ). Estrogen replacement was long believed to reduce the risk for development of coronary artery disease in women, based on the observation that estrogen producing women had fewer heart attacks than men of similar age and risk factor profile. Conflicting data has recently emerged that paradoxically demonstrates that women may have a higher incidence of recurrent myocardial infarction if started on HRT in the first years following their first heart attack; in later years however, a protective effect of HRT was observed in such women. At this time, the role of HRT in women with coronary artery disease, or at high risk for the development of coronary artery disease, remains somewhat controversial, and should be an individual decision between a women and her doctor.
Beta blockers : In patients who have sustained a myocardial infarction, the long-term administration of a class of drugs known as beta-blockers has been demonstrated to result in a much lower incidence of recurrent heart attacks, and may improve survival by as much as 40%. For this reason, use of these agents is considered in most patients.
Smoking cessation: Smoking cessation, by whatever means, has been clearly demonstrated to reduce future heart attacks and death in patients with known coronary artery disease, or who have other risk factors for the development of coronary artery disease. While many methods, both chemical and behavioral, have been used to aid smoking cessation, the initial success rate is often low, and the relapse rate is high. Certain medications which affect neurotransmitters in the brain, similar to agents often used to treat depression (e.g.: Bupropion ) have recently been demonstrated to be helpful in many patients trying to stop smoking. While effective, these agents may produce significant side effects, and should only be used under the close supervision of a doctor.
Are there alternative treatments?
Chelation therapy (which involves the removal of ions from the blood) with edetic acid (EDTA) has been practiced largely by those in the 'alternative medicine' community for about fifty years, going both in and out of vogue. In recent years, chelation therapy has been popularized with claims that it can treat and even reverse the process of atherosclerosis. Despite such claims, the effectiveness of chelation remains scientifically unproven and its use is controversial; for this reason, its use cannot be recommended at this time, particularly in lieu of more well-established proven effective therapies.
What are the screening tests for coronary artery disease?
In patients at risk for the development of coronary artery disease (one or more known risk factors), a variety of noninvasive tests are available to screen for the presence of underlying coronary artery disease before the occurrence of a heart attack. These tests include exercise treadmill testing, with or without simultaneous radionucleide or echocardiographic ( ultrasound ) imaging, and high resolution CT scans ("heart scans"). For information about Who should undergo such testing, and which test should be performed, please read the Screening Tests for Coronary Artery Disease article.
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