Low T(3) levels are an independent predictor of mortality in patients with chronic heart failure, adding prognostic information to conventional clinical and functional cardiac parameters.

In the absence of changes in clinical chemical parameters, tumor necrosis factor-alpha, interleukin-6, and acute-phase reactant proteins, these results confirm in a clinical setting the upregulation of endothelial adhesiveness observed in experimental hypercholesterolemia and suggest a direct role for cholesterol in regulating this phenomenon, at least in familial hypercholesterolemia.

Hepatitis C viruses (HCV) present in 110 Italian patients were characterized by genotype-specific PCRs. Among the 65 cases of community-acquired hepatitis, HCV genotype IT was dominant (60%o), followed by genotypes IV (15%), m (11%), and I (3%). Among the 45 hemophilia-associated cases, the distribution of the

In healthy conditions, the endothelium plays a pivotal role in maintaining vascular homeostasis, mainly by the production of the relaxing factor nitric oxide (NO), which protects the vessel wall from those mechanisms favouring the development of vascular atherosclerosis. Aging is a powerful cardiovascular risk factors associated with endothelial dysfunction. In details, an alteration in the NO substrate L-arginine is the major factor responsible for endothelial dysfunction with advancing age, while reactive oxygen species (ROS) excess generation, which in turn reduce NO availability, plays a role in oldest individuals only. NO inhibition by ROS excess is the main cause of endothelial dysfunction which occurs in many other clinical conditions including arterial hypertension. Although hypertension induces early vascular aging in several arterial districts, however vascular features of physiological aging and hypertension are not necessarily similar. While an impaired NO availability represents the common final effect, aging and hypertension seem to adopt different mechanisms, at least at the level of microcirculation. Indeed, physiological aging shows a progressive reduced NO availability, while in advanced age some degree of oxidative stress emerges. In hypertensive patients, NO availability is early reduced, but the progression rate with age appears to be similar. Whether the hypertensive- and age-related vascular alterations represent only a mere additive effect of two independent risk factors resulting in endothelial dysfunction awaits further clarification.