Acute coronary syndromes do not promote prolonged in vivo FXII-dependent prothrombotic activity.

Background: Coagulation FXII is activated on contact with lipoprotein particles. It has been suggested that contact with subendothelial tissue provides an alternative biological surface for FXII activation. Our aim was to investigate whether activated FXII (FXIIa) is elevated in patients with coronary atherosclerosis, and whether disease status (acute phase or stable state) affects circulating levels of FXIIa.

Carvedilol prevents doxorubicin-induced free radical release and apoptosis in cardiomyocytes in vitro.

The clinical use of doxorubicin, a highly active anticancer drug, is limited by its severe cardiotoxic side effects. Increased oxidative stress and apoptosis have been implicated in the cardiotoxicity of doxorubicin. Carvedilol is an adrenergic blocking agent with potent anti-oxidant activity.

Intense lipid peroxidation in premature clinical coronary atherosclerosis is associated with metabolic abnormalities.

Increased oxidative stress is associated with rapid progression of atherosclerosis. In this study we sought to determine whether premature onset of clinical coronary atherosclerosis is associated with increased levels of lipid peroxidation. We measured plasma levels of malondialdehyde (MDA), using high-pressure liquid chromatography, in 42 male patients with early- (<56 years) or late-onset (>64 years) unstable angina and in 2 age-matched control groups (n=20).