Mitral annular dynamics are influenced by left ventricular load and contractility in an acute animal model.

The purpose of this study was to investigate the effects of loading conditions and left ventricular (LV) contractility on mitral annular dynamics. In 10 anesthetized pigs, eight piezoelectric transducers were implanted equidistantly around the mitral annulus. High-fidelity catheters measured left ventricular pressures and the slope of the end-systolic pressure-volume relationship (Ees ) determined LV contractility. Adjustments of pre- and afterload were done by constriction of the inferior caval vein and occlusion of the descending aorta. Mitral annulus area indexed to body surface area (MAAi ), annular circularity index (ACI), and non-planarity angle (NPA) were calculated by computational analysis. MAAi was more dynamic in response to loading interventions than ACI and NPA. However, MAAi maximal cyclical reduction (-Δr) and average deformational velocity (- v ¯ $$ \overline{v} $$ ) did not change accordingly (p = 0.31 and p = 0.22). Reduced Ees was associated to attenuation in MAAi -Δr and MAAi - v ¯ $$ \overline{v} $$ (r2 = 0.744; p = 0.001 and r2 = 0.467; p = 0.029). In conclusion, increased cardiac load and reduced LV contractility may cause deterioration of mitral annular dynamics, likely impairing coaptation and increasing susceptibility to valvular incompetence.

Left ventricular venting during extracorporeal membrane oxygenation; the effects on cardiac performance in a porcine model of critical post-cardiotomy failure.

INTRODUCTION: Left ventricular distension is a major concern with postcardiotomy veno-arterial extracorporeal membrane oxygenation (VA-ECMO) supporting a critical heart failure after cardiac surgery. This porcine study evaluates the effects of left ventricular venting on cardiac function during ECMO-supported circulation and after weaning from ECMO. METHODS: Twenty anaesthetised open-chest pigs were put on cardiopulmonary bypass with aortic cross-clamping and suboptimal cardioplegic arrest for 40 min. After declamping and defibrillation, the animals were supported by VA-ECMO for 180 min either with or without additional left ventricular venting. Continuous haemodynamic evaluations were performed at baseline and at cardiac arrest, during VA-ECMO and for 120 min after weaning from circulatory support. Left ventricular perfusion and function were evaluated with microspheres, pressure-volume loops and epicardial echocardiography at baseline and after 1 and 2 h with unsupported circulation. RESULTS: In vented animals both mean aortic and left ventricular peak systolic pressure increased at the end of the ECMO-supported period compared to those not vented and remained increased also after weaning. Both at 60 min and 120 min after weaning from circulatory support, left ventricular stroke work and pressure-volume area were increased in vented compared to not vented animals. At 120 min left ventricular stroke volume was increased in vented compared to not vented animals, myocardial perfusion did not differ. The left ventricular mechanical efficiency, defined as the ratio between pressure volume area and myocardial perfusion, was increased (53.2 ± 5 vs 36.2 ± 2.1 J/mL/g, p = 0.011) in vented- compared to not vented hearts. CONCLUSION: This experimental study demonstrate that left ventricular venting during post-cardiotomy veno-arterial ECMO for 3 h attenuates deterioration of left ventricular function and haemodynamics early after weaning from circulatory support.

Myocardial perfusion and cardiac dimensions during extracorporeal membrane oxygenation-supported circulation in a porcine model of critical post-cardiotomy failure.

INTRODUCTION: Venoarterial extracorporeal membrane oxygenation is widely used as mechanical circulatory support for severe heart failure. A major concern with this treatment modality is left ventricular distension due to inability to overcome the afterload created by the extracorporeal membrane oxygenation circuit. The present porcine study evaluates coronary circulation, myocardial perfusion and ventricular distension during venoarterial extracorporeal membrane oxygenation. METHODS: Ten anesthetized open-chest pigs were cannulated and put on cardiopulmonary bypass. Heart failure was achieved by 90 minutes of aortic cross-clamping with insufficient cardioplegic protection. After declamping, the animals were supported by venoarterial extracorporeal membrane oxygenation for 3 hours. Continuous haemodynamic measurements were performed at baseline, during cardiopulmonary bypass/aortic cross-clamping and during venoarterial extracorporeal membrane oxygenation. Fluorescent microsphere injections at baseline and after 1, 2 and 3 hours on venoarterial extracorporeal membrane oxygenation evaluated myocardial perfusion. Left ventricular function and distension were assessed by epicardial echocardiography. RESULTS: The myocardial injury caused by 90 minutes of ischaemia resulted in a poorly contracting myocardium, necessitating venoarterial extracorporeal membrane oxygenation in all animals. The circulatory support maintained the mean arterial blood pressure within a satisfactory range. A hyperaemic left anterior descending coronary artery flow while on extracorporeal membrane oxygenation was observed compared to baseline. Myocardial tissue perfusion measured by microspheres was low, especially in the subendocardium. Echocardiography revealed myocardial tissue oedema, a virtually empty left ventricle, and a left ventricular output that remained negligible throughout the extracorporeal membrane oxygenation run. CONCLUSION: Coronary artery blood flow is maintained during venoarterial extracorporeal membrane oxygenation after cardiopulmonary bypass and cardioplegic arrest despite severely affected performance of the left ventricle. Myocardial perfusion decreases, however, presumably due to rapid development of myocardial tissue oedema.