[Physiopathology of heart failure]

In this paper we review pathophysiologic aspects of heart failure (HF). Mechanisms that normally act to prevent decrease in stroke volume and peripheral pressure are activated in HF and become maladaptive. These mechanisms lead to cardiac stimulation (inotropism, chronopism and lusotropism), peripheral vasoconstriction and sodium and water retention. HF progression is related to a) neurohumoral mechanisms, signaled by neurohumoral messengers; b) inflammatory activation; and c) ventricular remodeling that can be both cause and consequence of HF. We review the main neurohumoral mechanisms, some "regulators" (vasoconstrictors, antinatriuretics, inotropics and proliferatives) and some "counter-regulators" (vasodilators, natriuretics, negative inotropics and antiproliferatives). The first group includes the sympathetic nervous system, the renin angiotensin aldosterone system, arginine-vasopressive and endothelin, while in the second group natriuretic peptides, nitric oxide, bradykinin, vasodilator prostaglandins, the dopaminergic system, adrenomedullin and parasympathetic mechanisms are included. In inflammatory activation we review cytokines and oxidative stress. In ventricular remodeling we review modifications in myocyte function and morphology as well as modifications in the interstitium. Actions and interactions between these systems are the main factors leading to HF progression.