[Peripheral adaptation in chronic heart failure: therapeutic implications]

Systemic vasoconstriction is a hallmark in chronic heart failure and due to several compensatory mechanisms such as neural, humoral and local vascular factors. Peripheral vasoconstriction mediated by increased sympathetic tone and activated plasma renin-angiotensin system (RAS) may act primarily for short-term control. The effects of the vascular RAS, impaired endothelium-mediated dilation (possibly due to chronically reduced flow) and structural alterations of the vessel wall slowly emerge over time. In addition, fluid and sodium retention may contribute to increase vascular stiffness in chronic heart failure. Improved cardiac output with acute administration of vasodilators and inotropic agents appears to exert redistribution of blood flow without improving blood flow to working muscle during exercise. Even if such agents do improve blood flow to the exercising skeletal muscle with short-term administration, oxygen utilization of the skeletal muscle is not immediately increased because intrinsic abnormalities of skeletal muscle exist in chronic heart failure; e.g. due to chronic deconditioning, resulting in reduced oxidative capacity of skeletal muscle as suggested by ultrastructural analysis and NMR-spectroscopy. The reversal of the above delineated peripheral alterations develop slowly over time. Chronically increased flow may improve impaired endothelium-dependent relaxation of the vessel wall and the oxidative capacity may increase, in part, due to a training effect.(ABSTRACT TRUNCATED AT 250 WORDS)