Key result
OCT-detected lipid and cholesterol crystals in non-culprit lesions linked to ~3-fold higher MACE risk.
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Why the study?
Intraplaque hemorrhage contributes to plaque destabilization and is frequently co-located with cholesterol crystals, but the prevalence and impact of OCT-detected low-intensity area without attenuation plus cholesterol crystals in untreated non-culprit lesions on major adverse cardiac events were unclear.
Does the presence of OCT-detected low-intensity area without attenuation and cholesterol crystals in untreated non-culprit lesions increase the risk of subsequent MACE in patients undergoing OCT-guided PCI?
Cohort (n=566)
Does the presence of OCT-detected low-intensity area without attenuation and cholesterol crystals in untreated non-culprit lesions increase the risk of subsequent MACE in patients undergoing OCT-guided PCI?
Hazard Ratio: 3.09 (95% CI 1.27–7.5)
p-value: p=0.01
The presence of OCT-detected low-intensity area without attenuation and cholesterol crystals in untreated non-culprit lesions identifies vulnerable plaques at significantly higher risk for subsequent major adverse cardiac events.
May inform OCT-based risk stratification of non-culprit lesions; leaves open whether targeted intervention improves outcomes.
Background and aims Pathologists have shown that intraplaque hemorrhage contributes to plaque destabilization and is frequently co-located with cholesterol crystals (CC). Optical coherence tomography (OCT)-detected low-intensity area without attenuation (LIA) may represent intraplaque hemorrhage. We aimed to examine the prevalence and impact of OCT-detected LIA + CC in untreated non-culprit lesions (NCLs) on subsequent major adverse cardiac events (MACE). Methods OCT imaged NCLs in the culprit vessel in the patients who underwent OCT-guided percutaneous coronary intervention were included. An NCL was a lesion with >90° of diseased arc (≥0.5 mm intimal thickness), length ≥2 mm, and >5 mm away from stent edge. CC was defined as a thin linear region of high intensity. NCL-related MACE includes cardiac death, myocardial infarction, or ischemia-driven revascularization attributed to NCLs. Results We included 735 NCLs in 566 patients with 2.5 ± 0.7 years follow-up. The prevalence of concomitant LIA with CC (LIA + CC) was 15.5% (114/735). Three-year NCL-related MACE rate was 2.9% (20 events) at a lesion level and 15.6% (78 events) at a patient level. Untreated NCLs with LIA + CC had an increased risk for NCL-MACE (adjusted hazard ratio [HR] 3.09, 95% confidence interval [CI] 1.27–7.50, p = 0.01) along with thin-cap fibroatheroma (adjusted HR 4.38, 95% CI 1.44–13.30, p < 0.01) and minimum lumen area <3.5 mm 2 (adjusted HR 5.33, 95% CI 1.94–14.62, p < 0.01). Patients having ≥1 untreated NCL with LIA + CC had an increased risk for NCL-MACE (adjusted HR 1.95, 95% CI 1.19–3.19, p < 0.01). Conclusions An OCT-detected LIA + CC in an NCL was associated with subsequent NCL-MACE.
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Usui et al. (2021) conducted a cohort in Non-culprit lesions in patients undergoing OCT-guided percutaneous coronary intervention (n=566). OCT-detected low-intensity area without attenuation and cholesterol crystals (LIA + CC) vs. Absence of LIA + CC in non-culprit lesions was evaluated on NCL-related MACE (cardiac death, myocardial infarction, or ischemia-driven revascularization attributed to NCLs) (HR 3.09, 95% CI 1.27-7.50, p=0.01). Untreated non-culprit lesions with OCT-detected low-intensity area and cholesterol crystals had an increased risk for NCL-related MACE (HR 3.09; 95% CI 1.27-7.50; p=0.01).
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