[Diastolic function modulation by load. Physiological basis and clinical implications].

INTRODUCTION AND OBJECTIVES

Diastolic heart failure has emerged over the last decade as a separate clinical entity, but its pathophysiology is still largely unknown. Left ventricular (LV) relaxation is considered an important determinant of early, but not late, LV filling. We recently showed that a substantial afterload elevation induces a marked slowing of relaxation. In this study we investigated the repercussion of such slowing on late LV filling.

METHODS

The study was carried out on 7 open-chest, anaesthetised, New Zealand white rabbits, fully instrumented to evaluate cardiac function. The load was manipulated by transient occlusions of the ascending aorta and/or of the inferior vena cava.

RESULTS

We observed that the afterload elevations had a biphasic effect on the relaxation rate and diastolic pressure-dimension (P-D) relation: small elevations accelerated relaxation and did not affect the diastolic P-D relation, while greater elevations progressively decreased the relaxation rate and induced a divergent upward shift of the diastolic P-D. The magnitude of this upward shift was related to the relaxation rate and the time available for the ventricle to relax.

CONCLUSIONS AND IMPLICATIONS

Small to moderate afterload elevations are easily compensated by the normal ventricle, while greater elevations induce diastolic dysfunction even in normal hearts, which leads us to the concept of afterload reserve. This concept helps explain why diastolic dysfunction and pulmonary congestion, present in heart failure, may be reverted by decreasing the load (e.g. vasodilators and diuretics).