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 ± 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.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 ± 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.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.

Targeted Temperature Management at 33°C Versus 36°C and Impact on Systemic Vascular Resistance and Myocardial Function After Out-of-Hospital Cardiac Arrest

“…A recent porcine model in myocardial infarction supports this hypothesis because mixed venous saturation increased during hypothermia despite a progressive reduction in cardiac output, whereas mixed venous saturation decreased in normothermic controls. 26 This also implies that SVO 2 as a marker of cardiac output may not be as reliable at lower temperatures, corresponding to the weaker correlations between SVO 2 and CI seen in the TTM33 group. 27 However, overall levels of lactate were higher in the TTM33 group suggesting that the metabolic supply and demands may be slightly imbalanced at 33°C, but interestingly lactate concentrations remained elevated during rewarming.…”

Mild Hypothermia Attenuates Circulatory and Pulmonary Dysfunction During Experimental Endotoxemia*

“…The setup was described in detail before (12,13). Thirteen overnight-fasted landrace pigs (64 ± 1 kg) were sedated with 0.5 mg/kg midazolam and 20 mg/kg ketamine.…”

“…To calculate the end-systolic pressure-volume relationship, afterload was increased by brief aortic balloon catheter inflation as described before (12,13). LPS was infused for 4 hours, and the pigs were followed for another 4 hours, resulting in a total of 8 hours.…”

“…Cooling in vivo also induced LV diastolic dysfunction, as evidenced by slowed active LV relaxation (10,11) and a leftward shift of the end-diastolic pressure-volume relationship (10). However, such diastolic dysfunction was compensated by spontaneous bradycardia (10,12,13). The hypometabolic state induced by MH reduced systemic oxygen demand and improved SvO 2 during experimental myocardial infarction and cardiogenic shock in pigs (13,14).…”

“…However, such diastolic dysfunction was compensated by spontaneous bradycardia (10,12,13). The hypometabolic state induced by MH reduced systemic oxygen demand and improved SvO 2 during experimental myocardial infarction and cardiogenic shock in pigs (13,14). MH further improved survival in rodent models of sepsis (15,16) and attenuated lung injury after endotoxin and heatshock exposure (17,18) in rats.…”