Left ventricular diastolic dysfunction during acute myocardial infarction: effect of mild hypothermia
Standard
Left ventricular diastolic dysfunction during acute myocardial infarction: effect of mild hypothermia. / Schwarzl, Michael; Huber, Stefan; Maechler, Heinrich; Steendijk, Paul; Seiler, Sebastian; Truschnig-Wilders, Martie; Nestelberger, Thomas; Pieske, Burkert M; Post, Heiner.
In: RESUSCITATION, Vol. 83, No. 12, 12.2012, p. 1503-1510.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - Left ventricular diastolic dysfunction during acute myocardial infarction: effect of mild hypothermia
AU - Schwarzl, Michael
AU - Huber, Stefan
AU - Maechler, Heinrich
AU - Steendijk, Paul
AU - Seiler, Sebastian
AU - Truschnig-Wilders, Martie
AU - Nestelberger, Thomas
AU - Pieske, Burkert M
AU - Post, Heiner
N1 - Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
PY - 2012/12
Y1 - 2012/12
N2 - 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.
AB - 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.
KW - Animals
KW - Diastole
KW - Hypothermia, Induced
KW - Myocardial Infarction/complications
KW - Swine
KW - Ventricular Dysfunction, Left/etiology
U2 - 10.1016/j.resuscitation.2012.05.011
DO - 10.1016/j.resuscitation.2012.05.011
M3 - SCORING: Journal article
C2 - 22634434
VL - 83
SP - 1503
EP - 1510
JO - RESUSCITATION
JF - RESUSCITATION
SN - 0300-9572
IS - 12
ER -
