Post PCI hemorrhage Compromises Myocardial Salvage In MI and increases HF risk: JACC study
Incident heart failure following acute myocardial infarction (MI) is a preventable therapeutic target. Primary percutaneous coronary intervention (PCI) for acute ST-segment elevation myocardial infarction (STEMI) routinely achieves normal antegrade coronary artery blood flow in >90% of cases; yet, imaging evidence shows failed myocardial reperfusion, manifesting as microvascular obstruction and myocardial haemorrhage, in approximately 50% and 40%, respectively.
A recent study suggests that cardiac injury from myocardial infarction is not only the result of ischemia from a clogged artery but also the result of myocardial bleeding post-reperfusion. The study findings were published in the Journal of the American College of Cardiology on January 03, 2022.
Microvascular obstruction (MVO) is independently associated with an increased likelihood of death and heart failure, independent of the size of infarction. Reperfusion therapy for acute MI is lifesaving. However, the benefit of reperfusion therapy can be paradoxically diminished by reperfusion injury, which can increase MI size. To further examine, Dr Rohan Dharmakumar and his team conducted a study and evaluated whether haemorrhage plays a role in reperfusion-mediated MI expansion.
The researchers assessed the cardiac troponin kinetics in 70 patients treated by primary PCI for acute STEMI, and 70% had evidence of myocardial haemorrhage by cardiac magnetic resonance imaging (CMR)criteria. To isolate the effects of haemorrhage from the ischemic burden, they performed controlled canine studies (n = 25) and serially followed both cTn and MI size with time-lapse imaging.
Key findings of the study:
- Upon analysis, the researchers observed a difference in cTn before reperfusion; however, they found that troponin following primary PCI peaked earlier (12 hours vs 24 hours) and was higher in patients with haemorrhage.
- In hemorrhagic animal models, they found that reperfusion led to the rapid expansion of myocardial necrosis culminating in epicardial involvement, which was not present in nonhemorrhagic cases.
- They observed no difference in MI size and repair at 1-hour postreperfusion in animals with and without haemorrhage. However, within 72 hours of reperfusion, they noted a 4-fold greater loss in salvageable myocardium in hemorrhagic MIs.
- They noted this paralleled observations in patients with larger MIs occurring in hemorrhagic cases.
The authors concluded, "Myocardial haemorrhage is a determinant of MI size. It drives MI expansion after reperfusion and compromises myocardial salvage. This introduces a clinical role of haemorrhage in acute care management, risk assessment, and future therapeutics."
In the modern era of revascularization, this study asserts infarct size is not only determined by the restricted blood supply to the heart, but also by the effects of reperfusion therapy.
In an accompanying editorial, Dr Colin Berry and Dr Borja Ibáñez wrote, "We applaud the investigators for providing new, mechanistic insights into a difficult clinical problem that has an unmet therapeutic need. Only through mechanistic studies that are transferable to the clinic can therapeutic targets be identified…Further, future research should assess the validity of T2∗ for accurate sizing of intramyocardial haemorrhage, including at different time points, because T2∗ decay is influenced by the breakdown products of haemoglobin which evolve over time."
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