We thank Dr Hudzik for his interest in our study and the important points raised regarding non-culprit plaque rupture and thin-cap fibroatheroma (TCFA) in patients with ST-segment elevation myocardial infarction (STEMI).1 We appreciate the opportunity to respond.
In our study,2 patients with non-culprit plaque rupture had a higher incidence of non-culprit lesion-related major adverse cardiac events. As mentioned in the discussion section, this may be explained by differences in underlying mechanisms and baseline characteristics. Notably, all 35 non-culprit lesion-related events originated from lesions without plaque rupture at baseline, and multivariable analysis showed no independent association between non-culprit plaque rupture and adverse outcomes. Instead, our findings suggest that non-ruptured TCFA – not plaque rupture – is the key predictor of long-term clinical events, underscoring the importance of plaque phenotype rather than rupture status in disease progression.
We agree that optical coherence tomography (OCT)-defined TCFA is a structural surrogate, not a direct marker of biological instability. Nonetheless, OCT offers superior spatial resolution for fibrous cap measurement.3 Accumulating evidence supports the prognostic value of OCT-defined TCFA as a high-risk plaque phenotype.4
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