BACKGROUND: Relatively little is known about the plaque characteristics of border-zone infarcts and how they differ between cortical border-zone (CBZ) and internal border-zone (IBZ) infarcts.
METHODS: We conducted a retrospective observational cohort study of patients with intracranial atherosclerotic disease who underwent high-resolution magnetic resonance imaging (HR-MRI) examination. Individuals with border-zone infarcts in the middle cerebral artery (MCA) territory, detected by diffusion-weighted imaging, were enrolled. Plaque morphological and compositional parameters of both IBZ and CBZ groups were compared. Independent predictors were identified using a binary logistic regression model, and the sensitivity and specificity of the model were assessed using a receiver operating characteristic curve. Kaplan-Meier survival analysis further explored differences in stroke recurrence between BZ patients with mono or dual antiplatelet therapy.
RESULTS: We reviewed 101 symptomatic patients with border-zone infarcts (BZ) within the MCA territory in the study. Out of the patients meeting the imaging eligibility criteria, we detected 34 cases with isolated IBZ, 23 cases with isolated CBZ, and six cases with both IBZ and CBZ infarcts. Those with IBZ infarcts had a higher plaque burden than those without (p < 0.001), and those with CBZ infarcts exhibited a complicated plaque less frequently than those without (37.9% vs 67.6%, p = 0.018). In those with isolated IBZ or CBZ infarcts, plaque burden was independently associated with isolated IBZ infarcts (odd ratio=1.08; 95% CI, 1.02-1.15; p = 0.023). During the median follow-up period of 37 (27, 50) months, 13.8% of patients receiving early dual antiplatelet treatment and 30.4% of those on single antiplatelet therapy experienced stroke recurrence (p = 0.182).
CONCLUSIONS: Intracranial atherosclerotic plaque morphology and composition differ between patients with IBZ and those with CBZ infarcts. Higher plaque burden is more associated with IBZ infarcts.

Low-density lipoprotein cholesterol (LDL-C) levels are recommended according to the patient\'s risk factors based on guidelines. In patients achieving low LDL-C levels, the need for statins is uncertain, and the plaque characteristics of patients not treated with statins are unclear. In addition, the difference in plaque characteristics with and without statins is unclear in similarly high LDL levels. We evaluate the impact of statins on plaque characteristics on optical coherence tomography (OCT) in patients with very low LDL-C levels and high LDL-C levels. A total of 173 stable angina pectoris patients with 173 lesions undergoing OCT before percutaneous coronary intervention were evaluated. We divided the LDL-C levels into three groups: < 70 mg/dL (n = 48), 70 mg/dL ≤ LDL-C < 100 mg/dL (n = 71), and ≥ 100 mg/dL (n = 54). Among patients with LDL-C < 70 mg/dL, patients not treated with statins showed a significantly higher C-reactive protein level (0.27 ± 0.22 mg/dL vs. 0.15 ± 0.19 mg/dL, p = 0.049), and higher incidence of thin-cap fibroatheromas (TCFAs; 44% [7/16] vs. 13% [4/32], p = 0.021) than those treated with statins. Among patients with LDL-C level ≥ 100 mg/dL, patients treated with statins showed a significantly higher prevalence of familial hypercholesterolemia (FH) (38% [6/16] vs. 5% [2/38], p = 0.004), lower incidence of TCFAs (6% [1/16] vs. 39% [15/38], p = 0.013), healed plaques (13% [2/16] vs. 47% [18/38], p = 0.015), and higher incidence of fibrous plaques (75% [12/16] vs. 42% [16/38], p = 0.027) than patients not treated with statins. While patients achieved a low LDL-C, patients not treated with statins had high plaque vulnerability and high systemic inflammation. While patients had a high LDL-C level with a high prevalence of FH, patients treated with statins had stable plaque characteristics.

OBJECTIVE: To evaluate the predictive ability of plaque characteristics for long-term stroke recurrence among patients with symptomatic intracranial atherosclerotic disease (ICAD).
METHODS: This cohort study included 132 patients with acute ischemic stroke (AIS) attributed to ICAD who were recruited between July 2017 and December 2020 and followed until stroke recurrence or December 2021. Plaque surface irregularity, degree of stenosis, plaque burden, remodeling ratio, enhancement ratio, and intraplaque hemorrhage were assessed with 3-dimensional high-resolution magnetic resonance vessel wall imaging (3D HR-MRI). Data were analyzed using Cox models, receiver operating characteristic (ROC) curves, and Kaplan-Meier survival analysis.
RESULTS: Of the 132 patients, during a median follow-up of 2.8 years, stroke recurrence occurred in 35 patients. The multivariable-adjusted hazard ratio (95% confidence interval) of stroke recurrence was 3.15 (1.34-7.42) per 10% increase in plaque burden and 2.17 (1.27-3.70) for enhancement ratio. The area under the curve (AUC) to predict stroke recurrence was 0.725 (95% CI 0.629-0.822) for plaque burden, 0.692 (95% CI 0.593-0.792) for enhancement ratio, and only 0.595 (95% CI 0.492-0.699) for the Essen stroke risk score. The Kaplan-Meier survival analysis further demonstrated significant differences in survival of free recurrent stroke between patients with plaque burden or enhancement ratio below and above the optimum cut-offs (both p < 0.001).
CONCLUSIONS: Higher plaque burden and enhancement ratio are independent risk factors for long-term stroke recurrence among patients with symptomatic ICAD, and valuable imaging markers for predicting and stratifying risk of stroke recurrence.
CONCLUSIONS: In patients with symptomatic ICAD, the results of this high-resolution magnetic resonance vessel wall imaging study have potential implications for optimal management of intracranial plaques and secondary prevention of stroke recurrence based on plaque burden and enhancement ratio.
CONCLUSIONS: • Identification of intracranial plaque characteristics responsible for stroke recurrence is essential to preventing stroke recurrence in patients with symptomatic intracranial atherosclerotic disease. • Higher plaque burden and enhancement ratio are independent risk factors for stroke recurrence. • Plaque burden and enhancement ratio are valuable imaging markers in the prediction and stratification of the risk of stroke recurrence.

OBJECTIVE: To evaluate the diagnostic performance of fractional flow reserve (FFR) derived from coronary computed tomography angiography (CCTA; CT-FFR) and combined plaque characteristics for ischemia in different CCTA stenosis levels.
METHODS: This clinical trial analyzed 317 patients with 30 %-90 % coronary stenosis in 366 vessels from 5 centers undergoing CCTA and invasive FFR. 366 vessels were assigned into < 50 % (nonobstructive) and ≥ 50 % (obstructive) stenosis groups. Lesion length (LL), plaque burden (PB), diameter stenosis (DS), volume ratio of plaque subcomponents < 30 HU (VR < 30HU), and high-risk features were analyzed. Logistic regression models were used to identify plaque characteristic predictors for lesion-specific ischemia in different stenosis grades. The area under receiver operating characteristics curve (AUC) of integrated plaque characteristics and CT-FFR were calculated and compared.
RESULTS: In < 50 % stenosis lesions, PB (OR: 1.296, p = 0.002), LL (OR:1.075, p = 0.020), and DS (OR:1.085, p = 0.031) were independent predictors of ischemia. In ≥ 50 % stenosis lesions, VR < 30HU (OR:1.031, p = 0.005) and DS (OR: 1.020, p =  0.044) were independent predictors for ischemia. AUC of plaque characteristic (VR < 30HU plus DS) for ischemia was 0.67 (95 % CI: 0.61-0.72) in ≥ 50 % stenosis level, which was significantly lower than CT-FFR (AUC=0.90; 95 % CI: 0.86-0.93) (p <  0.001). For lesions causing < 50 % stenosis, AUC of combined plaque model (VR < 30HU plus DS) was 0.88 (95 % CI: 0.80-0.95), equivalent to AUC of CT-FFR (AUC = 0.88; 95 % CI: 0.80-0.96; p =  0.957).
CONCLUSIONS: CT-FFR is a powerful functional assessment tool for both obstructive and nonobstructive diseases. However, for nonobstructive CAD confirmed by CCTA, a model of a combination of plaque characteristics could be a valuable alternative to CT-FFR.

UNASSIGNED: Cardiovascular disease (CVD) poses a serious threat to human health. Research shows that ABO blood groups, especially non-O blood types, are closely related to the incidence of cardiovascular diseases (CVDs). This study aimed to determine the associations of blood types with non-culprit coronary plaque characteristics using optical coherence tomography (OCT).
UNASSIGNED: A total of 257 acute coronary syndrome (ACS) patients (average age, 59.39±10.08 years, 80% male) who underwent OCT of 3 vessels were identified. Subjects were divided into 2 groups: the O blood group (71 patients with 121 plaques) and the non-O group (186 patients with 329 plaques). The non-culprit coronary plaque features of the two groups were compared using OCT.
UNASSIGNED: The non-type O group had larger lipid arcs, thinner fibrous caps, and a greater number of thin-cap fibro atheromas (TCFAs). The type A, B, and AB blood groups had larger lipid arcs than the type O blood group, as well as thinner fibrous caps and more TCFAs. The type A blood group had thinner fibrous caps and a greater number of TCFAs than the type B and AB blood groups.
UNASSIGNED: ACS patients with type non-O blood had more non-culprit plaques. Patients with type A blood, in particular, had more vulnerable characteristics than those with type O blood.

OBJECTIVE: This study was designed to utilize frequency-domain optical coherence tomography (FD-OCT) for assessment of plaque characteristics and vulnerability in patients with acute coronary syndrome (ACS) compared to stable coronary artery disease (SCAD).
RESULTS: We enrolled 48 patients; divided into an ACS-group (27 patients) and SCAD-group (21 patients) according to their clinical presentation. Hypertension and diabetes mellitus were more prevalent in SCAD group. Patients with ACS showed higher frequency of lipid-rich plaques (96.3% vs. 66.7%, P = .015), lower frequency of calcium plaques (7.4% vs. 57.1%, P < .001), and fibrous plaques (14.8% vs. 81%, P < .001) when compared with SCAD patients. The TCFA (defined as lipid-rich plaque with cap thickness <65 μm) identified more frequently (33.3% vs. 14.3%, P = .185), with a trend towards thinner median fibrous cap thickness (70 (50-180) µm vs. 100 (50-220) µm, P = .064) in ACS group. Rupture plaque (52% vs. 14.3%, P = .014), plaque erosion (18.5% vs. 0%, P = .059) and intracoronary thrombus (92.6% vs. 14.3%, P < .001) were observed more frequently in ACS group, while cholesterol crystals were identified frequently in patients with SCAD (0.0% vs. 33.3%, P = .002).
CONCLUSIONS: The current FD-OCT study demonstrated the differences of plaque morphology and identified distinct lesion characteristics between patients with ACS and those with SCAD. These findings could explain the clinical presentation of patients in both groups.

BACKGROUND: Coronary computed tomography angiography (CCTA) not only provides information regarding luminal stenoses but also allows for visualization of mural atheromatous changes (coronary plaques).
OBJECTIVE: We sought to elucidate whether plaques seen on CCTA enable prediction of 2-year outcomes in patients with suspected and known coronary artery disease (CAD).
METHODS: Of 3015 patients who underwent CCTA, the images and 2-year clinical courses of 2802 patients were independently analyzed. The primary endpoint was the composite of all-cause death and acute coronary syndrome.
RESULTS: During the 2-year observation period, 49 (1.7%) patients developed the primary outcome. The 2-year rates of the primary outcome in the normal (n = 515, no mural lesions), calcium (n = 654, calcified lesion alone), and plaque groups (n = 1633, presence of noncalcified or partially calcified plaques) were 0.2%, 2.0%, and 2.1%, respectively (P = 0.0028). Adverse plaque features such as low attenuation, positive remodeling, spotty calcification, and the napkin-ring sign (low-attenuation core with a higher-attenuation rim) were assessed by an independent core laboratory. Stepwise multivariate Cox proportional hazard analysis showed that a plaque with two or more characteristics (adjusted hazard ratio, 1.98; 95% confidence interval, 1.09-3.60; P = 0.0254), age of ≥67 years (mean), statin treatment after CCTA, and obstructive stenosis remained independent predictors of the primary outcome.
CONCLUSIONS: Plaque imaging in CCTA has predictive value for the 2-year outcome and is a useful identifier for high-risk patients among those with known and suspected CAD.

UNASSIGNED: The purpose of this study is to elucidate the impact of out-stent plaque characteristics on vascular response after implantation of second generation drug-eluting stent (G2-DES).
UNASSIGNED: Enrolled were 37 patients with 39 coronary artery lesions into which three types of G2-DES were successfully implanted (9 Nobori biolimus-, BES; 15 Xience everolimus-, EES; 15 Resolute zotarolimus-eluting stents; R-ZES). Immediately after (baseline) and one year after the implantation (follow-up), iMAP-intravascular ultrasound (IVUS) was performed to measure out-stent plaque volume (OSPV) and its components. Percent OSPV and vulnerable plaque index (VPI) were defined as percentile of OSPV to vessel volume and as percentile of lipidic plus necrotic volume to OSPV. Coronary angioscopy at follow-up rated the degree of arterial repair by neointimal stent coverage (NSC).
UNASSIGNED: Poor NSC was found in approximately 60% of each G2-DES. In BES, % OSPV at baseline was significantly greater in poor NSC than in good NSC (36.2 ± 3.9 vs. 27.3 ± 4.0%, P = 0.01). In EES, %OSPV was significantly greater in poor NSC than in good NSC (41.0 ± 4.1 vs. 32.6 ± 2.7%, P < 0.01). In R-ZES implantation, there was no significant difference with regards to %OSPV between poor and good NSC. In BES, VPI at baseline was significantly greater in poor NSC than good NSC (54.0 ± 5.8 vs. 42.2 ± 5.1%, P = 0.02). There was no significant difference with regards to VPI between poor and good NCS in EES and R-ZES.
UNASSIGNED: Impact of out-stent plaque characteristics on vascular response was different among the three types of G2-DES.