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Prognostic impact of healed coronary plaque in non-culprit lesions assessed by optical coherence tomography

2020; Elsevier BV; Volume: 309; Linguagem: Inglês

10.1016/j.atherosclerosis.2020.07.005

1879-1484

Eisuke Usui, Gary S. Mintz, Tetsumin Lee, Mitsuaki Matsumura, Yiran Zhang, Masahiro Hada, Masao Yamaguchi, Masahiro Hoshino, Yoshihisa Kanaji, Tomoyo Sugiyama, Tadashi Murai, Taishi Yonetsu, Tsunekazu Kakuta, Akiko Maehara,

Acute Myocardial Infarction Research

Background and Aims We sought to investigate the characteristics and prognostic impact of healed plaque (HP) detected by optical coherence tomography (OCT) in non-culprit segments in treated vessels. Methods OCT analysis included HP having a different optical intensity with clear demarcation from underlying plaque, thin-cap fibroatheroma (TCFA), and minimal lumen area. Non-culprit lesion (NCL) was defined as a plaque with >90° arc of disease (≥0.5 mm intimal thickness), length ≥2 mm, and location >5 mm from the stent edges. Major adverse cardiac event (MACE) included cardiac death, myocardial infarction (MI), or ischemia-driven revascularization (IDR). Results We studied a total of 726 NCLs in 538 patients who underwent percutaneous coronary intervention with evaluable non-culprit segments by OCT. The prevalence of an HP was 17.8% (129/726) per lesion and 21.9% (118/538) per patient. At median follow-up of 2.2 years, there were 65 NCL-related MACE events, including 6 MIs and 65 IDRs of which 87.7% had a stable presentation. The presence of untreated HP was positively correlated with subsequent NCL-related MACE (hazard ratio [HR] 2.01, 95% confidence interval [CI], 1.20–3.37, p < 0.01). There were 16 IDRs with stable angina occurring at a specific OCT-imaged NCL where an untreated HP was positively associated with subsequent NCL-related MACE (HR 3.72, 95% CI 1.35–10.30, p = 0.01) along with TCFA (HR 10.0, 95% CI 3.20–31.40, p < 0.01) and minimal lumen area <3.5 mm2 (HR 7.42, 95% CI 2.07–26.60, p < 0.01). Conclusions An OCT-detected HP in an NCL is a marker for future (mostly) stable non-culprit-related MACE at both a patient- and lesion-level.