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Department faculty and hospital therapy of medical faculty and department internal diseases of medical prophylactic faculty. MYOCARDIAL INFARCTION. Prof. Rizamuhamedova M.Z. MYOCARDIAL INFARCTION. Acute focal necrosis of heart muscle due to absolute or relative failure coronary blood flow.
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Department faculty and hospital therapy of medical faculty and department internal diseases of medical prophylactic faculty. MYOCARDIAL INFARCTION Prof. Rizamuhamedova M.Z.
MYOCARDIAL INFARCTION • Acute focal necrosis of heart muscle due to absolute or relative failure coronary blood flow.
AETIOLOGY • Coronary artery thrombosis in an atherosclerotic plaque • Spasm of the coronary arteries of different etiologies • Vasculitis affecting medium-sized vessels - rheumatic fever, periarteritisnodosa, rheumatoid arthritis • Coronary embolism in infective endocarditis, diseases of the bloodAnemia, which developed against the background of coronary atherosclerosis
RISK FACTORS • Hypercholesterolemia • Heredity • Smoking • Diabetes mellitus • Arterial hypertension • Gout • Hypertriglyceridemia • Early gerontoxon • The diagonal earlobe crease
PATHOGENESIS • Rupture of an atherosclerotic plaque • Platelet activation • Acute coronary artery occlusion • The development of necrosis, arrhythmias • Dimensions foci of necrosis depends on the level of occlusion of a coronary artery
Period of myocardial infarction • Prodrome - 30 min. Up to 30 days. (Unstable angina) • The Island - from the attack of angina before the appearance of signs of necrosis of cardiac muscle. Duration hours • Acute - is characterized by resorption of necrotic masses, the beginning of the formation of scar around - 10 days • Subacute - reduced symptoms of heart failure, resorption necrotic syndrome. 3 to 8 weeks • Postinfarction –is not observed with a favorable course of clinical manifestations
CLASSIFICATION OF MYOCARDIAL INFARCTION BY ECG CHARACTERS • On pathological tooth Q - stable occlusive thrombus caused a coronary artery, an effective thrombolytic therapy • Equivalents wave Q - R wave amplitude changes • Any other changes in the QRS complex • Without pathological Q wave
Myocardial infarction with isolated T-wave changes - (small focal)- has a favorable course • Elevation myocardial infarction segment S-T (mural) - proceeds favorably, but with a high probability of recurrence, thrombolytic therapy • Myocardial infarction with S-segment depression T (subendocardial) has a severe course, predictive adverse
CLINICAL FORMS OF MYOCARDIAL INFARCTION • ANGINAL FORM • ATYPICAL FORMS OF MYOCARDIAL INFARCTION Gastroalgic form (2-3%)Asthmatic form (5-10%)Cerebral form (3-5%)Painless form (arrhythmic)edematous form
STUDIES IN MYOCARDIAL INFARCTION • ECG (awareness - 85%) • Echocardiography • Chest X-ray • Angiography (to assess the degree of recovery of myocardial perfusion) • Enzymatic diagnosis • ESR is increased after 12 hours of myocardial infarction • Leucocytosis - a few hours, peak 2-4 days a week - the normalization value
COMPLICATIONS OF MYOCARDIAL INFARCTION • Heart failure • Pulmonary edema • Cardiogenic shock • Myocardial rupture • Left ventricular aneurysm
Thromboembolism (including pulmonary embolism) • Pericarditis • Dysrhythmia • Dressler's syndrome • Cardiac arrest
Modern principles of treatment of acute myocardial infarction • Aspirin • Oxygen • Treatment of anginal pain • Reperfusion therapy (pharmacological, mechanical) • Beta-blockers
Intravenous infusion of nitroglycerin • Early use of ACE inhibitors • Anticoagulants • Lipid-lowering drugs • Metabolic therapy