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.