ECPR After Prolonged Cardiac Arrest: Targeting Mechanisms of the No-Reflow
Investigating mechanisms of “no-reflow” to improve outcomes of ECPR after prolonged cardiac arrest.
Project at a Glance
Product Type:
Therapeutic
Project Start Date:
June 1, 2017
Principal Investigators:
Robert Neumar, MD Robert Bartlett, MD
Solution Sheet:
Download Solution Sheet (PDF)
Funding History:
$3,067,247 in non-dilutive funding • 2017 $3,067,247 NIH • Substantial departmental, school and center based support
Overview
Dr. Neumar and Bartlett’s team hypothesizes that intravascular complications of total body ischemia and reperfusion, including microvascular coagulation, leukocyte adhesion, and neutrophil extracellular trap (NET) formation cause no-reflow and prevent recovery of heart and brain function when ECPR is used to treat prolonged cardiac arrest.
The team expects to identify effective strategies for treating the microvascular pathology of prolonged total body ischemia and reperfusion, with the longterm goal of improving the survival and neurologic outcomes of patients with sudden cardiac arrest that is refractory to standard care.
Image credit: ShutterStock
Significant Need
The “no-reflow phenomenon,” defined as inadequate vital organ reperfusion despite the restoration of normal cardiac output, is a fundamental barrier to the success of extracorporeal cardiopulmonary resuscitation (ECPR) after prolonged cardiac arrest. A University of Michigan research team led by Drs. Robert Neumar and Robert Bartlett aims to delineate the mechanistic barriers to recovery of cardiac and neurologic function with ECPR after prolonged total body ischemia nd reperfusion, as well as to develop therapeutic strategies to overcome these barriers.
Competitive Advantage
• Will improve survival and neurologic outcomes of patients with sudden cardiac arrest that is refractory to standard care • Will address a critical barrier to the efficacy of ECPR for refractory cardiac arrest, with the potential to save thousands of lives in the U.S. each year • Will generate new fundamental knowledge about the pathophysiology of prolonged total body ischemia and reperfusion and will potentially bring new technologies to the bedside • Will inform future prospective randomized clinical trials aimed at optimizing ECPR for refractory cardiac arrest
Funding Organization(s)
Publications
None at this time