In 1885, Oscar Langendorff was the first person to describe the increase in contractility ('Pulsverstärkung') that follows an extrasystole.1 Langendorff experimented with spontaneously beating isolated frog hearts. He recorded the heartbeats by using a lever that transferred the contractile movements of the heart to a rotating drum. Electrical stimulation resulted in premature contractions that were followed by compensatory pauses. In these experiments, he noticed that myocardial contractility during the first post-ectopic beats was typically stronger compared with the normal beats (see Figure 1A). Decades later, this phenomenon was termed postextrasystolic potentiation (PESP).2 PESP is present at the level of the myocardium, independently of pre-or afterload conditions. 3 The driving force behind the augmented post-extrasystolic contractility is augmented calcium release from the intracellular stores during the post-extrasystolic action potential. 4,5 Historically, PESP has been studied intensively with regard to two possible clinical applications (reviewed in Cooper 3 ):• PESP was induced during contrast ventriculography with the aim of identifying ischaemic but viable myocardial regions that might benefit from revascularisation.• PESP was elicited by paired pacing with the aim of augmenting myocardial contractility in heart failure patients.Besides these now widely abandoned applications, several studies have documented an interesting relationship between PESP and myocardial dysfunction.
Post-extrasystolic Potentiation and HeartDisease: A Forgotten Association?PESP can be measured as post-extrasystolic augmentation of the maximum left-ventricular pressure rise (LV dP/dt) or as systolic blood pressure potentiation. The parameter that is most closely related to myocardial contractility is LV dP/dt. At the level of LV dP/dt, PESP was observed both in healthy people and in heart failure patients.
6However, potentiation of LV dP/dt was typically more pronounced in failing than in healthy hearts. 7-10 At the level of blood pressure, it has to be taken into account that systolic blood pressure is not only determined by cardiac output, but also by vascular factors, such as peripheral vascular resistance. When PESP was measured at the level of maximum systolic blood pressure (or maximum LV pressure, which are roughly equivalent in the absence of aortic stenosis), the typical finding in healthy probands was that the first post-ectopic heartbeat elicited a lower pulse wave than the regular ones. By contrast, in heart failure patients, PESP of systolic blood pressure could generally be observed. [6][7][8][9][10] In a series of 100 consecutive patients with coronary artery disease, the pattern of post-extrasystolic blood pressure potentiation was associated with an increased prevalence of congestive heart failure and cardiomegaly as well as with higher left-ventricular end-diastolic pressure, lower cardiac output and lower left-ventricular ejection fraction (LVEF). 11At the cellular level, PESP of contractility is caused ...