15 myocardial infarction


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15 myocardial infarction

  1. 1. Myocardial infarction One distinguishes • Non—Q wave MI: Area of ischemic necrosis is limited to the inner one third to half of myocardial wall. • Q wave MI: Area of ischemic necrosis penetrates the entire thickness of the ventricular wall. ETIOLOGY Coronary atherosclerosis • Coronary artery spasm • Coronary embolism (caused by infective endocarditis, rheumatic heart disease, intracavitary thrombus) • Periarteritis and other coronary artery inflammatory diseases • Dissection into coronary arteries (aneurysmal or iatrogenic) • Congenital abnormalities of coronary circulation • MI with normal coronaries (MINC syndrome): more frequent in younger patients and cocaine addicts Clinical presentation: • Crushing substernal or retrosternal chest pain usually lasts longer than 30 min. • Pain is unrelieved by rest or sublingual nitroglycerin or is rapidly recurring. • Pain radiates to the left or right arm, neck, jaw, back, shoulders, or abdomen and is not pleuritic in character. • Pain may be associated with dyspnea, diaphoresis, nausea, or vomiting. • There is no pain in approximately 20% of infarctions (usually in diabetic or elderly patients). Physical findings: • Skin may be diaphoretic, with pallor (because of decreased oxygen). • Rales may be present at the bases of lungs (indicative of CHF).
  2. 2. • Cardiac auscultation may reveal an apical systolic murmur caused by mitral regurgitation secondary to papillary muscle dysfunction; S3 or S4 may also be present. • Physical examination may be completely normal. LABORATORY TESTS • Serum cardiac enzyme studies: damaged necrotic heart muscle releases cardiac isoenzymes (CK, LDH) into the blood stream in amounts that correlate with the size of the infarct. Electrophoretic fractionation of the enzymes can pinpoint certain isoenzymes (CK-MB and LDH-1) that are more sensitive indicators of MI than total CK or LDH. • Cardiac troponin levels: cardiac-specific troponin T (cTnT) and cardiac- specific troponin I (cTnI) are new markers for acute Ml. Rapid whole blood bedside assays are now available. Increases in serum levels of cTnT and cTnI may occur relatively early after muscle damage and may be present for several days after MI (up to 7 days for cTnI and up to 10 to 14 days for cTnT).  Fig.26. Time course of elevations of serum markers after MI. Traditionally total CK, CK-MB, and lactic dehydrogenase (LDH [with isoenzymes]) are measured. The smaller molecule myoglobin is released quickly from infarcted myocardium. Troponin I rises more slowly than myoglobin and may be useful for diagnosis of infarction even up to 3 to 4 days after the event. Assays for cardiac-specific troponin I
  3. 3. and troponin T using monoclonal antibodies are now available. ECG In Q wave infarction, there is development of:  a. Inverted T waves, indicating an area of ischemia  b. Elevated ST segment, indicating an area of injury  c. Q waves, indicating an area of infarction (usually develop over 12 to 36 hr) ECG in non-Q wave MI Q waves are absent, but:  a. History and myocardial enzyme elevations are compatible with MI.  b. ECG shows ST segment elevation, depression, or no change followed by T wave inversion. Superacute and acute stage of non-Q-wave MI IMAGING STUDIES • Chest radiography is useful to evaluate for pulmonary congestion. • Echocardiography can evaluate wall motion abnormalities and identify mural thrombus or mitral regurgitation, which can occur acutely after MI. NONPHARMACOLOGIC THERAPY • Limit patient’s activity: bed rest in the initial 24 hr; if the patient remains stable, gradually increase activity. • Diet: NPO until stable, then no added salt, low-cholesterol diet.
  4. 4. • Patient education to decrease the risk of subsequent cardiac events (proper diet, cessation of smoking, regular exercise) should be initial when the patient is medically stable. PHARMACOLOGIC THERAPY 1. Nasal oxygen 2. Nitrates 3. Adequate analgesia: morphine sulfate IV 4. Aspirin 5. β-Adrenergic blocking agents 6.Thrombolytic therapy 7. Primary angioplasty (PTCA) may be performed as an excellent alternative to thrombolytic therapy. Prompt access to emergency coronary artery bypass graft (CABG) surgery is mandatory if primary PTCA is to be undertaken. Prognosis after MI The prognosis after MI depends on multiple factors: • Presence of arrhythmias, • Use of β-blockers: the mortality of patients on a regular regimen of β- blockers is significantly decreased when compared with that of control groups. • Size of infarct: the larger it is, the higher the post-MI mortality rate. • Site of infarct: inferior wall MI carries a better prognosis than anterior wall MI. • Type of infarct: although the in-hospital mortality rate is higher for patients with Q wave infarcts, the long-term prognosis for non —Q wave MI may be worse because these patients have a higher incidence of sudden cardiac death after hospital discharge.