Congestive Heart Failure: Physiopathology, Etiology, and Therapeutics
Maurissen, Stéphanie L.C.
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Congestive Heart Failure (CHF) is a heart condition affecting millions of Americans each year. In patients with CHF, the heart's ejection fraction is low, which subsequently decreases oxygen flow to cells and results in dyspnea, and tachycardia. Clinical signs also include an enlarged heart, an enlarged liver, and edema in the lungs and extremities. CHF is a secondary disease caused by predisposing conditions that weaken the heart. Coronary artery disease, hypertension, age, and myocardial infarct are some of the most significant predisposing conditions leading to CHF. The renin-angiotensin system plays a major role in CHF. Renin cleaves angiotensinogen in the heart to form angiotensin I, which is cleaved by angiotensinconverting enzyme (ACE) to form angiotensin II. Angiotensin II binds to angiotensin receptors on the cell surface of heart cells and causes signal transduction cascades leading to hypertrophy, reduction in cell communication, and eventually cell death. There are many treatments for CHF. Aspirin can be prescribed to inhibit renin secretion from the liver; ACE inhibitors (such as enalapril and captopril) inhibit angiotensin I cleavage, Angiotensin Receptor Blockers (such as losartan and eprosartan) inhibit angiotensin II from binding to receptors on the cardiac cells; diuretics decrease fluid load in the body; and 𝛽-blockers block norepinephrine. Future research is needed to comprehend: 1) the role of alternative pathways of angiotensin II production in the development of CHF, 2) the role of the two angiotensin II receptors and how they differ in the induction of apoptosis, and 3) the role of angiotensinogen inhibitors in the progression of CHF.