Adalat

GENERIC NAME: nifedipine

BRAND NAMES: Adalat, Procardia, Afeditab, Nifediac

DRUG CLASS AND MECHANISM: Nifedipine belongs to a class of medications called calcium channel blockers (CCBs) that are used to treat angina (heart pain), high blood pressure, and abnormal heart rhythms. Other drugs in the same class include amlodipine (Norvasc), diltiazem (Cardizem LA, Tiazac), felodipine (Plendil), isradipine (Dynacirc), nicardipine (Cardene), nimodipine (Nimotop), and verapamil (Covera-HS, Veralan PM, Calan). Like other CCBs, nifedipine works by blocking the flow of calcium into the muscle cells surrounding the arteries that supply blood to the heart (coronary arteries) as well as other arteries of the body. Since the inflow of calcium is what causes the muscle cells to contract, blocking the entry of calcium relaxes the muscles and dilates (widens) the arteries. By dilating coronary arteries, nifedipine increases the flow of blood to the heart. This treats and prevents angina which occurs when the flow of blood to the heart is not adequate to supply the heart with enough oxygen necessary to pump blood. Relaxing the muscles surrounding other arteries of the body lowers blood pressure and thereby reduces the pressure against which the heart must pump blood and function. This reduces the demand of the heart for oxygen--another mechanism by which CCBs treat and prevent angina. In addition, nifedipine slows conduction of the electrical current that travels through the heart that causes the muscle of the heart to contract. This effect can be used to correct abnormally rapid heartbeats.

PRESCRIPTION: Yes

GENERIC AVAILABLE: Yes

PREPARATIONS: Capsules:10 and 20 mg. Tablets: 30, 60, and 90 mg

STORAGE: Tablets should be stored at room temperature 15-25 C (59-77 F). They should be protected from light, moisture, and humidity.

PRESCRIBED FOR: Nifedipine is used for the treatment and prevention of angina resulting from either an increased workload on the heart (as with exercise) or spasm of the coronary arteries. It is used in the treatment of high blood pressure, to treat abnormally fast heart rhythms such as atrial fibrillation, and in the prevention of episodes of rapid heart rhythm originating from the atria of the heart.

It also is used to dilate blood vessels that go into spasm such as those causing Raynaud's phenomenon, a painful condition of the hands caused by spasm of the arteries supplying blood to the hands. Non-FDA approved uses include anal fissures (applied to the fissures), prevention of migraine headaches in adults, ureteral stones (as secondary therapy) and wound healing (applied to the skin).

DOSING: The usual dose for nifedipine capsules is 10 to 20 mg three times daily. It is important to swallow capsules whole. For extended release tablets, the usual dose is 30 or 60 mg once daily. The tablets should be swallowed whole and not bitten or cut in half. Nifedipine can be taken with or without food.

DRUG INTERACTIONS: In rare instances, congestive heart failure has been associated with nifedipine, usually in patients already on a beta blocker, for example, propranolol (Inderal), metoprolol (Lopressor), etc. Excessive lowering of blood pressure (hypotension) during initiation of nifedipine treatment can occur, especially in patients already taking another blood pressure lowering drug.

Generally, nifedipine is avoided in children.

Nifedipine decreases the elimination of digoxin (Lanoxin) by the kidneys which can increase digoxin blood levels in the blood and give rise to digoxin toxicity. It is important, therefore, to monitor blood levels of digoxin in order to avoid toxicity.

Nifedipine interferes with the breakdown of tacrolimus (Prograf) by the liver, which in turn causes elevated blood levels of tacrolimus and may increase the risk of toxicity from tacrolimus.

Nifedipine reduces the blood levels of quinidine (Quinaglute, Quinidex, Quinora) which may reduce the effectiveness of quinidine. Conversely, blood levels of nifedipine are increased by quinidine and may lead to side effects from nifedipine.

Cimetidine (Tagamet) interferes with breakdown by the liver of nifedipine and increases nifedipine blood levels. Therefore, cautious dosing is necessary when both medications are administered concurrently.

Nifedipine should not be taken with grapefruit juice since grapefruit juice (one glass, approximately 200 ml) inhibits the breakdown of nifedipine by the liver and increases the levels of nifedipine in the blood.

PREGNANCY: There are no adequate studies of nifedipine in pregnant women, and in general, it is avoided during pregnancy.

NURSING MOTHERS: Nifedipine is excreted in human breast milk. Generally, nifedipine is avoided in nursing mothers.

SIDE EFFECTS: Side effects of nifedipine are generally mild, and reversible. Most side effects are expected consequences of the dilation of the arteries. The most common side effects include headache, dizziness, flushing, and edema (swelling) of the lower extremities. Less common side effects include dizziness, nausea and constipation.

Reference: FDA Prescribing Information

Heart Attack (Myocardial Infarction)

What is a heart attack?

A heart attack (also known as a myocardial infarction) is the death of heart muscle from the sudden blockage of a coronary artery by a blood clot. Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen. Blockage of a coronary artery deprives the heart muscle of blood and oxygen,causing injury to the heart muscle. Injury to the heart muscle causes chest pain and chest pressure sensation. If blood flow is not restored to the heart muscle within 20 to 40 minutes, irreversible death of the heart muscle will begin to occur. Muscle continues to die for six to eight hours at which time the heart attack usually is "complete." The dead heart muscle is eventually replaced by scar tissue.

Approximately one million Americans suffer a heart attack each year. Four hundred thousand of them die as a result of their heart attack.

What causes a heart attack?

Atherosclerosis

Atherosclerosis is a gradual process by which plaques (collections) of cholesterol are deposited in the walls of arteries. Cholesterol plaques cause hardening of the arterial walls and narrowing of the inner channel (lumen) of the artery. Arteries that are narrowed by atherosclerosis cannot deliver enough blood to maintain normal function of the parts of the body they supply. For example, atherosclerosis of the arteries in the legs causes reduced blood flow to the legs. Reduced blood flow to the legs can lead to pain in the legs while walking or exercising, leg ulcers, or a delay in the healing of wounds to the legs. Atherosclerosis of the arteries that furnish blood to the brain can lead to vascular dementia (mental deterioration due to gradual death of brain tissue over many years) or stroke (sudden death of brain tissue).

In many people, atherosclerosis can remain silent (causing no symptoms or health problems) for years or decades. Atherosclerosis can begin as early as the teenage years, but symptoms or health problems usually do not arise until later in adulthood when the arterial narrowing becomes severe. Smoking cigarettes, high blood pressure, elevated cholesterol, and diabetes mellitus can accelerate atherosclerosis and lead to the earlier onset of symptoms and complications, particularly in those people who have a family history of early atherosclerosis.

Coronary atherosclerosis (or coronary artery disease) refers to the atherosclerosis that causes hardening and narrowing of the coronary arteries. Diseases caused by the reduced blood supply to the heart muscle from coronary atherosclerosis are called coronary heart diseases (CHD). Coronary heart diseases include heart attacks, sudden unexpected death, chest pain (angina), abnormal heart rhythms, and heart failure due to weakening of the heart muscle.

Atherosclerosis and angina pectoris

Angina pectoris (also referred to as angina) is chest pain or pressure that occurs when the blood and oxygen supply to the heart muscle cannot keep up with the needs of the muscle. When coronary arteries are narrowed by more than 50 to 70 percent, the arteries may not be able to increase the supply of blood to the heart muscle during exercise or other periods of high demand for oxygen. An insufficient supply of oxygen to the heart muscle causes angina. Angina that occurs with exercise or exertion is called exertional angina. In some patients, especially diabetics, the progressive decrease in blood flow to the heart may occur without any pain or with just shortness of breath or unusually early fatigue.

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 one to 15 minutes and is relieved by rest or by taking nitroglycerin by placing a 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 artery disease. Chest pains that just last a few seconds rarely are due to coronary artery disease.

Angina also can occur at rest. Angina at rest more commonly indicates that a coronary artery has narrowed to such a critical degree that the heart is not receiving enough oxygen even at rest. Angina at rest infrequently may be due to spasm of a coronary artery (a condition called Prinzmetal's or variant angina). Unlike a heart attack, there is no permanent muscle damage with either exertional or rest angina.

Atherosclerosis and heart attack

Occasionally the surface of a cholesterol plaque in a coronary artery may rupture, and a blood clot forms on the surface of the plaque. The clot blocks the flow of blood through the artery and results in a heart attack (see picture below). The cause of rupture that leads to the formation of a clot is largely unknown, but contributing factors may include cigarette smoking or other nicotine exposure, elevated LDL cholesterol, elevated levels of blood catecholamines (adrenaline), high blood pressure, and other mechanical and biochemical forces.

Unlike exertional or rest angina, heart muscle dies during a heart attack and loss of the muscle is permanent, unless blood flow can be promptly restored, usually within one to six hours.

While heart attacks can occur at any time, more heart attacks occur between 4:00 A.M. and 10:00 A.M. because of the higher blood levels of adrenaline released from the adrenal glands during the morning hours. Increased adrenaline, as previously discussed, may contribute to rupture of cholesterol plaques.

Approximately 50% of patients who develop heart attacks have warning symptoms such as exertional angina or rest angina prior to their heart attacks, but these symptoms may be mild and discounted.

What are the symptoms of a heart attack?

Although chest pain or pressure is the most common symptom of a heart attack, heart attack victims may experience a variety of symptoms including:

• Pain, fullness, and/or squeezing sensation of the chest

• Jaw pain, toothache, headache

• Shortness of breath

• Nausea, vomiting, and/or general epigastric (upper middle abdomen) discomfort

• Sweating

• Heartburn and/or indigestion

• Arm pain (more commonly the left arm, but may be either arm)

• Upper back pain

• General malaise (vague feeling of illness)

• No symptoms (Approximately one quarter of all heart attacks are silent, without chest pain or new symptoms. Silent heart attacks are especially common among patients with diabetes mellitus.)

Even though the symptoms of a heart attack at times can be vague and mild, it is important to remember that heart attacks producing no symptoms or only mild symptoms can be just as serious and life-threatening as heart attacks that cause severe chest pain. Too often patients attribute heart attack symptoms to "indigestion," "fatigue," or "stress," and consequently delay seeking prompt medical attention. One cannot overemphasize the importance of seeking prompt medical attention in the presence of symptoms that suggest a heart attack. Early diagnosis and treatment saves lives, and delays in reaching medical assistance can be fatal. A delay in treatment can lead to permanently reduced function of the heart due to more extensive damage to the heart muscle. Death also may occur as a result of the sudden onset of arrhythmias such as ventricular fibrillation.

What are the complications of a heart attack?

Heart failure

When a large amount of heart muscle dies, the ability of the heart to pump blood to the rest of the body is diminished, and this can result in heart failure. The body retains fluid, and organs, for example, the kidneys, begin to fail.

Ventricular fibrillation

Injury to heart muscle also can lead to ventricular fibrillation. Ventricular fibrillation occurs when the normal, regular, electrical activation of heart muscle contraction is replaced by chaotic electrical activity that causes the heart to stop beating and pumping blood to the brain and other parts of the body. Permanent brain damage and death can occur unless the flow of blood to the brain is restored within five minutes.

Most of the deaths from heart attacks are caused by ventricular fibrillation of the heart that occurs before the victim of the heart attack can reach an emergency room. Those who reach the emergency room have an excellent prognosis; survival from a heart attack with modern treatment should exceed 90%. The 1% to 10% of heart attack victims who later die frequently had suffered major damage to the heart muscle initially or additional damage at a later time.

Deaths from ventricular fibrillation can be avoided by cardiopulmonary resuscitation (CPR) started within five minutes of the onset of ventricular fibrillation. CPR requires breathing for the victim and applying external compression to the chest to squeeze the heart and force it to pump blood. In 2008, the American Heart Association modified the mouth-to-mouth instruction of CPR, and recommends that chest compressions alone are effective if a bystander is reluctant to do mouth-to-mouth. When paramedics arrive, medications and/or an electrical shock (cardioversion) can be administered to convert ventricular fibrillation back to a normal heart rhythm and allow the heart to pump blood normally. Therefore, prompt CPR and a rapid response by paramedics can improve the chances of survival from a heart attack. In addition, many public venues now have automatic external defibrillators (AEDs) that provide the electrical shock needed to restore a normal heart rhythm even before the paramedics arrive. This greatly improves the chances of survival.

What are the risk factors for atherosclerosis and heart attack?

Factors that increase the risk of developing atherosclerosis and heart attacks include increased blood cholesterol, high blood pressure, use of tobacco, diabetes mellitus, male gender, and a family history of coronary heart disease. While family history and male gender are genetically determined, the other risk factors can be modified through changes in lifestyle and medications.

• High Blood Cholesterol (Hyperlipidemia). A high level of cholesterol in the blood is associated with an increased risk of heart attack because cholesterol is the major component of the plaques deposited in arterial walls. 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 would turn into a solid substance.) The cholesterol in blood is either combined with lipoproteins as very low-density lipoproteins (VLDL), low-density lipoproteins (LDL) or high-density lipoproteins (HDL).
  
  The cholesterol that is combined with low-density lipoproteins (LDL cholesterol) is the "bad" cholesterol that deposits cholesterol in arterial plaques. Thus, elevated levels of LDL cholesterol are associated with an increased risk of heart attack.
  
  The cholesterol that is combined with HDL (HDL cholesterol) is the "good" cholesterol that removes cholesterol from arterial plaques. Thus, low levels of HDL cholesterol are associated with an increased risk of heart attacks.
  
  Measures that lower LDL cholesterol and/or increase HDL cholesterol (losing excess weight, diets low in saturated fats, regular exercise, and medications) have been shown to lower the risk of heart attack. One important class of medications for treating elevated cholesterol levels (the statins) have actions in addition to lowering LDL cholesterol which also protect against heart attack. Most patients at "high risk" for a heart attack should be on a statin no matter what the levels of their cholesterol.

• High Blood Pressure (Hypertension). High blood pressure is a risk factor for developing atherosclerosis and heart attack. Both high systolic pressure (when the heart beats) and high diastolic pressure (when the heart is at rest) increase the risk of heart attack. It has been shown that controlling hypertension with medications can reduce the risk of heart attack.

• Tobacco Use (Smoking). Tobacco and tobacco smoke contain chemicals that cause damage to blood vessel walls, accelerate the development of atherosclerosis, and increase the risk of heart attack.

• Diabetes (Diabetes Mellitus). Both insulin dependent and non-insulin dependent diabetes mellitus (type 1 and 2, respectively) are associated with accelerated atherosclerosis throughout the body. Therefore, patients with diabetes mellitus are at risk for reduced blood flow to the legs, coronary heart disease, erectile dysfunction, and strokes at an earlier age than non-diabetic subjects. Patients with diabetes can lower their risk through rigorous control of their blood sugar levels, regular exercise, weight control, and proper diets.

• Male Gender. At all ages, men are more likely than women to develop atherosclerosis and coronary heart disease. Some scientists believe that this difference is partly due to the higher blood levels of HDL cholesterol in women than in men. However, this gender difference narrows as men and women grow older.

• Family History of Heart Disease. Individuals with a family history of coronary heart diseases have an increased risk of heart attack. Specifically, the risk is higher if there is a family history of early coronary heart disease, including a heart attack or sudden death before age 55 in the father or other first-degree male relative, or before age 65 in the mother or other female first-degree female relative.

How is a heart attack diagnosed?

When there is severe chest pain, suspicion that a heart attack is occurring usually is high, and tests can be performed quickly that will confirm the heart attack. A problem arises, however, when the symptoms of a heart attack do not include chest pain. A heart attack may not be suspected, and the appropriate tests may not be performed. Therefore, the initial step in diagnosing a heart attack is to be suspicious that one has occurred.

Electrocardiogram. An electrocardiogram (ECG) is a recording of the electrical activity of the heart. Abnormalities in the electrical activity usually occur with heart attacks and can identify the areas of heart muscle that are deprived of oxygen and/or areas of muscle that have died. In a patient with typical symptoms of heart attack (such as crushing chest pain) and characteristic changes of heart attack on the ECG, a secure diagnosis of heart attack can be made quickly in the emergency room and treatment can be started immediately. If a patient's symptoms are vague or atypical and if there are pre-existing ECG abnormalities, for example, from old heart attacks or abnormal electrical patterns that make interpretation of the ECG difficult, the diagnosis of a heart attack may be less secure. In these patients, the diagnosis can be made only hours later through detection of elevated cardiac enzymes in the blood.

Blood tests. Cardiac enzymes are proteins that are released into the blood by dying heart muscles. These cardiac enzymes are creatine phosphokinase (CPK), special sub-fractions of CPK (specifically, the MB fraction of CPK), and troponin, and their levels can be measured in blood. These cardiac enzymes typically are elevated in the blood several hours after the onset of a heart attack. A series of blood tests for the enzymes performed over a 24-hour period are useful not only in confirming the diagnosis of heart attack, but the changes in their levels over time also correlates with the amount of heart muscle that has died.

The most important factor in diagnosing and treating a heart attack is prompt medical attention. Rapid evaluation allows early treatment of potentially life-threatening abnormal rhythms such as ventricular fibrillation and allows early reperfusion (return of blood flow to the heart muscle) by procedures that unclog the blocked coronary arteries. The more rapidly blood flow is reestablished, the more heart muscle that is saved.

Large and active medical centers often have a "chest pain unit" where patients suspected of having heart attacks are rapidly evaluated. If a heart attack is diagnosed, prompt therapy is initiated. If the diagnosis of heart attack is initially unclear, the patient is placed under continuous monitoring until the results of further testing are available.

What about heart attacks in women?

What are the risk factors for heart attack in women?

Coronary artery disease (CAD) and heart attacks are erroneously believed to occur primarily in men. Although it is true that the prevalence of CAD among women is lower before menopause, the risk of CAD rises in women after menopause. At age 75, a woman's risk for CAD is equal to that of a man's. CAD is the leading cause of death and disability in women after menopause. In fact, a 50-year-old woman faces a 46% risk of developing CAD and a 31% risk of dying from coronary artery disease. In contrast, her probability of contracting and dying from breast cancer is 10% and 3%, respectively.

The risk factors for developing CAD in women are the same as in men and include:

• increased blood cholesterol,
  
  
• high blood pressure,
  
  
• smoking cigarettes,
  
  
• diabetes mellitus, and a
  
  
• family history of coronary heart disease at a young age.

Smoking cigarettes

Even "light" smoking raises the risk of CAD. In one study, middle-aged women who smoked one to 14 cigarettes per day had a twofold increase in strokes (caused by atherosclerosis of the arteries to the brain) whereas those who smoked more than 25 cigarettes per day had a risk of stroke 3.7 fold higher than that of nonsmoking women. Furthermore, the combination of smoking and the use of birth control pills increase the risk of heart attacks even further, especially in women over 35.

Quitting smoking immediately begins to reduce the risk of heart attacks. The risk gradually returns to the same risk of nonsmoking women after several years of not smoking.

Cholesterol treatment guidelines in women

Current NCEP (National Cholesterol Education Program) treatment guidelines for undesirable cholesterol levels are the same for women as for men.

What are the symptoms of heart attack in women and how is heart attack diagnosed?

Women are more likely to encounter delays in establishing the diagnosis of heart attack than men. This is in part because women tend to seek medical care later than men, and in part because diagnosing heart attacks in women can sometimes be more difficult than diagnosing heart attacks in men. The reasons include:

1. Women are more likely than men to have atypical heart attack symptoms such as:

• neck and shoulder pain,
  
  
• abdominal pain,
  
  
• nausea,
  
  
• vomiting,
  
  
• fatigue, and
  
  
• shortness of breath.

1. Silent heart attacks (heart attacks with little or no symptoms) are more common among women than among men.
   
   
2. Women have a higher occurrence than men of chest pain that is not caused by heart disease, for example chest pain from spasm of the esophagus.
   
   
3. Women are less likely than men to have the typical findings on the ECG that are necessary to diagnose a heart attack quickly.
   
   
4. Women are more likely than men to have angina (chest pain due to lack of blood supply to the heart muscle) that is caused by spasm of the coronary arteries or caused by disease of the smallest blood vessels (microvasculature disease). Cardiac catheterization with coronary angiograms (x-ray studies of the coronary arteries that are considered the most reliable tests for CAD) will reveal normal coronary arteries and therefore cannot be used to diagnose either of these two conditions.
   
   
5. Women are more likely to have misleading, or "false positive" noninvasive tests for CAD then men.

Because of the atypical nature of symptoms and the occasional difficulties in diagnosing heart attacks in women, women are less likely to receive aggressive thrombolytic therapy or coronary angioplasty, and are more likely to receive it later than men. Women also are less likely to be admitted to a coronary care unit.

What is the treatment for heart attack in women?

Thrombolytic (fibrinolytic or clot dissolving) therapy has been shown to reduce death from heart attacks similarly in men and women; however, the complication of strokes from the thrombolytic therapy may be slightly higher in women than in men.

Emergency percutaneous transluminal coronary angioplasty (PTCA) or coronary stenting for acute heart attack is as effective in women as in men; however women may have a slightly higher rate of procedure-related complications in their blood vessels (such as bleeding or clotting at the point of insertion of the PTCA catheter in the groin) and death. This higher rate of complications has been attributed to women's older age, smaller artery size, and greater severity of angina. The long-term outcome of angioplasty or stenting however, is similar in men and women, and should not be withheld due to gender.

The immediate mortality from coronary artery bypass graft surgery (CABG) in women is higher than that for men. The higher immediate mortality rate has been attributed to women's older age, smaller artery size, and greater severity of angina (the same as for PTCA). Long term survival, rate of recurrent heart attack and/or need for reoperation, however, are similar in men and women after CABG.

What about hormone therapy and heart attack in women?

After menopause, the production of estrogen by the ovaries gradually diminishes over several years. Along with this reduction, there is an increase in LDL ("bad" cholesterol) and a small decrease in HDL ("good" cholesterol). These changes in lipid levels are believed to be one of the reasons for the increased risks of developing CAD after menopause. Women who have had their ovaries surgically removed (oophorectomy) or experience an early menopause, also have an accelerated risk of CAD.

Since treatment with estrogen hormone results in higher HDL and lower LDL cholesterol levels, doctors thought for many years that estrogen would protect women against CAD (as well protect against dementia and stroke). Many studies have found that postmenopausal women who take estrogen have lower CAD rates than women who do not. Unfortunately many of the studies were observational studies (studies in which women are followed over time but decide on their own whether or not they wish to take estrogen). Observational studies have serious shortcomings because they are subject to selection bias; for example, women who choose to take estrogen hormones may be healthier and have a lower risk of heart attacks than those who do not. In other words, something else in the daily habits of women who take estrogen (such as exercise or healthier diet) may make them less likely to develop heart attacks. Therefore, only a randomized trial (a study in which women agree to be assigned to estrogen or a placebo or sugar pill at random but are not told which pills they took until the end of the study) can establish the whether hormone therapy after menopause can prevent CAD.

HERS trial results

The Heart and Estrogen/progestin Replacement Study (HERS), was a randomized placebo-controlled trial of the effect of the daily use of estrogens plus medroxyprogesterone (progestin) on the rate of heart attacks in postmenopausal women who already had CAD. The HERS trial did not find a reduction in heart attacks in women who took hormone therapy. This lack of benefit in preventing heart attacks occurred despite an 11% lower LDL and a 10% higher HDL cholesterol level in the women treated with hormones. The study also found that more women in the hormone-treated group experienced blood clots in the veins and gallbladder disease than women in the placebo-treated group. (Blood clots in the veins are dangerous because these clots can travel to the lungs and cause pulmonary embolism, a condition with chest pain, shortness of breath, and even shock and death.) However, the increase in gallbladder disease and blood clots among healthy users of estrogen who do not have heart disease is very small.

Based on the results of this study, researchers concluded that estrogen is not effective in preventing coronary artery disease and heart attacks in postmenopausal women who already have CAD. It should be noted, however, that the results of the HERS trial only apply to women who have known CAD prior to starting hormone therapy and not to women without known coronary artery disease.

WHI trial results

The Women's Health Initiative (WHI) was the first randomized controlled trial designed to determine the long-term benefits and risks of treatment with estrogens plus medroxyprogesterone (progestin) in healthy menopausal women (women without CAD). The results were reported in a series of articles in 2002, 2003, and 2004. The estrogen + progestin portion of the WHI study had to be stopped earlier than planned, after just 5.2 years, because the increase in coronary heart disease, stroke, and pulmonary embolism among women who use estrogen + progesterone outweighed the benefits of reduced bone fractures and colon cancer. The estrogen-alone portion of the WHI was stopped because women who took estrogen alone had no reduction in heart attack risk, yet there was a significant increase in stroke risk.

The increase in breast cancer became apparent after three to five years, but the increase in heart disease and pulmonary emboli occurred early on, in the first year.

Recommendations for the use of estrogens plus medroxyprogesterone (progestin) in women

Medicinenet Medical Editors believe that:

• Decision regarding use of hormone therapy has to be individualized, and all women should discuss with their physicians what is best for her.

• Estrogens plus medroxyprogesterone (progestin) is still the best therapy for hot flashes. Despite the WHI study, many women remain good candidates for estrogens plus medroxyprogesterone (progestin) therapy (or estrogen alone if they have had hysterectomy). This is especially true if hormone therapy is limited to the shortest duration, optimally less than five years.

• Estrogens with or without medroxyprogesterone (progestin) should not be used to prevent or treat either Alzheimer's disease, heart disease, or stroke.

While estrogens plus medroxyprogesterone (progestin) are effective in preventing osteoporosis and related bone fractures, women concerned about the risk of hormone therapy should discuss with their doctors, the use of other non-hormonal alternatives to prevent and treat osteoporosis.

What is new in heart attack?

Greater public awareness about heart attacks and changes in lifestyle have contributed to a dramatic reduction in the incidence of heart attacks during the last four decades. Improved anticoagulant drugs such as hirudin and hirulog, are being tested and may complement current therapies. The role of the "super aspirins" [abciximab (Reopro) and eptifibatide (Integrilin)] is currently being investigated as well.

More effective versions of TPA are being developed. Increasingly, paramedics can do ECGs in the field, diagnose a heart attack, and take patients directly to hospitals that have the ability to do PTCA and stenting. This can save time and reduce damage to the heart. At present, the accepted best treatment for a heart attack is identification promptly of the diagnosis, and transport to a hospital that can perform prompt catheterization and PTCA or stenting within the first 90 minutes of the cardiac event.

Recent data has shown that lowering blood LDL levels even further than previously suggested may further decrease the risk of heart attacks.

Research also has shown that inflammation may play a role in the development of atherosclerosis, and this is an active area of current investigation. There also is early evidence that with genetic engineering it may be possible to develop a drug that can be administered to clear plaques from arteries (a "scavenger molecule").

Heart Attack At A Glance

• A heart attack results when a blood clot completely obstructs a coronary artery supplying blood to the heart muscle and heart muscle dies.

• The blood clot that causes the heart attack usually forms at the site of rupture of an atherosclerotic, cholesterol plaque on the inner wall of a coronary artery.

• The most common symptom of heart attack is chest pain.
  
  
• The most common complications of a heart attack are heart failure, and ventricular fibrillation.

• The risk factors for atherosclerosis and heart attack include elevated cholesterol levels, increased blood pressure, tobacco use, diabetes, male gender and a family history of heart attacks at an early age.

• Heart attacks are diagnosed with electrocardiograms and measurement of cardiac enzymes in blood

• Early reopening of blocked coronary arteries reduces the amount of damage to the heart and improves the prognosis for a heart attack.

• Medical treatment for heart attacks may include anti-platelet, anti-coagulant, and clot dissolving drugs as well as angiotensin converting enzyme (ACE) inhibitors, beta blockers and oxygen.

• Interventional treatment for heart attacks may include coronary angiography with percutaneous transluminal coronary angioplasty (PTCA), coronary artery stents, and coronary artery bypass grafting (CABG).

• Patients suffering a heart attack are hospitalized for several days to detect heart rhythm disturbances, shortness of breath, and chest pain.

• Further heart attacks can be prevented by aspirin, beta blockers, ACE inhibitors, discontinuing smoking, weight reduction, exercise, good control of blood pressure and diabetes, following a low cholesterol and low saturated fat diet that is high in omega-3-fatty acids, taking multivitamins with an increased amount of folic acid, decreasing LDL cholesterol, and increasing HDL cholesterol.

amiodarone

GENERIC NAME: amiodarone

BRAND NAME: Cordarone

DRUG CLASS AND MECHANISM: Amiodarone is used to correct abnormal rhythms of the heart. (It is an antiarrhythmic medication.) Amiodarone was discovered in 1961 and approved by the FDA in December of 1985. Although amiodarone has many side effects, some of which are severe and potentially fatal, it has been successful in treating many arrhythmias where other antiarrhythmic drugs have failed. Amiodarone is considered a "broad spectrum" antiarrhythmic medication, that is, it has multiple and complex effects on the electrical activity of the heart which is responsible for the heart's rhythm. Among its most important electrical effects are:

1. a delay in the rate at which the heart's electrical system "recharges" after the heart contracts (repolarization);
2. a prolongation in the electrical phase during which the heart's muscle cells are electrically stimulated (action potential);
3. a slowing of the speed of electrical conduction (how fast each individual impulse is conducted through the heart's electrical system);
4. a reduction in the rapidity of firing of the normal generator of electrical impulses in the heart (the heart's pacemaker);
5. a slowing of conduction through various specialized electrical pathways (called accessory pathways) which can be responsible for arrhythmias.

In addition to being an antiarrhythmic medication, amiodarone also causes blood vessels to dilate (enlarge). This effect can result in a drop in blood pressure. Because of this effect, it also may be of benefit in patients with congestive heart failure.

PRESCRIPTION: Yes

GENERIC AVAILABLE: Yes

PREPARATIONS: Tablets (pink), round in shape: 200 mg.

STORAGE: Tablets should be kept at room temperature, less than 30°C (86°F).

PRESCRIBED FOR: Amiodarone is used for many serious arrhythmias of the heart including ventricular fibrillation, ventricular tachycardia, atrial fibrillation, and atrial flutter.

DOSING: Amiodarone usually is given in several daily doses to minimize stomach upset which is seen more frequently with higher doses. For this same reason, it is also recommended that amiodarone be taken with meals.

DRUG INTERACTIONS: Amiodarone may interact with beta-blockers such as atenolol (Tenormin), propranolol (Inderal), metoprolol (Lopressor), or certain calcium channel blockers, such as verapamil (Calan, Isoptin, Verelan, Covera-HS) or diltiazem (Cardizem, Dilacor, Tiazac), resulting in an excessively slow heart rate or a block in the conduction of the electrical impulse through the heart.

Amiodarone increases the blood levels of digoxin (Lanoxin) when the two drugs are given together. It is recommended that the dose of digoxin be cut by 50% when amiodarone therapy is started.

Flecainide (Tambocor) blood concentrations increase by more than 50% with amiodarone. Procainamide (Procan-SR, Pronestyl) and quinidine (Quinidex, Quinaglute) concentrations increase by 30%-50% during the first week of amiodarone therapy. Additive electrical effects occurs with these combinations, and worsening arrhythmias may occur as a result. Some experts recommend that the doses of these other drugs be reduced when amiodarone is started.

Amiodarone can result in phenytoin (Dilantin) toxicity because it causes a two- or three-fold increase in blood concentrations of phenytoin. Symptoms of phenytoin toxicity including unsteady eye movement (temporary and reversible), tiredness and unsteady gait.

Ritonavir (Norvir) can inhibit the enzyme that is responsible for the metabolism of amiodarone. Although no clinical problems have been recognized as a result of this interaction yet, it would be prudent to avoid this combination for fear of the potential for amiodarone toxicity.

Amiodarone also can interact with tricyclic antidepressants (for example, amitriptyline, Elavil), or phenothiazines (for example, chlorpromazine, Thorazine) and potentially cause serious arrhythmias.

Amiodarone interacts with warfarin (Coumadin) and increases the risk of bleeding. The bleeding can be serious or even fatal. This effect can occur as early as 4-6 days after the start of the combination of drugs or can be delayed by a few weeks.

Amiodarone can interact with some cholesterol-lowering medicines of the "statin" class, such as simvastatin (Zocor), atorvastatin (Lipitor), and lovastatin (Mevacor), increasing the risk of severe muscle breakdown and kidney failure or liver disease. This interaction is dose-related, meaning that lower doses of statins are safer than higher doses when used with amiodarone. An alternative statin, pravastatin (Pravachol), does not share this interaction and is safer in patients taking amiodarone.

Amiodarone inhibits the metabolism of dextromethorphan, the cough suppressant found in most over-the-counter (and some prescription) cough and cold medications (for example, Robitussin-DM). Although the significance of the interaction is unknown, these two drugs probably should not be taken together if possible.

Reference: FDA Prescribing Information

amlodipine

GENERIC NAME: amlodipine

BRAND NAME: Norvasc

DRUG CLASS AND MECHANISM: Amlodipine belongs to a class of medications called calcium channel blockers. These medications block the transport of calcium into the smooth muscle cells lining the coronary arteries and other arteries of the body. Since calcium is important in muscle contraction, blocking calcium transport relaxes artery muscles and dilates coronary arteries and other arteries of the body. By relaxing coronary arteries, amlodipine is useful in preventing chest pain (angina) resulting from coronary artery spasm. Relaxing the muscles lining the arteries of the rest of the body lowers the blood pressure, which reduces the burden on the heart as it pumps blood to the body. Reducing heart burden lessens the heart muscle's demand for oxygen, and further helps to prevent angina in patients with coronary artery disease. For more detailed information related to coronary artery disease, please read the Chest Pain, Cholesterol, and Heart Attack articles.

PRESCRIPTION: yes

GENERIC AVAILABLE: no

PREPARATIONS: Tablets ( 2.5mg, 5mg, 10mg.)

STORAGE: Amlodipine should be stored at room temperature in a tight, light resistant container.

PRESCRIBED FOR: Chest pain (angina) occurs because of insufficient oxygen delivered to the heart muscles. Insufficient oxygen may be a result of coronary artery blockage or spasm, or because of physical exertion which increases heart oxygen demand in a patient with coronary artery narrowing. Amlodipine is used for the treatment and prevention of angina resulting from coronary spasm as well as from exertion. Amlodipine is also used in the treatment of high blood pressure.

DOSING: Amlodipine can be taken with or without food. Amlodipine is metabolized mainly by the liver and dosages may need to be lowered in patients with liver dysfunction.

DRUG INTERACTIONS: In patients with severe coronary artery disease, amlodipine can increase the frequency and severity of angina or actually cause a heart attack on rare occasions. This phenomenon usually occurs when first starting amlodipine, or at the time of dosage increase. Excessive lowering of blood pressure during initiation of amlodipine treatment can occur, especially in patients already taking another blood pressure lowering medication. In rare instances, congestive heart failure has been associated with amlodipine, usually in patients already on a beta blocker. For further information on beta blockers, please read the propranolol (Inderal) article.

PREGNANCY: Generally, amlodipine is avoided in pregnancy, and by nursing mothers and children.

NURSING MOTHERS: Generally, amlodipine is avoided in pregnancy, and by nursing mothers and children.

SIDE EFFECTS: Side effects of amlodipine are generally mild and reversible. The two most common side effects are headache and edema (swelling) of the lower extremities. Less common side effects include dizziness, flushing, fatigue, nausea, and palpitations.

Reference: FDA Prescribing Information

atenolol

GENERIC NAME: atenolol

BRAND NAME: Tenormin

DRUG CLASS AND MECHANISM: Atenolol is a beta-adrenergic blocking agent that blocks the effects of adrenergic drugs, for example, adrenaline or epinephrine, on nerves of the sympathetic nervous system. One of the important functions of beta-adrenergic stimulation is to stimulate the heart to beat more rapidly. By blocking the stimulation of these nerves, atenolol reduces the heart rate and is useful in treating abnormally rapid heart rhythms. Atenolol also reduces the force of contraction of heart muscle and lowers blood pressure. By reducing the heart rate, the force of muscle contraction, and the blood pressure against which the heart must pump, atenolol reduces the work of heart muscle and the need of the muscle for oxygen. Since angina occurs when oxygen demand of the heart muscle exceeds the supply, atenolol is helpful in treating angina. Atenolol was approved by the FDA in August 1981.

PRESCRIPTION: Yes

GENERIC AVAILABLE: Yes

PREPARATIONS: Tablets: 25, 50, 100 mg. Injection: 5 mg/10 ml

STORAGE: Store at room temperature 20°to 25°C (68° to 77°F).

PRESCRIBED FOR: Atenolol is prescribed for patients with high blood pressure (hypertension). It is also used to treat chest pain (angina pectoris) related to coronary artery disease. Atenolol also is useful in slowing and regulating certain types of abnormally rapid heart rates (tachycardias). It is also prescribed for acute myocardial infarction (heart attack). Other uses for atenolol include the prevention of migraine headaches and the treatment of certain types of tremors (familial or hereditary essential tremors).

DOSING: Atenolol should be taken before meals or at bedtime.

The dose for treating high blood pressure or angina is 50-100 mg once daily.

Acute myocardial infarction (heart attack) is treated with two 5 mg injections administered 10 minutes apart followed by treatment with 100 mg oral atenolol for 6-9 days. If atenolol injections are not advisable, patients may be treated with 100 mg daily of oral atenolol for 7 days.

DRUG INTERACTIONS: Calcium channel blockers and digoxin (Lanoxin) can cause lowering of blood pressure and heart rate to dangerous levels when administered together with atenolol. Atenolol can mask the early warning symptoms of low blood sugar (hypoglycemia), and should be used with caution in patients receiving treatment for diabetes.

PREGNANCY: Atenolol may cause harm and growth retardation in the fetus when given to pregnant women.

NURSING MOTHERS: Atenolol is excreted in breast milk and my cause adverse effects in the breastfed infant.

SIDE EFFECTS: Atenolol is generally well tolerated, and side effects are mild and transient. Rare side effects include abdominal cramps, diarrhea, constipation, fatigue, insomnia, nausea, depression, dreaming, memory loss, fever, impotence, lightheadedness, slow heart rate, low blood pressure, numbness, tingling, cold extremities, and sore throat.

Atenolol can aggravate breathing difficulties in patients with asthma, chronic bronchitis, or emphysema. In patients with existing slow heart rates (bradycardias) and heart blocks (defects in the electrical conduction of the heart), atenolol can cause dangerously slow heart rates, and even shock. Atenolol reduces the force of heart muscle contraction and can aggravate symptoms of heart failure.

In patients with coronary artery disease, abruptly stopping atenolol can suddenly worsen angina, and occasionally precipitate heart attacks. If it is necessary to discontinue atenolol, its dosage can be reduced gradually over several weeks.

Reference: FDA Prescribing Information

Coronary Artery Bypass Graft Surgery (CABG)

What is coronary artery bypass graft (CABG) surgery?

According to the American Heart Association 427,000 coronary artery bypass graft (CABG) surgeries were performed in the United States in 2004, making it one of the most commonly performed major operations. CABG surgery is advised for selected groups of patients with significant narrowings and blockages of the heart arteries (coronary artery disease). CABG surgery creates new routes around narrowed and blocked arteries, allowing sufficient blood flow to deliver oxygen and nutrients to the heart muscle.

How does coronary artery disease develop?

Coronary artery disease (CAD) occurs when atherosclerotic plaque (hardening of the arteries) builds up in the wall of the arteries that supply the heart. This plaque is primarily made of cholesterol. Plaque accumulation can be accelerated by smoking, high blood pressure, elevated cholesterol, and diabetes. Patients are also at higher risk for plaque development if they are older (greater than 45 years for men and 55 years for women), or if they have a positive family history for early heart artery disease.

The atherosclerotic process causes significant narrowing in one or more coronary arteries. When coronary arteries narrow more than 50 to 70%, the blood supply beyond the plaque becomes inadequate to meet the increased oxygen demand during exercise. The heart muscle in the territory of these arteries becomes starved of oxygen (ischemic). Patients often experience chest pain (angina) when the blood oxygen supply cannot keep up with demand. Up to 25% of patients experience no chest pain at all despite documented lack of adequate blood and oxygen supply. These patients have "silent" angina, and have the same risk of heart attack as those with angina.

When a blood clot (thrombus) forms on top of this plaque, the artery becomes completely blocked causing a heart attack.

When arteries are narrowed in excess of 90 to 99%, patients often have accelerated angina or angina at rest (unstable angina). Unstable angina can also occur due to intermittent blockage of an artery by a thrombus that eventually is dissolved by the body's own protective clot-dissolving system.

How is coronary artery disease diagnosed?

The resting electrocardiogram (EKG) is a recording of the electrical activity of the heart, and can demonstrate signs of oxygen starvation of the heart (ischemia) or heart attack. Often, the resting EKG is normal in patients with coronary artery disease and angina. Exercise treadmill tests are useful screening tests for patients with a moderate likelihood of significant coronary artery disease (CAD) and a normal resting EKG. These stress tests are about 60 to 70% accurate in diagnosing significant CAD.

If the stress tests do not reveal the diagnosis, greater accuracy can be achieved by adding a nuclear agent (thallium or Cardiolite) intravenously during stress tests. Addition of thallium allows nuclear imaging of the blood flow to different regions of the heart, using an external camera. An area of the heart with reduced blood flow during exercise, but normal blood flow at rest, signifies significant artery narrowing in that region.

Combining echocardiography (ultrasound imaging of the heart muscle) with exercise stress testing (stress echocardiography) is also a very accurate technique to detect CAD. When a significant blockage exists, the heart muscle supplied by this artery does not contract as well as the rest of the heart muscle. Stress echocardiography and thallium stress tests are both at least 80% to 85% accurate in detecting significant coronary artery disease.

When a patient cannot undergo exercise stress test because of nervous system or joint problems, medications can be injected intravenously to simulate the stress on the heart due to exercise and imaging can be performed with a nuclear camera or ultrasound.

Cardiac catheterization with angiography (coronary arteriography) is the most accurate test to detect coronary artery narrowing. Small hollow plastic tubes (catheters) are advanced under x-ray guidance to the openings of the two main heart arteries (left and right). Iodine contrast, "dye," is then injected into the arteries while an x-ray video is recorded. Sometimes, an exercise study is then done to determine whether a moderate narrowing (40 - 60%) is actually causing ischemia and, therefore, requires treatment.

A newer modality, high speed CT scanning angiography has recently become available. This procedure uses powerful x-ray methods to visualize the arteries to the heart. Its role in the evaluation of CAD is currently being evaluated.

How is coronary artery disease (CAD) treated?

Medicines used to treat angina reduce the heart muscle demand for oxygen in order to compensate for the reduced blood supply. Three commonly used classes of drugs are the nitrates, beta blockers and calcium blockers. Nitroglycerin (Nitro-Bid) is an example of a nitrate. Examples of beta blockers include propranolol (Inderal) and atenolol (Tenormin). Examples of calcium blockers include nicardipine (Cardene) and nifedipine (Procardia, Adalat). Unstable angina is also treated with aspirin and the intravenous blood thinner heparin. Aspirin prevents clumping of platelets, while heparin prevents blood clotting on the surface of plaques in a critically narrowed artery. When patients continue to have angina despite maximum medications, or when significant ischemia still occurs with exercise testing, coronary arteriography is usually indicated. Data collected during coronary arteriography help doctors decide whether the patient should be considered for percutaneous coronary intervention, or percutaneous transluminal angioplasty (PTCA), whereby a small balloon is used to inflate the blockage. Angioplasty (PTCA) is usually followed by placement of a stent or coronary artery bypass graft surgery (CABG) to increase coronary artery blood flow.

Angioplasty can produce excellent results in carefully selected patients. Under x-ray guidance, a wire is advanced from the groin to the coronary artery. A small catheter with a balloon at the end is threaded over the wire to reach the narrowed segment. The balloon is then inflated to push the artery open, and a steel mesh stent is generally inserted.

CABG surgery is performed to relieve angina in patients who have failed medical therapy and are not good candidates for angioplasty (PTCA). CABG surgery is ideal for patients with multiple narrowings in multiple coronary artery branches, such as is often seen in patients with diabetes. CABG surgery has been shown to improve long-term survival in patients with significant narrowing of the left main coronary artery, and in patients with significant narrowing of multiple arteries, especially in those with decreased heart muscle pump function.

How is CABG surgery done?

The cardiac surgeon makes an incision down the middle of the chest and then saws through the breastbone (sternum). This procedure is called a median (middle) sternotomy (cutting of the sternum). The heart is cooled with iced salt water, while a preservative solution is injected into the heart arteries. This process minimizes damage caused by reduced blood flow during surgery and is referred to as "cardioplegia." Before bypass surgery can take place, a cardiopulmonary bypass must be established. Plastic tubes are placed in the right atrium to channel venous blood out of the body for passage through a plastic sheeting (membrane oxygenator) in the heart lung machine. The oxygenated blood is then returned to the body. The main aorta is clamped off (cross clamped) during CABG surgery to maintain a bloodless field and to allow bypasses to be connected to the aorta.

The most commonly used vessel for the bypass is the saphenous vein from the leg. Bypass grafting involves sewing the graft vessels to the coronary arteries beyond the narrowing or blockage. The other end of this vein is attached to the aorta. Chest wall arteries, particularly the left internal mammary artery, have been increasingly used as bypass grafts. This artery is separated from the chest wall and usually connected to the left anterior descending artery and/or one of its major branches beyond the blockage. The major advantage of using internal mammary arteries is that they tend to remain open longer than venous grafts. Ten years after CABG surgery, only 66% of vein grafts are open compared to 90% of internal mammary arteries. However, artery grafts are of limited length, and can only be used to bypass diseases located near the beginning (proximal) of the coronary arteries. Using internal mammary arteries may prolong CABG surgery because of the extra time needed to separate them from the chest wall. Therefore, internal mammary arteries may not be used for emergency CABG surgery when time is critical to restore coronary artery blood flow.

CABG surgery takes about four hours to complete. The aorta is clamped off for about 60 minutes and the body is supported by cardiopulmonary bypass for about 90 minutes. The use of 3 (triple), 4 (quadruple), or 5 (quintuple) bypasses are now routine. At the end of surgery, the sternum is wired together with stainless steel and the chest incision is sewn closed. Plastic tubes (chest tubes) are left in place to allow drainage of any remaining blood from the space around the heart (mediastinum). About 5% of patients require exploration within the first 24 hours because of continued bleeding after surgery. Chest tubes are usually removed the day after surgery. The breathing tube is usually removed shortly after surgery. Patients usually get out of bed and are transferred out of intensive care the day after surgery. Up to 25% of patients develop heart rhythm disturbances within the first three or four days after CABG surgery. These rhythm disturbances are usually temporary atrial fibrillation, and are felt to be related to surgical trauma to the heart. Most of these arrhythmias respond to standard medical therapy that can be weaned one month after surgery. The average length of stay in the hospital for CABG surgery has been reduced from as long as a week to only three to four days in most patients. Many young patients can even be discharged home after two days.

A new advance for many patients is the ability to do CABG with out going on cardiopulmonary bypass ("off pump"), with the heart still beating. This significantly minimizes the occasional memory defects and other complications that may be seen after CABG, and is a significant advance.

How do patients recover after CABG surgery?

Sutures are removed from the chest prior to discharge and from the leg (if the saphenous vein is used) after 7 to 10 days. Even though smaller leg veins will take over the role of the saphenous vein, a certain degree of swelling (edema) in the affected ankle is common. Patients are advised to wear elastic support stockings during the day for the first four to six weeks after surgery and to keep their leg elevated when sitting. This swelling usually resolves after about six to eight weeks. Healing of the breastbone takes about six weeks and is the primary limitation in recovering from CABG surgery. Patients are advised not to lift anything more than 10 pounds or perform heavy exertion during this healing period. They are also advised not to drive for the first four weeks to avoid any injury to the chest. Patients can return to normal sexual activity as long as they minimize positions that put significant weight on the chest or upper arms. Return to work usually occurs after the six week recovery, but may be much sooner for non-strenuous employment.

Exercise stress testing is routinely done four to six weeks after CABG surgery and signals the beginning of a cardiac rehabilitation program. Rehabilitation consists of a 12 week program of gradually increasing monitored exercise lasting one hour three times a week. Patients are also counseled about the importance of lifestyle changes to lower their chance of developing further CAD. These include stopping smoking, reducing weight and dietary fat, controlling blood pressure and diabetes, and lowering blood cholesterol levels.

What are the risks and complications of CABG surgery?

Overall mortality related to CABG is 3-4%. During and shortly after CABG surgery, heart attacks occur in 5 to 10% of patients and are the main cause of death. About 5% of patients require exploration because of bleeding. This second surgery increases the risk of chest infection and lung complications. Stroke occurs in 1-2%, primarily in elderly patients. Mortality and complications increase with:

• age (older than 70 years),

• poor heart muscle function,

• disease obstructing the left main coronary artery,

• diabetes,

• chronic lung disease, and

• chronic kidney failure.

Mortality may be higher in women, primarily due to their advanced age at the time of CABG surgery and smaller coronary arteries. Women develop coronary artery disease about 10 years later than men because of hormonal "protection" while they still regularly menstruate (although in women with risk factors for coronary artery disease, especially smoking, elevated lipids, and diabetes, the possibility for the development of coronary artery disease at a young age is very real). Women are generally of smaller stature than men, with smaller coronary arteries. These small arteries make CABG surgery technically more difficult and prolonged. The smaller vessels also decrease both short and long-term graft function.

What are the long-term results after CABG surgery?

A very small percentage of vein grafts may become blocked within the first two weeks after CABG surgery due to blood clotting. Blood clots form in the grafts usually because of small arteries beyond the insertion site of the graft causing sluggish blood run off. Another 10% of vein grafts close off between two weeks and one year after CABG surgery. Use of aspirin to thin the blood has been shown to reduce these later closings by 50%. Grafts become narrowed after the first five years as cells stick to the inner lining and multiply, causing formation of scar tissue (intimal fibrosis) and actual atherosclerosis. After 10 years, only 2/3 of vein grafts are open and 1/2 of these have at least moderate narrowings. Internal mammary grafts have a much higher (90%) 10 year rate of remaining open. This difference in longevity has caused a shift in surgical practices toward greater use of internal mammary and other arteries as opposed to veins for bypasses.

Recent data has shown that in CABG patients with elevated LDL cholesterol (bad cholesterol) levels, use of cholesterol-lowering medications (particularly the statin family of drugs) to lower LDL levels to below 80 will significantly improve long-term graft patency as well as improve survival benefit and heart attack risk. Patients are also advised about the importance of lifestyle changes to lower their chance of developing further atherosclerosis in their coronary arteries. These include stopping smoking, exercise, reducing weight and dietary fat, as well as controlling blood pressure and diabetes. Frequent monitoring of CABG patients with physiologic testing can identify early problems in grafts. PTCA (angioplasty) with stenting, in addition to aggressive risk factor modification, may significantly limit the need for repeat CABG years later. Repeat CABG surgery is occasionally necessary, but may have a higher risk of complication.

How do CABG surgery and angioplasty (PTCA) compare?

Ongoing studies are comparing the treatment results of angioplasty (PTCA) versus bypass (CABG surgery) in patients who are candidates for either procedure. Both procedures are very effective in reducing angina symptoms, preventing heart attacks, and reducing death. Many studies have either shown similar benefits or slight advantage to CABG (primarily in severe diabetics), although current studies are evaluating the two procedures utilizing the most current improved techniques (for example, newer "medicated" stents and the off-pump CABG); this data is still being collected. The best choice for an individual patient is best made by their cardiologist, surgeon, and primary doctor.

Coronary Artery Bypass Graft At A Glance

• Coronary artery disease develops because of hardening of the arteries (arteriosclerosis) that supply blood to the heart muscle.

• In the diagnosis of coronary artery disease, helpful tests include EKG, stress test, echocardiography, and coronary angiography.

• Coronary artery bypass graft (CABG) surgery reestablishes sufficient blood flow to deliver oxygen and nutrients to the heart muscle.

• The bypass graft for a CABG can be a vein from the leg or an inner chest wall artery.