Myocardial infarction means death of myocardial cells secondary to ischaemia induced by obstruction of a coronary artery. This term must be distinguished from “myocardial cell necrosis”. Although cell death and necrosis are synonymous, the term myocardial cell necrosis is best applied to death of single cells or tiny groups of cells which still have an intact blood supply. Conversely, myocardial infarction should be restricted to an area of cell death secondary to ischaemia. This distinction is important because the features and time sequence of cell death as well as the duration of the healing phase depend on the presence or absence of a freely flowing blood supply. In myocardial infarction, the healing phase is retarded by the persistent reduction of blood flow.
The term ischaemia literally means to hold back blood. The general definition of myocardial ischaemia reflects this idea: myocardial ischaemia develops whenever the flow of arterial blood through the diseased vessels is reduced to a volume below that required by the myocardium for adequate function. However, it is difficult to correlate quantitatively ischaemia and depressed myocardial function. It is impossible to measure local changes in myocardial blood flow. Hence, the precise relationship between decreases in arterial blood flow and depression in function is impossible, to establish, which means that the above definition of ischaemia is useful only as a concept. During acute experimental coronary occlusions, the overall arterial flow is reduced to about 5 to 10 per cent of normal in the most, ischaemic parts of the heart, although it theoretically could reach zero and later probably does reach zero. Zero flow is best referred to as total ischaemia.
Coronary arterial occlusion leads to death of cardiac muscle due to decreased blood supply. Death tissue stop functioning, heart contractility is weaken, and the heart could completely stop.
When the size of acute myocardial infarction is over 2,5-3 sm, typical clinical signs are presented: prolonged acute left-sided chest pain with irradiation to the left hand and characteristic electrocardiographic changes. Pain is not influenced by vasodilators.
Necrosis starts just about 20-40 minutes after the initial symptoms.
This is the optimum period for intensive thrombolytic therapy and coronary surgery. If reperfusion is acheaved ( restored blood supply), necrosis isn’t occur and the incident isn’t end with myocardial infarction.
The earliest signs in prenecrotic phase are wave-like contractions of injured myofibrilles (with disturbed striation), which are pressed under the influence of the adjacent cardiomyocytes with save function. Myocardial infarction about to 18-th-24-th shows lack of nuclei, contractility bands and coagulative necrosis. Coagulative necrosis ends with erased nuclei. Leucocytes enter in the first hours in the area of necrosis. Their infiltration reach the maximum between 4 and 7 day. After 7-th day leucocytes are replaced by macrophages. They phagocytose necrotic fragments. At the periphery of infarction zone is found so called miocitolisis: vacuole degeneration of ischemic cardiomyocytes. Between 2-th and 4-th week at the periphery of infarction zone grows granulation tissue. It matures (increasing of fibrous connective tissue, and reduced capillaries and cell proliferation) and between the end of 6-th and 8-th week a fibrous cicatrices is made.
Possible complications of myocardial infarction:
- Laceration of papillary muscle
- Laceration of heart wall with hemopeicardium and heart tamponade
- Laceration of interventricular septum with development of acute right-sided heart insufficiency
- Wall thrombosis towards the inner heart’s surface
- Acute and chronic aneurysm of left ventricle
- Dilation (relaxion and dilation) of the left ventricle with development of heart insufficiency
- Thromboembolism with development of infarctions in brain, spleen and kidneys.
- Energy weakness with cardiogenic shock in wide transmural infarction.
- Severe rhythm and conductive disturbances (particulary in damaging of interventricular septum) with sudden heart death.
- Pulmonary edema.
- Rupture (tearing) of myocard and heart tamponade.
- Endocardial thrombosis with following thromboembolism in cerebral artery and development of brain infarction.
Hippocrates wrote: “It appears to me a most excellent thing to cultivate prognosis.”
The prognosis in myocardial infarction cannot be accurately made ; some patients apparently making an uneventful recovery die suddenly: others pass through a stormy convalescence but do well. It is best not to be too precise in judgement.
The most frequent early approach to the problem was to estimate the severity and prognosis of the acute myocardial infarction by listing the presence or absence of certain factors. In general, advanced age, history of hypertension, angina pectoris or previous myocardial infarction, heart failure, hypotension, serious arrhythmia, persistent chest pain, high fever, and mafked leucocytosis have been associated with poor prognosis.
Insufficient data are available regarding a large group of patients who die suddenly outside the hospital. Most of these patients probably develop ventricular fibrillation within 1 to 2 hours after the onset of symptoms.