Pathophysiology of chronic heart failure.

Heart failure is a medical condition characterized by reduced cardiac output (CO) and increased venous pressure, associated with underlying molecular changes and subsequent damage to and death of cardiac muscle cells. The body has its own ways of increasing lowered CO, which together make up the neurohumoral response. This is composed of three basic elements: (1) a hemodynamic defense reaction which maintains perfusion pressure in the major organs by increasing circulating blood volume, inducing vasoconstriction and stimulating the heart; (2) an inflammatory response (in which the body organs act as if they were facing an exogenous agent), in which inflammatory cytokines and reactive oxygen species play an important role; (3) a hypertrophic response and ventricular remodeling, with structural changes in cardiac muscle cells and in the shape of the ventricular chamber. Neurohumoral mechanisms are classified according to their effects: regulatory (increasing vasoconstriction, sodium retention, inotropism and proliferation); and counter-regulatory (with the opposite effects). Ultimately, they are responsible for the failing heart. Our aim is to bring together data on the mechanisms of progression to heart failure, elucidating the relationships between the biological agents involved, particularly those susceptible to pharmacological modification.