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with lipid-rich or vulnerable plaque characteristics, including in non-flow-limiting non-culprit lesions of patients with MI. 3,4 Conversely, from a prognostic standpoint, lower PPG or diffuse disease patterns have also been associated with adverse vessel-related outcomes after PCI. 5 Thus, plaque vulnerability and clinical prognosis may represent related but distinct aspects of coronary disease.Our original discussion was intended to raise the hypothesis that a lower QFR-PPG phenotype may reflect a broader disease burden in AMI non-IRA lesions, rather than to establish a direct mechanistic link between low QFR-PPG and vulnerable plaque morphology.Further studies integrating coronary physiology with systematic intravascular imaging are needed to clarify the underlying plaque phenotype.Taken together, we agree that QFR-PPG <0.78 should be interpreted as a data-derived prognostic threshold rather than as a definitive biological definition of diffuse disease or plaque vulnerability.At the same time, the additional analyses demonstrate that QFR-PPG provides prognostic information not fully captured by QFR within the nonischemic range, particularly when combined with relatively lower QFR values.We therefore believe that the QFR/ QFR-PPG phenotype is best interpreted as a prognostic physiological risk-stratification tool for deferred, functionally insignificant intermediate non-IRA lesions after AMI.
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Nakao et al. (2026) studied this question.
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