Loading Sequence Plays an Important Role in Enhanced Load Sensitivity of Left Ventricular Relaxation in Conscious Dogs With Tachycardia-Induced Cardiomyopathy

Author:

Ishizaka Shinji1,Asanoi Hidetsugu1,Wada Osamu1,Kameyama Tomoki1,Inoue Hiroshi1

Affiliation:

1. From the Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan.

Abstract

Background Left ventricular relaxation rate in the failing heart depends more on the systolic load than in the normal heart. To elucidate the mechanisms for the enhanced load sensitivity of left ventricular relaxation in heart failure, we examined the relative contributions of changes in end-systolic volume and loading sequence to the left ventricular relaxation rate. Methods and Results In seven conscious dogs, the time constant (T d ) of left ventricular pressure decay, end-systolic volume, systolic circumferential force, and time to peak force during caval occlusion were compared before and after development of tachycardia-induced heart failure. Rapid ventricular pacing decreased the slope of the end-systolic pressure-volume relation from 4.5 to 2.8 mm Hg/mL ( P <.01) and prolonged T d from 33 to 49 ms ( P <.01). In normal conditions, caval occlusion reduced end-systolic force (−580 g, P <.01) and end-systolic volume (−7 mL, P <.01) but did not change T d or time to peak force. In heart failure, however, caval occlusion shortened T d (−11 ms, P <.01), with a concomitant decrease in the time to peak force (−30 ms, P <.01), while end-systolic volume and force declined slightly. Consequently, for a comparable reduction in end-systolic force, T d decreased more in heart failure than in normal hearts, suggesting enhanced load sensitivity. Moreover, changes in T d correlated well with those in the time to peak force ( r =.79, P <.01) but not with those in end-systolic volume. Conclusions Loading sequence rather than elastic recoil seems to play the predominant role in the enhanced load sensitivity of left ventricular relaxation in heart failure.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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