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Heart Attack
(Myocardial Infarction)


What is a heart attack?

A heart attack (also called a myocardial infarction) is the death of part of the heart muscle due to its sudden loss of blood supply. Typically, the loss of blood supply is caused by a complete blockage of a coronary artery by a blood clot. A coronary artery is an artery that supplies blood (along with essential nutrients) to the heart muscle. Death of the heart muscle often causes chest pain and electrical instability of the heart muscle tissue. Electrical instability of the heart causes ventricular fibrillation (chaotic electrical disturbance). Orderly transmission of electrical signals in the heart is important for the regular beating (pumping) of the heart. A heart undergoing ventricular fibrillation simply quivers, and cannot pump or deliver oxygenated blood to the brain. Permanent brain damage and death can occur unless oxygenated blood flow is restored within five minutes.

Approximately one million Americans suffer a heart attack annually. Four hundred thousand of these victims die as a result. Many of the heart attack deaths are due to ventricular fibrillation of the heart that occurs before the victim can reach any medical assistance or the emergency room. These electrical disturbances of the heart can often be successfully treated with medications or other means by paramedics in the “field,” or upon arrival to the hospital. Approximately 90% to 95% of heart attack victims who reach the hospital survive. The 5% to 10% who later die are those who have suffered major heart muscle damage, or who suffer an “extension” or enlargement of their heart attack.
Early heart attack deaths can be avoided if a bystander starts CPR (cardiopulmonary resuscitation) within five minutes of the onset of ventricular fibrillation. CPR involves breathing for the victim and applying external chest compression to make the heart pump. When paramedics arrive, medications and/or electrical shock (cardioversion) to the heart can be administered to convert ventricular fibrillation to a normal heart rhythm. Therefore, prompt CPR and rapid paramedic response can improve the survival chances from a heart attack.

What causes a heart attack?

A heart attack is caused by the formation of a blood clot on a cholesterol plaque located on the inner wall of an artery to the heart (coronary artery). Cholesterol is a fatty chemical which is part of the outer lining of cells in the body. Cholesterol plaque is the formation of a hard, thick substance within the artery walls which is caused by deposits of cholesterol in the artery walls; a process that begins in the late teens. Over time, the accumulation of cholesterol plaque causes thickening of the artery walls and narrowing of the arteries; a process called atherosclerosis. Plaque accumulation can be accelerated by smoking, high blood pressure, elevated cholesterol, and diabetes. Ultimately, atherosclerosis causes significant narrowing of the coronary arteries. During exercise or excitement, the narrowed coronary arteries cannot increase the blood supply to meet the increased oxygen demand of the heart muscle. When the heart muscle is thus deprived of blood oxygen, a condition called ischemia results; ischemia may be associated with chest pain (angina pectoris). Typically, angina occurs with exertion, and subsides with rest. When the narrowing in the artery becomes critical, angina at rest or “unstable” angina may result. Unstable angina can be the harbinger of a heart attack in the near future.

Occasionally the surface of the cholesterol plaque in the artery may rupture, which leads to the formation of blood clot on the surface of the plaque, which then completely occludes blood flow in the vessel and results in a heart attack (see diagram). The cause of this “plaque rupture” is largely unknown, but contributing factors may include cigarette smoking, elevated LDL cholesterol, elevated levels of blood catecholamines (adrenaline), high blood pressure, and other mechanical and biochemical forces. Unlike exertional angina, death of the heart muscle from a heart attack is permanent. For more information, please see the Cholesterol article of MedicineNet.com.

What are the symptoms of a heart attack?

Chest pain or pressure is a common symptom of heart attack. Cardiac chest pain is often vague, or dull, and may be described as a pressure or band-like sensation, squeezing, heaviness, or other discomfort. Heart attacks frequently occur from 4:00 A.M. to 10:00 A.M. due to higher adrenaline amounts released from the adrenal glands during the morning hours. Increased adrenaline in the bloodstream can contribute to the above mentioned plaque rupture. Interestingly, heart attacks do not usually happen during exercise, although exercise is commonly associated with exertional angina. Approximately one quarter of all heart attacks are silent, without chest pain. In diabetics, the incidence of “silent” heart attacks may be much higher.

Heart attack victims may complain of:
  • chest pressure
  • sweating
  • jaw pain
  • heartburn and/or indigestion
  • arm pain (more commonly the left arm, but may be either)
  • upper back pain
  • general malaise (vague feeling of illness)
  • nausea
  • shortness of breath

How is a heart attack diagnosed?

The initial diagnosis of a heart attack is made by a combination of clinical symptoms and characteristic electrocardiogram (EKG) changes. An EKG is a recording of the electrical activity of the heart, and can detect areas of ischemic heart muscle (muscle which is deprived of oxygen) and/or dead tissue in the heart. However, confirmation of a heart attack can only be made hours later through detection of elevated cardiac enzymes in the blood. Cardiac enzymes are muscle proteins which are released into the blood circulation by dying heart muscles when their surrounding membranes dissolve. Such enzymes include creatine kinase (CK), special subforms of CK, and troponin. Achieving PROMPT MEDICAL ATTENTION is the THE MOST IMPORTANT FACTOR for an improved prognosis with a heart attack. Rapid evaluation allows early treatment of potentially life-threatening arrhythmias, and permits early “reperfusion” (return of blood flow) of the heart muscle, as described below. The sooner that reperfusion is established, the smaller the resultant heart attack will be. Large and active cardiac centers often have a “chest pain unit”, where patients are rapidly screened for the presence of a heart attack, and prompt therapy is initiated. If the diagnosis of heart attack is initially unclear, the patient is observed in a monitored setting, until the results of further testing are available.

What are the treatment options for a heart attack?

The immediate 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, the heart attack is generally halted and the patient becomes pain free. Early reperfusion minimizes the extent of heart muscle damage and preserves the pumping function of the heart. Delay in establishing reperfusion can result in irreversible death to the heart muscle cells and reduced pumping force of the remaining heart muscle. The amount and health of the remaining heart muscle is the major determinant of the future quality of life and longevity for a patient after a heart attack. Optimal benefit is obtained if reperfusion can be established in the first 4- 6 hours of a heart attack.

he most direct method of opening a blocked artery, provided the hospital has a cardiac catheterization facility, is to perform an immediate coronary angiogram and PTCA (percutaneous transluminal coronary angioplasty). Under X-ray guidance, a tiny plastic catheter with a balloon at the end is advanced over a fine guide wire to the blockage site and inflated, thus pushing the clot and plaque out of the way. PTCA can be effective in opening up to 95% of arteries, usually within 60 minutes. In addition, the angiogram allows evaluation of the status of the other coronary arteries, so that long- term treatment plans may be formulated. Recently, it has been demonstrated that the placement of a coronary stent (a tiny hollow cylinder) at the time of PTCA results in even better long term outcomes, with a lower recurrence rate and lower risk of repeat heart attack. These results may be further enhanced by the addition of newer “super aspirins” (potent blood thinners that work to antagonize the blood-clotting effects of platelets in the blood and in the cholesterol plaque), which are given at the time of PTCA or coronary stenting. For further information, please see the Angioplasty article of MedicineNet.com.
As an alternative to PTCA or stenting for an acute heart attack, certain clot dissolving medicines (thrombolytic agents) such as tissue plasminogen activator (TPA) or streptokinase given intravenously can successfully open up to 80% of acutely occluded coronary arteries. The earlier these agents are administered, the better the success at opening the artery, and the more effective the preservation of heart muscle. If thrombolytic administration is given too late (more than 6 hours after the onset of the heart attack), most of the muscle damage may have already occurred. When there will be a potential delay in the ability to perform PTCA, either if the hospital does not have a catheterization laboratory with the ability to perform PTCA, or if there are logistic reasons why PTCA will be delayed, thrombolytic therapy is then be promptly administered to allow prompt reperfusion. PTCA may then be performed in patients who fail to respond to thrombolytic therapy. Thrombolytic therapy carries a significant bleeding risk, such that some patients are not candidates for this therapy (patients with recent surgery or major trauma, recent stroke, bleeding ulcer, or other related conditions. Anti-platelet agents, like aspirin, reduce the tendency of platelets in the blood to clump and clot. These agents work in conjunction with the above-mentioned reprefusion therapies to decrease the possibility of recurrent closure of the artery and improves the chances of survival. Aspirin is given to ALL patients with a heart attack, unless there is a history of significant intolerance to aspirin. An anti-coagulant, heparin, is given intravenously in the hospital as a blood-thinning agent to prevent blood clots and to maintain an open artery during the initial 24-72 hours. Nitroglycerin a vasodilator (blood vessel dilator), which opens the blood vessel by relaxing the muscular wall of the blood vessel, is given intravenously to prevent blood vessel spasm and to minimize the size of the heart attack. ACE (angiotensin converting enzyme) inhibitors, another class of vasodilators, are often given orally after a large heart attack to improve the heart muscle healing process. Examples of ACE inhibitors include captopril (Capoten), enalapril (Vasotec), lisinopril (Zestril and Prinvil). These medications reduce the stress load to the heart, thereby helping the damaged heart muscle to recover. Beta blocking agents, such as propanalol, metoprolol, and atenelol, are also often given during the acute heart attack to decrease the amount of muscle damage. Long-term administration of these agents following a heart attack has been shown to improve survival and reduce the risk of future heart attacks.

In some patients, PTCA can be technically difficult or dangerous to perform. In others, PTCA and thrombolytic medications may fail to achieve reperfusion or maintain open arteries. These patients may be considered for coronary artery bypass graft (CABG) surgery. For more information, please see the Coronary Artery Bypass Graft article of MedicineNet.com.

How does a patient recover from a heart attack?

Heart attack patients are monitored in the hospital for 3 or more days prior to discharge home. Rhythm disturbances, shortness of breath due to heart failure, or recurrent pain are indications for further therapy such as balloon angioplasty or coronary stenting, additional medications, or bypass surgery. Patients gradually increase their activity under observation. Before discharge, low level stress testing may be performed to detect significant residual narrowing in the coronary arteries, exercise-induced rhythm changes, heart muscle failure, and to help guide the physicians in prescribing activity regimens after discharge. 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 indication that angiography should be performed. Before resuming full activity or work, several weeks are needed for the area of the heart attack to heal. After a small heart attack, which is measured by the size of heart muscle damage, patients can usually resume normal activities after two weeks. These activities include returning to work as well as normal sexual activity. A moderate heart attack requires limited, gradually increasing activity for up to four weeks, while a large heart attack may result in a recovery period of six weeks or longer. These time frames are necessary 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 which causes shortness of breath or undue fatigue. 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 individually tailored to each patient.

How can I prevent a second heart attack?

Aspirin and beta blockers (propranolol, metoprolol, atenolol) have been shown to reduce chances of a second heart attack and improve future survival. Beta blockers antagonize the action of adrenaline and relieve stress to the heart muscles. Stopping smoking, reducing weight and dietary fat, controlling blood pressure and diabetes, and a reduction of serum cholesterol, along with regular, carefully prescribed exercise can all improve the quality of life and longevity after a heart attack. Reduction of LDL cholesterol to a value below 100 mg/dl has been particularly demonstrated to have a beneficial effect on long-term prognosis. ACE inhibitor medication (mentioned above) aids in the healing process and improves long-term survival in selected patients.


In the months following a heart attack, further cardiac stress testing, with or without adjunctive 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 for the risk of developing cardiac arrhythmias. All such testing should be discussed with the patient’s health care team.

What is in the future for heart attack sufferers?

Greater public awareness and lifestyle changes have contributed to a dramatic reduction in the incidence of heart attacks over the last 4 decades. Improved blood-thinning agents, such as Hirudin and Hirulog, are being tested to complement current therapies. The role of the “super aspirins” (Reopro, Integrellin, and Aggrastat) is currently being investigated as well. Newer versions of t-PA are being developed to achieve a higher percentage of open arteries to the heart. Emergency medical teams which rapidly respond, and are able to diagnose heart attacks and administer emergency drugs in non- hospital settings, as well as performing electrical defibrillation, have been shown in test cities, such as Seattle, to improve outcome and save heart muscle. With the widespread application of modern in-hospital and out of hospital programs for heart attack patients, the long-term prognosis following a heart attack will only improve.

Heart Attack At A Glance

  • A heart attack results when a blood clot completely obstructs a coronary artery supplying blood to the heart muscle.
  • A heart attack causes death of part of the heart muscle.
  • The site of blood clot formation during a heart attack is usually a cholesterol plaque on the inner wall of a coronary artery.
  • A heart attack can cause chest pain, heart failure, and electrical instability of the heart.
  • arm pain (more commonly the left arm, but may be either)
  • Electrical instability of the heart can cause life threatening abnormal heart rhythm.
  • Treatment of a heart attack includes:
    • Prompt administration of drugs to dissolve and prevent blood clots
    • Performance of angioplasty or intracoronary stenting to open an obstructed artery
  • Medications that open (dilate) blood vessels.
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