Key result
Pre-infarction angina in STEMI patients was independently associated with a lower prevalence of culprit-lesion plaque rupture (OR 0.44; 95% CI 0.268-0.725; P=0.001).
Why the study?
The association between pre-infarction angina and culprit plaque characteristics assessed by optical coherence tomography in acute myocardial infarction patients remains unclear.
Does pre-infarction angina associate with different culprit-lesion morphology in patients with STEMI?
Observational (n=279)
Does pre-infarction angina associate with different culprit-lesion morphology in patients with STEMI?
Odds Ratio: 0.44 (95% CI 0.268–0.725)
Absolute Event Rate: 40.5% vs 61.9%
p-value: p=0.001
Pre-infarction angina in STEMI patients is associated with a lower incidence of plaque rupture and lipid-rich plaques, suggesting different underlying mechanisms of infarction.
PIA associated with fewer TCFA and ruptures in STEMI culprits; extends prior protection observations but leaves causal mechanisms open for prospective study.
Background Previous studies reported the cardiac protection effect of pre-infarction angina (PIA) in patients with acute myocardial infarction (AMI). However, the association between PIA and culprit plaques characteristics in AMI patients through optical coherence tomography (OCT)assessment remains unclear. Purpose We sought to identify culprit-plaque morphology associated with PIA in patients with ST-segment elevation myocardial infarction (STEMI) using OCT. Methods A total of 279 STEMI patients who underwent intravascular OCT of culprit-lesion were included. Baseline clinical data and culprit-plaque characteristics were compared between the PIA group the non-PIA group. Results Patients with PIA represented 54.8% of the study population (153 patients). No differences were observed in clinical and angiographic data between two groups, except STEMI onset with exertion was significantly less common in PIA group (24.2% versus 40.5%, P=0.004). Patients with PIA exhibited a significantly lower incidence of plaque rupture (40.5% versus 61.9%, P<0.001) and lipid-rich plaques (48.4% versus 69.0%, P=0.001). The thin-cap fibroatheroma (TCFA) prevalence was lower in PIA group, presenting a thicker fibrous cap thickness, although statistically significant differences were not observed (20.3% versus 30.2%, P=0.070; 129.1±92.0μm versus 111.4±78.1μm, P=0.088; respectively). Multivariate logistic regression analysis indicated that PIA was an independent negative predictor for plaque rupture (odds ratio: 0.44, 95% confidence interval: 0.268–0.725, P=0.001). Conclusion STEMI patients with PIA showed a significantly lower prevalence of plaque rupture and lipid-rich plaques in culprit-lesion than non-PIA group, implying different mechanisms of STEMI attack. Flow chart + Bar graphs of OCT findings Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): Association between pre-infarction angina and culprit-lesion morphology in patients with ST-segment elevation myocardial infarction: An optical coherence tomography study
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Wang et al. (2020) conducted an observational in ST-segment elevation myocardial infarction (n=279). Pre-infarction angina vs. No pre-infarction angina was evaluated on Plaque rupture (OR 0.44, 95% CI 0.268-0.725, p=0.001). Pre-infarction angina in STEMI patients was independently associated with a lower prevalence of culprit-lesion plaque rupture (OR 0.44; 95% CI 0.268-0.725; P=0.001).
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