Targeting the vicious inflammation-oxidative stress cycle for the management of heart failure.

Oxidative stress and inflammation are each implicated independently in the development and progression of heart failure. Their interaction, however, is also evident throughout the process from initial injury to cardiac remodeling and failure. In the failing heart, the linkage between excessive reactive oxygen species (ROS) and the cytokine elaboration is manifested in shared elements and cross-promotion within downstream signaling pathways.

Hibernating myocardium: pathophysiology, diagnosis, and treatment.

Comprehensive management of patients with chronic ischemic disease is a critically important component of clinical practice. Cardiac myocytes have the potential to adapt to limited flow conditions by adjusting contractile function, reducing metabolism, conserving resources, and preserving myocardial integrity to cope with an oxygen and (or) nutrition shortage. A prime metabolic feature of cardiac myocytes affected by chronic ischemia is the return to a fetal gene pattern with predominance of carbohydrates as the substrate for energy.

Biology of TNFalpha and IL-10, and their imbalance in heart failure.

Our understanding of the multiple in vivo functions of the proinflammatory cytokine, tumor necrosis factor (TNFalpha), is advancing at a rapid pace. In addition to its antitumor effects, overproduction of TNFalpha provokes tissue injury and organ failure. TNFalpha has also been shown to be cardiodepressant and responsible for various cardiovascular complications.