Despite its high prevalence and significant rates of associated morbidity and mortality, the syndrome of decompensated heart failure (HF) remains poorly defined and vastly understudied. HF is due to several mechanisms including pump dysfunction disorder, neurohormonal activation disorder, and salt-water retention disorder. The first step of the syndrome includes cardiac damage and remodeling in terms of coronary disease systo diastolic dysfunction and myocardial metabolism alterations. Neurohormonal activation and hydrosaline retention occur during successive steps in response to cardiac injury for compensatory reasons. Both mechanisms provide inotropic support to the failing heart increasing stroke volume, and peripheral vasoconstriction to maintain mean arterial perfusion pressure. However, they are deleterious to cardiocirculatory homeostasis in the late stage. Further factors involve structural changes, such as loss of myofilaments, apoptosis and disorganization of the cytoskeleton, as well as disturbances in Ca homeostasis, alteration in receptor density, signal transduction, and collagen synthesis. Each disorder contributes at a different time to HF development and worsening. Clinical presentation depends on pulmonary congestion, organ perfusion, presence of coronary disease, fluid retention and systemic pressure. For these reasons, the picture of HF is widely varied.
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|Titolo:||Heart failure: pathophysiology and clinical picture.|
|Rivista:||CONTRIBUTIONS TO NEPHROLOGY|
|Citazione:||Palazzuoli, A., & Nuti, R. (2010). Heart failure: pathophysiology and clinical picture. CONTRIBUTIONS TO NEPHROLOGY, 164, 1-10.|
|Appare nelle tipologie:||1.1 Articolo in rivista|
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