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Subendocardial ischemic myocardial lesions associated with severe coronary atherosclerosis
Insights
Severe chronic subendocardial ischemia causes distinct morphologic changes in the heart muscle. These changes in subendocardial myocardium differ from those seen in acute myocardial infarction.
Area of Science:
- Cardiovascular Pathology
- Ischemic Heart Disease Research
- Myocardial Histopathology
Background:
- Subendocardial myocardium is vulnerable to ischemic damage.
- Distinguishing chronic ischemic changes from acute events is clinically important.
Purpose of the Study:
- To characterize morphologic changes in the subendocardial myocardium caused by severe, chronic subendocardial ischemia.
- To differentiate these lesions from those resulting from acute myocardial infarction.
Main Methods:
- Histopathologic examination of subendocardial myocardium from 13 patients with fatal ischemic heart disease.
- Correlation of morphologic findings with clinical data, including unstable angina and congestive heart failure.
Main Results:
- Patients exhibited severe coronary artery stenosis without acute occlusion.
- Subendocardial myocardium showed pallor, hyperemia, or fibrosis, with preserved myofibers near the endocardium.
- Microscopically, lesions featured vacuolar change and coagulation necrosis without significant neutrophil infiltration or stromal collapse.
Conclusions:
- The observed subendocardial myocardial lesions are distinctive to severe chronic ischemia.
- These morphologic patterns can be differentiated from myocardial necrosis associated with acute coronary artery occlusion.
Abstract:
Morphologic changes in the subendocardial myocardium that appeared to be caused by severe, chronic subendocardial ischemia were studied in patients with fatal ischemic heart disease admitted to the Specialized Center of Research for Ischemic Heart Disease at the University of Alabama in Birmingham in the period 1970--1977. Thirteen patients were selected for this report on the basis that they had the lesions in the subendocardial myocardium we believe to have been caused by subendocardial ischemia and had no evidence of acute or remote myocardial infarction or other conditions that may have contributed to their terminal illness or death. Clinical findings were unstable angina, congestive heart failure, usually no increase in plasma enzymes indicative of myocardial damage, and electrocardiographic changes consistent with subendocardial ischemia. All 13 patients had 75% or greater stenosis of the three major coronary arteries; none had acute thrombotic or embolic coronary artery occlusion. The left ventricle in all cases was hypertrophied. The subendocardial myocardium showed circumferential pallor, hyperemia, or focal fibrosis without perceptible loss of volume in papillary muscles or trabeculae carneae. Microscopically, acute lesions showed one to two layers of preserved myofibers adjacent to the endocardium, vacuolar change in the deeper fibers, and focal areas of coagulation necrosis of variable size in the myocardium external to the fibers with vacuolar change. Coagulation necrosis was extensive in some cases and usually was not associated with infiltration of neutrophils. The repair reaction involved removal of necrotic sarcoplasm by mononuclear phagocytes, resulting in a reticular-appearing tissue without evidence of stromal collapse. Granulation tissue was not seen. Collagen fibers appeared to be deposited within the area of previous sarcolemmal sheaths. The distribution and morphology of subendocardial myocardial lesions associated with severe coronary atherosclerosis are distinctive and can be distinguished from myocardial necrosis or fibrosis associated with acute total occlusion of a coronary artery.