© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Load sensitivity of left ventricular relaxation in normal and failing hearts: evidence of a nonlinear biphasic response
aDepartment of Medicine, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284, USA
bAudie Murphy Memorial Veterans Hospital, San Antonio, TX 78284, USA
* Tel.: +1-210-567-4600; fax: +1-210-567-6960 prabhu{at}uthscsa.edu
Objective: This investigation sought to define the effect of heart failure (HF) on the load sensitivity of left ventricular (LV) relaxation and to correlate alterations in load sensitivity with the variables of ejection timing, systolic load profile and elastic recoil. Methods: Nine dogs instrumented with LV micromanometers and piezoelectric crystals were studied before and after HF produced by prolonged rapid LV pacing. After pharmacologic autonomic blockade and atrial pacing at 160 bpm, hemodynamic measurements were recorded at steady-state and during vena caval occlusion. LV relaxation for individual beats during caval occlusion was assessed using tau, the monoexponential time constant, and systolic load was estimated using end-systolic circumferential force (ESF). Results: The tau–ESF relation was nonlinear and biphasic, with an initial decrease in tau followed by a delayed increase, and was described by a parabolic equation with a curvilinearity coefficient a. Examination of ejection variables and systolic load profile indicated that the initial acceleration of relaxation reflected the influence of increased elastic recoil, whereas the late slowing reflected the influence of earlier end-ejection and delayed systolic loading. HF produced significant baseline prolongations of tau (P<0.005), time to relaxation onset (P<0.001) and time to peak force (P<0.015) compared to control. The curvilinearity coefficient of the tau–ESF relation was significantly increased (18.1±20.1·10–5 vs. 3.99±2.89·10–5 g–2, P=0.048), indicating increased load sensitivity of relaxation. This increased load sensitivity correlated with delayed onset but increased overall magnitude of the effects of earlier end-ejection and late systolic loading on relaxation. Conclusions: The tau–ESF relationship during transient load reduction is nonlinear and biphasic with an initial acceleration of relaxation, reflecting the impact of elastic recoil, and delayed slowing, reflecting changes in ejection timing and systolic loading sequence. This relation is more curvilinear in the failing heart, indicating increased load sensitivity of LV relaxation. These changes primarily occur due to alterations in the impact of ejection timing and systolic load profile rather than increased elastic recoil.
KEYWORDS Heart failure; Ventricular function; Cardiomyopathy; Contractile function; Hemodynamics