Int J Cardiovasc Imaging. 2026 Feb 4. doi: 10.1007/s10554-026-03633-9. Online ahead of print.
ABSTRACT
This study aims to investigate the impact of intravascular ultrasound (IVUS)-detected attenuated plaque (AP) on coronary microvascular dysfunction (CMVD) in patients with unstable angina undergoing percutaneous coronary intervention (PCI). The primary endpoints were the incidence of the no-reflow phenomenon, peri-procedural myocardial injury (PMI), post-procedural Thrombolysis in Myocardial Infarction (TIMI) myocardial perfusion frame count (TMPFC), and myocardial perfusion assessed by single-photon emission computed tomography (SPECT). This single-center, observational study, conducted in accordance with the STROBE guidelines, enrolled patients with unstable angina who underwent PCI with IVUS guidance. Based on IVUS findings, patients were retrospectively categorized into an AP group and a non-AP group. We compared the incidence of intraprocedural no-reflow, post-PCI cardiac biomarkers (cTnI and CK-MB), post-PCI TMPFC, and SPECT findings at baseline and 3 days post-PCI. Multivariable logistic regression analysis was performed to identify independent predictors of no-reflow, adjusting for confounders such as plaque burden. Secondary outcomes included major adverse cardiovascular and cerebrovascular events (MACCE) at 6-month follow-up. A total of 563 patients were included (229 in the AP group, 334 in the non-AP group). Baseline clinical and lesion characteristics were largely comparable, except for higher total cholesterol in the AP group (5.11 ± 0.37 vs. 4.98 ± 0.86 mmol/L, P = 0.031) and a significantly higher plaque burden in the AP group (76.8 ± 9.4% vs. 68.5 ± 10.2%, P < 0.001). The incidence of no-reflow was significantly higher in the AP group compared to the non-AP group (37.1% vs. 12.8%, P < 0.001). Post-PCI levels of cTnI (0.42 ± 0.28 vs. 0.15 ± 0.09 ng/mL) and CK-MB were significantly elevated in the AP group (P < 0.001), indicating greater peri-procedural myocardial injury. Post-PCI TMPFC was prolonged in the AP group (107.55 ± 24.19 vs. 89.86 ± 18.91 frames, P < 0.001), indicating impaired myocardial perfusion. While pre-procedural SPECT results were similar, at 3 days post-PCI, the AP group exhibited significantly greater stress ischemic segment counts, higher resting and stress perfusion total scores, and larger abnormal perfusion areas compared to the non-AP group (all P < 0.05). Multivariable analysis confirmed that the presence of AP was an independent predictor of no-reflow (OR 3.12, 95% CI 1.85-5.26, P < 0.001), independent of plaque burden. At 6-month follow-up, the incidence of MACCE was not statistically different between the two groups (8.2% vs. 6.2%, P = 0.357). In patients with unstable angina undergoing PCI, the presence of IVUS-detected attenuated plaque is strongly associated with an increased incidence of intraprocedural no-reflow, peri-procedural myocardial injury, and objective evidence of post-procedural coronary microvascular dysfunction. Although this did not translate to a significant difference in 6-month clinical outcomes in this cohort, AP serves as a critical independent imaging marker for identifying patients at higher risk for periprocedural microvascular injury.
PMID:41636976 | DOI:10.1007/s10554-026-03633-9
