Postextrasystolic potentiation and echocardiography: the effect of varying basic heart rate, extrasystolic coupling interval and postextrasystolic interval.

Abstract

SUMMARY The purpose of this study was to determine whether echocardiography can be used to monitor postextrasystolic potentiation (PESP) and, if so, which of the echocardiographic variables are valid indicators of PESP and under what conditions. An implantable M-mode echocardiographic transducer was sewn to the right ventricular outflow tract of the dog heart to record continuously across the minor diameter of the left ventricle. The sinus node pacemaking region was excised and a pacing protocol was used to vary the basic heart rate, the extrasystolic coupling interval and the postextrasystolic interval. The decreases in ejection time and diastolic dimension as well as the increases in the mean rate of circumferential fiber shortening (Vcf) and fractional shortening (%FS) that occur with increasing heart rate were detected by echocardiography. There were also increases in posterior wall maximal velocity and excursion and an increase in the rate of diastolic relaxation. Shortening the coupling interval of the extrasystole resulted in the expected potentiation of Vcf, %FS and the excursion, maximal velocity and rate of diastolic relaxation of the posterior wall. No correlation was observed for percent thickening of the posterior wall or interventricular septum, either because the technique was too insensitive or because wall thickening does not reflect the rapid-phase force-frequency perturbation of PESP. Allowing a full compensatory pause for the postextrasystolic interval resulted in a greater potentiation of all variables than if the postextrasystolic interval was timed to occur when postextrasystolic diastolic pressure and dimension were identical to preextrasystolic diastolic pressure and dimension (isolength). However, only at isolength was potentiation highly predictable, and then only if the heart rate and the coupling interval were known. We conclude that most of the variables measured echocardiographically can be used to determine whether the PESP response is equivalent to a predicted value, provided all intervals are known or carefully controlled.

Electrical management of heart failure: from pathophysiology to treatment

“… 4 , 16–18 An important aspect of irregular rhythm is PESP, a phenomenon that refers to an increase in contractility that is associated with Ca 2+ overload. 16 , 19 , 20 The role of PESP as a trigger for the development of HF is supported by a study in isolated myocytes and intact myocardium showing that irregular cycles of excitation and contraction induce an altered profile of gene and protein expression including down-regulation of sarcoplasmic reticulum ATPase 2a pump (SERCA) and an abnormal ratio of phosphorylated to total phospholamban (PLB). 21 Using a combination of echocardiographic imaging and computer simulations, Lyon et al .…”

Abnormal Left Ventricular Mechanics of Ventricular Ectopic Beats

“…; 2) post-extrasystolic potentiation (increase in contractility that follows an atrial or ventricular extrasystole) associated with acute intracellular Ca 2+ overload and increased myocardial oxygen consumption 11, 12 , which has an inverse relationship to PVC coupling interval (shorter coupling intervals have a greater intracellular Ca 2+ and post-extrasystolic potentiation 12,9, 13 ; 3) autonomic dysregulation; and 4) “tachycardia” due to a short R-to-PVC interval. However, tachycardia as a single mechanism of PVC-induced CM is unlikely, not only because the mean heart rate in our PVC-induced CM model was significantly lower (130±13 bpm) than described in tachycardia-induced CM models (heart rate >180 bpm 14, 15 ), but also due to the absence of histological and mitochondrial abnormalities characteristic of tachycardia-induced CM and other HF models 16 .…”

Assessment of subtle cardiac dysfunction induced by premature ventricular contraction using two dimensional strain echocardiography and the effects of successful ablation

“…Some authors consider postextrasystolic potentiation (PEP) as a mechanism for PVC-CM. PEP signi cantly increases myocardial oxygen consumption [33][34], and when frequent this increased energy consumption may cause systolic dysfunction. However, this hypothesis has never been investigated.…”