Elevated preload is critical for synchronization of myocardial lengthening (é) and mitral inflow (E) in acute ischemic acute heart failure

Abstract

BackgroundTachycardia in ischemic acute heart failure (AHF) is believed to be a compensatory response to sustain cardiac output and perfusion pressure. Little is known about early diastole in this setting.MethodsIn a pig model (n=8, mean±SD) we simultaneously measured myocardial strain (sonometric crystals), mitral‐inflow (conductance‐catheter) and mitral‐pressure difference MITRP (LV‐LA micromanometer). Pacing‐induced tachycardia was induced in the control state and in ischemic AHF (following coronary microembolization).ResultsTachycardia (160 bpm) shortened the long axis é‐delay (see Figure) from 43±30 to 20±21 ms (p=0.0066), compared to E wave in control, but not in AHF (22±13 to 25±17 ms). Interestingly, by reducing preload to similar levels as control, the é‐delay became evident also in the AHF condition (22±13 vs 48±23 ms p=0.0067). Additionally, tachycardia increased peak MITRP from 4±1 to 9±4 (p=0.007) mmHg in control, but not in AHF (6±2 to 7±2 mmHg). The enhanced relaxation following tachycardia caused a maintained potential energy across the mitral valve in early filling phase (MITRPINTG) in control (0.4±0.2 to 0.4±0.2 mmHg*s), which was reduced following tachycardia in AHF (0.6±0.2 to 0.4±0.2 mmHg*s p=0.0246).ConclusionTachycardia during AHF fails to hasten é and thereby amplifying the pressure driving force across the mitral valve.