Ischemic cardiomyopathy, microscopic.
Laboratory Diagnosis of Myocardial Infarction A number of laboratory biomarkers for myocardial injury are available. None is completely sensitive and specific for myocardial infarction, particularly in the hours following onset of symptoms.
Timing is important, as are correlation with patient symptoms, electrocardiograms, and angiographic studies. The following biomarkers have been described in association with acute myocardial infarction: Troponins: Troponin I and T are structural components of cardiac muscle.
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They are released into the bloodstream with myocardial injury. They are highly specific for myocardial injury--more so than CK-MB--and help to exclude elevations of CK with skeletal muscle trauma. However, the rate of dating heart disease for early infarction may not be as dramatic as for CK-MB. Troponins will remain elevated longer than CK--up to 14 days. This makes troponins a superior marker for diagnosing myocardial infarction in the recent past--better than lactate dehydrogenase LDH.
However, this continued elevation has the disadvantage of making it more difficult to diagnose reinfarction or extension of infarction in a patient who has already suffered an initial MI.
Troponin T lacks some specificity because elevations can appear with skeletal myopathies and with renal failure. However, an elevation in total CK is not specific for myocardial injury, because most CK is located in skeletal muscle, and elevations are possible from a variety of non-cardiac conditions.
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It tends to increase within 3 to 4 hours of myocardial necrosis, then peak in a day and return to normal within 36 hours. It is less sensitive than troponins.
Saenger and Jaffe, Kumar and Cannon, Part I, The CK-MB is also useful for diagnosis of reinfarction or extensive of an MI because it begins to disease after a day, so subsequent elevations are indicative of another event. Chattington et al, Myoglobin: Myoglobin is a protein found in skeletal and cardiac muscle which binds oxygen. It is a very sensitive indicator of muscle injury. However, it is not specific for cardiac muscle, and can be elevated with any form of injury to skeletal muscle.
The rise in myoglobin can help to determine the size of an infarction.
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A negative myoglobin can help to rule out myocardial infarction. It is elevated even before CK-MB.
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BNP release can be stimulated by systolic and diastolic left ventricular dysfunction, acute coronary syndromes, stable coronary heart disease, valvular heart dating heart disease, acute and chronic right ventricular failure, and left and right ventricular hypertrophy secondary to arterial or pulmonary hypertension. BNP is a marker for heart failure. Since inflammation is part of atheroma formation, then CRP may reflect the extent of atheromatous plaque formation and predict risk for acute coronary events.
However, CRP lacks specificity for vascular events. Saenger and Jaffe, Copeptin: Arginine vasopressin AVP is secreted as a prohormone from the dating heart disease pituitary and then cleaved to form a C-terminal part called copeptin. A rapid increase in copeptin can be associated with stroke, sepsis, or acute myocardial injury. In conjunction with troponin, copeptin has high negative predictive value to rule out myocardial injury.
Ischemic cardiomyopathy: pathophysiologic mechanisms. Ischmic cardiomyopathy: myocyte cell loss, myocyte hypertrophy, and myocyte cellular hyperplasia.
Timed sequential analysis of creatine kinase in the diagnosis of myocardial infarction in patients over 65 years of age. Acute coronary syndromes: diagnosis and management, part I. Acute coronary syndromes: Diagnosis and management, part II. A strategy for the use of cardiac injury markers in the diagnosis of acute myocardial infarction.
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Biomarkers and acute coronary syndromes: an update. Pathology of coronary atherosclerosis and thrombosis. Cardiovasc Diagn Ther. The use of biomarkers for the evaluation and treatment of patients with acute coronary syndromes.
Acute myocardial infarction.
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