To clarify the mechanisms of afterload reduction on left ventricular diastolic function, the influence of nitroglycerin upon ventricular diastolic pressure-volume relations was studied in 22 patients during catheterization. After nitroglycerin, average ventricular systolic pressure declined by 25 mm Hg (18%) and end-diastolic pressure by 7 mm Hg (28%) (P less than 0.005). End-systolic and diastolic ventricular volumes decreased by 37% and 23% respectively (P less than 0.005). Although peak negative dP/dt fell by 22% (P less than 0.0005), "T", an index of the time course of isovolumic diastolic ventricular relaxation, was insignificantly changed. Diastolic pressure-volume curves were significantly displaced downward and leftward without significant change in slope, suggesting that a family of pressure-volume curves for each ventricle with similar slope but positions depend upon immediate loading conditions. Absence of change in slope or of "T" suggests that this displacement may be mediated indirectly, perhaps by relaxation of extracardiac constraints to ventricular distensibility. Accordingly, improvement in ventricular function by vasodilators may be partly due to downward displacement of the pressure-volume relation, with associated reduction of wall tension and myocardial oxygen consumption.

SUMMARY To clarify the mechanism of displacement of the left ventricular diastolic pressure-volume function with alteration of loading conditions, the effects of nitroglycerin on pressure-volume relations in 13 patients were compared with those of amyl nitrite in 13 other patients during cardiac catheterization. After nitroglycerin, average systemic mean arterial pressure declined by 15.1 mm Hg (17%) and left ventricular enddiastolic pressure by 9.4 mm Hg (49%); right ventricular systolic and end-diastolic pressures fell 11.6 mm Hg (36%) and 5 mm Hg (41%), respectively. In all patients diastolic pressure-volume curves were significantly displaced downward and leftward. After amyl nitrite, average systemic mean arterial pressure fell 20.1 mm Hg (22%), but left ventricular end-diastolic pressure and right ventricular systolic and end-diastolic pressures were not significantly reduced. No significant displacement of diastolic pressure-volume curves occurred. Both the rate constant of the exponentially fit diastolic pressure-volume curve, and the rate of diastolic isovolumic relaxation (T) were unchanged after each drug. Thus downward displacement of diastolic pressure-volume functions after nitroglycerin appears to be dependent more upon reduction of right ventricular filling dynamics than coronary perfusion pressures. More favorable effects upon left ventricular function may be associated with reduction of both left ventricular filling pressures and systemic impedance (reflecting both "preload" and "afterload") than of systemic arterial pressures ("afterload") alone.

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SUMMARY To determine if asynchronous segmental relaxation is associated with altered left ventricular (LV) diastolic function, we examined systolic and diastolic wall motion and function indexes in 16 patients without and 16 with asynchronous relaxation (groups 1 and 2, respectively). The segment with asynchronous relaxation was observed most frequently in the free anterior LV wall and was not consistently related geographically to coronary stenosis, nor to systolic asynergy in the same region, but was frequently accompanied by simultaneous segmental inward motion elsewhere in the ventricle.LV chamber volume stiffness during diastolic filling and at end-diastole was statistically similar in each group. Conversely, both T (58.3 ± 2.3 msec vs 41.0 ± 3.6 msec) and the isovolumic relaxation period (140.9 ± 7.5 msec vs 116 ± 6 msec) were significantly more prolonged, peak negative dP/dt was lower (1314 ± 57 mm Hg/sec vs 1604 ± 114 mm Hg/sec), and the y-axis intercept of the diastolic pressure-volume curve was higher in group 2 patients (7.96 ± 0.98 mm Hg vs 4.88 ± 0.93 mm Hg) (p < 0.05 for each), indicating impaired relaxation and altered diastolic tone.With improved systolic function and relaxation properties after nitroglycerin, both the asynchronous outward relaxation and the inferior segment of simultaneous inward motion were ameliorated. Conversely, with increased ventricular preload and afterload induced by isometric exercise, both the asynchronous segmental outward motion anteriorly and the inward motion inferiorly were exaggerated.Asynchronous segmental relaxation may represent a compensatory mechanism in areas of normal contraction that offsets abnormal inward motion elsewhere, tending to maintain isovolumic status of the ventricle.OUTWARD segmental left ventricular (LV) wall motion during the isovolumic relaxation period of diastole is frequently observed in left ventriculograms of patients who undergo diagnostic cardiac catheterization. Gooch et al. ' initially described this phenomenon in patients with mitral valve prolapse, and attributed it to a functional myocardiopathy; however, it has more recently been reported both in normal subjects2 and patients with coronary artery disease.

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