Troponin kinetics can be used to identify hemorrhagic MI, a dangerous condition after PCI
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Key takeaways:
- Troponin kinetics can be used to detect hemorrhagic MI after PCI for STEMI.
- Hemorrhagic MI is linked to elevated risk for in-hospital and 30-day mortality, readmission and acute heart failure.
Hemorrhagic MI is associated with poor outcomes after PCI for STEMI and can be diagnosed via troponin kinetics, not necessarily requiring cardiac MRI, researchers reported at Cardiovascular Research Technologies.
“In primary PCI after STEMI, hemorrhagic MI occurs in about 40% of patients. It is a high number,” Ankur Kalra, MD, FACP, FACC, FSCAI, interventional cardiologist at Franciscan Health, primary investigator at Krannert Cardiovascular Research Center and adjunct clinical associate professor of medicine at Indiana University School of Medicine, who presented the findings, told Healio. “It is something that the interventional community is not familiar with. It’s incredibly important because hemorrhage within the myocardium is a function of not delayed reperfusion but just of reperfusion. In a subset of patients that is not small, this transformation occurs and leads to infarct expansion. Independent of area at risk and ischemic time, there are patients who develop hemorrhagic conversion or transformation of myocardial infarction. Why exactly they go on to develop hemorrhagic conversion or transformation, we do not know. There are certainly risk factors like being a man and smoking and other established risk factors for heart disease like diabetes and high blood pressure. But we have a lot of work to do to determine why it happens in this subset.”
The standard method for diagnosing hemorrhagic MI after PCI is cardiac MRI, but that is not always feasible, Rohan Dharmakumar, PhD, Charles Fisch Endowed Chair in Cardiology, executive director of the Krannert Cardiovascular Research Center, professor of medicine, radiology and imaging sciences, anatomy, cell biology & physiology, director for cardiovascular imaging research, Indiana Institute for Biomedical Imaging Sciences, associate director for research IU Health/IUSM Cardiovascular Institute, Indiana University School of Medicine, adjunct professor of biomedical engineering at Purdue University and principal investigator of the study, told Healio.
“Patients with hemorrhagic MI can be identified within hours of PCI compared to cardiac MRI, which is only indicated 3 to 5 days after PCI, even in those who are not contraindicated, and assuming cardiac MRI is accessible,” he said. “The blood troponin-based assessment of hemorrhagic MI is a significantly cheaper and widely accessible, allowing for every STEMI patient to be characterized as hemorrhagic or non-hemorrhagic. In cases where cardiac MRI is necessary to characterize hemorrhagic MI patients further, troponin-based identification can be a ‘gatekeeper’ to cardiac MRI.”
“The understanding of post-PCI troponin levels has never been understood in terms of post-reperfusion myocardial injury, and these findings give clarity in terms of fundamental pathophysiological changes and adverse outcomes even after timely reperfusion therapy. Also, the ability to diagnose hemorrhagic MI without cardiac MRI will provide more clinical insights for appropriate STEMI care protocols,” Keyur Vora, MD, FACC, the lead clinical investigator of the study, advanced imaging cardiologist and assistant professor of medicine at Krannert Cardiovascular Research Center, told Healio.
The researchers conducted a prospective trial, MIRON-TROP, of patients who had PCI for STEMI, to determine whether troponin kinetics could predict hemorrhagic MI similar to cardiac MRI, and a retrospective analysis, MIRON-ACUTE, comparing clinical outcomes between patients who had hemorrhagic MI and those who did not.
Troponin indicates hemorrhagic MI
MIRON-TROP was conducted in a discovery cohort of 154 patients and a validation cohort of 53 patients.
“In the discovery cohort, we analyzed using cardiac MRI which patients had hemorrhagic transformation following reperfusion,” Kalra told Healio. “Then we looked at the troponin kinetics. These were troponin levels which were drawn hourly up to 12 hours, and then at 16, 18 and 24 hours, up to 72 hours. And what we found was, the troponin increase is precipitous in the first 12 hours in patients who have hemorrhagic MI.”
“The concentration of troponin surges in hemorrhagic patients within hours of PCI compared to those without hemorrhagic MI. In particular, the troponin concentration in hemorrhagic patients peaks higher (multifold) and earlier (within 6 hours compared to 16+ hours) than in non-hemorrhagic MIs,” Dharmakumar told Healio.
Hemorrhagic MI confers poor outcomes
MIRON-ACUTE included 6,180 patients who had PCI for STEMI, of whom 1,323 had hemorrhagic MI after their procedure and the rest did not.
Compared with those without it, those who had hemorrhagic MI were at elevated risk for in-hospital mortality (6.58% vs. 2.37%; adjusted OR = 2.795; P < .0001), 30-day mortality (8.54% vs. 3.11%; aOR = 2.85; P < .0001), 30-day readmission (10.05% vs. 7%; aOR = 1.481; P < .0001) and acute HF (2.65% vs. 1.03%; aOR = 2.519; P < .0001), Kalra said during the presentation.
“We need to start rethinking STEMIs, and dichotomizing them as hemorrhagic or non-hemorrhagic. With this novel troponin kinetics study using high-sensitivity troponin, you can actually diagnose hemorrhagic MI at the bedside just by doing hourly troponins post-PCI,” Kalra told Healio. “The first thing we can do is closely watch these patients ... don’t discharge them after 2 days. Maybe they need longer hospitalization to make certain that they are not getting readmitted or dying. And there is a potential therapeutic target here. Some of the mechanistic studies that our group has done have shown elegantly that the hemorrhage is occurring because of microvascular obstruction, and the vessels are bursting into the infarcted cardiomyocytes. And there is iron deposition. If we can chelate the iron deposition so a lot of the injury has been mediated by iron, then potentially we can completely abate scar formation.”
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Kalra A, et al. Late-breaking clinical science | Hot topics. Presented at: Cardiovascular Research Technologies; March 9-12, 2024; Washington, D.C.
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