Coronary microembolisation induces acute and progressive diastolic heart failure

Ventricular Dysfunction & Heart Failur

DOCA/salt-induced hypertension plus high-cholesterol/high-lipid diet: A large animal model of concentric LV hypertrophy with increased LV stiffness

Cardiolog

The Induction of Mild Hypothermia Prevents Sympathetic Activation but Preserves Systemic Vascular Resistance During Endotoxemia in Pigs

Cardiac Dysfunction and Arrhythmia

The induction of mild hypothermia prevents acute pulmonary failure during endotoxemia in pigs

Cardiolog

The Induction of Mild Hypothermia Prevents Acute Respiratory Failure During Endotoxemia in Pigs

Cardiac Dysfunction and Arrhythmia

The induction of mild hypothermia improves systolic function of the resuscitated porcine heart at no further sympathetic activation

Cardiac Dysfunction and Arrhythmia

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

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.Cardiolog