Ability of left ventricular stress-shortening relations, end-systolic stress/volume ratio and indirect indexes to detect severe contractile failure in ischemic or idiopathic dilated cardiomyopathy

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The ability of several proposed indirect and direct indexes of left ventricular (LV) systolic performance and contractility to detect clinically important LV dysfunction was evaluated in 42 patients with refractory dilated cardiomyopathy studied with right-sided heart catheterization and M-mode echocardiography. Hemodynamic evaluation demonstrated elevated filling pressure (mean pulmonary artery wedge pressure 24 ± 6 mm Hg) and depressed function (cardiac index 1.68 ± 0.43 liters/min/m 2). Echocardiographic LV end-diastolic dimension (7.3 ± 1.0 cm), mass (182 ± 60 gm/m 2) and end-systolic stress (163 ± 44 × 10 3 dynes/cm 2) were increased whereas fractional shortening was depressed in all (mean 12 ± 4%). During follow-up 88% of patients died at a median interval of 16 months after study. Indirect measurements of LV function (mitral E point-septal separation and the ratio of preejection period to LV ejection time) were abnormal in 100 and 88% of patients, respectively. Contractility was classified as depressed in 36 (86%) patients by the end-systolic stress/volume index ratio and in 31 (74%) by the relation between fractional shortening and end-systolic stress. In contrast, the relation between end-systolic stress and velocity of circumferential shortening identified only 7 (17%) patients as having subnormal contractility and classified 9 (21%) as having supernormal contractility. Rate correction of velocity of circumferential shortening only modestly improved the ability of the relation to identify depressed contractility (abnormal in 16 patients or 38%). Thus, relatively simple indirect and direct (stress-shortening relation and end-systolic stress/volume index ratio) indexes appear useful in identifying severe, prognostically important LV contractile dysfunction, whereas methods that successfully correct for variations in preload and heart rate in normal subjects result in artifactual normalization of function in most patients with dilated cardiomyopathy.