OBJECTIVES: Aortic valve regurgitation, fusion and thrombosis are commonly reported clinical complications after continuous flow ventricular assist device implantations; however, the complex interaction between reduced pulsatile flow physiology and aortic valve functions has not been studied experimentally. To address this, a continuous flow left ventricular assist device was implanted in four swine ex vivo beating hearts and then operated at baseline (device off, no flow) and at device speeds ranging between 8500 and 11,500 rpm under healthy and experimentally created failing heart conditions. METHODS: At baseline and after each speed increase, aortic, left ventricular, left atrial and pulse pressure signals were monitored to assess the haemodynamic status of the ex vivo heart, aortic valve opening time and the transvalvular pressure changes. Aortic root and device flows were recorded with flow probes. Left ventricular pressure-volume loops were measured with a conductance catheter. Changes in aortic leaflet motion and end-diastolic aortic root diameter were recorded with epicardial echocardiography. RESULTS: A two-chamber healthy and failing ex vivo beating heart model was successfully created. At increasing device flows, aortic valve open time steadily decreased from 36±7% of the baseline cardiac cycle to 0% at 11,500 rpm in the healthy heart and from 18±16 to 0% in failing heart mode (P<0.05). Aortic transvalvular pressure increased from 25±5 mmHg (baseline) to 67±7 mmHg (11,500 rpm) in the healthy heart and from 10±9 mmHg (baseline) to 73±8 mmHg (11,500 rpm) in failing heart mode (P<0.05). Aortic root diameters were significantly increased at speeds exceeding 10 500 rpm in the healthy heart mode (P<0.05 vs baseline) and approached statistical significance in failing hearts. CONCLUSIONS: Increasing assist device flows resulted in pressure overload above the aortic leaflets, impaired leaflet functions, caused aortic root dilatation and altered leaflet coaptation at the central portion of the aortic valve in both modes. We conclude that the deleterious effect of the reduced pulsatile flow on the aortic valve functions and haemodynamics is immediate and such an insult may explain the structural changes of the aortic valve causing leaflet fusion and/or regurgitation in the chronic phase.
OBJECTIVES: Aortic valve regurgitation, fusion and thrombosis are commonly reported clinical complications after continuous flow ventricular assist device implantations; however, the complex interaction between reduced pulsatile flow physiology and aortic valve functions has not been studied experimentally. To address this, a continuous flow left ventricular assist device was implanted in four swine ex vivo beating hearts and then operated at baseline (device off, no flow) and at device speeds ranging between 8500 and 11,500 rpm under healthy and experimentally created failing heart conditions. METHODS: At baseline and after each speed increase, aortic, left ventricular, left atrial and pulse pressure signals were monitored to assess the haemodynamic status of the ex vivo heart, aortic valve opening time and the transvalvular pressure changes. Aortic root and device flows were recorded with flow probes. Left ventricular pressure-volume loops were measured with a conductance catheter. Changes in aortic leaflet motion and end-diastolic aortic root diameter were recorded with epicardial echocardiography. RESULTS: A two-chamber healthy and failing ex vivo beating heart model was successfully created. At increasing device flows, aortic valve open time steadily decreased from 36±7% of the baseline cardiac cycle to 0% at 11,500 rpm in the healthy heart and from 18±16 to 0% in failing heart mode (P<0.05). Aortic transvalvular pressure increased from 25±5 mmHg (baseline) to 67±7 mmHg (11,500 rpm) in the healthy heart and from 10±9 mmHg (baseline) to 73±8 mmHg (11,500 rpm) in failing heart mode (P<0.05). Aortic root diameters were significantly increased at speeds exceeding 10 500 rpm in the healthy heart mode (P<0.05 vs baseline) and approached statistical significance in failing hearts. CONCLUSIONS: Increasing assist device flows resulted in pressure overload above the aortic leaflets, impaired leaflet functions, caused aortic root dilatation and altered leaflet coaptation at the central portion of the aortic valve in both modes. We conclude that the deleterious effect of the reduced pulsatile flow on the aortic valve functions and haemodynamics is immediate and such an insult may explain the structural changes of the aortic valve causing leaflet fusion and/or regurgitation in the chronic phase.
Entities:
Keywords:
Aortic valve; Cardiac assist device; Continuous flow; Ex vivo beating heart; Leaflet functions