[Chronic heart failure as a crisis event of the family].

The family greatly influences any of its members and significantly contributes to the patient rehabilitation. A limited and superficial interest from the family as well as an overprotective and anxiogenic behavior may lead to chronicization, relapse or even to progression of the disease. The close relationship between the patient and the physician is an illusion, since family members deeply affect this interaction.

Effects of endotoxic shock on neuronal NOS and calcium transients in rat cardiac myocytes.

Objective: The effects of endotoxic shock on transcriptional and translational pattern of nitric oxide synthase isoforms (NOSs) and cytoplasmic calcium were investigated.

Methods: Male SD rats injected with lipopolysaccharides or saline were sacrificed after 6 and 20 h. Cardiac myocytes were enzimatically isolated from the excised hearts and evaluated for: (1) expression of constitutive (e and n) and inducible (i) NOSs by RT-PCR; (2) NOSs protein levels by Western blot, enzymatic activities by a radioimmunometric assay and nitric oxide metabolites by spectrophotometry; (3) calcium transients by Indo-1 fluorescence.

[Anxiety, depression, and stressed life in patients awaiting heart transplantation: are these factors to be considered?].

Rationale: Heart transplantation is a therapeutic procedure in which biological, psychological, social and ethical aspects play an important role, none of them has to be underestimated. It is known that the waiting period up to heart transplantation is extremely stressful for patients and their families, causing psychopathological and disadaptive reactions. Aim of the present study was to investigate psychological tract characteristics, stress reactions and quality of life in a group of patients registered for heart transplantation.

TNFalpha in patients with congestive heart failure.

It is now generally accepted that chronically extensive stimulation of the cytokine system-and of TNFalpha in particular-is detrimental to the heart and to peripheral tissue and that such stimulation may contribute to the pathogenesis of congestive heart failure of various causes. During the past decade, basic and clinical research has provided growing evidence for the role of systemic and local inflammatory responses that, however, have so far failed to translate into new treatments for patients. The present paper represents an attempt to critically review the general concepts that lie behind the dichotomy existing between an impressive bulk of biologic research showing the role of TNFalpha as a pathogen in congestive heart failure and the difficulties in translating this evidence into patients' treatment.

Oxidative stress in cardiovascular disease: myth or fact?

Oxidative stress is a mechanism with a central role in the pathogenesis of atherosclerosis, cancer, and other chronic diseases. It also plays a major role in the aging process. Ischemic heart disease is perhaps the human condition in which the role of oxidative stress has been investigated in more detail: reactive oxygen species and consequent expression of oxidative damage have been demonstrated during post-ischemic reperfusion in humans and the protective role of antioxidants has been validated in several experimental studies addressing the pathophysiology of acute ischemia.

Skeletal muscle abnormalities in rats with experimentally induced heart hypertrophy and failure.

Background: In congestive heart failure (CHF), function and metabolism of skeletal muscles are abnormal.

Aim: To evaluate whether the reduced oxidative capacity of skeletal muscles in CHF is due to impaired O(2) utilisation.

Methods: CHF was induced in rats by injecting 50 mg/Kg monocrotaline.

Future strategies of reverse remodeling prevention of hibernation.

A complex interrelationship exists among chronic ischemic left ventricular dysfunction, persistence of myocardial viability and possibility to limit progression of chronic heart failure. Cardiac remodeling is influenced by several factors still under investigation. Hibernation is basically an adaptive mechanism to chronically abnormal coronary blood flow, characterized by metabolic and structural alterations of the cardiac tissue, that are fully recovered upon revascularization.