NONUNIFORM COURSE OF LEFT-VENTRICULAR PRESSURE FALL AND ITS REGULATION BY LOAD AND CONTRACTILE STATE

Background Effects of systolic left ventricular pressure (LVP) on rate s of-pressure fall remain incompletely understood. This study analyzed phase-plane dP/dt versus LVP plots to differentiate between accelerat ing and decelerating effects and to investigate the variability in rep orted load effects on rates of LVP fall. Methods and Results Abrupt ao rtic occlusions were performed by inflating a balloon positioned in th e ascending aorta of anesthetized open-chest dogs (n=17). The occlusio ns resulted in clamp elevations of systolic LVP. In protocol A, the el evations of systolic LVP induced by total aortic occlusions were timed at early, mid, and late ejection. The magnitude of the elevations was 36.0+/-3.6 mm Hg for early, 11.6+/-0.6 mm Hg for mid, and negligible for late occlusions. The course of LVP fall appeared to be more comple x than previously appreciated. Pressure fall might be subdivided in an initial accelerative phase, an intermediate decelerative phase, and a terminal decelerative phase. The initial phase accelerated with mid a nd late occlusions. The intermediate phase slowed down with early and to a lesser extent with mid occlusions. The terminal phase was never a ffected by aortic clamp occlusions. In protocol B, early elevations of systolic LVP were obtained with multiple graded aortic occlusions. Th e effects of matched LVP elevations of 12 mm Hg on rate of LVP fall we re evaluated with the time constant of LVP fall (tau) and showed an in teranimal variability ranging from acceleration and a 20% decrease in tau to deceleration and a 35% increase in tau. Changes in tau were mod erately correlated with commonly used indexes of contractility (peak dP/dt, r=-.78; regional, fractional shortening, r=-.63). These changes in tau showed a close correlation with the systolic LVP of the test b eat, expressed as a percentage of the peak isovolumetric LVP, obtained with total aortic occlusion (r=.984). This suggested that the contrac tion-relaxation coupling should be analyzed in terms of peak force dev elopment rather than contraction velocity or ejection fraction. Conclu sions LVP fall could be subdivided into an initial accelerative phase, an intermediate decelerative phase, and a terminal decelerative phase . Effects of elevations in systolic LVP on rate of LVP fall could be p redicted by knowing peak isovolumetric LVP. Nonuniformity of LVP fall and adequate interpretation of load effects should be taken into accou nt when clinical situations or pharmacological interventions are consi dered. In congestive heart failure, slow LVP fall could mainly reflect working conditions close to isovolumetric rather than relaxation dist urbances.