Obstructive non-culprit lesions increased MACE risk (17.7% vs 12.8%; HR 1.39, 95% CI 1.02-1.91), but underlying thin-cap fibroatheroma was the independent predictor of recurrent MACEs.
Cohort (n=1,312)
Does the presence of angiographic obstructive non-culprit lesions or underlying high-risk morphology (TCFA) predict recurrent MACEs in patients with acute myocardial infarction?
In patients with acute myocardial infarction, the long-term prognostic risk of non-culprit lesions is driven by underlying high-risk morphology (TCFA) rather than angiographic stenosis severity.
Hazard Ratio: 1.39 (95% CI 1.02–1.91)
Absolute Event Rate: 17.7% vs 12.8%
BACKGROUND: Patients with acute myocardial infarction and angiographically obstructive non-culprit lesions are at high risk for recurrent major adverse cardiac events (MACEs). However, it remains largely unknown whether events are due to stenosis severity or due to the underlying high-risk lesion morphology. METHODS: Between January 2017 and December 2021, 1312 patients with acute myocardial infarction underwent optical coherence tomography of all the 3 main epicardial arteries after successful percutaneous coronary intervention. Patients and lesions were categorized according to the presence or absence of (1) 1 or more non-culprit angiographic obstructive stenoses with a visual diameter stenosis of ≥50% and (2) 1 or more lesions with an underlying high-risk morphology defined as an optical coherence tomography thin-cap fibroatheroma (TCFA). Patients were followed for up to 5 years (median 4.1 interquartile range: 3.0-5.0 years). MACEs comprised cardiac death, non-fatal myocardial infarction, and unplanned coronary revascularization. RESULTS: Overall, 492 patients had at least 1 obstructive non-culprit lesion, 352 had a single lesion, and 140 had multiple obstructive non-culprit lesions. The presence and number of angiographic obstructive non-culprit lesions correlated with the proportion and number of optical coherence tomography-derived TCFAs. At the lesion level, the prevalence of TCFA was twice as high in obstructive lesions compared with nonobstructive lesions. Patients with obstructive non-culprit lesions had an increased risk of overall MACEs (17.7% versus 12.8%; hazard ratio, 1.39 95% CI, 1.02-1.91) and non-culprit lesion-related MACEs (8.7% versus 3.9%; HR, 2.13 [95% CI, 1.26-3.59). Results were similar when patients were categorized on the basis of the underlying TCFA. A proportionally higher rate of overall and non-culprit lesion-related MACEs was observed as the number of obstructive stenoses or TCFAs in non-culprit segments increased. The lesion-specific HRs for obstructive lesion and TCFA were 2.03 (95% CI, 1.06-3.89) and 2.39 (95% CI, 1.29-4.43), respectively. Optical coherence tomography-derived TCFA, but not angiographic obstructive stenosis, was independently predictive of recurrent MACEs in both patient-level and lesion-level multivariable models in which these 2 characteristics were introduced simultaneously. CONCLUSIONS: The long-term prognostic implications of the presence and extent of angiographic obstructive non-culprit lesions in patients with acute myocardial infarction are primarily due to their correlation with the underlying high-risk morphology, which confers an increased risk of recurrent MACEs.
Dai et al. (Fri,) conducted a cohort in Acute myocardial infarction (n=1,312). Obstructive non-culprit lesions vs. Absence of obstructive non-culprit lesions was evaluated on Overall MACEs (cardiac death, non-fatal myocardial infarction, and unplanned coronary revascularization) (HR 1.39, 95% CI 1.02-1.91). Obstructive non-culprit lesions increased MACE risk (17.7% vs 12.8%; HR 1.39, 95% CI 1.02-1.91), but underlying thin-cap fibroatheroma was the independent predictor of recurrent MACEs.