The cause of death was attributed as being cardiac due to the presence of myocardial changes similar to those seen in cardiomyopathies and small intramural artery disease and to the absence of other relevant pathological changes in other organs/tissues. In chronic AAS-related cardiac damage, the echocardiographic features are also similar to those seen in heart failure and cardiomyopathies [4,5]. Enlargement and thickening of the left ventricle with loss of diastolic properties and mass increase have been documented at echocardiography [4]. The left ventricular hypertrophy persists several years after discontinuation of AAS abuse [5]. An endomyocardial biopsy study documented abnormal cardiac hypertrophy and fibrosis [6]. Prior pathologic studies documented similar histopathologic findings without mention to the small vessel status. In our four cases, the small arteriolar vessel disease was prominent. Small arteriolar vessels were thickened and showed intimal hyperplasia. These vascular lesions could play a role in causing chronic ischemic damage and arrhythmogenic potential. This small vessel disease could constitute a key point for future in vivo investigation with functional imaging tools.

Sudden anabolic steroid abuse-related death in athletes

BUZZI, FABIO;
2007-01-01

Abstract

The cause of death was attributed as being cardiac due to the presence of myocardial changes similar to those seen in cardiomyopathies and small intramural artery disease and to the absence of other relevant pathological changes in other organs/tissues. In chronic AAS-related cardiac damage, the echocardiographic features are also similar to those seen in heart failure and cardiomyopathies [4,5]. Enlargement and thickening of the left ventricle with loss of diastolic properties and mass increase have been documented at echocardiography [4]. The left ventricular hypertrophy persists several years after discontinuation of AAS abuse [5]. An endomyocardial biopsy study documented abnormal cardiac hypertrophy and fibrosis [6]. Prior pathologic studies documented similar histopathologic findings without mention to the small vessel status. In our four cases, the small arteriolar vessel disease was prominent. Small arteriolar vessels were thickened and showed intimal hyperplasia. These vascular lesions could play a role in causing chronic ischemic damage and arrhythmogenic potential. This small vessel disease could constitute a key point for future in vivo investigation with functional imaging tools.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11571/417133
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