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Aims To investigate local haemodynamics in the setting of acute coronary plaque rupture and erosion. Methods and Results Intracoronary optical coherence tomography performed in 37 patients with acute coronary syndromes caused by plaque rupture (n = 19) or plaque erosion (n = 18) was used for 3D reconstruction and computational fluid dynamic simulation. Endothelial shear stress (ESS), spatial ESS gradient (ESSG), and oscillatory shear index (OSI) were compared between plaque rupture and erosion through mixed-effects logistic regression. Lipid, calcium, macrophages, layered plaque, and cholesterol crystals were also analysed. By multivariable analysis, only high ESSG (odds ratio [OR] 5.29, 95% confidence interval [CI] 2.57-10.89, p < 0.001), lipid (OR 12.98, 95% CI 6.57-25.67 p < 0.001), and layered plaque (OR 3.17, 95% CI 1.82-5.50, p < 0.001) were independently associated with plaque rupture. High ESSG (OR 13.28, 95% CI 6.88-25.64, p < 0.001), ESS (OR 2.70, 95% CI 1.34-5.42, p = 0.005) and OSI (OR 2.18, 95% CI 1.33-3.54, p = 0.002) independently associated with plaque erosion. ESSG was higher at rupture sites than erosion sites (median (interquartile range): 5.78 (2.47, 21.15) versus 2.62 (1.44, 6.18) Pa/mm, p = 0.009), OSI was higher at erosion sites than rupture sites (1.04x10−2 (2.3x10−3, 4.74x10−2) versus 1.29x10−3 (9.39x10−5, 3.0x10−2), p < 0.001), but ESS was similar (p = 0.29). Conclusions High ESSG is independently associated with plaque rupture while high ESSG, ESS, and OSI associate with plaque erosion. While ESSG is higher at rupture sites than erosion sites, OSI is higher at erosion sites and ESS was similar. These results suggest that ESSG and OSI may play critical roles in acute plaque rupture and erosion, respectively. Translational Perspective Plaque rupture and erosion are distinct pathological and clinical entities with possibly different optimal treatments. This study demonstrates that high endothelial shear stress gradient is independently associated with site of both rupture and erosion, and is significantly higher in rupture. High oscillatory shear index is independently associated with the site of erosion only, and is higher in erosion than rupture. Larger studies are necessary to determine whether these indices may detect and distinguish plaque rupture and erosion in a clinical setting or to assess overall risk for acute coronary syndromes.

Objective: Healed plaques, signs of previous plaque destabilization, are frequently found in the coronary arteries. Healed plaques can now be diagnosed in living patients. We investigated the prevalence, angiographic, and optical coherence tomography features of healed plaques in patients with stable angina pectoris. Approach and Results: Patients with stable angina pectoris who had undergone optical coherence tomography imaging were included. Healed plaques were defined as plaques with one or more signal-rich layers of different optical density. Patients were divided into 2 groups based on layered or nonlayered phenotype at the culprit lesion. Among 163 patients, 87 (53.4%) had layered culprit plaque. Patients with layered culprit plaque had more multivessel disease (62.1% versus 44.7%, P =0.027) and more angiographically complex culprit lesions (64.4% versus 35.5%, P <0.001). Layered culprit plaques had higher prevalence of lipid plaque (83.9% versus 64.5%, P =0.004), macrophage infiltration (58.6% versus 35.5%, P =0.003), calcifications (78.2% versus 63.2%, P =0.035), and thrombus (28.7% versus 14.5%, P =0.029). Lipid index ( P =0.001) and percent area stenosis ( P =0.015) were greater in the layered group. The number of nonculprit plaques, evaluated using coronary angiograms, tended to be greater in patients with layered culprit plaque (4.2±2.5 versus 3.5±2.1, P =0.053). Nonculprit plaques in patients with layered culprit lesion had higher prevalence of layered pattern ( P =0.002) and lipid phenotype ( P =0.005). Lipid index ( P =0.013) and percent area stenosis ( P =0.002) were also greater in this group. Conclusions: In patients with stable angina pectoris, healed culprit plaques are common and have more features of vulnerability and advanced atherosclerosis both at culprit and nonculprit lesions.

Aims  Layered plaques represent signs of previous plaque destabilization. A recent study showed that acute coronary syndrome (ACS) patients with layered culprit plaque have more vulnerability at the culprit lesion and systemic inflammation. We aimed to compare the characteristics of non-culprit plaques between patients with or without layered plaque at the culprit lesion. We also evaluated the characteristics of layered non-culprit plaques, irrespective of culprit plaque phenotype. Methods and results We studied ACS patients who had undergone pre-intervention optical coherence tomography (OCT) imaging. The number of non-culprit lesions was evaluated on coronary angiogram and morphological characteristics of plaques were studied by OCT. In 349 patients, 99 (28.4%) had layered culprit plaque. The number of non-culprit plaques in patients with or without layered culprit plaque was similar (3.2 ± 0.8 and 2.8 ± 0.8, P = 0.23). Among 465 non-culprit plaques, 145 from patients with layered culprit plaque showed a higher prevalence of macrophage infiltration (71.0% vs. 60.9%, P = 0.050). When analysed irrespective of culprit plaque phenotype, layered non-culprit plaques showed higher prevalence of lipid (93.3% vs. 86.0%, P = 0.028), thin cap fibroatheroma (29.7% vs. 13.7%, P &lt; 0.001), and macrophage infiltration (82.4% vs. 54.0%, P &lt; 0.001) than non-layered plaques. Plaques with layered phenotype at both culprit and non-culprit lesions had the highest vulnerability. Conclusion  In ACS patients, those with layered phenotype at the culprit lesion demonstrated greater macrophage infiltration at the non-culprit sites. Layered plaque at the non-culprit lesions was associated with more features of plaque vulnerability, particularly when the culprit lesion also had a layered pattern.

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A 24-year-old male visited our hospital because of pain in both flanks. His biochemistry profile showed an elevated serum creatinine level and low serum uric acid level. History taking revealed that he had undertaken exercise prior to the acute kidney injury (AKI) event, and he stated that family members had a history of urolithiasis. His renal profile improved after hydration and supportive care during hospitalization. Although the patient was subsequently admitted again due to AKI, his status recovered with similar treatment. Since the diagnosis of the patient was familial renal hypouricemia with exercise-induced AKI, we performed genotyping of SLC22A12, which encodes human urate transporter 1. The diagnosis was confirmed by the detection of a homozygous mutation of W258X. We herein, report a case of familial renal hypouricemia confirmed by genotyping of SLC22A12, and review the relevant literature.