Heart Failure Syndrome

Extract

[...] The left ventricle progressively dilates and changes from the normal ellipsoid shape to a more spherical geometry. This "remodeling" is accompanied by changes in the cardiac interstitium, leading to altered orientation of the myofibrils and progressive fibrosis. The result is more discoordinate and less effective contraction. ACE inhibitors and ß-blockers slow, halt, or reverse this remodeling process, preventing left ventricular dilation, geometric distortion, and deterioration in contractile function. Conclusions Chronic heart failure is a multifaceted syndrome with diverse presentations. The initial manifestations of [...]

[...] ACE inhibitors and ß-blockers slow, halt, or reverse this remodeling process, preventing left ventricular dilation, geometric distortion, and deterioration in contractile function. Conclusions Chronic heart failure is a multifaceted syndrome with diverse presentations. The initial manifestations of hemodynamic dysfunction are a reduction in stroke volume and a rise in ventricular filling pressures, perhaps in the basal state but consistently under conditions of increased systemic demand for blood flow. Bibliography Cecil Textbook of Medicine 22th.Ed Current Cardiology 2nd.Ed Hurst's The Heart 10th.Ed Current Medical Diagnosis & Treatment 2007 Listras HEART FAILURE SYNDROME Chronic heart failure is a multifaceted syndrome with diverse presentations. [...]

[...] Endothelin and arginine vasopressin are elevated in many heart failure patients, and interference with their actions may promote vasodilation and diuresis. Arginine vasopressin induces vasoconstriction through a vascular receptor and reduces free water clearance through a renal tubular receptor. The endothelins cause prolonged vasoconstriction, reductions in glomerular filtration, mesangial hypertrophy, bronchoconstriction, and pulmonary arteriolar constriction. The endothelins are particularly attractive targets for therapy. CYTOKINE ACTIVATION Circulating levels of many proinflammatory cytokines, including tumor necrosis factor-a, interleukin-1ß, and interleukin-6, are elevated in patients with relatively severe heart failure and may be involved in the syndrome of cardiac cachexia. [...]

[...] It is this constellation of responses that leads to the characteristic pathophysiology of the heart failure syndrome. Recognition of the role of neurohormonal activation in heart failure has grown with the increasing understanding of its pathophysiology and with evidence that blockade of some of these responses can have a profound effect on the natural history of the disease. The number of hormonal systems that are known to be activated in heart failure continues to grow. Neurohumoral Responses SYMPATHETIC NERVOUS SYSTEM Initial activation of the sympathetic nervous system probably results from reduced pulse pressures, which stimulate arterial baroreceptors, and renal hypoperfusion. [...]

[...] Endothelin and arginine vasopressin are elevated in many heart failure patients, and interference with their actions may promote vasodilation and diuresis. Arginine vasopressin induces vasoconstriction through a vascular receptor and reduces free water clearance through a renal tubular receptor. The endothelins cause prolonged vasoconstriction, reductions in glomerular filtration, mesangial hypertrophy, bronchoconstriction, and pulmonary arteriolar constriction. The endothelins are particularly attractive targets for therapy. CYTOKINE ACTIVATION Circulating levels of many proinflammatory cytokines, including tumor necrosis factor-a, interleukin-1ß, and interleukin-6, are elevated in patients with relatively severe heart failure and may be involved in the syndrome of cardiac cachexia. [...]