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Heart Disease: A Case Study

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Mitral valve insufficiency causes regurgitation of stroke volume back to the low pressure left atrium and remodeling of the heart walls. Remodeling of the heart walls leads to progressive left-sided cardiomegaly in an attempt to compensate for decreased stroke volume but becomes a cascade of continued dysfunctional changes with no return to normal stroke volume. Stretching of the mitral annulus from remodeling increases the regurgitant orifice and regurgitant volume. A vicious cycle ensues in an attempt to compensate for dysfunctional changes by further remodeling.3,11 The majority of remodeling occurs prior to the onset of clinical signs with the most rapid changes occurring in the six months prior to onset of CHF.3,7 Animal models for mitral …show more content…
Although the role of hormones in progression of heart disease is controversial, they become the target of mainstay therapies for heart disease management.3 Initially, decreased blood pressure leads to an increase in sympathetic tone and the release of norepinephrine. Stimulation of the β-1 receptors increases heart rate and contractility. The β-1 receptors are down regulated within a few days, but norepinephrine continues to be released in increasing amounts as heart failure worsens.14 The renin-aldosterone-angiotensin system (RAAS) is stimulated by renal hypoxemia which is a result of decreased renal blood flow in heart failure. Renin release from the juxtaglomerular apparatus initiates aldosterone release from the adrenal cortex. Aldosterone increases sodium and water reabsorption in the distal tubules of the nephron which increases blood volume, venous pressure, and preload. The result is ultimately increased workload on an already failing heart. Angiotensin II is a potent vasoconstrictor which will increase vascular resistance and afterload. Antidiuretic hormone (vasopressin) release is stimulated by the increased plasma osmolality of heart failure and has similar effects as RAAS. The results of these pathways can play a significant role in remodeling and attempt at compensation in acute or chronic CHF and become a target for therapies following

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