Acute Myocardial Infarction (MI) can be defined as condition in which, there is death or necrosis of myocardial cells. It is generally diagnosed at the end of the ambit of myocardial ischemia or acute coronary condition. Myocardial infarction occurs once myocardial ischemia oversteps a critical threshold and overcomes myocardial cellular repairing mechanism that is contrived for maintaining normal operating function and hemostasis. Ischemia at such critical threshold level for quite a longer period ends up in irreversible myocardial cell damage or in worst cases, even its death.
Classical symptoms of acute MI include fulminant chest pain (a typical radiating pain that travels from the left arm or left side of the neck to the heart), dyspnea (shortness of breath), nausea and/or vomiting, palpitation, profuse perspiration and anxiety (often called as sense of impending doom). Statistics say that women might experience less typical symptoms as compared to that of the men, most commonly dyspnea, weakness, gastrointestinal disturbance, and tiredness. Roughly, about one quarter of all myocardial infarctions are silent i.e. they do not show any chest pain or other signs.
Most of the cases of myocardial infarction are caused due to a commotion in the vascular endothelium that is linked with unstable atherosclerotic plaques those stimulate the formation of an intracoronary thrombus that ultimately ends up in coronary artery blood flow block. If such blockage persists for longer duration (approximately 20 to 40 min) there will be irreversible myocardial cell damage and cell death. The development of atherosclerotic plaques occurs over a period of years and even to the decades. However, the reason for initial vascular lesion that leads to the development of atherosclerotic plaques is still illusive.
Generally, it is high level of cholesterols in the bloodstream that restrict the blood flow to the cardiac tissues. Excessive body fats, high cholesterol and/or lipid profiles can be few of the main culprits for myocardial infarction. The blood vessels are nothing but the hollow pipe or tube-like cylindrical structure that allows the blood to flow flawlessly. High cholesterol levels start accumulating onto the walls of blood vessels and this, in turn, results in narrowing of the blood vessels. The blood supply is reduced and over the times, it could be cut-off for a while (ischemic conditions, where there is transient loss of blood supply). When the affected organ is heart, it is ischemic heart attack.
The severity of myocardial infarction is dependent on three main factors: the degree of the occlusion in the coronary arteries, the tenure of time of occlusions, and the presence or absence of circulation of the collateral blood. Usually, if there is more proximal the coronary occlusion, there will be more extensive chances of myocardium at risks of necrosis. Simply putting, larger the myocardial infarction, greater is the chance of death because of mechanical complications or pumping failure. If vessel occlusion is for prolonged period, there are more chances of permanent myocardial damage distal to that occlusion.
As the continuance of the occlusion will increase, the area of myocardial cell death will expand that finally extends from the endocardium to the myocardium (middle layer) and finally to the epicardium (innermost layer). The area of myocardial cell death will then spread laterally to area of watersheds or collateral perfusion and usually, after 6-8 hours have passed of coronary occlusion, most of the distal myocardium would have died. The magnitude of myocardial cell death reflects the extent of the myocardial infarction. If blood flow is successfully restored before the major damage to the myocardium, more heart muscle can be saved from the permanent damage or death and the life can be saved.