Congestive Heart Failure: Physiopathology, Etiology, and Therapeutics
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Authors
Maurissen, StƩphanie L.C.
Issue Date
2004
Type
Thesis
Language
en_US
Keywords
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Abstract
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 š¯›½-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.
Description
v, 98 p.
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