Dexrazoxane Reduces Heart Muscle Bleeding After Heart Attack: Study

Indiana University researchers have found that administering intravenous dexrazoxane before, during and after reopening a blocked coronary artery in heart attack patients reduced intramyocardial hemorrhage, a serious form of reperfusion-related heart muscle injury. The findings suggest that dexrazoxane may offer a potential cardioprotective strategy to limit myocardial damage following restoration of blood flow after acute myocardial infarction.

This promising result has potential to prevent heart failure and death for millions of people suffering severe heart attacks around the world each year.

Participants treated with dexrazoxane also demonstrated greater myocardial preservation and higher left ventricular ejection fraction — a metric that indicates how well the heart’s main chamber is pumping. Findings from the phase 2 SHIELD-MI clinical trial were presented at ESC Congress 2026, the world’s leading cardiology conference in Munich, Germany Monday, and simultaneously published in the European Heart Journal.

IMH is a life-threatening complication of a heart attack that can occur after percutaneous coronary intervention (PCI) or coronary angioplasty, a procedure for emergency reopening of the blocked coronary artery.

This past Friday at the 2026 ESC Congress, IMH was identified as the most serious form of heart muscle injury in the 5th Universal Definition of Myocardial Infarction (UDMI), in a joint statement released by the American College of Cardiology, American Heart Association, European Society of Cardiology and World Heart Federation.

IMH affects about 40% of patients with treated for STEMI, who could face an increased risk of heart failure and death.

Dexrazoxane is an FDA-approved drug used in oncology to reduce doxorubicin-associated cardiomyopathy. SHIELD-MI investigated a new cardiovascular application of dexrazoxane: limiting myocardial injury associated with reperfusion after STEMI.

Dexrazoxane prevents heart muscle death

"SHIELD-MI is the first clinical trial to show that a therapy delivered during the peri-reperfusion period can directly reduce intramyocardial hemorrhage while also limiting infarct size after STEMI," said Keyur Vora, MD, lead author, clinical investigator and CIRC’s director of Clinical Cardiovascular Imaging and Trials at IU School of Medicine. "This is important because restoring blood flow with PCI is only the first step; severe microvascular and hemorrhagic injury can continue to damage the myocardium even after the artery has been opened."

Vora said Dexrazoxane was well tolerated in the trial, with no serious adverse events, and the reductions in hemorrhagic injury and infarct size, together with preservation of left ventricular function, provide an encouraging signal that targeting intramyocardial hemorrhage itself may represent a new therapeutic strategy for patients with STEMI.

"Our goal is to take what we have learned from decades-long research of hemorrhagic myocardial infarction and apply it toward practical solutions that can reduce incidents of major adverse cardiovascular events, including heart failure or death," said senior and corresponding author Rohan Dharmakumar, PhD, executive director of the IU Medical Imaging Research Institute and vice chair for research for the Department of Radiology and Imaging Sciences at IU School of Medicine. "Through our cardiac magnetic resonance imaging research, we now understand the influence of how microvascular injury leading to intramyocardial hemorrhage can render a 6-fold greater risk of a major adverse cardiovascular event-or MACE."

Dharmakumar notes the damaging impact of red blood cells leaking into the heart muscle, including the release of the regulatory protein troponin, extensive heart tissue death, microvascular obstruction and near or complete loss of the salvaged myocardium, of which he helped identify and define in 2023 — and also this year as part of the Fifth UDMI Task Force.

The IU CIRC research team also developed a scoring system to help interventional cardiologists identify which patients might be at greatest risk for intramyocardial hemorrhage before reperfusion therapy is implemented.

About the SHIELD-MI Trial

The Phase II SHIELD-MI trial was a single-center, double-blind, placebo-controlled, sequential-cohort clinical trial in adults with STEMI undergoing primary PCI. Participants received intravenous dexrazoxane or placebo. Dexrazoxane was administered as a fixed four-dose regimen designed to target the period when reperfusion injury is developing, with the first dose given immediately before primary PCI and subsequent doses administered at four, eight and 12 hours after PCI. A total of 123 STEMI patients participated in the trial, with a final analytic cohort of 50 clinically matched for a comparison study, with 25 participants receiving Dexrazoxane and 25 receiving a placebo.

Cardiac magnetic resonance imaging (CMR) was performed 48 to 72 hours after primary PCI to assess intramyocardial hemorrhage, infarct size, microvascular injury and left ventricular function. Images were analyzed by two experienced cardiovascular magnetic resonance physicians, each with more than 10 years of CMR experience, who were blinded to treatment allocation and clinical data.

In patients receiving dexrazoxane, SHIELD MI reported a 68% reduction in intramyocardial hemorrhage burden, and a 34% reduction in infarct size and higher left ventricular ejection fraction, a measure of the heart’s pumping function. Together, these findings support further investigation in a randomized, multi-center, study of whether targeting intramyocardial hemorrhage following reperfusion can translate into improved long-term cardiovascular outcomes.

Reference:

Keyur P Vora, Kinjal Bhatt, Shrenik Doshi, Vishal Poptani, Andreas Kumar, Robert Finney, Cynthia Taub, Grant Reed, Rishi Puri, Balaji Tamarappoo, Edward Fry, Timothy Henry, Jay Traverse, Ankur Kalra, Rohan Dharmakumar, Intravenous dexrazoxane for haemorrhagic myocardial infarction: the SHIELD-MI study, European Heart Journal, 2026;, ehag715, https://doi.org/10.1093/eurheartj/ehag715