Abstract

Coronary plaque rupture is the most common cause of vessel thrombosis and acute coronary syndrome. The accurate early detection of plaques prone to rupture may allow prospective, preventative treatment; however, current diagnostic methods remain inadequate to detect these lesions. Established imaging features indicating vulnerability do not confer adequate specificity for symptomatic rupture. Similarly, even though experimental and computational studies have underscored the importance of endothelial shear stress in progressive atherosclerosis, the ability of shear stress to predict plaque progression remains incremental. This review examines recent advances in image-based computational modelling that have elucidated possible mechanisms of plaque progression and rupture, and potentially novel features of plaques most prone to symptomatic rupture. With further study and clinical validation, these markers and techniques may improve the specificity of future culprit plaque detection.

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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.

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 < 0.001), and macrophage infiltration (82.4% vs. 54.0%, P < 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.

Objective There are no societal ultrasound (US) guidelines detailing appropriate patient selection for deep vein thrombosis (DVT) imaging in patients with COVID-19, nor are there protocol recommendations aimed at decreasing exposure time for US technologists. We aimed to provide COVID-19-specific protocol optimization recommendations limiting US technologist exposure while optimizing patient selection. Methods A novel two-pronged algorithm was implemented to limit the DVT US studies on patients with COVID-19 prospectively, which included direct physician communication with the care team and a COVID-19-specific imaging protocol was instated to reduce US technologist exposure. To assess the pretest risk of DVT, the sensitivity and specificity of serum d -dimer in 500-unit increments from 500 to 8000 ng/mL and a receiver operating characteristic curve to assess performance of serum d -dimer in predicting DVT was generated. Rates of DVT, pulmonary embolism, and scan times were compared using t -test and Fisher's exact test (before and after implementation of the protocol). Results Direct physician communication resulted in cancellation or deferral of 72% of requested examinations in COVID-19-positive patients. A serum d -dimer of >4000 ng/mL yielded a sensitivity of 80% and a specificity of 70% (95% confidence interval, 0.54-0.86) for venous thromboembolism. Using the COVID-19-specific protocol, there was a significant (50%) decrease in the scan time ( P < .0001) in comparison with the conventional protocol. Conclusions A direct physician communication policy between imaging physician and referring physician resulted in deferral or cancellation of a majority of requested DVT US examinations. An abbreviated COVID-19-specific imaging protocol significantly decreased exposure time to the US technologist.

The haemodynamic behaviour of blood inside a coronary artery after stenting is greatly affected by individual stent features as well as complex geometrical properties of the artery including tortuosity and curvature. Regions at higher risk of restenosis, as measured by low wall shear stress (WSS < 0.5 Pa), have not yet been studied in detail in curved stented arteries. In this study, three-dimensional computational modelling and computational fluid dynamics methodologies were used to analyse the haemodynamic characteristics in curved stented arteries using several common stent models. Results in this study showed that stent strut thickness was one major factor influencing the distribution of WSS in curved arteries. Regions of low WSS were found behind struts, particularly those oriented at a large angle relative to the streamwise flow direction. These findings were similar to those obtained in studies of straight arteries. An uneven distribution of WSS at the inner and outer bends of curved arteries was observed where the WSS was lower at the inner bend. In this study, it was also shown that stents with a helical configuration generated an extra swirling component of the flow based on the helical direction; however, this extra swirl in the flow field did not cause significant changes on the distribution of WSS under the current setup.

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.