The heart muscle needs a constant supply of oxygen-rich blood. The coronary arteries, which branch off the aorta just after it leaves the heart, deliver this blood. An acute coronary syndrome occurs when a sudden blockage in a coronary artery greatly reduces or cuts off the blood supply to an area of the heart muscle (myocardium). The lack of blood supply to any tissue is termed ischemia. If the supply is greatly reduced or cut off for more than a few minutes, heart tissue dies. A heart attack, also termed myocardial infarction (MI), is death of heart tissue due to ischemia. (See also Overview of Coronary Artery Disease.)
The complications of acute coronary syndromes depend on how much of the heart muscle is damaged, which is a direct result of where a coronary artery was blocked and how long this artery was blocked. If the blockage affects a large amount of heart muscle, the heart will not pump effectively. If the blockage shuts off blood flow to the electrical system of the heart, the heart rhythm may be affected.
In a heart attack, part of the heart muscle dies. Unlike muscle, dead tissue, and the scar tissue that eventually replaces it, does not contract. The scar tissue sometimes even expands or bulges when the rest of the heart contracts. Consequently, there is less muscle to pump blood. If enough muscle dies, the heart’s pumping ability may be so reduced that the heart cannot meet the body’s need for blood and oxygen. Heart failure, low blood pressure (hypotension), and/or shock develop. If more than half of the heart tissue is damaged or dies, the heart generally cannot function, and severe disability or death is likely.
Drugs such as beta-blockers and especially angiotensin-converting enzyme (ACE) inhibitors can reduce the extent of the abnormal areas by reducing the workload of and the stress on the heart (see table Drugs Used to Treat Coronary Artery Disease). Thus, these drugs help the heart maintain its shape and function more normally.
The damaged heart may enlarge, partly to compensate for the decrease in pumping ability (up to a point, a larger heart beats more forcefully). Enlargement of the heart makes abnormal heart rhythms more likely.
Abnormal heart rhythms (arrhythmias) occur in more than 90% of people who have had a heart attack. These abnormal rhythms may occur because the heart attack damaged part of the heart’s electrical system. Sometimes there is a problem with the part of the heart that triggers the heartbeat, so heart rate may be too slow (bradycardia). Other problems can cause the heart to beat rapidly or irregularly (for example, atrial fibrillation). Sometimes the signal to beat is not conducted from one part of the heart to the other, and the heartbeat may slow or stop (heart block).
In addition, areas of heart muscle that have poor blood flow but that have not died can be very irritable. This irritability can cause heart rhythm problems, such as ventricular tachycardia or ventricular fibrillation. These rhythm problems greatly interfere with the heart’s pumping ability and may cause the heart to stop beating (cardiac arrest). A loss of consciousness or death can result. These rhythm disturbances are a particular problem in people who have an imbalance in blood chemicals, such as a low potassium level.
Pericarditis (inflammation of the two-layered sac that envelops the heart) may develop in the first day or two after a heart attack. Pericarditis is more common in people who have not had the blocked artery opened by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). People seldom notice symptoms of early developing pericarditis because their heart attack symptoms are more prominent. However, pericarditis produces a scratchy rhythmic sound that can sometimes be heard through a stethoscope 2 to 3 days after a heart attack. Sometimes, the inflammation causes a small amount of fluid to collect in the space between the two layers of the pericardium (pericardial effusion).
Post-myocardial infarction (Dressler) syndrome is pericarditis that develops 10 days to 2 months after a heart attack. This syndrome causes fever, pericardial effusion (extra fluid in the space surrounding the heart), inflammation of the membranes covering the lungs, pleural effusion (extra fluid in the space between the two layers of the pleura), and joint pain. Diagnosis is based on the symptoms it causes and on the time it occurs.
People who develop pericarditis are usually given a nonsteroidal anti-inflammatory drug. Colchicine is often rapidly effective. Even with treatment, the syndrome can recur. If post-myocardial infarction syndrome is severe, a corticosteroid or a different nonsteroidal anti-inflammatory drug may be needed for a short time.
Rarely, the heart muscle ruptures under the pressure of the heart’s pumping action because the damaged heart muscle is weak. Rupture usually occurs 1 to 10 days after a heart attack and is more common among women. The wall separating the two ventricles (septum), the external heart wall, and the muscles that open and close the mitral valve are particularly susceptible to rupture during or after a heart attack.
Rupture of the septum results in too much blood being diverted to the lungs, causing accumulation of fluid (pulmonary edema). A rupture of the septum can sometimes be repaired surgically.
Rupture of the external wall almost always causes rapid death. Doctors rarely have time to attempt surgery, and even then, surgery is rarely successful.
If the mitral valve muscles rupture, the valve cannot function—the result is sudden and severe heart failure. Doctors can sometimes repair the damage surgically.
The damaged muscle may form a thin bulge (aneurysm) on the wall of the ventricle. Doctors may suspect an aneurysm based on abnormal results of electrocardiography (ECG), but echocardiography is done to be sure. These aneurysms may cause episodes of abnormal heart rhythms and may reduce the heart’s pumping ability. Because blood flows more slowly through aneurysms, blood clots can form in the heart’s chambers. If heart failure or abnormal heart rhythms develop, the aneurysm may be removed surgically.
Historically, about 20% of people who have had a heart attack form clots inside the heart, over the area of dead heart muscle. More recently, clot formation is less common. In about 10% of these people, parts of the clots break off, travel through the bloodstream, and lodge in smaller blood vessels throughout the body. They may block the blood supply to part of the brain (causing a stroke) or to other organs.
Echocardiography may be done to detect clots forming in the heart or to determine whether a person has factors that make clots more likely to form. For example, an area of the left ventricle may not be beating as well as it should.
For people who have clots, doctors often prescribe anticoagulants (sometimes called blood thinners) such as heparin and warfarin. Heparin is given intravenously in the hospital for at least 2 days. Then, warfarin is given by mouth for 3 to 6 months. Aspirin also is taken indefinitely.
Other complications after a heart attack include leakage of the mitral valve (mitral valve regurgitation).
Nervousness and depression are common after a heart attack. Depression after a heart attack may be significant and may persist.
Drugs Mentioned In This Article
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