Left ventricular diastolic dysfunction during acute myocardial infarction: Effect of mild hypothermia

Abstract

BackgroundMild hypothermia (MH) decreases infarct size and mortality in experimental reperfused myocardial infarction, but may potentiate ischaemia-induced left ventricular (LV) diastolic dysfunction. MethodsIn anaesthetized pigs (70±2kg), polystyrol microspheres (45μm) were infused repeatedly into the left circumflex artery until cardiac power output decreased >40%. Then, pigs were assigned to normothermia (NT, 38.0°C, n=8) or MH (33.0°C, n=8, intravascular cooling) and followed for 6h (CME 6h). *p<0.05 vs baseline, †p<0.05 vs NT. ResultsIn NT, cardiac output (CO) decreased from 6.2±0.3 to 3.4±0.2*l/min, and heart rate increased from 89±4 to 101±6*bpm. LV end-diastolic volume fell from 139±8 to 64±4ml*, while LV ejection fraction remained constant (49±1 vs 53±4%). The corresponding end-diastolic pressure–volume relationship was progressively shifted leftwards, reflecting severe LV diastolic dysfunction. In MH, CO fell to a similar degree. Spontaneous bradycardia compensated for slowed LV relaxation, and the leftward shift of the end-diastolic pressure–volume relationship was less pronounced during MH. MH increased systemic vascular resistance, such that mean aortic pressure remained higher in MH vs NT (69±2† vs 54±4mmHg). Mixed venous oxygen saturation at CME 6h was higher in MH than in NT (59±4† vs 42±2%) due to lowered systemic oxygen demand during cooling. ConclusionWe conclude that (i) an acute loss of end-diastolic LV compliance is a major component of acute cardiac pump failure during experimental myocardial infarction, and that (ii) MH does not potentiate this diastolic LV failure, but stabilizes haemodynamics and improves systemic oxygen supply/demand imbalance by reducing demand.