Late-era enrollment (2018-2022) was associated with a significantly lower risk of culprit lesion-attributed revascularization compared to 2013-2017 (sHR 0.56), while non-culprit events remained unchanged.
Observational (n=6,363)
Yes
Does contemporary treatment (2018-2022) compared to earlier treatment (2013-2017) reduce the incidence of culprit- and non-culprit lesion-attributed revascularization in patients with AMI undergoing primary PCI?
While culprit lesion-attributed revascularization after AMI has decreased in recent years, non-culprit lesion-attributed events remain relatively unchanged, highlighting residual coronary risk.
Hazard Ratio: 0.56 (95% CI 0.44–0.71)
Absolute Event Rate: 3.5% vs 6.2%
p-value: p=<0.001
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.
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 significantly lower risk of culprit lesion-attributed revascularization compared to 2013-2017 (sHR 0.56), while non-culprit events remained unchanged.