Heart Attack

Heart attack (myocardial infarction) is a feared condition of heart muscle cells damage due to a sudden lack of oxygen. Oxygen and nutrients supply the myocardial cells thanks to two coronary arteries that arise from aorta. A closure of the coronary artery or its branches causes severe ischemia in the relevant myocardial area and that (if not urgently solved) leads to necrosis of myocardial cells.


The most common underlying cause is the atherosclerosis of the coronary arteries. The arteries narrow due to deposits of fats in their walls and this can manifest as the angina pectoris. If this process of atherosclerotic narrowing lasts for a long time, it is rather positive as the arteries have ability to slowly form side branches that can bypass the narrowed areas and to ensure the oxygen supply. In a heart attack, there is usually a rupture of an atherosclerotic plate. This hurts the arterial wall and causes formation of a blood clot. Such blood clot causes a sudden obstruction of the artery. When the body is unable to dissolve the clot or when the patient does not get adequate help, the lack of oxygen leads to irreversible necrosis of myocardial cells.

Risk factors

Risk factors of heart attack are very similar to risk factors of atherosclerosis (see related article) and of ischemic stroke.


The most typical symptom is a sudden lasting pain located behind the breastbone. It can occur at rest or during physical exercise (the rupture of the vessel wall and clot formation can occur at any time). The pain is stronger than in angina pectoris and unlike that, the pain does not improve when at rest. The affected person is usually very restless, anxious and suffers from excessive sweating. The pain may radiate to the back or limbs and sometimes it may even mimic the abdominal pain. Sometimes the heart attack may be completely painless (“silent infarction”) and manifest just by symptoms of heart failure, especially by shortness of breath.


Time is the main issue in an acute myocardial infarction. Myocardial cells are able to live without oxygen for few hours, and then they succumb to necrosis. The treatment of a heart attack should therefore starts as soon as possible, in ideal case within 4 hours of the onset of pain. When the therapy is successful, the damage may be minor or even not present at all. The lasting unpleasant pain is basically a good sign, because that what hurts is still alive. After few hours the pain disappears marking the cell necrosis.


The diagnosis is based on the patient's symptoms, specific ECG changes and elevation of cardiac enzymes. These enzymes are substances, whose concentration elevates during myocardial damage as they leak from damaged myocardial cells. The echocardiography can confirm disruption of heart movements in area damaged by the infarction and the ultimate examination method is the coronary angiography.


Complications of an acute myocardial infarction are variable and include arrhythmias, heart aneurysm and its rupture (leading to cardiac tamponade and rapid death), heart valve damage and signs of heart failure


The treatment of an acute myocardial infarction must be complex and urgent. The approach is different in various countries. In the first place, the patient is usually treated with anticoagulants to prevent the growth of the blood clot. Further approach may include administration of thrombolysis – special drugs dissolving the blood clot (rarer) or endovascular treatment (classical approach). The endovascular treatment means a therapeutic coronary angiography with angioplasty (dilation of a narrowed or obstructed artery by a special balloon) and implantation of stent. The stent is a tube-shaped hollow device that prevents local reocclusion. Some findings are untreatable endovascularly and the patients must undergo cardiosurgical intervention – creation of a coronary bypass.