Key result
Late-era treatment is linked to ~44% less culprit lesion revascularization, with non-culprit events unchanged.
Why the study?
Recurrent ischemic events after AMI can arise from culprit or non-culprit lesions, but temporal trends in culprit- and non-culprit lesion-attributed revascularization in contemporary practice remain unclear.
Does treatment in the contemporary era (2018-2022) reduce culprit and non-culprit lesion-attributed revascularization compared to the early era (2013-2017) in patients with AMI undergoing primary PCI?
Observational (n=6,363)
Yes
Does treatment in the contemporary era (2018-2022) reduce culprit and non-culprit lesion-attributed revascularization compared to the early era (2013-2017) in patients with AMI undergoing primary PCI?
While contemporary PCI practices have significantly reduced recurrent revascularizations attributed to treated culprit lesions, untreated non-culprit lesions remain a persistent source of residual ischemic risk after AMI.
Answers are grounded in this paper and cite their sources.
Supports culprit optimization in contemporary AMI practice; leaves open optimal non-culprit strategies in multivessel disease.
Background: Recurrent ischemic events after acute myocardial infarction (AMI) may arise from treated culprit lesions (CLs) or untreated non-CLs (NCLs). However, temporal trends in CL- and NCL-attributed revascularization in contemporary clinical practice remain unclear. Methods and Results: We analyzed data from the Mie ACS Registry, a multicenter registry enrolling patients with AMI who underwent primary percutaneous coronary intervention. Patients with previous coronary artery bypass grafting were excluded. The coprimary endpoints were the times to the first CL- and NCL-attributed revascularization over a 2-year follow-up period. Death was treated as a competing event. Temporal trends and predictors were evaluated using competing-risk analyses. Among 6,363 patients, 2,860 were enrolled in 2013–2017 and 3,503 were enrolled in 2018–2022. The cumulative incidence of CL-attributed revascularization was significantly lower in the later era (6.2% vs. 3.5%; P<0.001), whereas NCL-attributed revascularization showed only modest temporal improvement from 2013–2017 to 2018–2022 (6.6% vs. 5.5%, respectively; P=0.091). In multivariable analyses, late-era (2018–2022) enrollment was independently associated with a lower risk of CL-attributed revascularization (subdistribution hazard ratio [sHR] 0.56; 95% confidence interval [CI] 0.44–0.71; P<0.001), whereas multivessel disease was the strongest predictor of NCL-attributed revascularization (sHR 2.31; 95% CI 1.84–2.91; P<0.001). Conclusions: Despite temporal reductions in CL-attributed revascularization, NCL-attributed events remained relatively unchanged. NCLs continue to represent an important source of residual coronary risk after AMI.
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Takasaki et al. (2026) conducted an observational in Acute myocardial infarction (n=6,363). Late-era enrollment (2018-2022) vs. Early-era enrollment (2013-2017) was evaluated on Time to first culprit lesion-attributed revascularization over a 2-year follow-up period (sHR 0.56, 95% CI 0.44-0.71, p=<0.001). Late-era enrollment (2018-2022) was associated with a lower risk of culprit lesion-attributed revascularization compared to 2013-2017, while non-culprit events remained unchanged.
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