POSTEXTRASYSTOLIC LEFT-VENTRICULAR ISOVOLUMIC PRESSURE DECAY IS NOT MONOEXPONENTIAL

Objective: The relationship between the left ventricular (LV) relaxati on time constant and early diastolic filling is not fully defined. Thi s study provides additional evidence that LV isovolumic pressure fall in the normal intact heart in response to certain interventions is not adequately described by a model of monoexponential decay and that its relationship to filling is complex. Methods and results: To gain furt her insight into the relationship between LV relaxation and early rapi d filling we measured LV isovolumic relaxation rate, peak early fillin g velocity (E), LV volumes, and transmitral pressures at baseline and in the first postextrasystolic beat after a short-coupled extrasystole in 9 anesthetized dogs. Postextrasystolic isovolumic relaxation rate was slowed as measured by 3 commonly used time constants, while E was increased 32%. LV contractility and peak pressure were also increased, while LV end-systolic volume was decreased. LV minimum pressure was d eceased, while the early diastolic transmitral pressure gradient was i ncreased. Although all relaxation time constants measured over the ent ire isovolumic relaxation phase indicated slowed relaxation, direct me asurement of isovolumic relaxation time indicated no change in relaxat ion rate. Calculation of the time constants and direct measurement of isovolumic relaxation time during early isovolumic pressure decay indi cated slowed postextrasystolic pressure decay rate compared with basel ine, while calculation of time constants and direct measurement of iso volumic relaxation time during late isovolumic relaxation indicated au gmented postextrasystolic pressure decay rate versus baseline. Conclus ions: This non-exponential behavior of LV isovolumic pressure decay in postextrasystolic beats after short-coupled extrasystoles provides fu rther evidence that the relationship that exists between ventricular r elaxation and early filling is not simple. The results an interpreted in terms of current theoretical formulations that attribute control of myocardial relaxation to the interaction between inactivation-depende nt and load-dependent mechanisms. (C) 1997 Elsevier Science B.V.