OCT identified vessel wall abnormalities like fibrocalcific plaques and thrombi in 85% of coronary artery lesions in adults 22 years post-Kawasaki disease.
Does optical coherence tomography identify coronary vessel wall abnormalities in adults long after Kawasaki disease with severe coronary involvement?
OCT identifies significant subclinical coronary vessel wall abnormalities, including vulnerable plaques and thrombi, in adults decades after severe Kawasaki disease, highlighting the need for optimized long-term monitoring.
Absolute Event Rate: 0% vs 0%
Background Children with a history of Kawasaki disease (KD) and severe coronary involvement are at risk for acute coronary syndrome later in adulthood even in the absence of severe luminal lesions. We therefore investigated whether the coronary vessel walls in such adults are accompanied by potential substrates for acute coronary syndrome using optical coherence tomography (OCT), a high-resolution imaging modality. Methods OCT was performed in patients who were followed up by serial coronary angiogram (CAG) and cardiac multi-detector computed tomography (MDCT) for ≥ 15 years after the diagnosis of acute KD with coronary artery aneurysms (≥ 6 mm in diameter). Results Eleven patients (6 males, 55%) with median age 25.3 years (IQR: 22.7–30.3) and median interval 22.6 years (19.9–25.8) after acute KD were recruited. We investigated 51 coronary segments, comprising 43 coronary artery lesions (CALs) (19 regressed aneurysms, 37.2%; 16 persistent aneurysms, 31.4%; and 8 localized stenoses, 15.7%) and 8 normal segments (15.7%). OCT findings revealed fibrocalcific plaque in 20 segments (39.2%), fibroatheroma in 16 (31.4%), superficial signal-rich regions with attenuation in 14 (27.5%), microvessels in 18 (35.3%), luminal thrombi in 13 (25.5%), and ruptured plaque in 4 (7.8%). Qualitatively, all but one normal segment showed no OCT-derived abnormalities, whereas CALs, including regressed aneurysms, exhibited fibrocalcific plaques, fibroatheroma, and microvessels, along with luminal thrombi and ruptured plaques. Quantitatively, CAG-derived advanced lesions (persistent aneurysms and localized stenoses) and MDCT-derived calcified plaques were associated with OCT-detected vessel wall abnormalities. Conclusions The present study showed that CALs in adults long after acute KD with severe coronary involvement are associated with OCT-derived vessel wall abnormalities, which are correlated with luminal lesions and MDCT-detected calcified plaques. Although these results do not demonstrate causality and may not be generalizable to milder cases, they warrant further studies to optimize screening and monitoring of adult KD-related coronary sequelae.
Ohashi et al. (Wed,) reported a other. OCT identified vessel wall abnormalities like fibrocalcific plaques and thrombi in 85% of coronary artery lesions in adults 22 years post-Kawasaki disease.