Why the study?
Does postextrasystolic potentiation alter left ventricular performance mechanics differently in normal subjects compared to patients with valvular heart disease?
Does postextrasystolic potentiation alter left ventricular performance mechanics differently in normal subjects compared to patients with valvular heart disease?
Postextrasystolic potentiation enhances ventricular performance through increased inotropic state across all groups, but relies on preload reserve only in normal subjects and those with aortic stenosis, not in chronic volume overload.
Caution against assuming preload contribution to PESP in regurgitation; leaves open mechanism-targeted research in valvular disease.
To determine the relative influence of preload, afterload, and inotropic state on postextrasystolic potentiation (PESP) of ventricular performance in man, we computed angiographic left ventricular volume and wall stress frame by frame for a control and potentiated beat in each of 31 patients. In 10 normal subjects, PESP increased ejection fraction by 14%, while left ventricular end-diastolic volume increased by 8% (p less than .001) and end-systolic stress fell by 21% (p less than .005). Enhanced diastolic filling (+6%, p less than .005) with a small decline in end-systolic stress (-8%, p = NS) likewise contributed to potentiation of ejection fraction (+14%, p less than .001) in seven patients with aortic stenosis. Diastolic filling was not significantly augmented during the compensatory pause in six patients with isolated mitral regurgitation, nor in eight patients with aortic regurgitation (+2%, p = NS for both). Although afterload tended to fall for potentiated beats in patients with aortic (-11%, p = NS) and mitral regurgitation (-23%, p = NS), analysis of ejection fraction-end-systolic stress relationships demonstrated an independent effect of inotropic state on potentiated ejection performance. Thus, utilization of preload reserve contributed to PESP in normal subjects and patients with aortic stenosis, but not in those with volume overload imposed by chronic valvular regurgitation. Enhanced inotropic state independent of small changes in afterload was demonstrated in all subgroups.
No takes yet. Share an insight, caveat, or question.
Wisenbaugh et al. (1986) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: