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Heart attack
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Heart Attack

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 pressure. If blood flow is not restored within 20 to 40 minutes, irreversible death of the heart muscle will begin to occur. Muscle continues to die for 6-8 hours at which time the heart attack usually is "complete." The dead heart muscle is replaced by scar tissue.

Causes Of Heart Attack:

Atherosclerosis

Atherosclerosis is a gradual process in 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 cannot 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 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 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 diagram 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.

While heart attacks can occur at any time, most 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.

The Symptoms OfA Heart Attack:

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

  • 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.

The Complications Of A Heart Attack:

Heart failure If 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 die later include those victims who suffer major damage to the heart muscle initially or who suffer 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. 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 defibrillators that provide the electrical shock needed to restore a normal heart rhythm even before the paramedics arrive. This greatly improves the chances of survival.

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. For more, please see the Cholesterol and Your Heart article.

  • 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. For more, please see the High Blood Pressure article.
  • 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. For more, please see the Smoking and Quitting Smoking article.
  • 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. For more, please see the Diabetes article.
  • 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.
Diagnosis for A Heart Attack:

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.

How is a heart attack treated?

Treatment of heart attacks include:

  • Anti-platelet medications to prevent formation of blood clots in the arteries
  • Anti-coagulant medications to prevent growth of blood clots in the arteries
  • Coronary angiography with either percutaneous transluminal coronary angioplasty (PTCA) with or without stenting to open blocked coronary arteries
  • Clot-dissolving medications to open blocked arteries
  • Supplemental oxygen to increase the supply of oxygen to the heart's muscle
  • Medications to decrease the need for oxygen by the heart's muscle
  • Medications to prevent abnormal heart rhythms
The primary goal of treatment is to quickly open the blocked artery and restore blood flow to the heart muscle, a process called reperfusion. Once the artery is open, damage to heart muscle ceases, and the patient becomes pain free. By minimizing the extent of heart muscle damage, early reperfusion preserves the pumping function of the heart. Optimal benefit is obtained if reperfusion can be established within the first 4-6 hours of a heart attack. Delay in establishing reperfusion can result in more widespread damage to heart muscle and a greater reduction in the ability of the heart to pump blood. Patients with hearts that are unable to pump sufficient blood develop heart failure, decreased ability to exercise, and abnormal heart rhythms. Thus, the amount of healthy heart muscle remaining after a heart attack is the most important determinant of the future quality of life and longevity.

Anti-platelet agents
Anti-platelet agents are medications that prevent blood clots from forming by inhibiting the aggregation of platelets. Platelets are fragments of cells that circulate in the blood. Platelets begin the formation of blood clots by clumping together (a process called aggregation). Platelet clumps are then strengthened and expanded by the action of clotting factors (coagulants) that result in the deposition of protein (fibrin) among the platelets. Aggregation of platelets occurs at the site of any injury or laceration, but it also occurs at the site of rupture of cholesterol plaques in the walls of coronary arteries. Formation of clots at the site of an injury or laceration is desirable because it prevents excessive loss of blood, but formation of clots inside coronary arteries blocks the arteries and causes heart attacks. There are three types of anti-platelet agents -- aspirin, thienopyridines, and the glycoprotein IIb/IIIa inhibitors. These agents differ in their mode of action, anti-platelet potency, speed of onset of action, and cost. Aspirin Aspirin inhibits the activity of the enzyme cyclo-oxygenase inside platelets. Cyclo-oxygenase is an enzyme whose activity is necessary for the formation of a chemical, thromboxane A2, that causes platelets to aggregate. Aspirin, by inhibiting the formation of thromboxane A2, prevents platelets from aggregating and thereby prevents the formation of blood clots. Aspirin alone has its greatest impact on improving survival among patients with heart attacks. Numerous studies have shown that aspirin reduces mortality (by 25%) when given to patients with heart attacks. Aspirin is easy to use, safe at the low doses used for anti-platelet action, fast acting (with an onset of action within 30 minutes), and cheap. Aspirin is given at a dose of 160 mg to 325 mg immediately to almost all patients as soon as a heart attack is recognized. It also is continued on a daily basis indefinitely after the heart attack. The only reason for not using aspirin is a history of intolerance or allergy to aspirin. Aspirin is taken daily following a heart attack to reduce the risk of another heart attack. (Preventing further heart attacks is called secondary prevention, while preventing the first heart attack is called primary prevention). The ideal daily dose of aspirin for secondary prevention has not been established. Some doctors recommend 160 mg; others recommend 81 mg. The reason for this difference has to do with aspirin's occasional long-term side effect of bleeding (for example from stomach ulcers). Even though the risk of major bleeding with long-term, moderate dose aspirin (325 mg/day) is low (less than 1%), this risk can be lowered slightly by using an even lower dose (160 or 81 mg/day). Aspirin also benefits patients with forms of coronary heart disease other than an acute heart attack. Aspirin has been shown to reduce heart attacks and improve survival in the following patients:
  • Aspirin improves survival among patients with unstable angina. Patients with unstable angina experience chest pains at rest or with minimal exertion. These patients have critically narrowed coronary arteries and are at imminent risk of having a heart attacks
  • Aspirin improves survival among patients with stable exertional angina. (These are patients who experience chest pain only with exertion.)
  • Aspirin prevents formation of blood clots at the site of the PTCA (see below).
  • Aspirin prevents the formation of blood clots that can occlude surgical bypass grafts. (Occlusion of bypass grafts can lead to heart attacks.)
  • Aspirin in low doses (81 mg/day) has been shown to prevent first heart attacks (primary prevention)
The thienopyridines

The thienopyridines such as ticlopidine (Ticlid) and clopidogrel (Plavix) inhibit the ADP receptor on the surface of platelets. Inhibiting the ADP receptors on the platelets prevent the platelets from aggregating and causing blood clots to form. The theinopyridines are more potent anti-platelet agents than aspirin. Clopidogrel (Plavix) is used far more commonly than ticlopidine (Ticlid) because ticlopidine can, in rare instances, cause low platelet and/or white blood cell counts. Clopidogrel plays an important role in the treatment of heart attacks and is used in the following situations:

  • Clopidogrel is used instead of aspirin in patients who have an allergy to aspirin.
  • Clopidogrel often is given together with aspirin in treating heart attacks. Studies have shown that the combination of aspirin and clopidogrel is more effective than aspirin alone in improving survival and limiting damage to heart muscle among patients with heart attacks.
  • Clopidogrel is given together with aspirin to patients undergoing PTCA with or without coronary stenting (see later discussion). Studies have shown that the combination of aspirin and clopidogrel is more effective than aspirin alone in preventing formation of blood clots that can re-occlude the coronary artery unblocked by PTCA and in preventing blood clots within recently placed stents.
  • After a heart attack or after PTCA, aspirin is given indefinitely. The optimal duration of clopidogrel has not been established, and duration of use by physicians varies from weeks to months.
Patients who receive the combination of clopidogrel and aspirin are more likely than patients who receive aspirin alone to develop complications of major bleeding following coronary artery bypass surgery. Therefore, ideally clopidogrel should be stopped 3-7 days before surgery.
Glycoprotein IIb/IIIa inhibitors The glycoprotein IIb/IIIa inhibitors such as abciximab (Reopro) and eptifibatide (Integrilin) prevent aggregation of platelets by inhibiting the glycoprotein receptors on the platelets. They are the most potent anti-platelet agents, approximately 9 times more potent than aspirin, and three times more potent than the thienopyridines. The glycoprotein IIb/IIIa inhibitors are also the most expensive anti-platelet agents. The currently FDA-approved glycoprotein IIb/IIIa inhibitors have to be given intravenously. They usually are given along with aspirin and heparin. They are quick acting; their maximal anti-platelet effects are achieved within minutes of infusion. These inhibitors have become important in the treatment of patients with heart attacks, patients with unstable angina, and patients undergoing PTCA with or without stenting. Numerous studies have shown that glycoprotein IIb/IIIa inhibitors:
  • Decrease the size of the blood clot blocking the coronary arteries, thus improving blood flow, limiting damage to heart muscle, and improving survival among patients with heart attacks
  • Decrease the incidence of heart attacks and improve survival among patients with unstable angina
  • Prevent the formation of blood clots inside coronary stents and in coronary arteries unblocked by PTCA, thus decreasing the incidence of heart attacks and improving survival, specifically, when given intravenously at the time of PTCA and stenting and followed by oral aspirin and clopidogrel
The major risk of glycoprotein IIb/IIIa inhibitors is bleeding. Therefore, patients on heparin, aspirin, and glycoprotein IIb/IIIa inhibitors have to be monitored closely for bleeding. Recent studies have demonstrated equal efficacy of abciximab and eptifibatide. Eptifibatide is shorter acting than abciximab. In the event of major bleeding, the anti-platelet effect of eptifibatide can be reversed within hours of stopping the intravenous infusion, while the anti-platelet effect of abciximab will last much longer. Sometimes, transfusions of platelets are necessary to treat major bleeding due to abciximab. An uncommon side effect of glycoprotein IIb/IIIa inhibitors is the development of low platelet counts (thrombocytopenia). Thrombocytopenia can increase the risk for bleeding and, in rare instances, may actually cause blood to clot. Thus, patients receiving glycoprotein IIb/IIIa inhibitors should have their platelet counts monitored closely.
Anti-coagulants Coagulants (clotting factors) are proteins produced by the liver. Clotting factors are responsible for "cementing" clumps of platelets together to form a stronger and larger clot. Anti-coagulants such as intravenous or subcutaneous heparin, subcutaneous low molecular weight heparin, and oral warfarin (Coumadin), prevent the formation of blood clots either by inhibiting the production of clotting factors or by interfering with the action of the clotting factors.
Heparin. Heparin prevents the formation and growth of blood clots by inhibiting the action of clotting factors that cement the clumps of platelets together. Heparin is given either intravenously or as a subcutaneous (under the skin) injection.

Heparin commonly is given intravenously, usually with aspirin, anti-platelet agents, or fibrinolytic (clot-dissolving) medications for treating heart attacks. Intravenous heparin is given (usually with aspirin or an anti-platelet agent) to patients with heart attacks who are undergoing PTCA with or without stenting. Heparin also is given to patients who are at risk of developing blood clots within the chambers (atria and ventricles) of the heart. (For example, patients with atrial fibrillation can develop blood clots in the atria. Patients with large heart attacks and major damage to the heart muscle also can develop blood clots in the ventricles.) Heparin's anti-coagulant effect is fast acting (beginning shortly after the start of the infusion) and dose-related (greater with higher doses). The duration of heparin treatment for heart attacks is approximately 48 hours.

Heparin's major side effect is bleeding, and the most serious bleeding complication is intracranial hemorrhage (bleeding into the brain). The risk of bleeding is higher with higher doses. Thus, patients receiving heparin will undergo frequent blood testing to measure APPT levels. The APPT level is a measure of the degree of anti-coagulation. The goal is to keep the patient's APPT level in a safe range and to avoid abnormally high APPT levels that signify excessive anti-coagulation and a greater risk of bleeding. If there is bleeding, heparin has the advantage of having a short duration of action, and its anti-coagulant effects disappears rapidly after stopping the intravenous infusion.
Low molecular weight heparin. Low molecular weight heparins such as enoxaparin (Lovenox) and dalteparin (Fragmin), are sub-fractions of heparin with longer-lasting effects than heparin. They can be given every 12-24 hours as subcutaneous injections (like insulin). Studies have shown enoxaparin and dalteparin to be equivalent to intravenous heparin in patients with many conditions such as heart attacks, unstable angina, and blood clots in the veins or arteries of the lungs. The effects of low molecular weight heparins generally wear off after 6-12 hours. They are not used in place of intravenous heparin in patients undergoing PTCA or stenting.
Warfarin. Warfarin (Coumadin) prevents the formation of blood clots by inhibiting the production of clotting factors by the liver. Warfarin must be taken orally and is slow acting; it can take days to achieve an adequate anti-coagulant effect. Warfarin's anti-coagulant effect is dose-related, that is, it's effect is greater with larger doses.

Because of its slow onset of action, Coumadin is not commonly used immediately for the treatment of heart attacks. Instead, it is used orally on a long-term basis in selected patients after heart attacks to prevent blood clots. For example, patients with atrial fibrillation or patients with major damage to ventricular muscle will take warfarin daily on a long-term basis to prevent blood clots in the atria and ventricles, respectively. Warfarin also is commonly used to prevent blood clots in veins of the legs in patients who are likely to develop them.

The risk with warfarin is abnormal bleeding, and the risk of bleeding is higher with higher doses. Thus, patients on warfarin should have their blood tested frequently (often weekly) to measure their prothrombin time and INR. Like APPT, the prothrombin time and INR measure the degree of anti-coagulation. The goal of treatment is to keep the prothrombin time and INR in a safe range, avoiding excessively high prothrombin time and INR levels that indicate too much anti-coagulation and a greater risk of bleeding. The effects of warfarin may be increased or decreased greatly by many other medications or foods, and it is crucial to review these medications and foods with the doctor.

Warfarin has a long duration of action, and it's anti-coagulation effect can last several days after it is stopped. Therefore, transfusions of clotting factors and/or vitamin K (to stimulate the liver to produce the clotting factors depleted by treatment with warfarin) must be given to reverse the anti-coagulation in the event of serious bleeding.
Clot-dissolving drugs While anti-platelet agents and anti-coagulants prevent the formation of blood clots, they cannot dissolve existing blood clots and hence cannot be relied upon to open blocked arteries rapidly. Clot-dissolving drugs (also called fibrinolytic or thrombolytic medications) actually dissolve blood clots and can rapidly open blocked arteries. Intravenous administration of clot-dissolving drugs such as tissue plasminogen activator (TPA) or TNK can open up to 80% of acutely blocked coronary arteries. The earlier these drugs are administered, the greater the success at opening the artery and the more effective the preservation of heart muscle. If clot-dissolving drugs are given too late (more than 6 hours after the onset of the heart attack), most of the muscle damage already may have occurred.

If a hospital does not have a catheterization laboratory with the ability to perform PTCA, or if there are logistic reasons why PTCA will be delayed, clot-dissolving drugs can be promptly administered to achieve reperfusion. PTCA then may be performed in patients who fail to respond to the clot-dissolving drugs. (If prompt PTCA and stenting are available, it has been demonstrated that they are preferable to clot-dissolving drugs to open arteries.)

Clot-dissolving drugs increase the risk of bleeding enough so that some patients cannot be treated with them, for example, patients with recent surgery or major trauma, recent stroke, bleeding ulcer, or other conditions that increases the risk of bleeding.

Coronary angiography and percutaneous transluminal coronary angioplasty

Coronary angiography and percutaneous transluminal coronary angioplasty (PTCA) is the most direct method of opening a blocked coronary artery. The procedures are performed in the catheterization laboratory in a hospital. Under x-ray guidance, a tiny plastic catheter with a balloon on its end is advanced over a guide wire from a vein in the groin or the arm and into the blocked coronary artery. Once the balloon reaches the blockage, it is inflated, pushing the clot and plaque out of the way to open the artery. PTCA can be effective in opening up to 95% of arteries. In addition, the angiogram (x-ray pictures taken of the coronary arteries) allows evaluation of the status of the other coronary arteries so that long-term treatment plans may be formulated. For optimal benefits, coronary angiography and PTCA should be performed as soon as possible. Most cardiologists recommend that the time interval between the patient's arrival at the hospital and the deployment of the angioplasty balloon to open the artery should be less than 60-90 minutes. For best results, the coronary angiogram and PTCA should be performed by an experienced cardiologist in a well-equipped cardiac catheterization laboratory. The cardiologist is considered experienced if he or she performs more than 75 such procedures a year. The catheterization laboratory personnel are considered experienced if the facility performs more than 200 such procedures a year. It also is important that there be a surgical team to perform immediate open-heart surgery (coronary artery bypass grafting) in the event that PTCA is unsuccessful in opening the blocked artery or if there is a serious complication of PTCA. For example, in a small number of patients, PTCA cannot be performed because of technical difficulties in passing the guide wire or the balloon across the narrowed arterial segment. Open-heart surgery also will be necessary if there is a serious complication such as coronary artery injury during PTCA or an abrupt closure of the coronary artery shortly after PTCA. These complications may occur in 1-2% of patients. The most serious complication of PTCA is an abrupt closure of the coronary artery within the first few hours after PTCA. Abrupt coronary artery closure (that can lead to further heart damage) occurs in 5% of patients after simple balloon angioplasty (without stenting). Abrupt closure is due to a combination of tearing (dissection) of the inner lining of the artery, blood clotting at the site of the balloon, and constriction (spasm) or elastic recoil of the artery at the site where the balloon is inflated. Individuals at an increased risk for abrupt closure include women, patients with unstable angina, and patients having heart attacks. The risk of abrupt closure of the coronary arteries can be reduced if:

  • Aspirin is given during or after PTCA to prevent blood clotting. In fact, virtually all patients are maintained on aspirin indefinitely after PTCA to prevent arterial clots.
  • Anticoagulants such as intravenous heparin are given during PTCA to further prevent blood clotting.
  • Combinations of nitrates and calcium channel blockers are used to minimize coronary artery spasm (see discussion that follows).
  • Coronary artery stents are deployed to minimize coronary artery closure.
  • The glycoprotein IIb/IIIa inhibitors are given.
Coronary artery stents

Coronary artery stents are small hollow cylinders that can be deployed over the angioplasty balloons and left within the coronary arteries to keep the arteries open. Stents help prevent abrupt closure of arteries shortly after PTCA . They also prevent restenosis (recurrent narrowing of the arteries) several months after PTCA. Coronary stents decrease the risks of arterial dissections, elastic recoil, and artery spasm that can occur after PTCA and cause re-occlusion of the artery. Studies have shown that the incidence of abrupt coronary artery closure after PTCA has declined dramatically with the introduction of coronary stents. Coronary stents also help to keep the coronary arteries open in the longer-term. After a successful PTCA, as many as 30-40% of patients will develop recurrent narrowing (restenosis) at the site of inflation of the balloon, usually within 6 months following PTCA. Restenosis may or may not be accompanied by symptoms such as angina. Thus, restenosis often is detected by exercise stress tests performed 4 to 6 months after PTCA. The widespread use of coronary stents has reduced this incidence of restenosis by as much as 50%. The recent introduction of coated stents (stents that are coated with chemicals to further reduce restenosis) has reduced the incidence of restenosis to well under 10% and has been a major improvement in treatment. Patients with coronary artery stents usually are maintained on full doses of daily aspirin. For the first 4-12 weeks after the placement of stents, patients are given an additional anti-platelet drug such as ticlopidine or clopidogrel because the metal surface of the stents may promote the formation of blood clots in the first several weeks after the stent is inserted.

Nitrates

Nitroglycerin is the most common nitrate used in the treatment of heart attacks. It can be given sublingually (under the tongue), as a spray, as a paste applied over skin, and intravenously. Intravenous nitroglycerine has a rapid onset of action and is commonly used in the initial (first 48 hours) treatment of heart attacks. Nitroglycerine is a vasodilator (blood vessel dilator), which opens arteries by relaxing the muscular wall of the artery. Nitroglycerine dilates coronary arteries as well as other blood vessels throughout the body. By dilating blood vessels, nitroglycerine lowers blood pressure, decreases the work that the heart must do, lowers the demand by the heart for oxygen, prevents coronary artery spasm, improves blood flow to the heart muscle, and potentially minimizes the size of the heart attack. Nitroglycerine is especially helpful in patients with heart attacks who also have heart failure or high blood pressure. The common side effects of nitrates are headaches and low blood pressure. Low blood pressure can cause weakness, dizziness, and, sometimes, even fainting. Nitrates should not be given in patients who have taken medicines for erectile dysfunction such as sildenafil (Viagra) and vardenafil (Levitra) in the preceding 24 hours, since severe low blood pressure may result. Nitrates should not be given in patients who have taken tadalafil (Cialis) in the preceding 36-48 hours because the effects of Cialis last longer than either sildenafil or vardenafil.

Angiotensin converting enzyme inhibitors Angiotensin converting enzyme (ACE) inhibitors, another class of blood vessel dilators, often are given orally after a large heart attack to improve the healing of heart muscle. Examples of ACE inhibitors include captopril (Capoten), enalapril (Vasotec), lisinopril (Zestril and Prinivil), and ramipril (Altace). These medications lower the blood pressure and reduce the workload of the heart, thereby helping the damaged heart muscle to recover. They are especially helpful in patients who have recovered from heart attacks but have high blood pressure, heart failure, major damage to the left ventricle, and diabetes mellitus. For additional information, please see the Beta Blockers article.
Beta-blockers Beta-blockers such as propranolol (Inderal), metoprolol (Lopressor, Toprol XL), and atenolol (Tenormin) usually are given early during a heart attack and are continued long-term. Beta blockers antagonize the action of adrenaline and relieve stress on the muscles of the heart. Beta-blockers decrease the workload of the heart by slowing the heart rate and decreasing the force of contraction of heart muscle. Decreasing the workload decreases the demand for oxygen by the heart and limits the amount of damage to the heart muscle. Long-term administration of beta-blockers following a heart attack has been shown to improve survival and reduce the risk of future heart attacks. Beta-blockers also improve survival among patients with heart attacks by decreasing the incidence of life-threatening abnormal heart rhythms, for example, ventricular fibrillation. Beta-blockers can be given intravenously in the hospital and then can be taken orally for long-term treatment.

The side effects of beta-blockers are wheezing (worsening of breathing in patients with asthma), abnormally slow heart rate, and exacerbation of heart failure (especially in patients with significant damage to their heart muscle); however, in patients with chronic heart failure, beta blockers have recently been demonstrated to be helpful in decreasing symptoms and prolonging life.

Oxygen Oxygen also is commonly administered during the acute phase of a heart attack as are narcotics such as morphine; these agents aid in the reduction of discomfort and actually help minimize the amount of heart damage.

Coronary artery bypass In some patients, PTCA can be technically difficult or dangerous to perform. In others, PTCA and clot-dissolving medications may fail to achieve reperfusion or maintain open arteries. These patients may be considered for coronary artery bypass grafting surgery. For more information.

What can a patient expect during recovery from a heart attack?

Heart attack patients are monitored in the hospital for three or more days prior to discharge home. Rhythm disturbances, shortness of breath due to heart failure, or recurrent chest pain are reasons for further therapy such as balloon angioplasty or coronary stenting, additional medications, or bypass surgery. Patients gradually increase their activity under observation. Before discharge, a low-level exercise stress test may be performed to detect important residual narrowing in the coronary arteries, exercise-induced cardiac rhythm abnormalities, and heart muscle failure, and to help guide the doctor in prescribing an activity regimen after hospitalization. An abnormal stress test prior to hospital discharge following a heart attack predicts a high risk for subsequent cardiac events; if the patient has not yet had a coronary angiogram, an abnormal pre-discharge stress test is a strong reason for doing angiography. Since most patients usually receive angiography early, the use of pre-discharge stress testing has declined. Before resuming full activity or work, several weeks may be needed for the heart muscle to heal. After a small heart attack (little damage to heart muscle), patients usually can resume normal activities after two weeks. These activities include returning to work as well as normal sexual activity. A moderate heart attack (moderate damage to heart muscle) requires limited, gradually increasing activity for up to four weeks, while a large heart attack (much damage to heart muscle) may result in a recovery period of six weeks or longer. These time frames are necessary in order for the dead heart muscle to substantially complete the scarring process. During this healing period, patients should avoid vigorous exertion and heavy lifting (over 20 pounds) or any strenuous activity that causes shortness of breath or undue fatigue. Cardiac rehabilitation typically begins during hospitalization and continues during the months following a heart attack. Cardiac rehabilitation programs provide a helpful transition to a safe and full return to a normal lifestyle. In addition, cardiac rehabilitation allows the prescription of a long-term exercise program tailored to each patient and helps patients and their families adjust to lifestyle changes and the difficult and conflicting emotions that often follow a heart attack.

How can a second heart attack be prevented?

  • Take aspirin and beta-blockers (propranolol, metoprolol, atenolol) that have been shown to reduce the chances of a second heart attack and improve survival.
  • Stop smoking cigarettes.
  • Reduce excess weight, and exercise regularly.
  • Control blood pressure and diabetes.
  • Follow a diet that is low in cholesterol (less than 200 mg daily) and saturated fat (less than 7% of total calories). For more, please see the Therapeutic Lifestyle Changes (TLC) Daily Food Guide, Eating Heart Healthy.
  • Reduce LDL (bad) cholesterol and increase HDL (good) cholesterol. Reduction of LDL cholesterol to a value below 100 mg/dl, particularly with the statin group of medications, has been demonstrated to prevent further heart attacks. Patients with low HDL (less than 35 mg/dl) are encouraged to exercise regularly and to take medications to increase HDL. For more in-depth information about cholesterol, LDL, and HDL, please see the Cholesterol article.
  • Take ACE inhibitors that aid the healing process and improve long-term survival in selected patients, particularly those with major damage to heart muscle.
  • Take a daily multivitamin that has 400-800 microgram of folic acid. This helps to reduce homocysteine levels in the blood that may aggravate atherosclerosis.
  • Eat a diet rich in omega-3-fatty acids by eating more fish or take fish oil supplements. (See the fish oil article). High intake of omega-3-fatty acids decreases the risk of sudden death from heart attacks
  • Undergo further testing. In the months following a heart attack, further cardiac stress testing, with or without nuclear or echocardiographic imaging, may be prescribed to determine if additional therapy will be necessary to prevent future heart attacks. In addition, special testing may be required to evaluate the risk of developing cardiac arrhythmias. All such testing should be discussed with the doctor.
Heart Attacks In Women:

Risk of heart attacks in womenCoronary 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; they are increased blood cholesterol, high blood pressure, smoking cigarettes, diabetes mellitus, and a family history of coronary heart disease at a young age.
Smoking cigarettesEven "light" smoking raises the risk of CAD. In one study, middle-aged women who smoked 1 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 decreases back down to the same risk of nonsmoking women after several years of not smoking.

Cholesterol treatment guidelines in womenCurrent NCEP (National Cholesterol Education Program) treatment guidelines for undesirable cholesterol levels are the same for women as for men. For more information about the NCEP guidelines, please read The Guidelines on Cholesterol for Adults article.

Diagnosis Of Heart Attacks In Women: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 are:

  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.
  2. Silent heart attacks (heart attacks with little or no symptoms) are more common among women than among men.
  3. 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.
  4. Women are less likely than men to have the typical findings on the ECG that are necessary to diagnose a heart attack quickly.
  5. 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 most reliable tests for CAD) will reveal normal coronary arteries and therefore cannot be used to diagnose either of these two conditions.
  6. 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.

Treatment of heart attacks in womenThrombolytic (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.

Estrogen and coronary heart disease 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 3-5 years, but the increase in heart disease and pulmonary emboli occurred early on, in the first year.

For additional information on the WHI results, please read the article, The Women's Health Initiative in Perspective: The Last Straw for Estrogen Therapy?

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 5 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" (Reopro and 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. 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.
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