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A Pre-Clinical Porcine Model of Orthotopic Heart Transplantation
Published on: April 27, 2019
Left Ventricular Physiology and Ventricular-Vascular Interactions in Young Patients After Heart Transplantation
Heiner Latus1,2, Ramona Raap1, Karin Klingel3
1Pediatric Heart Centre, Centre for Congenital Heart Disease Giessen Germany.
Insights
Heart transplant recipients exhibit impaired ventriculo-arterial coupling, with increased arterial elastance (Ea) negatively impacting graft function. This highlights vascular dysfunction as a key factor in late graft failure.
Area of Science:
- Cardiovascular Physiology
- Transplantation Medicine
- Vascular Biology
Background:
- Systemic arterial hypertension and aortic stiffness increase ventricular afterload in heart transplant recipients, potentially causing graft dysfunction.
- Understanding ventriculo-arterial coupling is crucial for assessing cardiovascular health post-transplantation.
Purpose of the Study:
- To characterize systemic arterial elastance (Ea) and its impact on left ventricular function and ventriculo-arterial coupling in pediatric and young adult heart transplant survivors.
- To evaluate these parameters using invasive conductance catheter technique.
Main Methods:
- Invasive cardiac catheterization and pressure-volume loop analysis were performed on 30 heart transplant recipients.
- Load-independent parameters including ventricular elastance (Ees) and ventricular compliance were assessed at rest and during dobutamine infusion.
- Systemic arterial elastance (Ea) and ventriculo-arterial coupling (Ea/Ees) were calculated.
Main Results:
- Ventricular elastance (Ees) increased appropriately with dobutamine, but ventricular compliance remained unchanged.
- Ventriculo-arterial coupling (Ea/Ees) was abnormal at rest and did not improve with dobutamine due to a significant rise in systemic arterial elastance (Ea).
- Both Ees and ventricular compliance were significantly associated with Ea.
Conclusions:
- Heart transplant recipients demonstrate impaired ventriculo-arterial coupling, even with preserved left ventricular contractile reserve.
- Increased afterload, driven by abnormal vascular function, is a significant factor contributing to late graft failure.
- Monitoring vascular elastance and coupling is essential for managing long-term outcomes in heart transplant patients.
Abstract:
Background In patients after heart transplantation, systemic arterial hypertension and enhanced central aortic stiffness contribute to increased ventricular afterload, which might lead to graft dysfunction. The aim of our study was to characterize systemic arterial elastance and its impact on left ventricular function and ventriculo-arterial coupling in a cohort of children, adolescents, and young adults after heart transplantation using invasive conductance catheter technique. Methods and Results Thirty patients who had heart transplants (age, 20.0±6.5 years, 7 female) underwent invasive cardiac catheterization including pressure-volume loop analysis. Load-independent parameters of systolic (ventricular elastance [Ees]) and diastolic (ventricular compliance) function as well as systemic arterial elastance (Ea, end-systolic pressure/stroke volume) and ventriculo-arterial coupling (Ea/Ees) were assessed at baseline level and during dobutamine infusion (10 μg/kg/min). Ees showed an appropriate increase under inotropic stimulation from 0.43 (0.11-2.52) to 1.00 (0.20-5.10) mm Hg/mL/m2 (P<0.0001), whereas ventricular compliance remained rather unchanged (0.16±0.10 mm Hg/mL/m2 to 0.12±0.07 mm Hg/mL/m2; P=0.10). Ventriculo-arterial coupling Ea/Ees was abnormal at rest and did not improve significantly under dobutamine (1.7 [0.6-6.7] to 1.3 [0.5-4.9], P=0.70) due to a simultaneous rise in Ea from 0.71 (0.37-2.82) to 1.10 (0.52-4.03) mm Hg/mL/m2 (P<0.0001). Both Ees and ventricular compliance were significantly associated with Ea at baseline and under dobutamine infusion. Conclusions Patients who underwent heart transplantation show impaired ventriculo-arterial coupling at rest and under inotropic stimulation despite preserved left ventricular contractile reserve. An abnormal response in vascular function resulting in increased afterload seems to represent an important factor that may play a role for the development of late graft failure.
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