MEDICAL INFORMATION
HEART ATTACK (MYOCARDIAL INFARCTION)
Heart attack usually means that there is a sudden impairment of the blood flow to the heart muscle which results in damage (myocardial infarction) to the heart muscle. The result may be permanent loss of muscle (necrosis) in the affected area of the heart leading to impaired function of the heart and may then be associated with irregularities of electrical patterns (arrhythmias) of the heart, enlargement of the heart, congestive heart failure, rupture of the heart, and disability and death. Heart attacks usually occur in the condition of coronary artery arteriosclerosis (hardening or narrowing of the arteries in the heart muscle). The lining of coronary artery is known as the endothelium. When the arteries become narrowed or the endothelium becomes rough and irregular, there is an interference and slowing of blood flow through the arteries. This is associated with a tendency of the body to form blood clots at these abnormal areas of the arteries. Most heart attacks are caused by blood clots (thrombosis) at these abnormal areas. In more than half of patients who have episodes of decreased blood flow to the heart muscle, there is an associate pain (angina pectoris) in the chest and sometimes radiating to the neck and arms, and there may be sweating, anxiety, and large changes in blood pressure and heart rate, and patients may faint, fall and even have strokes, or become confused. However, there may be no pain at all, perhaps abdominal discomfort, belching, or very little physical findings. During an attack of angina, the individual may become very weak and have greatly impaired ability to walk. So individuals may have very serious heart attacks without much pain. The syndrome of angina with or without heart attack is frequently referred to as Unstable Coronary Syndrome.
Every year more than four million patients are admitted to hospitals worldwide with the diagnosis of unstable coronary syndrome. Millions more suffer the syndrome at home, never going to the hospital, or experiencing death before they can get to a hospital. As indicated, the initiating event of unstable coronary syndrome is a local thrombosis in the coronary artery. The major acute therapy in the United States and many other countries of the world is thrombolytic and antithrombotic therapy. Thrombolytic therapy is designed to dissolve the blood clot. This is done by drugs that act on the protein of the clot to breakdown the clot: such drugs include streptokinase, tissue plasminogen activator, urokinase, and others. Antithrombotic therapy medications prevent further clot formation while the usual defense mechanisms of the body dissolve the clot. The main drugs of this class are heparin, low molecular weight heparins, ticlopidine and aspirin, although there are others. A major mechanism of some antithrombotic drugs is designated anti-platelet effect. Platlets are very small white blood cells that stick to rough endothelium of arteries or stick to endothelium of narrowed arteries and are an essential component of the blood clot. The area on the platelet responsible for combining to form clots is known as the 2b/3a receptor, and therefore a major class of anti-platelet drugs are known as "2b/3a antagonists".
Coronary artery dilation by certain medications can clinically reverse or modify the acute coronary syndrome. These medications include the potent vasodilator nitroglycerin and various nitrate drugs, as well as drugs known as calcium channel blockers. Mild, readily reversible attacks of chest pain from contriction or spasm of coronary arteries, or decreased blood flow to the heart, is known as STABLE ANGINA PECTORIS. Stable angina pectoris is treated by long-acting nitrates, nitroglycerin spray or pills under the tongue, and various other medications. Controlling high blood pressure is a major preventive measure against episodes of Stable Angina, and the most important of all is complete abstinance from smoking tobacco products. The reason for abstinance from tobacco is because the nicotine in the smoke causes severe vasoconstriction in the arteriosclerosed arteries. Finally, when medications fail, or as an adjunct to medications, the coronary artery clotted area or narrowed or blocked area may be mechanically dilated (balloon percutaneous coronary artery angioplasty, PTCA), or reemed out (directional coronary artery atherectomy, or rotational coronary artery atherectomy known as rotoblator). PTCA is often carried out in association with placement of an intracoronary artery stent, which is a coiled device made of steel to keep the artery open. In many cases PTCA/STENTING either fail or are not possible, so the blocked coronary arteries are bypassed with grafts from the aorta using veins or arteries and this is known as coronary artery bypass grafting (CABG). Most patients do not realize that the actual size of the coronary arteries are very small and it is only the very large ones that can undergo PTCA/STENTING or CABG surgery: only the very large arteries which are only about 1/8th inch in diameter. The problem with all PTCA/STENT and CABG procedures is RESTENOSIS.
RESTENOSIS occurs in all PTCA/STENT & CABG procedures. With PTCA it occurs in about 40 percent of patients by one year. Presently, consideration is being given to placing a STENT in the affected coronary artery stenosis on a routine basis whenever PTCA is performed on the affected artery. PTCA/STENT usually lasts longer before restenosis. CABG does not repair the stenosed artery, but bypasses it. However, other arteries become stenosed with CABG, so that the procedure often must be followed in 1 to 8 years with PTCA. Furthermore, most patients have more than one area of narrowed coronary artery, usually many. However, the cardiologist or cardiovascular surgeon only work on those arteries that are at least narrowed by 50%, and usually only those narrowed by more than 90%. Therefore these procedures are never as successful as one desires because there are always other areas of the coronary arteries coming along with more artersiosclerosis, narrowing and tendencies to the Acute Coronary Syndrome. Therefore, major research effort in the medical community is designed to develop new medications to DECREASE RESTENOSIS. The major medications presently believed to decrease restenosis are aspirin and ticlopidine, and strong evidence suggests cholesterol lowering drugs and the angiotensin converting enzyme inhibitor (ACEI) antihypertensive drugs are also effective to decrease restenosis. Among the very active clinical research areas are various 2b/3a antagonist drugs under clinical investigation, anti-inflammatory drugs, radiation therapy to the coronary artery and many therapies.
The information provided in this section of HEART ATTACK should not be taken as an authoritative source of clinicopathlogical characteristics of HEART ATTACK or an authoritative source of the current standard medical therapy or philosophy of treatment of HEART ATTACK. Individuals should consult their physician concerning treatment of this condition.