Non-ischemic Cardiomyopathy Secondary to Left Ventricular Hypertrophy due to Long-term Anabolic-androgenic Steroid Use in a Former Olympic Athlete.

Currently, the cardiovascular risk associated with the use of anabolic steroids is not well documented. Recent studies have shown that its use may potentiate the development of cardiac dysfunction in the short term. This case report describes an encounter that supports a causal link between anabolic-androgenic steroid use (AAS) and cardiomyopathy later in life.

Thrombin Generation and Activity During Coronary Angioplasty: Influence of Angiographic Lesion Morphology.

OBJECTIVE: To investigate the relationships between coronary atherosclerotic plaque injury, lesion morphology, and activation of the coagulation cascade. BACKGROUND: Balloon angioplasty of coronary lesions may result in intracoronary thrombin generation and activity. It is unknown whether the angiographic morphology of the lesion prior to intervention, an indicator of the presence of thrombus in the lesion, is a determinant of the degree of coagulation cascade activation.

Thrombosis in ischemic heart disease.

Thrombus formation on a fissured or disrupted atherosclerotic plaque is the main pathogenetic mechanism for the acute coronary syndromes of myocardial infarction and unstable angina. Myocardial infarction results from an acute total occlusion of the artery, while unstable angina is secondary in most cases to mural thrombus formation. Thrombus formation has also been implicated in chronic atherosclerotic disease progression and in restenosis following coronary angioplasty.

Low density lipoprotein receptor-independent hepatic uptake of a synthetic, cholesterol-scavenging lipoprotein: implications for the treatment of receptor-deficient atherosclerosis.

The metabolism of infused 111In-labeled phospholipid liposomes was examined in Watanabe heritable hyperlipidemic (WHHL) rabbits, which lack low density lipoprotein (LDL) receptors, and in normal control rabbits. The half-times (t1/2) for clearance of 111In and excess phospholipid from plasma were 20.8 +/- 0.