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Near-infrared spectroscopy intravascular ultrasounds (NIRS-IVUSs) can identify high-risk plaque morphologies associated with future event risk. However, the usage of NIRS-IVUSs is not universal. We report a case with insignificant coronary angiography (CAG) and high-risk NIRS-IVUS findings. A 58-year-old man with exertional dyspnea was admitted for a CAG evaluation. The CAG of the patient demonstrated mild angiographic stenosis in the mid-left anterior descending artery. However, NIRS-IVUS revealed a high maximum lipid core burden index at 4 mm (MaxLCBI4mm) and an intraluminal calcific protrusion with severe luminal stenosis at the lesion. Therefore, the patient was diagnosed as stable angina, and a drug-eluting stent was implanted in the lesion. A post-stent NIRS-IVUS demonstrated improved MaxLCBI4mm and significantly improved luminal stenosis. The patient did not have any procedural complications. In the present case, a patient with insignificant CAG demonstrated multiple high-risk features on NIRS-IVUS. Therefore, a percutaneous coronary intervention was performed. The presented case highlights the utility of NIRS-IVUS in nonobstructive CAG.

Carotid plaque is often an important factor in ischemic stroke after it changes from stable to vulnerable, and low-density lipoprotein cholesterol (LDL-c) and high-density lipoprotein cholesterol (HDL-c) are associated with plaque vulnerability. We aimed to investigate whether the LDL-c/HDL-c ratio, an easily available and novel biomarker, is associated with vulnerable plaques and enhances the warning effect on vulnerability compared to LDL-c or HDL-c alone.
We conducted a retrospective study of 187 patients with severe CAS admitted to the Department of Vascular Surgery at the Nanjing Drum Tower Hospital from January 2019 to July 2021. They were divided into a stable plaque group and a vulnerable plaque group according to carotid ultrasonography, carotid angiography (CTA), and plaque pathology. Baseline information was collected and compared between the two groups. Correlation analysis was used to determine the degree of correlation between clinical variables. Univariate and multifactor logistic regression analyses were used to examine independent risk factors for vulnerable plaque in patients with severe CAS. Receiver operating characteristic (ROC) curves were used to assess the capacity of LDL-c/HDL-c to predict the occurrence of vulnerable plaque.
The age of the vulnerable plaque group was 68.12 ± 8.90 years, with 85 males (89.91%); the age of the stable plaque group was 68.77 ± 8.43 years, with 70 males (89.74%). Multivariate logistic regression analysis showed that LDL-c/HDL-c, smoking and diabetes were independent risk factors for vulnerable plaque (all P <0.05). The risk of vulnerable plaque was 4.78-fold greater in the highest LDL-c/HDL-c quartile (≥ 2.63) than in the lowest quartile (≤ 1.31) (P-trend <0.001), and the area under the ROC curve for LDL-c/HDL-c (AUC=0.681, P <0.001) was higher than that for LDL-c and HDL-c.
LDL-c/HDL-c, smoking and diabetes were independent risk factors for vulnerable plaque in patients with severe CAS, and LDL-c/HDL-c had a higher predictive value for the presence of vulnerable plaque compared with other lipid parameters.

BACKGROUND: Matrix metalloproteinase 10 (MMP-10) has a close relationship with carotid atherosclerosis (CAS) and cerebral infarction. The MMP-10 rs17435959 polymorphism causes a leucine to valine transition at codon 4 in exon 1 of the MMP-10 gene and may have functional effects.
OBJECTIVE: To investigate the relationship between the MMP-10 rs17435959 polymorphism and the formation and stability of CAS plaques.
METHODS: The present case-control study contains 738 visitors who came to our health examination center for the first time. According to the carotid ultrasound examinations, visitors were classified into the vulnerable plaque group (41-86 years old, 141 male, 105 female), the stable plaque group (41-86 years old, 141 male, 105 female) and the no plaque group (41-85 years old, 141 male, 105 female). All visitors in the three groups were sex- and- age-matched, and cardiovascular and cerebrovascular diseases were absent. The polymorphism was genotyped by real-time polymerase chain reaction- restriction.
RESULTS: Compared to the GG genotype, the frequency of the CC and CG genotypes was significantly more common in the vulnerable plaque group than in the no plaque group (18.7% vs. 7.7%, unadjusted P = 0.002). Moreover, compared to the G allele, the frequency of the C allele was significantly more common in the vulnerable plaque group than in the no plaque group (10.4% vs. 3.9%, unadjusted P = 0.000) and in the vulnerable plaque group than in the stable plaque group (10.4% vs. 5.1%, unadjusted P = 0.008). Binary logistic regression showed that the CC and CG genotype was independent risk factor for the formation (P = 0.019, OR = 1.961, 95% CI [1.117, 3.444]) and vulnerability (P = 0.035, OR = 1.842, 95% CI [1.045, 3.247]) of CAS plaques. Moreover, individuals who have the C allele showed a higher level of fibrinogen, which was an independent risk factor for the formation of CAS plaques (P = 0.000, OR = 2.425, 95% CI [1.475, 3.985]).
CONCLUSIONS: The rs17435959 polymorphism was associated with the formation and vulnerability of CAS plaques. Individuals who had variant-type MMP-10 showed higher levels of fibrinogen, which promoted the formation of CAS plaques.

BACKGROUND: Lipid-rich plaques (LRP) in the non-culprit lesions (NCL) in patients with the acute coronary syndrome may trigger lesion-related, adverse cardiovascular events. Aggressive lipid-lowering therapy may stabilize LRP; however, the times of stabilization remain undefined.
METHODS: A 60-year-old man presented with unstable angina. Coronary angiography revealed a severely stenotic lesion (culprit lesion) in the left descending artery, and another non-obstructive lesion in the distal left main trunk artery. Near-infrared spectroscopy (NIRS) imaging showed LRP with a maximum lipid core burden index (LCBI)4mm of 422. Optical coherence tomographic (OCT) imaging showed the vulnerable plaque as a thin cap fibroatheroma with a thickness of 50 µm. We prescribed aggressive lipid-lowering treatment with a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor, and serially observed this lesion for 24 months. The NIRS imaging showed that the LCBI gradually decreased over time (max LCBI4mm of 422, 417, 318, 265, and 106 conducted at index percutaneous coronary intervention, 3, 8, 12, and 24 months, respectively). As plaque regression and stabilization of high-risk LRP were observed, we promptly discontinued treatment with the PCSK9i inhibitor.
CONCLUSIONS: During the long-term, 24-month, follow-up using serial NIRS-IVUS imaging, we observed the gradual decrease in LCBI over time, due to aggressive lipid-lowering therapy. Compared with the lowering of low-density lipoprotein cholesterol, the stabilization of vulnerable plaques may require longer times of about 2 years. Evaluation of NCL-related adverse cardiac events by serial intravascular imaging over time, using NIRS-IVUS or OCT, may be warranted in such cases.

Carotid atherosclerosis is one of the main underlying inducements of stroke, which is a leading cause of disability. The morphological feature and biomechanical environment have been found to play important roles in atherosclerotic plaque progression. However, the biomechanics in each patient\'s blood vessel is complicated and unique.
To analyse the biomechanical risk of the patient-specific carotid stenosis, this study used the fluid-structure interaction (FSI) computational biomechanical model. This model coupled both structural and hemodynamic analysis. Two patients with carotid stenosis planned for carotid endarterectomy were included in this study. The 3D models of carotid bifurcation were reconstructed using our in-house-developed protocol based on multisequence magnetic resonance imaging (MRI) data. Patient-specific flow and pressure waveforms were used in the computational analysis. Multiple biomechanical risk factors including structural and hemodynamic stresses were employed in post-processing to assess the plaque vulnerability.
Significant difference in morphological and biomechanical conditions between 2 patients was observed. Patient I had a large lipid core and serve stenosis at carotid bulb. The stenosis changed the cross-sectional shape of the lumen. The blood flow pattern changed consequently and led to a complex biomechanical environment. The FSI results suggested a potential plaque progression may lead to a high-risk plaque, if no proper treatment was performed. The patient II had significant tandem stenosis at both common and internal carotid artery (CCA and ICA). From the results of biomechanical factors, both stenoses had a high potential of plaque progression. Especially for the plaque at ICA branch, the current 2 small plaques might further enlarge and merge as a large vulnerable plaque. The risk of plaque rupture would also increase.
Computational biomechanical analysis is a useful tool to provide the biomechanical risk factors to help clinicians assess and predict the patient-specific plaque vulnerability. The FSI computational model coupling the structural and hemodynamic computational analysis, better replicates the in vivo biomechanical condition, which can provide multiple structural and flow-based risk factors to assess plaque vulnerability.

Coronary artery disease rarely manifests itself in the first decades of life, which explains why this population is underrepresented in clinical studies. The mechanisms and natural history of the disease seem to differ between this population and older patients. Recent studies suggest a more rapid disease progression in youth, presenting more unstable atherosclerotic plaques, although this correlation has yet to be proven. In this paper, we present the case of a 41-year-old man who presented with a non-ST elevation myocardial infarction, with percutaneous coronary intervention of the culprit lesion (70-90% lesion at bifurcation of the circumflex artery with the first marginal obtuse artery and a sub-occlusive lesion of the ramus intermedius). There was also a non-significant lesion (estimated at 30%) located in the left anterior descending coronary artery. Ten days after discharge, the patient suffered another non-ST elevation myocardial infarction. The coronary angiography revealed a surprising sub-occlusive lesion of the left anterior descending coronary artery. Regarding this case, the authors reviewed the literature on the pathophysiology of rapidly progressive coronary artery disease and the approach for non-significant lesions in patients with acute coronary syndrome, especially in the younger population.