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

RESUSCITATION

卷:83

Article

Huber, Stefan²  Maechler, Heinrich²  Steendijk, Paul³  Truschnig-Wilders, Martie^4,5  Post, Heiner¹ 

[1] Med Univ Graz, Klin Abt Kardiol, Dept Cardiol, A-8036 Graz, Austria

[2] Med Univ Graz, Dept Cardiothorac Surg, A-8036 Graz, Austria

[3] Leiden Univ, Med Ctr, Dept Cardiol, NL-2300 RC Leiden, Netherlands

[4] Med Univ Graz, Inst Clin Med, A-8036 Graz, Austria

[5] Med Univ Graz, Chem Lab Diagnost, A-8036 Graz, Austria

关键词: Hypothermia;    No-reflow;    Myocardial infarction;    Systolic function;    Diastolic function;    Pressure-volume analysis;   

DOI  :  10.1016/j.resuscitation.2012.05.011

来源: Elsevier

【 摘 要 】

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 mu m) were infused repeatedly into the left circumflex artery until cardiac power output decreased >40%. Then, pigs were assigned to normothermia (NT, 38.0 degrees C, n = 8) or MH (33.0 degrees C, n = 8, intravascular cooling) and followed for 6 h (CME 6 h). *p < 0.05 vs baseline, dagger 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 dagger vs 54 +/- 4 mmHg). Mixed venous oxygen saturation at CME 6 h was higher in MH than in NT (59 +/- 4 dagger vs 42 perpendicular to 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. (c) 2012 Elsevier Ireland Ltd. All rights reserved.

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