Abstract

Because of the relation between left ventricular (LV) chamber elastance and heart size, it has been hypothesized that maximum time-varying elastance (Emax) must be standardized to differentiate between preserved and depressed LV systolic performance. To test this hypothesis, we studied 66 patients, of whom 25 had a normal LV, 20 had aortic regurgitation, 14 had mitral regurgitation, and seven had cardiomyopathy, with micromanometer-determined LV pressures and radionuclide angiograms during multiple LV loading conditions. Multiple regression analysis established that Emax was independently related to LV end-diastolic volume (r = -0.69). When the Emax and LV end-diastolic volume (EDV) data from all patients were plotted, a curvilinear relation was evident. Data transformation to the base e identified two distinct linear relations, one in the normal patients of lnEmax = -0.60 (lnEDV) +4.34 (r = -0.67, p less than 0.001); and one in the patients with cardiac pathology of lnEmax = -1.06 (lnEDV) +6.12 (r = -0.73, p less than 0.001), which differed from each other (p less than 0.01). When a mathematical standardization was applied to these data to eliminate the independent contribution of heart size to the reduction in lnEmax, the normal patients had a standardized lnEmax versus lnEDV slope of 0, whereas that in the patients with cardiac pathology remained negative and continued to differ from that in the normal patients (p less than 0.001). Dichotomization of patients with cardiac pathology into those with preserved and depressed LV chamber elastance by lnEmax or standardized lnEmax provided highly concordant data (k = 0.73, p less than 0.001). Moreover, the estimated contribution of LVEDV to the reduction in Emax in patients with cardiac pathology averaged only 14 +/- 7%. We conclude from these data that LV chamber elastance calculated with radionuclide angiography has an independent relation with LVEDV, that a mathematical standardization of Emax for heart size does not significantly alter the dichotomization of patients with cardiac pathology into those with preserved and depressed LV systolic performance, and that heart size makes a relatively small contribution to the reduction in this index of LV systolic performance. Thus, standardization for heart size may not be necessary to identify whether preserved or depressed LV chamber elastance exists in an individual adult patient with cardiac pathology compared with normal adult patients.

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