Abstract 16636: Superior Vena Caval Occlusion: A Novel Approach to Improve Cardiac Function in Heart Failure
Cardiac preload is a primary target of drug therapy for heart failure. No device based approaches to limit preload in heart failure exist. The inferior (IVC) and superior vena cava (SVC) provide two-thirds and one-third of venous return, respectively. We hypothesized that mechanical occlusion of the SVC improves biventricular function in heart failure by reducing ventricular preload. Methods and Results: To test this hypothesis, 4 adult swine underwent 60 minutes of left anterior descending artery occlusion followed by 60 minutes of reperfusion. 1 animal expired due to ventricular fibrillation after reperfusion. The acute hemodynamic effects of transient sequential percutaneous balloon occlusion of the SVC or IVC (n=4) were studied using conductance catheters before the onset of left ventricular (LV) injury. Transient IVC occlusion significantly reduced biventricular volumes, reduced LV stroke volume, and reduced LV peak-systolic pressure (Figure). In contrast, transient SVC occlusion reduced biventricular volumes but increased LV stroke volume, without decreasing LV peak-systolic pressure (Figure). IVC occlusion increased renal vein pressure from 10 to 24 mmHg, whereas SVC occlusion did not alter renal vein pressure. One week after LV injury, the hemodynamics of prolonged SVC occlusion were studied (n=3). Full SVC occlusion for 2 hours reduced biventricular volumes, and increased LV stroke volume, without decreasing LV peak-systolic or systemic blood pressure. Conclusions: SVC occlusion represents a novel device based approach that targets cardiac preload. In contrast to IVC occlusion, transient and prolonged full SVC occlusion was well tolerated. SVC occlusion reduces biventricular volume, while increasing cardiac output and sustaining systemic blood pressure, without adversely affecting renal hemodynamics. Future studies will test the clinical utility of continuous and intermittent SVC occlusion in acute and chronic heart failure.
Author Disclosures: N.K. Kapur: Research Grant; Modest; MD Start. V. Paruchuri: None. S. Annamalai: None. L. Buiten: None. M.A. Konstam: None. R.H. Karas: None.
- © 2015 by American Heart Association, Inc.