Abstract 4145275: Demonstrating Pulmonary Hypertension Reversibility Before Heart Transplantation: A Novel Bedside Technique Using Postural Change

Introduction: Pre-transplant pulmonary hypertension (PH) increases the risk of post-heart transplant right ventricular failure and as a result, morbidity, and mortality. Irreversible pulmonary hypertension is a contraindication to heart-only transplantation. Invasive and non-invasive methods to show PH reversibility include temporary and durable mechanical circulatory support (MCS), pulmonary vasodilators, diuretics, and inotropes. We herein describe a novel bedside technique to show PH reversibility and discuss its potential implications. Case: A 58-year-old female with advanced nonischemic cardiomyopathy was evaluated for heart transplant. There was no history of diabetes or dysautonomia. Supine right heart catheterization showed significant PH with the following data: PA 70/37 mmHg (48 mmHg); PCWP 25 mmHg; CO 4.03 L/min; PVR 5.7 WU. Diuretic therapy and sodium nitroprusside (SNP) were started, however due to hypotension SNP was stopped, and milrinone was initiated. Incidentally, we noticed that while seated in a chair her pulmonary hemodynamics dramatically improved without additional intervention: BP 111/73 (85) mmHg; PA 36/20 (25 mmHg); CO 3.91L/min. Once back in the supine position, the PA pressures returned to baseline. The findings were reproducible (Figure). Management: The patient continued IV diuretic and milrinone. SNP was not reintroduced, and IABP unloading was avoided as we felt reassured that the postural change in PA pressure was equivalent to vasodilator associated PH reversibility and identified a favorable phenotype for transplant. The patient underwent heart transplant and did not require an RVAD, or prolonged inotrope wean. Conclusion: To our knowledge this is the first case to describe the utility and predictive value of postural reversibility in PH in heart transplant. This is a simple bedside technique that can be performed at no extra cost using gravity to change cardiac loading conditions and may be as effective as more expensive and invasive treatments. Implications include the use of lower body negative pressure (LBNP) to prevent PH while supine during sleep or in bed. LBNP decreases venous return, leading to reduced preload and afterload, and thus reduces PH and in theory may avoid the need for durable MCS to treat PH in those needing heart transplant. We encourage further studies to determine the cost-effectiveness, clinical utility, and predictability of this novel technique for both RV failure post heart transplant and post-LVAD.