Coronary Plaque Phenotypes According to Physiological Disease Severity and Pullback Pressure Gradient

Background Coronary pressure pullback characterizes both the overall physiological severity and longitudinal distribution of coronary artery disease. However, the respective relationships of physiological disease severity and longitudinal disease distribution with local and vessel‐wide plaque phenotypes remain incompletely understood. Aims To investigate the relationships of physiological disease severity and longitudinal disease distribution with coronary plaque characteristics assessed by optical coherence tomography (OCT). Methods We studied 216 patients with left anterior descending coronary artery disease who underwent OCT and angiography‐based physiological assessment. Quantitative flow ratio (QFR) represented overall physiological disease severity, whereas the pullback pressure gradient (PPG) index characterized longitudinal disease distribution. Associations with local OCT characteristics and whole‐vessel burden of plaque features were assessed using regression models, with physiological indices standardized per 1 SD increase. Results Median QFR and PPG were 0.88 [0.73–0.95] and 0.76 [0.69–0.83], respectively. Lower QFR was strongly associated with greater maximum lipid arc ( β per 1 SD increase, −39.16°; 95% CI, −52.01 to −26.31; p < 0.001). PPG was not associated with maximum lipid arc in univariable analysis ( β , −9.18°; p = 0.19). After accounting for QFR, however, higher PPG was associated with greater lipid arc index ( β , 112.26 °·mm; p = 0.012) and smaller minimum lumen area ( β , −0.42 mm 2 ; p = 0.011), with a similar association observed for maximum lipid arc ( β , 16.60°; p = 0.045). Conversely, lower PPG was associated with greater whole‐vessel counts of adverse plaque features in unadjusted analyses, but these associations were attenuated after accounting for QFR. Conclusions At comparable physiological disease severity, a more focal physiological pattern was associated with greater local lipid concentration and lumen compromise, whereas a more diffuse pattern was associated with greater whole‐vessel counts of plaque features in unadjusted analyses. These findings suggest that physiological disease severity and longitudinal disease distribution provide complementary information on the spatial phenotype of coronary atherosclerosis.