Noninvasive determination of left ventricular end-systolic stress: validation of the method and initial application.

End-systolic left ventricular (LV) meridional wall stress is a quantitative index of true myocardial afterload that can be plotted against LV end-systolic diameter to give an index of contractility independent of loading conditions. We developed a noninvasive method for estimating end-systolic LV meridional wall stress based on M-mode LV echographic end-systolic diameter (LVID) and posterior wall thickness (PWT) and cuff systolic arterial pressure and compared it to simultaneous invasive LV wall stress derived from micromanometer LV pressure recordings and continuously digitized echograms in 12 subjects (four with atypical chest pain, six with severe aortic regurgitation (AR) and two with congestive cardiomyopathy), before and after load manipulation with nitroprusside, nitroglycerin, phenylephrine or saline. Cuff systolic pressure correlated well with end-systolic LV micromanometer pressure (r = 0.89, n = 31, range 96-160 mm Hg) and noninvasive end-systolic stress (0.334 P(LVID)/PWT [1 + PWT/LVID]) correlated extremely well with invasive stress (r = 0.97, n = 31, range 36-213 X 109 dyn/cm2). Invasive and noninvasive slopes (r = 0.91, n = 7) and LVID intercepts (r 0.89, n = 7) of the stress-diameter plots also correlated well. Noninvasive stressdiameter plots in nine normal subjects showed a range of slopes of 50-93 X 101 dyn/cm and intercepts of 1.8-2.8 cm. Mean basal end-systolic noninvasive stress in 22 normal subjects (64.8 ± 19.5 X 10W dyn/cm2) and 14 treated hypertensives (56.3 ± 26.7 X 103 dyn/cm2) was significantly lower than in nine patients with symptomatic aortic regurgitation who had reduced ejection fraction (142.2 ± 53.2 X 10o dyn/cm2,p < 0.01) or four patients with congestive cardiomyopathy (187.3 ± 49.8 X 103 dyn/cm2, p < 0.01), while a mild elevation of stress in symptomatic aortic regurgitation with normal ejection fraction was not statistically significant (91.1 ± 20.7 X 103 dyn/cm2, n = 6). Thus, afterload excess contributed to ejection fraction reduction. We conclude that end-systolic stress may be determined noninvasively and may be a useful approach to quantitation of LV afterload and contractility.