Key result
Drug-eluting stents placed for acute myocardial infarction exhibit substantially delayed vessel healing at culprit sites compared with stable lesions, potentially increasing late stent thrombosis risk.
Why the study?
Do drug eluting stents increase the risk of late stent thrombosis and mortality compared to bare metal stents in patients with acute myocardial infarction?
Do drug eluting stents increase the risk of late stent thrombosis and mortality compared to bare metal stents in patients with acute myocardial infarction?
Delayed endothelialization at plaque rupture sites provides a pathophysiologic mechanism for the potential long-term risks of late stent thrombosis with drug-eluting stents in acute myocardial infarction.
Despite the widespread use of coronary artery stenting for the treatment of ST-elevation acute myocardial infarction (STEMI), little information exists about the long-term outcomes of drug eluting stents (DES) in this setting. Although DES result in a marked reduction in the rate of restenosis, concern still exists about the long-term safety of this technology, especially with respect to late stent thrombosis (LST), a catastrophic event associated with significant morbidity and mortality. Observational studies have shown that this risk continues at a constant rate up to at least 4 years after stenting.1 Our lab has demonstrated that delayed healing (i.e. lack of complete endothelialization) is the primary pathologic substrate underlying these events and that >50% of stent struts in humans are not covered by endothelium up to 24 months after DES placement.2 Given that myocardial infarction is one of the only clinical presentations in which percutaneous coronary intervention has been shown to decrease the risk of death compared with medical therapy alone, the long-term outcomes after DES for acute myocardial infarction (AMI) is of immense clinical importance.3,4 Recent data from our laboratory in patients dying after DES placement for the treatment of AMI vs. stable angina demonstrated vessel healing at culprit sites (CSs) of plaque rupture is substantially delayed compared with CSs of stable lesions, emphasizing the importance of plaque morphology in the arterial response to DES.5 While randomized trials and observational studies of patients receiving DES for AMI have yielded inconsistent results regarding the safety of this practice, our data offer a pathophysiologic underpinning for the possibility that the benefits of opening an infarct-related artery in this setting might be outweighed by long-term risks of death and myocardial infarction associated with DES-driven LST.
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Finn et al. (2009) conducted an editorial in ST-elevation acute myocardial infarction (STEMI). Drug eluting stents vs. Bare metal stents was evaluated. Drug-eluting stents placed for acute myocardial infarction exhibit substantially delayed vessel healing at culprit sites compared with stable lesions, potentially increasing late stent thrombosis risk.
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