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Updated: May 22, 2026
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Left ventricular diastolic dysfunction during acute myocardial infarction: effect of mild hypothermia
Michael Schwarzl1, Stefan Huber, Heinrich Maechler
1Department of Cardiology, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria.
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 microm) 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.
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 mm Hg). 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.
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.
Insights
Mild hypothermia (MH) did not worsen left ventricular (LV) diastolic dysfunction after myocardial infarction in pigs. MH stabilized hemodynamics and improved oxygen supply by reducing demand.
Area of Science:
- Cardiology
- Therapeutic Hypothermia
Background:
- Mild hypothermia (MH) shows promise in reducing infarct size and mortality in experimental myocardial infarction.
- However, MH's potential to exacerbate ischemia-induced left ventricular (LV) diastolic dysfunction requires further investigation.
Purpose of the Study:
- To investigate the effects of mild hypothermia (MH) on left ventricular (LV) diastolic dysfunction following experimental myocardial infarction.
- To assess whether MH potentiates or mitigates diastolic LV failure and its impact on hemodynamic stability.
Main Methods:
- Anesthetized pigs underwent repeated left circumflex artery infusions of microspheres to induce myocardial infarction.
- Pigs were then assigned to normothermia (NT, 38.0°C) or mild hypothermia (MH, 33.0°C) for 6 hours, with hemodynamic and cardiac function parameters monitored.
Main Results:
- Both NT and MH groups experienced decreased cardiac output. MH mitigated the leftward shift of the end-diastolic pressure-volume relationship, indicating less pronounced diastolic dysfunction compared to NT.
- Mild hypothermia increased systemic vascular resistance, maintaining higher mean aortic pressure, and improved mixed venous oxygen saturation by reducing systemic oxygen demand.
Conclusions:
- Acute loss of LV end-diastolic compliance is a key factor in cardiac pump failure during myocardial infarction.
- Mild hypothermia does not potentiate diastolic LV failure; instead, it stabilizes hemodynamics and improves systemic oxygen supply/demand balance by reducing metabolic demand.
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