Difference between revisions of "Arrhythmogenic Right Ventricular Cardiomyopathy - Feline Cardiomyopathies"
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Little is known about he cause of ARVC in cats. In humans and Boxer dogs, ARVC is caused by mutations in various components of the desmosome (necessary for cell-cell adhesion). The resultant loss of mechanical coupling predisposes to arrhythmias. | Little is known about he cause of ARVC in cats. In humans and Boxer dogs, ARVC is caused by mutations in various components of the desmosome (necessary for cell-cell adhesion). The resultant loss of mechanical coupling predisposes to arrhythmias. | ||
==Pathophysiology== | ==Pathophysiology== | ||
| + | Reduced myocardial contractility predominantly involves the right ventricle. This results in reduced stroke volume and increased ventricular filling pressure due to increased end-systolic ventricular diameter. This eventually leads to congestive heart failure (CHF). | ||
| + | |||
==Clinical Signs== | ==Clinical Signs== | ||
===Signalment=== | ===Signalment=== | ||
Revision as of 11:02, 14 January 2013
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This article is still under construction. |
Overview
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) is a rare form of cardiomyopathy in cats and is more commonly seen in humans and dogs. ARVC is characterised by fibrofatty infiltration replacement of cardiomyocytes predominantly in the right ventricle and right atrium; this may also effect the left ventricle to a lesser degree in some cases. Pathophysiological sequelae include severe right ventricular myocardial failure, life-threatening ventricular arrhythmias and sudden death.
Aetiology
Little is known about he cause of ARVC in cats. In humans and Boxer dogs, ARVC is caused by mutations in various components of the desmosome (necessary for cell-cell adhesion). The resultant loss of mechanical coupling predisposes to arrhythmias.
Pathophysiology
Reduced myocardial contractility predominantly involves the right ventricle. This results in reduced stroke volume and increased ventricular filling pressure due to increased end-systolic ventricular diameter. This eventually leads to congestive heart failure (CHF).