Hemodynamic Effects of Mechanical Circulatory Support Devices in Ventricular Septal Defect

Author:

Pahuja Mohit1,Schrage Benedikt2,Westermann Dirk2,Basir Mir B.3,Garan Arthur Reshad4,Burkhoff Daniel45

Affiliation:

1. Division of Cardiology, Department of Internal Medicine, Detroit Medical Center/Wayne State University Medical School of Medicine, Detroit, MI (M.P.).

2. Department of Cardiology, University Heart Centre Hamburg Eppendorf, Hamburg, Germany (B.S., D.W.).

3. Division of Cardiology, Department of Medicine, Henry Ford Health System, Detroit, MI (M.B.B.).

4. Division of Cardiology, Department of Medicine, Columbia University Medical Center, New York, NY (A.R.G., D.B.).

5. Cardiovascular Research Foundation, New York, NY (D.B.).

Abstract

Background: Ventricular septal defect (VSD) is a lethal complication of acute myocardial infarction (AMI) and is often associated with cardiogenic shock. The optimal form of percutaneous mechanical circulatory support (MCS) for AMI-VSD is unknown. Methods and Results: We used a previously validated cardiovascular model to simulate AMI-VSD with parameters adjusted to replicate average hemodynamics reported in the literature, including a pulmonary-to-systemic blood flow ratio of 3.0. We then predicted effects of different types of percutaneous MCS (including intra-aortic balloon pumping, Impella, TandemHeart, and extracorporeal membrane oxygenation) on pressures and flows throughout the cardiovascular system. The simulation replicated all major hemodynamic parameters reported in the literature with AMI-VSD. Inotropes and vasopressors worsened left-to-right shunting, whereas vasodilators decreased shunting at the expense of worsening hypotension. All MCS devices increased forward blood flow and arterial pressure but other effects varied among devices. Impella 5.0 provided the greatest degree of pulmonary capillary wedge pressure reductions and decreased left-to-right shunting. Extracorporeal membrane oxygenation worsened pulmonary capillary wedge pressure and shunting, which could be improved by adding Impella or passive left ventricular vent. Pulmonary-to-systemic blood flow ratio could not be reduced below 2.0, and pulmonary flows remained high with all forms of MCS. Conclusions: Although no form of percutaneous MCS normalized hemodynamics in AMI-VSD, pulmonary capillary wedge pressure and shunting were worsened by extracorporeal membrane oxygenation and improved by Impella. Accordingly, based on hemodynamics alone, Impella provides the optimal form of support in AMI-VSD. However, other factors, including team experience, device availability, potential for tissue ingestion, and clinical characteristics, need to be considered when choosing a percutaneous MCS device for AMI-VSD.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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