Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Schwarzl, M; Huber, S; Maechler, H; Steendijk, P; Seiler, S; Truschnig-Wilders, M; Nestelberger, T; Pieske, BM; Post, H.
Left ventricular diastolic dysfunction during acute myocardial infarction: effect of mild hypothermia.
Resuscitation. 2012; 83(12):1503-10
Doi: 10.1016/j.resuscitation.2012.05.011
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- Führende Autor*innen der Med Uni Graz
- Post Heiner
- Schwarzl Michael
- Co-Autor*innen der Med Uni Graz
- Huber Stefan
- Mächler Heinrich
- Nestelberger Thomas
- Pieske Burkert Mathias
- Truschnig-Wilders Martini
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- Abstract:
- 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 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.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals - administration & dosage
- Diastole - administration & dosage
- Hypothermia, Induced - administration & dosage
- Myocardial Infarction - complications, therapy
- Swine - administration & dosage
- Ventricular Dysfunction, Left - etiology
- Find related publications in this database (Keywords)
- Hypothermia
- No-reflow
- Myocardial infarction
- Systolic function
- Diastolic function
- Pressure-volume analysis