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      Long-term serial changes in left ventricular function and reversal of ventricular dilatation after valve replacement for chronic aortic regurgitation.

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          Abstract

          In most patients with aortic regurgitation, valve replacement results in reduction in left ventricular dilatation and an increase in ejection fraction. To determine the relation between serial changes in ventricular dilatation and changes in ejection fraction, we studied 61 patients with chronic severe aortic regurgitation by echocardiography and radionuclide angiography before, 6-8 months after, and 3-7 years after aortic valve replacement. Between preoperative and early postoperative studies, left ventricular end-diastolic dimension decreased (from 75 +/- 6 to 56 +/- 9 mm, p less than 0.001), peak systolic wall stress decreased (from 247 +/- 50 to 163 +/- 42 dynes x 10(3)/cm2), and ejection fraction increased (from 43 +/- 9% to 51 +/- 16%, p less than 0.001). Between early and late postoperative studies, diastolic dimension and peak systolic wall stress did not change, but ejection fraction increased further (to 56 +/- 19%, p less than 0.001). The increase in ejection fraction correlated with magnitude of reduction in diastolic dimension between preoperative and early postoperative studies (r = 0.63), between early and late postoperative studies (r = 0.54), and between preoperative and late postoperative studies (r = 0.69). Late increases in ejection fraction usually represented the continuation of an initial increase occurring early after operation. Thus, short-term and long-term improvement in left ventricular systolic function after operation is related significantly to the early reduction in left ventricular dilatation arising from correction of left ventricular volume overload. Moreover, late improvement in ejection fraction occurs commonly in patients with an early increase in ejection fraction after valve replacement but is unlikely to occur in patients with no change in ejection fraction during the first 6 months after operation.

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          Wall stress and patterns of hypertrophy in the human left ventricle.

          It is generally recognized that chronic left ventricular (LV) pressure overload results primarily in wall thickening and concentric hypertrophy, while chronic LV volume overload is characterized by chamber enlargement and an eccentric pattern of hypertrophy. To assess the potential role of the hemodynamic factors which might account for these different patterns of hypertrophy, we measured LV wall stresses throughout the cardiac cycle in 30 patients studied at the time of cardiac catheterization. The study group consisted of 6 subjects with LV pressure overload, 18 with LV volume overload, and 6 with no evidence of heart disease (control). LV pressure, meridional wall stress (sigman), wall thickness (h), and radius (R) were measured in each patient throughout the cardiac cycle. For patients with pressure overload, LV peak systolic and end diastolic pressures were significantly increased (220 plus or minus 6/23 plus or minus 3 mm Hg) compared to control (117 plus or minus 7/10 plus or minus 1 mm Hg, P less than 0.01 for each). However, peak systolic and end diastolic (sigman) were normal (161 plus or minus 24/23 plus or minus 3 times 10-3 dyn/cm-2) compared to control (151 plus or minus 14/17 plus or minus 2 times 10-3 dyn/cm-2, NS), reflecting the fact that the pressure overload was exactly counterbalanced by increased wall thickness (1.5 plus or minus 0.1 cm for pressure overload vs. 0.8 plus or minus 0.1 cm for control, P less than 0.01). For patients with volume overload, peak systolic (sigman) was not significantly different from control, but end diastolic (sigmam) was consistently higher than normal (41 plus or minus 3 times 10-3 dyn/cm-2 for volume overload, 17 plus or minus 2 times 10-3 dyn/cm-2 for control, P less than 0.01). LV pressure overload was associated with concentric hypertrophy, and an increased value for the ratio of wall thickness to radius (h/R ratio). In contrast, LV volume overload was associated with eccentric hypertrophy, and a normal h/R ratio. These data suggest the hypothesis that hypertrophy develops to normalize systolic but not diastolic wall stress. We propose that increased systolic tension development by myocardial fibers results in fiber thickening just sufficient to return the systolic stress (force per unit cross-sectional area) to normal. In contrast, increased resting or diastolic tension appears to result in gradual fiber elongation or lengthening which improves efficiency of the ventricular chamber but cannot normalize the diastolic wall stress.
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            Noninvasive determination of left ventricular end-systolic stress: validation of the method and initial application

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              Differences in myocardial performance and load between patients with similar amounts of chronic aortic versus chronic mitral regurgitation.

              It is not known if the favorable changes in preload and afterload that augment ejection performance in acute experimental aortic and mitral regurgitation are also present in patients with chronic regurgitation. Additionally, observations that patients with mitral versus aortic regurgitation respond differently to valve replacement suggest that differences exist preoperatively between these two types of volume overload. Therefore, ventricular mechanics were compared in nine patients with severe aortic regurgitation, eight patients with severe mitral regurgitation and seven normal subjects. The amount of volume overload was similar in both groups with regurgitation. In both aortic and mitral regurgitation, ejection performance was reduced compared with findings in normal subjects. Preload estimated as enddiastolic stress was comparably elevated above normal in both groups with regurgitation: 69 +/- 24 dynes X 10(3)/cm2 in mitral regurgitation compared with 81 +/- 34 dynes X 10(3)/cm2 in aortic regurgitation and 36 +/- 11 dynes X 10(3)/cm2 in normal subjects. However, afterload estimated as mean systolic stress was normal in mitral regurgitation (186 +/- 34 dynes X 10(3)/cm2) but markedly elevated in aortic regurgitation (260 +/- 41 dynes X 10(3)/cm2) (p less than 0.01). Contractile depression tended to be more severe in mitral regurgitation despite similar ejection performance in mitral and aortic regurgitation. Thus, in mitral regurgitation favorable loading conditions may mask contractile dysfunction, and in aortic regurgitation excessive afterload contributes to poor pump performance, possibly accounting for previously observed differences in the response to valve replacement.
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                Author and article information

                Journal
                Circulation
                Circulation
                Ovid Technologies (Wolters Kluwer Health)
                0009-7322
                1524-4539
                November 1988
                November 1988
                : 78
                : 5
                : 1108-1120
                Affiliations
                [1 ]Cardiology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892.
                Article
                10.1161/01.CIR.78.5.1108
                2972417
                4223c07e-4059-4928-b443-415c7a4ef19c
                © 1988
                History

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