When a blocked coronary artery is suddenly reopened, the rescue itself can wound the heart in a second, quieter way — blood seeping into the muscle, destroying what was just saved. Researchers at Indiana University have found that dexrazoxane, a drug long used to shield cancer patients from chemotherapy's cardiac toll, may now serve a new purpose: administered during emergency heart attack intervention, it reduced this internal bleeding by nearly two-thirds in a phase 2 clinical trial. The finding, presented at ESC Congress 2026 in Munich and published in the European Heart Journal, arrives at
Drug trial shows dexrazoxane cuts heart bleeding by 68% in severe heart attacks
Intramyocardial hemorrhage affects approximately 40% of severe heart attack patients and increases risk of heart failure and death if untreated.
Severe injury can continue even after the artery opens
Mark
So dexrazoxane is a cancer drug. Why would it help with heart bleeding during a heart attack?
Mimi
It works by preventing cell death and reducing oxidative stress—damage from harmful molecules. In cancer patients, it protects the heart from chemotherapy toxicity. In a heart attack, the same mechanism seems to limit the damage that happens when blood flow is suddenly restored.
Luke
But this is a phase 2 trial with 50 patients total, 25 in each group. That's small. We don't know yet if this translates to fewer deaths or better long-term outcomes.
Mimi
That's exactly right. The trial shows the drug reduces bleeding and preserves heart function in the acute phase. But whether that prevents heart failure or death down the road—that's what the larger multicenter trial will test.
Mark
The 68% reduction in bleeding sounds remarkable. Is that the kind of number that usually holds up?
Luke
It's a real reduction in a measurable outcome—the amount of blood in the heart muscle on imaging. But imaging findings don't always predict clinical outcomes. A patient could have less bleeding and still have the same risk of heart failure if other mechanisms are at play.
Mimi
True. But the researchers also found a 34% reduction in infarct size—the area of dead tissue—and better ejection fraction. Those are multiple markers pointing the same direction.
Mark
Why is intramyocardial hemorrhage only now being recognized as the most serious form of heart injury?
Mimi
The imaging technology to detect and measure it precisely is relatively recent. For years, doctors could see that some heart attack patients did worse than others, but they couldn't always see why. Cardiac MRI made it visible.
Luke
And the researchers here helped define it. Dharmakumar's team identified the mechanisms in 2023 and contributed to the official definition this year. So this trial is partly validating their own framework.
Mark
Does that create a conflict of interest?
Luke
Not necessarily. But it's worth noting that the trial was single-center, run by the same group that defined the condition. A multicenter trial with independent investigators will be important for confirmation.
Mimi
The fact that they developed a scoring system to identify high-risk patients before treatment is interesting. That could help target the drug to people most likely to benefit.
Mark
When would this drug actually be given if it's approved?
Mimi
During the emergency procedure itself—the first dose right before the artery is reopened, then three more doses over the next 12 hours. It's a narrow window, but that's when the damage happens.
Le Pouls
- Roughly 40% of severe heart attack patients suffer internal bleeding into the heart muscle after emergency artery reopening — a complication that raises their risk of heart failure or death sixfold.
- Major cardiology organizations designated intramyocardial hemorrhage the most serious form of heart muscle injury just this week, signaling an urgent shift in how the field understands what happens after a blocked artery is cleared.
- The SHIELD-MI trial found that four intravenous doses of dexrazoxane — given before, during, and after the emergency procedure — cut internal heart bleeding by 68% and reduced dead tissue by 34%, with no serious side effects reported.
- Patients who received the drug also showed better preservation of the heart's pumping chamber and higher ejection fraction, suggesting the benefit extends beyond stopping bleeding to protecting overall function.
- The trial involved only 50 closely matched patients at a single center, so researchers are calling the results a promising signal rather than a conclusion — the path forward runs through larger, multicenter studies.
When a blocked coronary artery is suddenly reopened, the rescue itself can wound the heart in a second, quieter way — blood seeping into the muscle, destroying what was just saved. Researchers at Indiana University have found that dexrazoxane, a drug long used to shield cancer patients from chemotherapy's cardiac toll, may now serve a new purpose: administered during emergency heart attack intervention, it reduced this internal bleeding by nearly two-thirds in a phase 2 clinical trial. The finding, presented at ESC Congress 2026 in Munich and published in the European Heart Journal, arrives at a moment when cardiology's leading bodies have only just named intramyocardial hemorrhage the most serious form of heart muscle injury — suggesting that medicine is beginning to reckon with a harm it has long struggled to name.
Researchers at Indiana University have discovered that an existing cancer drug, given intravenously during emergency heart attack treatment, can cut internal heart bleeding by nearly two-thirds. The trial focused on STEMI patients — those suffering a severe heart attack caused by a suddenly blocked coronary artery. When that artery is reopened through emergency intervention, a dangerous secondary injury can follow: blood leaks into the heart muscle itself, triggering a cascade of destruction that kills tissue, blocks vessels, and can erase much of what the procedure worked to save.
This condition, intramyocardial hemorrhage, affects roughly 40% of STEMI patients worldwide and was just formally designated the most serious form of heart muscle injury by major cardiology organizations. Patients who experience it face a sixfold greater risk of heart failure or death. Until now, no treatment has directly targeted it.
Dexrazoxane has been FDA-approved for decades to protect cancer patients from the cardiac side effects of chemotherapy. The SHIELD-MI trial tested whether it could serve a second purpose — limiting the damage that unfolds when blood flow returns to a starved heart. Among 50 closely matched patients, those who received four intravenous doses of the drug — beginning just before the emergency procedure and continuing at four, eight, and twelve hours after — showed 68% less internal bleeding, 34% smaller areas of dead tissue, and better overall heart function compared to those who received a placebo.
Lead investigator Dr. Keyur Vora noted that reopening a blocked artery is only the first step: microvascular and hemorrhagic injury can continue damaging the heart muscle long after the procedure ends. The drug was well tolerated, with no serious adverse events reported. The research team, led by Dr. Rohan Dharmakumar, has spent years using cardiac MRI to map how this hemorrhage causes harm — work that also contributed to the Fifth Universal Definition of Myocardial Infarction released this year.
The results were presented at ESC Congress 2026 in Munich and published simultaneously in the European Heart Journal. Researchers describe the findings as a compelling early signal, not a final answer. The next step is a larger, multicenter randomized trial to determine whether reducing acute bleeding translates into fewer heart failures, fewer deaths, and better long-term quality of life for the millions who suffer severe heart attacks each year.
Researchers at Indiana University have found that an existing cancer drug, given intravenously during emergency heart attack treatment, cuts internal heart bleeding by nearly two-thirds. The finding comes from a phase 2 clinical trial of dexrazoxane in patients with STEMI—a severe form of heart attack in which a major coronary artery is suddenly blocked. When the artery is reopened through emergency intervention, a dangerous complication can follow: blood leaks into the heart muscle itself, a condition called intramyocardial hemorrhage. The trial showed that patients who received dexrazoxane before, during, and after the artery was reopened experienced a 68% reduction in this internal bleeding, along with a 34% smaller area of dead heart tissue and better overall heart function.
The stakes are substantial. Intramyocardial hemorrhage occurs in roughly 40% of STEMI patients—millions of people worldwide each year. Just this past week, major cardiology organizations jointly designated it as the most serious form of heart muscle injury, a recognition that underscores how much damage it causes. When blood cells leak into the heart muscle, they trigger a cascade of harm: the protein troponin spills out, tissue dies extensively, blood vessels become blocked, and salvaged heart muscle can be nearly or completely lost. Patients who experience this complication face a sixfold greater risk of major adverse cardiovascular events, including heart failure or death.
Dexrazoxane is not new. The FDA approved it decades ago to protect cancer patients from heart damage caused by the chemotherapy drug doxorubicin. What is new is using it for a different purpose: limiting the injury that occurs when blood flow is restored to a starved heart. The SHIELD-MI trial tested this idea in 123 STEMI patients at a single center. Fifty of them—25 receiving dexrazoxane and 25 receiving placebo—were closely matched and analyzed. The drug was given as four intravenous doses: one immediately before the emergency artery-opening procedure, then three more at four, eight, and twelve hours afterward. Cardiac imaging performed 48 to 72 hours later showed the dramatic difference.
Dr. Keyur Vora, the trial's lead investigator and director of clinical cardiovascular imaging at Indiana University's Cardiovascular Imaging Research Center, emphasized that reopening a blocked artery is only the beginning. "Severe microvascular and hemorrhagic injury can continue to damage the myocardium even after the artery has been opened," he said. The trial found that dexrazoxane was well tolerated, with no serious adverse events reported. Patients who received it showed not only less bleeding but also better preservation of the heart's main pumping chamber and higher ejection fraction—the percentage of blood the heart ejects with each beat, a key measure of function.
The research team, led by Dr. Rohan Dharmakumar, the executive director of Indiana University's Medical Imaging Research Institute, has spent years mapping how intramyocardial hemorrhage causes its damage. Using cardiac magnetic resonance imaging, they identified the mechanisms and helped define the condition as part of the Fifth Universal Definition of Myocardial Infarction released this year. They also developed a scoring system to help cardiologists identify which patients face the highest risk before treatment begins.
The trial results were presented Monday at ESC Congress 2026, the world's largest cardiology conference, held in Munich, and published simultaneously in the European Heart Journal. The findings are being framed as preliminary but encouraging—a signal that directly targeting intramyocardial hemorrhage itself could become a new treatment strategy for the most severe heart attacks. The next step is a larger, multicenter randomized trial to determine whether reducing bleeding and preserving heart muscle in the acute phase actually translates into better long-term outcomes: fewer heart failures, fewer deaths, better quality of life for the millions of people who suffer STEMI each year.
Citations marquantes
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.— Dr. Keyur Vora, lead investigator, Indiana University
Through our cardiac magnetic resonance imaging research, we now understand how microvascular injury leading to intramyocardial hemorrhage can result in a sixfold greater risk of a major adverse cardiovascular event.— Dr. Rohan Dharmakumar, executive director, IU Medical Imaging Research Institute
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