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The development of optical coherence tomography (OCT) has revolutionized our understanding of coronary artery disease. In vivo OCT research has paralleled with advances in computational fluid dynamics, providing additional insights in the various hemodynamic factors influencing plaque growth and stability. Recent OCT studies introduced a new concept of plaque healing in relation to clinical presentation. In addition to known mechanisms of acute coronary syndromes such as plaque rupture and plaque erosion, a new classification of calcified plaque was recently reported. This review will focus on important new insights that OCT has provided in recent years into coronary plaque development, progression, and destabilization, with a focus on the role of local hemodynamics and endothelial shear stress, the layered plaque (signature of previous subclinical plaque destabilization and healing), and the calcified culprit plaque.

Background Previous pathology studies demonstrated that thin-cap fibroatheroma (TCFA) is localized in specific segments of the epicardial coronary arteries. A detailed description of in vivo coronary plaques of various phenotypes has not been reported. Objectives We performed a comprehensive analysis on the distribution of coronary plaques with different phenotypes from our 3-vessel optical coherence tomography (OCT) database. Methods OCT images of all 3 coronary arteries in 131 patients were analyzed every 1 mm to assess plaque phenotype and features of vulnerability. In addition, plaques were divided into tertiles according to percent area stenosis (%AS). Results Among 534 plaques identified in 393 coronary arteries, 27.0% were fibrous plaques, 13.3% fibrocalcific plaques, 40.8% thick-cap fibroatheromas, and 18.9% thin-cap fibroatheromas (TCFA). TCFAs showed clustering in the proximal segment, particularly in the left anterior descending (LAD) artery. On the other hand, fibrous plaques were relatively evenly distributed throughout the entire length of the coronary arteries. In patients with acute coronary syndromes (ACS), TCFAs showed stronger proximal clustering in the LAD, two clustering peaks in the right coronary artery, and one clustering peak in the circumflex artery. The pattern of TCFA distribution was less obvious in non-ACS patients. The prevalence of TCFA was higher in the highest %AS tertile, compared to the lowest %AS tertile (30% vs. 9%, p Conclusions The present 3-vessel OCT study demonstrated that TCFAs cluster at specific locations in the epicardial coronary arteries, especially in ACS patients. TCFA was more prevalent in segments with tight stenosis.

Ethnic differences in the pathobiology of acute coronary syndromes (ACS) have not been systematically studied. We compared the underlying mechanisms of ACS between Asians and Whites. ACS patients with the culprit lesion imaged by optical coherence tomography were included. Patients were stratified into ST-elevation myocardial infarction (STEMI) and non-ST-elevation-ACS (NSTE-ACS), and baseline characteristics, underlying mechanisms of ACS, and culprit plaque characteristics were compared between Asians and Whites. Of 1,225 patients, 1,019 were Asian (567 STEMI and 452 NSTE-ACS) and 206 were White (71 STEMI and 135 NSTE-ACS). Asians had more diabetes and hypertension among STEMI patients; among NSTE-ACS patients, Asians had higher prevalence of diabetes and renal insufficiency, and lower prevalence of hyperlipidemia. There were no differences in the incidence of plaque rupture, plaque erosion and calcified plaque between Asians and Whites with STEMI (61.2%, 28.6%, 10.2% vs 46.5%, 38.0%, 15.5%, respectively, p = 0.055). Among NSTE-ACS patients, there was a significant difference between Asians and Whites (40.5%, 47.6%, 11.9% vs 27.4%, 48.9%, 23.7%, respectively, p = 0.001). After adjustment for clinical confounders, the risk of plaque rupture (p = 0.713), plaque erosion (p = 0.636), and calcified plaque (p = 0.986) was similar between the groups with STEMI. In NSTE-ACS patients, the only difference was an increased risk of calcified plaque in Whites (odds ratio: 2.125, 95% confidence interval: 1.213 to 3.723, p = 0.008). In conclusion, after adjustment for clinical confounders, Asian and White patients presenting with STEMI and NSTE-ACS showed similar underlying mechanisms of ACS, except for a higher risk of calcified plaque in Whites with NSTE-ACS.

Objective Coronavirus disease 2019 (COVID-19) is associated with abnormal inflammatory and coagulation markers, potentially mediating thrombotic events. Our objective was to investigate the incidence, time course, laboratory features, and in-hospital outcomes of COVID-19 patients with suspected venous thromboembolism (VTE). Methods A retrospective observational cohort study was conducted of patients hospitalized with COVID-19 who had undergone ultrasound imaging for suspected VTE from March 13 to May 18, 2020. The medical records of the included patients were reviewed for D-dimer, fibrinogen, prothrombin time, partial thromboplastin time, platelet count, C-reactive protein (CRP), and high-sensitivity troponin T at admission and at up to seven time points before and after ultrasound examination. The clinical outcomes included superficial venous thrombosis, deep vein thrombosis, pulmonary embolism, intubation, and death. Mixed effects logistic, linear, and Cox proportional hazards methods were used to evaluate the relationships between the laboratory markers and VTE and other in-hospital outcomes. Results Of 138 patients who had undergone imaging studies, 44 (31.9%) had evidence of VTE. On univariable analysis, an elevated admission CRP (odds ratio [OR], 1.05; 95% confidence interval [CI], 1.01-1.09; P = .02; per 10-U increase in CRP), platelet count (OR, 1.48; 95% CI, 1.04-2.12; P = .03; per 1000-U increase in platelet count), and male sex (OR, 2.64; 95% CI, 1.19-5.84; P = .02), were associated with VTE. However only male sex remained significant on multivariable analysis (OR, 2.37; 95% CI, 1.01-5.56; P = .048). The independent predictors of death included older age (hazard ratio [HR], 1.04; 95% CI, 1.00-1.07; P = .04), active malignancy (HR, 4.39; 95% CI, 1.39-13.91; P = .01), elevated admission D-dimer (HR, 1.016; 95% CI, 1.003-1.029; P = .02), and evidence of disseminated intravascular coagulation (HR, 4.81; 95% CI, 1.76-13.10; P = .002). Conclusions Male sex, elevated CRP, and elevated platelet count at admission were associated with VTE on univariable analysis. However, only male sex remained significant on multivariable analysis. Older age, active malignancy, disseminated intravascular coagulation, and elevated D-dimer at admission were independently associated with death for patients hospitalized with COVID-19.

Postmortem studies reported plaque erosion is frequent in young women. Recent in vivo studies failed to show age and sex differences in the plaque erosion prevalence. The aim of this study was to investigate the prevalence of plaque erosion by age and sex among acute coronary syndromes (ACS) patients. From 1699 ACS patients, 1083 with plaque erosion or rupture were analyzed. Patients were categorized as 5 age groups (≤ 50, 51-60, 61-70, 71-80, ≥ 81 years). Overall prevalence of plaque erosion was similar between males and females (p = 0.831). Males age ≤ 50 had higher (p = 0.018) and age 71-80 had lower (p = 0.006) prevalence of plaque erosion. Females age 61-70 had higher (p = 0.021) and age 71-80 had lower (p = 0.045) prevalence of plaque erosion. In advanced age groups (≥ 71 years), rupture was the dominant etiology in both sexes. In multivariate analysis of males, age ≤ 50 demonstrated a trend to increase (OR 1.418, 95% CI 0.961-2.093, p = 0.078) the erosion risk. Females age ≤ 70 independently increased (OR 2.138, 95% CI 1.249-3.661, p = 0.006) the risk for erosion. The prevalence of plaque erosion was similar between males and females. Plaque erosion risk was increased in the males age ≤ 50 and in the females age ≤ 70 among ACS patients.

Although an in vivo diagnosis of coronary plaque erosion has become possible by optical coherence tomography (OCT), angiographic characteristics of erosion have not been studied. The aim of this study was to investigate the angiographic features of plaque erosion in patients with non-ST elevation acute coronary syndromes (NSTE-ACS).Patients with NSTE-ACS who underwent OCT of the culprit lesion were collected at 11 institutions from 6 countries. Patients were classified as erosion or non-erosion based on OCT images. Angiographic features of both groups were compared.Among 494 cases with NSTE-ACS, 242 had plaque erosion and 252 had non-erosion. Compared to non-erosion group, erosion patients had less multivessel disease (28.5% vs. 49.6%, p 0.001), lower Jeopardy score (4.2 vs. 5.0, p 0.001), lower Gensini score (21.3 vs. 25.6, p = 0.014), and lower Syntax score (8.9 vs. 11.5, p 0.001). With regard to the culprit lesion morphology, plaque erosion group had smaller reference diameter (2.8 mm vs. 3.0 mm, p = 0.032), less frequent type B2/C lesions (51.2% vs. 71.8%, p 0.001), and lower prevalence of calcification (4.1% vs. 13.9%, p 0.001) and thrombus (16.5% vs. 28.2%, p = 0.002). In the mid left anterior descending artery (LAD), erosion was significantly more frequent than non-erosion (30.2% vs. 21.8%, p = 0.034).Patients with NSTE-ACS caused by plaque erosion have less complex angiographic features both at the 3-vessel level and at the culprit lesion level. Plaque erosion was frequently found in the mid LAD.

Diabetes mellitus (DM) increases cardiovascular morbidity and mortality. A statin is routinely prescribed to patients with DM. However, whether a statin therapy is equally effective in plaque stabilization in DM patients compared with non-DM patients is unknown. A total of 117 lipid-rich plaques were imaged in 90 patients (54 plaques in 41 DM patients and 63 plaques in 49 non-DM patients) with coronary artery disease, those who were treated with a statin and underwent serial optical coherence tomography imaging were included in this study (mean follow-up period, 362 ± 38 days). The changes in minimum fibrous cap thickness (FCT) and lipid index between baseline and 1-year follow-up were compared between the 2 groups. Minimum FCT increased and lipid index decreased with statin therapy in both groups. No significant differences were observed in percent changes of minimum FCT (p = 0.796) and lipid index (p = 0.336) between DM and non-DM patients. Statin therapy induced a significant increase in FCT and a significant decrease in lipid index in both groups. Vascular response to statin therapy was similar between the 2 groups irrespective of DM status.

Statins are widely used to lower cholesterol and to reduce cardiovascular events. Whether all statins have similar effects on plaque stabilization is unknown. We aimed to investigate coronary plaque response to treatment with different statins that result in similar lipid reduction using serial multimodality intracoronary imaging. Patients with de novo coronary artery disease requiring intervention were randomized to rosuvastatin 10mg (R10) or atorvastatin 20mg (A20) daily. Optical coherence tomography and intravascular ultrasound were performed at baseline, 6 months, and 12 months. Untreated nonculprit plaques were analyzed by optical coherence tomography for thin-cap fibroatheroma, minimum fibrous cap thickness, lipid arc, and lipid length. Total and percent atheroma volume, respectively were analyzed by intravascular ultrasound. Forty-three patients completed the protocol (R10: 24 patients, 31 plaques; A20: 19 patients, 30 plaques). The decrease in serum lipids was similar. From baseline to 6 months to 12 months, minimum fibrous cap thickness increased in the R10 group (61.4 ± 15.9 µm to 120.9 ± 57.9 µm to 171.5 ± 67.8 µm, p0.001) and the A20 group (60.8 ± 18.1 µm to 99.2 ± 47.7 µm to 127.0± 66.8 µm, p0.001). Prevalence of thin-cap fibroatheroma significantly decreased in the R10 and A20 groups (-48% and -53%, respectively, p0.001 for intragroup comparisons). Only the R10 group had a decrease in macrophage density (-23%, p = 0.04) and microvessels (-12%, p = 0.002). Total atheroma volume decreased in the R10 group (109.2 ± 62.1 mm

Endothelial shear stress (ESS) identifies coronary plaques at high risk for progression and/or rupture leading to a future acute coronary syndrome. In this study an optimized methodology was developed to derive ESS, pressure drop and oscillatory shear index using computational fluid dynamics (CFD) in 3D models of coronary arteries derived from non-invasive coronary computed tomography angiography (CTA). These CTA-based ESS calculations were compared to the ESS calculations using the gold standard with fusion of invasive imaging and CTA. In 14 patients paired patient-specific CFD models based on invasive and non-invasive imaging of the left anterior descending (LAD) coronary arteries were created. Ten patients were used to optimize the methodology, and four patients to test this methodology. Time-averaged ESS (TAESS) was calculated for both coronary models applying patient-specific physiological data available at the time of imaging. For data analysis, each 3D reconstructed coronary artery was divided into 2 mm segments and each segment was subdivided into 8 arcs (45°).TAESS and other hemodynamic parameters were averaged per segment as well as per arc. Furthermore, the paired segment- and arc-averaged TAESS were categorized into patient-specific tertiles (low, medium and high). In the ten LADs, used for optimization of the methodology, we found high correlations between invasively-derived and non-invasively-derived TAESS averaged over segments (n = 263, r = 0.86) as well as arcs (n = 2104, r = 0.85, p

Objectives There are no societal ultrasound guidelines detailing appropriate patient selection for deep vein thrombosis (DVT) imaging in COVID-19 patients nor are there protocol recommendations aimed at decreasing exposure time for ultrasound technologists. We aimed to provide COVID-19 specific protocol optimization recommendations limiting ultrasound technologist exposure while optimizing patient selection. Methods A novel two-pronged algorithm was implemented to limit the DVT ultrasound studies on COVID-19 patients prospectively which included direct physician communication with the care team and a COVID-19 specific imaging protocol was instated to reduce ultrasound technologist exposure. In order to assess pretest risk of DVT, sensitivity and specificity of serum D-Dimer in 500-unit increments from 500 to 8000 ng/mL and a receiver operating characteristic curve (ROC) to assess performance of serum D-Dimer in predicting DVT was generated. Rates of DVT, pulmonary embolism (PE) 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 exams in COVID-19 positive patients. A serum D-Dimer > 4000ng/mL yielded a sensitivity of 80% and a specificity of 70% (CI: 0.54-0.86) for venous thromboembolism. Using the COVID-19 specific protocol, there was a significant (50%) reduction in scan time (p

Introduction: Endothelial shear stress (ESS) identifies coronary plaques at high risk for progression and rupture leading to a future acute coronary syndrome. We developed an optimized methodology to derive ESS using computational fluid dynamics (CFD) in 3D models of coronaries from noninvasive computed tomography angiography (CTA). We hypothesized that ESS based on CTA has a high correlation with ESS based on the gold standard fusion of intravascular ultrasound (IVUS)/optimical coherence tomography (OCT) and CTA. Methods: In 14 patients, paired patient-specific CFD models based on invasive and CTA imaging of the left anterior descending (LAD) coronaries were created. 10 were used to optimize, and 4 patients to test the methodology. Time averaged ESS (TAESS) was calculated for both coronary models applying physiological data at the time of imaging. Each 3D reconstructed coronary was divided into 2 mm segments and further subdivided into 8 arcs (45 o ). TAESS was averaged per segment and arc. The paired segment and arc averaged TAESS were categorized into patient-specific tertiles (low, medium and high). Results: In the 10 LADs, used for optimization of the methodology, we found high correlations between invasively- and noninvasively-derived TAESS averaged over segments (n=263, r=0.86) and arcs (n=2104,r= 0.85,p Conclusions: We showed that we can accurately assess the TAESS distribution noninvasively from CTA and demonstrated a high correlation with TAESS using IVUS/OCT 3D models. Future studies should prove the prognostic value of CTA-based TAESS for plaque progression and clinical events.

Healed coronary plaques, morphologically characterized by a layered pattern, are signatures of previous plaque disruption and healing. Recent optical coherence tomography (OCT) studies showed that layered plaque is associated with vascular vulnerability. However, factors associated with layered plaques have not been studied. The aim of this study was to investigate predictors for layered plaque at the culprit plaques and at non-culprit plaques. Patients with coronary artery disease who underwent pre-intervention OCT imaging of the culprit lesion were included. Layered plaques were defined as plaques with one or more layers of different optical density and a clear demarcation from underlying components. Among 313 patients, layered plaque at the culprit lesion was observed in 18.8% of ST-segment elevation myocardial infarction patients, 36.3% of non-ST-segment elevation acute coronary syndrome patients, and 53.4% of stable angina pectoris (SAP) patients (p 0.001). In the multivariable model, SAP, multivessel disease, type B2/C lesion, and diameter stenosis 70% were independent predictors for layered plaque at the culprit lesion. In addition, 394 non-culprit plaques in 190 patients were assessed to explore predictors for layered plaques at non-culprit lesions. SAP, and thin-cap fibroatheroma and layered plaque at the culprit lesion were independent predictors for layered plaques at non-culprit lesions. In conclusion, clinical presentation of SAP was a strong predictor for layered plaque at both culprit plaques and non-culprit plaques. Development and biologic significance of layered plaques may be related to a balance between pan-vascular vulnerability and endogenous anti-thrombotic protective mechanism.

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 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.

Improvements in spatial and temporal resolution now permit robust high quality characterization of presence, morphology and composition of coronary atherosclerosis in computed tomography (CT). These characteristics include high risk features such as large plaque volume, low CT attenuation, napkin-ring sign, spotty calcification and positive remodeling. Because of the high image quality, principles of patient-specific computational fluid dynamics modeling of blood flow through the coronary arteries can now be applied to CT and allow the calculation of local lesion-specific hemodynamics such as endothelial shear stress, fractional flow reserve and axial plaque stress. This review examines recent advances in coronary CT image-based computational modeling and discusses the opportunity to identify lesions at risk for rupture much earlier than today through the combination of anatomic and hemodynamic information.

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 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.

Incomplete stent apposition (ISA, also known as malapposition) is a complication that affects day-to-day coronary stenting procedures. ISA is more prominent in complex arterial geometries, such as curvature, asa result of the limited conformability of coronary stents. These malapposed struts disturb the otherwise near-wall laminar blood flow and form a micro-recirculation environment. The micro-recirculation environment is often associated with low wall shear stress (WSS) and upsets the delicate balance of vascular biology, providing possible nidus for thrombosis and restenosis. In this study, a three-dimensional (3D) stent model was virtually deployed into an idealised curved coronary artery. Computational fluid dynamics (CFD) simulations were carried out to systematically analyse the haemodynamic effects of increasing maximum ISA distances, ranging from 180 (moderate), 400 (intermediate) to 910μm (severe) in an artery with decreasing radius of curvature (ROC). Micro-recirculations around both proximal and distal malapposed struts become more pronounced as compared to fully-apposed struts. The accompanying areas of low temporally-averaged WSS (AL-TAWSS) can increase twofold compared to the fully-apposed condition. Furthermore, substantial regions (∼5.2% and 9.0%) of AL-TAWSS are detached from the distal end of the malapposed struts in both moderate and intermediate cases respectively. Malapposed stents also induce more variation of TAWSS at the inner bend of the artery. At the stent surface, maximum WSS increases threefold from the fully-apposed case to intermediate ISA. High WSS on the strut surface is known to activate platelets which when exposed to the micro-recirculation environment may lead to their deposition and thrombosis.

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

The aim of this manuscript is to provide guidelines for appropriate use of CFD to obtain reproducible and reliable wall shear stress maps in native and instrumented human coronary arteries. The outcome of CFD heavily depends on the quality of the input data, which include vessel geometrical data, proper boundary conditions, and material models. Available methodologies to reconstruct coronary artery anatomy are discussed in ‘Imaging coronary arteries: a brief review’ section. Computational procedures implemented to simulate blood flow in native coronary arteries are presented in ‘Wall shear stress in native arteries’ section. The effect of including different geometrical scales due to the presence of stent struts in instrumented arteries is highlighted in ‘Wall shear stress in stents’ section. The clinical implications are discussed in ‘Clinical applications’ section, and concluding remarks are presented in ‘Concluding remarks’ section.

Acute coronary thrombosis with plaque erosion is responsible for about one-third of patients with acute coronary syndromes. The relationship between endothelial shear stress (ESS) and plaque erosion has not been systematically studied in patients so far. A total of 18 acute coronary syndrome

Coronary stent malapposition is a risk factor for complications like restenosis and thrombosis and can be identified using intravascular optical coherence tomography (OCT). It has been suggested that blood flow disturbances (e.g. shear rate, viscosity, etc.) near stent struts may play a role. However, the physical motion and aggregation of activated platelets across malapposed stent struts remain unknown. Abnormal tissue surrounding struts seen in OCT imaging (Panel D) may be linked to platelet behaviour.

Percutaneous coronary intervention (PCI) has shown a high success rate in the treatment of coronary artery disease. The decision to perform PCI often relies on the cardiologist's visual interpretation of coronary lesions during angiography. This has inherent limitations, particularly due to the low resolution and two-dimensional nature of angiography. State-of-the-art modalities such as three-dimensional quantitative coronary angiography, optical coherence tomography and invasive fractional flow reserve (FFR) may improve clinicians' understanding of both the anatomical and physiological importance of coronary lesions. While invasive FFR is the gold standard technique for assessment of the haemodynamic significance of coronary lesions, recent studies have explored a surrogate for FFR derived solely from three-dimensional reconstruction of the invasive angiogram, and therefore eliminating need for a pressure wire. Utilizing advanced computational fluid dynamics research, this virtual fractional flow reserve (vFFR) has demonstrated reasonable correlation with invasive measurements and remains an intense area of ongoing study. However, at present, several limitations and computational fluid dynamic assumptions may preclude vFFR from widespread clinical use. This review demonstrates the tight integration of advanced three-dimensional imaging techniques and vFFR in assessing coronary artery disease, reviews the advantages and disadvantages of such techniques and attempts to provide a glimpse of how such advances may benefit future clinical decision-making during PCI.

Pioneering histology-based studies performed at the beginning of the last century have demonstrated that the culprit lesions responsible for sudden death have specific morphological characteristics [1-4]. More recently, Davies and Thomas have shown that plaque disruption was the main cause of coronary thrombosis and is associated with crescendo angina, myocardial infarction, and sudden death [5,6]. These landmark studies have attracted attention and efforts were made to identify features associated with plaque vulnerability. Today it is known that the high-risk lesions have a specific phenotype called thin cap fibroatheroma (TCFA) that exhibits an increased plaque burden, with a necrotic core that is covered by a thin fibrous cap and is rich in macrophages [7-10]. More recent evidence has shown that vulnerable lesions also have micro-calcifications and are rich in neo-vessels and cholesterol crystals [11-13].

One particular complexity of coronary artery is the natural tapering of the vessel with proximal segments having larger caliber and distal tapering as the vessel get smaller. The natural tapering of a coronary artery often leads to proximal incomplete stent apposition (ISA). ISA alters coronary hemodynamics and creates pathological path to develop complications such as in-stent restenosis, and more worryingly, stent thrombosis (ST). By employing state-of-the-art computer-aided design software, generic stent hoops were virtually deployed in an idealized tapered coronary artery with decreasing malapposition distance. Pulsatile blood flow simulations were carried out using computational fluid dynamics (CFD) on these computer-aided design models. CFD results reveal unprecedented details in both spatial and temporal development of microrecirculation environments throughout the cardiac cycle (CC). Arterial tapering also introduces secondary microrecirculation. These primary and secondary microrecirculations provoke significant fluctuations in arterial wall shear stress (WSS). There has been a direct correlation with changes in WSS and the development of atherosclerosis. Further, the presence of these microrecirculations influence strongly on the local levels of blood viscosity in the vicinity of the malapposed stent struts. The observation of secondary microrecirculations and changes in blood rheology is believed to complement the wall (-based) shear stress, perhaps providing additional physical explanations for tissue accumulation near ISA detected from high resolution optical coherence tomography (OCT).

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.

Coronary optical coherence tomography (OCT) is now an established imaging technique in many catheterization laboratories worldwide. With its near-histological view of the vessel wall and lumen interface, it offers unprecedented imaging quality to improve our understanding of the pathophysiology of atherosclerosis, plaque vulnerability, and vascular biology. Not only is OCT used to accurately detect atherosclerotic plaque and optimize stent position, but it can further characterize plaque composition, quantify stent apposition, and assess stent tissue coverage. Given that its resolution of 15 μm is well above that of angiography and intravascular ultrasound, OCT has become the invasive imaging method of choice to examine the interaction between stents and the vessel wall. This review focuses on the application of OCT to examine coronary stents, the mechanisms of stent complications, and future directions of OCT-guided intervention.

A 3.0 × 18 mm Absorb bioresorbable vascular scaffold (Abbott Vascular, Santa Clara, California) was implanted in the midsegment of the left anterior descending coronary artery of a patient with stable angina pectoris. Optical coherence tomography was performed following scaffold implantation (

Incomplete stent apposition (ISA) is sometimes found in stent deployment at complex lesions, and it is considered to be one of the causes of post-stenting complications, such as late stent thrombosis and restenosis. The presence of ISA leads to large recirculation bubbles behind the stent struts, which can reduce shear stress at the arterial wall that retards neointimal formation process and thus lead to complications. Computational fluid dynamics (CFD) simulations are performed on simplified two-dimensional axisymmetric arterial models with stents struts of square and circular cross-sectional shapes at a malapposition distance of 120 μm from the arterial wall. To investigate the effects of pulsatile flow period on the dynamics of the recirculation bubbles, high fidelity simulations are carried out with pulsatile flows of period 0.4 s and 0.8 s. Under the condition of the same flow rate, both square and circular strut cases show that shorter period provides greater flow deceleration, leading to the formation of a larger recirculation bubble. With the same thickness, circular strut has a significant improvement over the square strut in terms of the size of the recirculation bubble, and therefore less likely to lead to complications.