Myocardial infarction

• Coronary arterial occlusion is a common cause of myocardial infarction (MI).
• Myocardial demand is a crucial factor in the development of MI.
• Severe coronary atherosclerosis is a significant risk factor for MI.
• Inadequate production of high-energy phosphates (creatinine phosphate and ATP) occurs in the absence of oxygen.
• Decreased aerobic glycolysis and onset of anaerobic glycolysis occur in the absence of oxygen.
• Platelet activation plays a role in the progression of MI.
• Acute transmural myocardial infarction is characterized by hemodynamic changes.
• Thrombosis is a common complication of MI.
• Hemodynamic changes are a characteristic of MI.
• Decreased blood supply induces profound functional, biochemical, and morphologic changes in the myocardium.
• MI can be caused by vasospasm, which is intense, relatively prolonged, and can occur with or without coronary atherosclerosis, and platelet aggregation.
• In one-third patients, small intramural coronary vessel disease or hematological abnormalities, such as hemoglobinopathies, may lead to acute coronary episodes.
• The clinical features of acute MI include chest pain, rapid thready pulse, dyspnea due to pulmonary congestion/pulmonary edema or impaired contractility of the heart, indigestion and apprehension, and may be asymptomatic, discovered on ECG.
• Emboli, which may arise from the left atrium due to atrial fibrillation, left-sided mural thrombosis, vegetative endocarditis, paradoxical embolus from the right side of heart or peripheral veins, are a potential cause of MI.
• Time of onset of changes in myocardial infarction can be categorized as 0-4 hours, 4-12 hours, 12-24 hours, and 2-8 weeks.
• Gross changes in myocardial infarction can include none, dark mottling, hyperemia around a yellow-tan infarct center, and maximally yellow-tan and soft with a well-delineated hyperemic border.
• Microscopic changes in myocardial infarction can include waviness of fibers at the border, beginning of coagulation necrosis and edema, coagulative necrosis with pyknosis of nuclei, neutrophilic infiltration, myocyte hypereosinophilia, and marginal contraction band necrosis.
• In the early stages of myocardial infarction, there is disintegration of dead myofibrils followed by phagocytosis of dead cells by macrophages at the infarct border.
• Early formation of fibrovascular granulation tissue at the margins is a characteristic of myocardial infarction.
• Well-established granulation tissue with new blood vessels and collagen deposition is a feature of myocardial infarction.
• Increased collagen deposition with decreased cellularity is a characteristic of myocardial infarction.
• A dense collagenous scar forms in the final stages of myocardial infarction.
• Laboratory diagnosis of acute myocardial infarction involves meeting two or three of the World Health Organization (WHO) criteria.
• A patient is diagnosed with myocardial infarction if two probable or three definite criteria are met.
• Clinical history of ischemic type of chest pain lasting for more than 20 min. is a criteria for diagnosing myocardial infarction.
• Changes in serial ECG tracings such as ST elevation/inverted T wave/appearance of Q wave are criteria for diagnosing myocardial infarction.
• Rise in levels of serum cardiac biomarkers or enzymes, which leak out of the damaged myocardium into the blood, such as: Creatinine kinase (CK), Troponins (Tn), and Lactate dehydrogenase (LD), are criteria for diagnosing myocardial infarction.
• Different isoenzymes of CK include: MM (skeletal muscle and heart), MB (principally from myocardium, particularly MB2), and BB (brain and lung).
• CK activity begins rising in 2-4 hours, peaks in 24 hours, and falls in 72 hours.
• KMV: More specific, begins rising in 4-8 hours, peaks in 18 hours, and falls in 48-72 hours.
• CKMB2/CKMBI ratio >1.5 is a highly sensitive indicator of myocardial injury.
• Troponins are of two types, namely, TnI and TnT.
• Troponins are not normally detectable in serum.
• Troponins are elevated in MI.
• Troponins of different origins can be distinguished by specific antibodies, which can also be used for quantitative assays.
• Troponins are the most sensitive and specific cardiac markers, being as sensitive as CKMB.
• Troponin levels remain elevated for 7-10 days permitting a late diagnosis evaluation of progression of infarct.
• Lactate dehydrogenase (LDH) is myocardium specific.
• LDH1 rises after 24 hours, reaches a peak in 3-6 days and returns to normal in 14.
• Myoglobin is the first cardiac marker to become elevated.