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

BACKGROUND: Mild hypothermia (MH) decreases infarct size and mortality in experimental reperfused myocardial infarction, but may potentiate ischaemia-induced left ventricular (LV) diastolic dysfunction. METHODS: In anaesthetized pigs (70 ± 2 kg), polystyrol microspheres (45 μm) 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 6 h (CME 6 h). *p < 0.05 vs baseline, †p < 0.05 vs NT. RESULTS: In 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 ± 4 ml*, 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 ± 4 mmHg). Mixed venous oxygen saturation at CME 6 h was higher in MH than in NT (59 ± 4† vs 42 ± 2%) due to lowered systemic oxygen demand during cooling. CONCLUSION: We 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.