Atlas of Heart Failure: Cardiac Function and Dysfunction by Arnold M. Katz (auth.), Wilson S. Colucci MD (eds.)

By Arnold M. Katz (auth.), Wilson S. Colucci MD (eds.)

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E E E .... ,, :J .... c.. 40 0 lum •, mL A 40 RO B 120 lhO 2l \ >lurn •, ml volume diagrams can be used to characterize systolic dysfunction, altered diastolic compliance, and the influence of loading conditions on cardiac function. A, A series of pressure-volume loops obtained from a patient with normal cardiac function. Each loop represents a cardiac cycle sampled during inflation of a balloon in the inferior vena cava to alter loading conditions. The slope of the end-systolic pressurevolume loop relationship (ESPVR, solid line) reflects end-systolic ventricular elastance, a relatively load-independent index of contractility.

I• ' . .... ~·' ........ , . ... ' ... ' .. -. . ~ ~. . • ,·, ' · .... . ~ ,? ' · ... ,: ' t :' .. . '· . . .. :_ . FIGURE 3-4. Histology of ischemic cardiomyopathy demonstrating replacement fibrosis. Myocyte hypertrophy occurs secondarily in response to increases in pressure or volume loads [9]. Fibrosis, the increased deposition of collagen, results from either repair of parenchymal myocyte injury (replacement fibrosis) or pathologic deposition in the interstitium. Histologic studies reveal that patients with ischemic cardiomyopathy display more replacement fibrosis but less myocyte hypertrophy than those with idiopathic cardiomyopathy.

When mitral regurgitation is acute, it may produce symptomatic pulmonary edema as well as pulmonary hypertension and right heart failure. Mitral regurgitation can also cause chronic left ventricular (LV) dysfunction, which, if left untreated, can lead to the development of dilated cardiomyopathy. Incompetence of the mitral valve reduces ventricular afterload and increases the velocity of contractile element shortening; thus, the LV ejection fraction may be normal despite significant LV dysfunction.

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