Plaque In Asymptomatic Patients Research Articles

Non-calcified plaque in asymptomatic patients with zero coronary artery calcium score: A systematic review and meta-analysis

BackgroundThere is growing interest in understanding the coronary atherosclerotic burden in asymptomatic patients with zero coronary artery calcium score (CACS). In this population, we aimed to investigate the prevalence and severity of non-calcified coronary plaques (NCP) as detected by coronary CT angiography (CCTA), and to analyze the associated clinical predictors. MethodsThis was a systematic review with meta-analysis of studies indexed in PubMed/Medline and Web of Science from inception of the database to March 31st, 2023. Using the random-effects model, separate Forest and Galbraith plots were generated for each effect size assessed. Heterogeneity was assessed using the I2 statistics whilst Funnel plots and Egger's test were used to assess for publication bias. ResultsFrom a total of 14 studies comprising 37808 patients, we approximated the pooled summary estimates for the overall prevalence of NCP to be 10% (95%CI: 6%–13%). Similarly, the pooled prevalence of obstructive NCP was estimated at 1.1% (95%CI: 0.7%–1.5%) from a total of 10 studies involving 21531 patients. Hypertension [OR: 1.46 (95%CI:1.31–1.62)] and diabetes mellitus [OR: 1.69 (95%CI: 1.41–1.97)] were significantly associated with developing any NCP, with male gender being the strongest predictor [OR: 3.22 (95%CI: 2.17–4.27)]. ConclusionThere is a low burden of NCP among asymptomatic subjects with zero CACS. In a subset of this population who have clinical predictors of NCP, the addition of CCTA has a potential to provide a better insight about occult coronary atherosclerosis, however, a risk-benefit approach must be factored in prior to CCTA use given the low prevalence of NCP.

Elevated EMMPRIN Serum Levels Indicate Plaque Vulnerability in Patients With Asymptomatic High Grade Carotid Stenosis

Carotid atherosclerosis is an important cause of cerebral ischaemic stroke. Sonographic plaque characteristics are inappropriate for exact prediction of possible future ischaemic events. Additional markers are needed to predict the clinical outcome in high grade carotid stenosis. This study aimed to test extracellular matrix metalloproteinase inducer (EMMPRIN), due to its involvement in plaque formation and destabilisation, as a potential marker of high risk vulnerable plaques. EMMPRIN was analysed in pre-operative serum samples from patients with symptomatic and asymptomatic carotid artery stenosis by a specific ELISA. Pre-operative duplex sonography classified the atherosclerotic plaque due to echogenicity. Histopathological analysis of vulnerable and non-vulnerable plaques was based on the American Heart Association (AHA) classification. The study included 265 patients undergoing carotid endarterectomy: 90 (m:f, 69:21) patients with symptomatic and 175 (m:f, 118:57) with asymptomatic disease. Analysis of circulating EMMPRIN revealed significantly higher levels in patients with echolucent plaques (4 480; IQR 3 745, 6 144 pg/mL) compared with echogenic plaques (4 159; IQR 3 418, 5 402 pg/mL; p= .025). Asymptomatic patients with vulnerable plaques had significantly higher levels of EMMPRIN (4 875; IQR 3 850, 7 016 pg/mL) compared with non-vulnerable plaques (4 109; IQR 3 433, 5 402 pg/mL; p < .001). In logistic regression analysis, duplex sonography combined with age, gender, and clinical risk factors predicted vulnerable plaques in asymptomatic patients with an AUC of 0.71 (95% CI 0.61 - 0.80). EMMPRIN significantly improved the AUC in asymptomatic patients (AUC 0.79; 95% CI 0.71 - 0.87; p= .014). Patients with high risk plaques according to ultrasound and histopathological characteristics demonstrated increased serum EMMPRIN levels. EMMPRIN on top of clinical risk factors, including age, gender, and duplex sonography may be used for pre-operative risk stratification in asymptomatic patients.

Translational Molecular Imaging Tool of Vulnerable Carotid Plaque: Evaluate Effects of Statin Therapy on Plaque Inflammation and American Heart Association–Defined Risk Levels in Cuff-Implanted Apolipoprotein E–Deficient Mice

Identification of high-risk carotid plaques in asymptomatic patients remains a challenging but crucial step in stroke prevention. The challenge is to accurately monitor the development of high-risk carotid plaques and promptly identify patients, who are unresponsive to best medical therapy, and hence targeted for carotid surgical interventions to prevent stroke. Inflammation is a key operator in destabilisation of plaques prior to clinical sequelae. Currently, there is a lack of imaging tool in routine clinical practice, which allows assessment of inflammatory activity within the atherosclerotic plaque. Herein, we have used a periarterial cuff to generate a progressive carotid atherosclerosis model in apolipoprotein E–deficient mice. This model produced clinically relevant plaques with different levels of risk, fulfilling American Heart Association (AHA) classification, at specific timepoints and locations, along the same carotid artery. Exploiting this platform, we have developed smart molecular magnetic resonance imaging (MRI) probes consisting of dual-targeted microparticles of iron oxide (DT-MPIO) against VCAM-1 and P-selectin, to evaluate the anti-inflammatory effect of statin therapy on progressive carotid atherosclerosis. We demonstrated that in vivo DT-MPIO-enhanced MRI can (i) quantitatively track plaque inflammation from early to advanced stage; (ii) identify and characterise high-risk inflamed, vulnerable plaques; and (iii) monitor the response to statin therapy longitudinally. Moreover, this molecular imaging–defined therapeutic response was validated using AHA classification of human plaques, a clinically relevant parameter, approximating the clinical translation of this tool. Further development and translation of this molecular imaging tool into the clinical arena may potentially facilitate more accurate risk stratification, permitting timely identification of the high-risk patients for prophylactic carotid intervention, affording early opportunities for stroke prevention in the future.

Vulnerable Carotid Artery Plaques in Asymptomatic Patients—A Narrative Review

AbstractOver the last two decades, medical management of carotid artery patients has improved significantly. Most patients remain stable on best medical therapy (BMT), making interventions unnecessary in all patients. “Selective” intervention is advocated for only those few patients who are having vulnerable or unstable carotid artery plaques. Literature search was done to explore current concept and role of available investigations to identify vulnerable carotid plaques. Vulnerable plaque is defined as those plaques having active inflammation, high large necrotic lipid content, neovascularity, thin capsule, surface irregularity, or intraplaque hemorrhage. Ultrasound (US) is the simple, noninvasive, cost-effective investigation to differentiate soft (echolucent) from fibrocalcified (echogenic) plaques. It can also comment on other high-risk plaque features such as plaque volume and area. Contrast-enhanced US can visualize neovascularization and plaque surface irregularities better than conventional US. Computed tomography is limited in identifying most high-risk plaque features and is not useful. High-resolution magnetic resonance imaging is the most accurate and externally validated investigation to characterize most high-risk plaque components. Positron emission tomography has emerged as the most promising dynamic investigation to identify and quantify inflammatory plaques and will be clinically very useful in decision making.

Serum Biomarkers in Carotid Artery Disease.

Carotid artery disease is considered a major cause of strokes and there is a need for early disease detection and management. Although imaging techniques have been developed for the diagnosis of carotid artery disease and different imaging-based markers have been proposed for the characterization of atherosclerotic plaques, there is still need for a definition of high-risk plaques in asymptomatic patients who may benefit from surgical intervention. Measurement of circulating biomarkers is a promising method to assist in patient-specific disease management, but the lack of robust clinical evidence limits their use as a standard of care. The purpose of this review paper is to present circulating biomarkers related to carotid artery diagnosis and prognosis, which are mainly provided by statistical-based clinical studies. The result of our investigation showed that typical well-established inflammatory biomarkers and biomarkers related to patient lipid profiles are associated with carotid artery disease. In addition to this, more specialized types of biomarkers, such as endothelial and cell adhesion, matrix degrading, and metabolic biomarkers seem to be associated with different carotid artery disease outputs, assisting vascular specialists in selecting patients at high risk for stroke and in need of intervention.

High-risk coronary artery plaque in asymptomatic patients with type 2 diabetes: clinical risk factors and coronary artery calcium score

BackgroundHigh-risk coronary artery plaque (HRP) is associated with increased risk of acute coronary syndrome.We aimed to investigate the prevalence of HRP in asymptomatic patients with type 2 diabetes (T2D), and its relation to patient characteristics including cardiovascular risk factors, diabetes profile, and coronary artery calcium score (CACS).MethodsAsymptomatic patients with T2D and no previous coronary artery disease (CAD) were studied using coronary computed tomography angiography (CCTA) in this descriptive study. Plaques with two or more high-risk features (HRP) defined by low attenuation, positive remodeling, spotty calcification, and napkin-ring sign were considered HRP. In addition, total atheroma volume (TAV), proportions of dense calcium, fibrous, fibrous-fatty and necrotic core volumes were assessed. The CACS was obtained from non-enhanced images by the Agatston method. Cardiovascular and diabetic profiles were assessed in all patients.ResultsIn 230 patients CCTA was diagnostic and 161 HRP were detected in 86 patients (37%). Male gender (OR 4.19, 95% CI 1.99–8.87; p < 0.01), tobacco exposure in pack years (OR 1.02, 95% CI 1.00–1.03; p = 0.03), and glycated hemoglobin (HbA1c) (OR 1.04, 95% CI 1.02–1.07; p < 0.01) were independent predictors of HRP. No relationship was found to other risk factors. HRP was not associated with increased CACS, and 13 (23%) patients with zero CACS had at least one HRP.ConclusionA high prevalence of HRP was detected in this population of asymptomatic T2D. The presence of HRP was associated with a particular patient profile, but was not ruled out by the absence of coronary artery calcium. CCTA provides important information on plaque morphology, which may be used to risk stratify this high-risk population.Trial registration This trial was retrospectively registered at clinical trials.gov January 11, 2017 trial identifier NCT03016910.

P.48 Ultrasound-Based Velocity and Acceleration of the Carotid Atheromatous Plaque in Asymptomatic Patients with Moderate and Severe Stenosis

PurposeThe purpose of this study was to investigate differences in ultrasound-based velocities and accelerations of the carotid atheromatous plaque between asymptomatic patients with moderate and severe stenosis, based on the assumption that plaque motion features are sensitive to cardiovascular health status.MethodsThe dataset used consists of 38 sequences of B-mode images (videos) of carotid atheromatous plaque of asymptomatic patients. Among the examined carotid arteries, 27 had severe stenosis degrees (>70%) and 11 had moderate stenosis degrees (<70%). Plaque motion estimation was based on an adaptive block matching methodology which incorporates Kalman filtering update strategies. Plaque velocity and acceleration were calculated by differentiating displacement and velocity, respectively. The two-tailed t-test was used to assess statistically significant differences.ResultsFigure shows examples of plaque velocity and acceleration waveforms. Radial and longitudinal plaque velocities were similar between moderate and severe cases (0.43 ± 0.15 mm/s and 0.73 ± 0.18 mm/s, respectively, vs. 0.37 ± 0.21 mm/s and 0.65 ± 0.20 mm/s, respectively; p-values 0.35 and 0.27, respectively). Radial and longitudinal plaque accelerations were significantly higher in moderate compared to severe stenosis cases (7.07 ± 4.64 mm/s2 and 10.08 ± 5.22 mm/s2, respectively, vs. 3.17 ± 2.25 mm/s2 and 5.05 ± 2.96 mm/s2, respectively; p-values = 0.00 for both cases). In moderate stenoses, longitudinal velocities, but not accelerations, were significantly higher than radial ones, whereas in severe stenoses, longitudinal velocities and accelerations were significantly higher than radial ones.ConclusionUltrasound-based velocities and accelerations can characterise biomechanical phenomena of the carotid plaque. Accelerations can differentiate between moderate and severe plaque.Figure(a) Example of ultrasound image of the carotid artery with the atheromatous plaque outlined in white. (b), (c) waveforms of radial and longitudinal velocities, respectively, of the plaque in (a). (d), (e) waveforms of radial and longitudinal accelerations, respectively, of the plaque in (a).

Early identification of carotid vulnerable plaque in asymptomatic patients

BackgroundThis study was to explore the influencing factors of atherosclerotic plaque formation and stability in patients with asymptomatic carotid atherosclerotic plaques, so as to identify the vulnerable plaques at early stage, and then find high-risk group of cardio-cerebrovascular events for early clinical intervention to reduce related mortality and disability.MethodsA total of 302 enrolled patients with asymptomatic carotid atherosclerotic plaques were divided into 3 groups based on the results of carotid artery color Doppler ultrasound: atherosclerotic unstable plaque (UP) group, atherosclerotic stable plaque (SP) group, and control group without plaques. Serum markers were measured by ELISA. χ2 test, t test, Pearson correlation analysis, and Logistic multivariate regression analysis were used in the analysis, and P < 0.05 was considered statistically significant.ResultsIt revealed that high MMP-9, LOX-1and YKL-40 were independent risk factors for unstable plaque formation. The area under the curve (AUC) of serum markers combined with MMP-9, LOX-1 and YKL-40 was 0.850, with sensitivity 87.67%, specificity 81.13%, and diagnostic accuracy 84.92%, which was significantly better than the individual diagnostic efficacy of other three factors. The accuracy rate of Crouse Plaque Score (CPS) in the diagnosis of vulnerable plaques was 61.90%, the 10-year ICVD diagnosis accuracy rate was 56.75%, and the diagnostic accuracy of serum markers was significantly better than CPS and 10-year ICVD.ConclusionNoninvasive cervical color Doppler ultrasound combined with serum markers MMP-9, LOX-1 and YKL-40 have significant early recognition effect on asymptomatic carotid vulnerable plaque patients.

An age-matched computed tomography angiographic study of coronary atherosclerotic plaques in patients with familial hypercholesterolaemia

Background and aimsFamilial hypercholesterolaemia (FH) is characterised by a high, but variable risk of premature coronary artery disease (CAD). Cardiac computed tomography angiography (CCTA) can be employed to assess subclinical coronary atherosclerosis. We investigated the features and distribution of coronary artery plaques in asymptomatic patients with and without genetically confirmed heterozygous FH. MethodsWe undertook an aged-matched case-control study of asymptomatic phenotypic FH patients with (cases, M+) and without (controls, M–) an FH-causing mutation. Coronary atherosclerosis was assessed by CCTA and calcium scoring. Coronary segments were evaluated for global and vessel-level coronary plaques and degree of stenosis. ResultsWe studied 104 cases and 104 controls (mean age 49.9 ± 10.4 years), who had a similar spectrum of non-cardiovascular risk factors. Pre-treatment plasma LDL-cholesterol was higher in the M+ than M– group (7.8 ± 2.1 vs 6.2 ± 1.2 mmol/L, p<0.001). There was a greater proportion of patients with mixed and calcified plaque, as well as a higher coronary artery calcium score and segment stenosis score (all p<0.05), in the M+ compared with the M– group. M+ patients also had a significantly higher frequency of coronary artery calcium in the left main and anterior descending and right coronary arteries (all p<0.05), but not in the left circumflex. ConclusionsAmong patients with phenotypic FH, those with a genetically confirmed diagnosis had a higher frequency and severity of coronary atherosclerotic plaques, and specifically more advanced calcified plaques.

Neutrophil Gelatinase Associated Lipocalin (NGAL) for Identification of Unstable Plaques in Patients with Asymptomatic Carotid Stenosis

Neutrophil gelatinase associated lipocalin (NGAL) and matrix metalloproteinase (MMP)-9/NGAL complex were investigated in asymptomatic patients with carotid artery stenosis including gender specific differences aiming at vulnerable plaques prone to embolisation. Serum NGAL and MMP-9/NGAL levels were analysed in 83 patients with asymptomatic carotid artery stenosis. Pre-operative ultrasound and post-endarterectomy histology of carotid atherosclerotic lesions were evaluated. Patients with vulnerable plaques, as determined by ultrasound (plaques with decreased echogenicity) and histological analysis (type VI according to the classification of the American Heart Association), displayed the highest levels of NGAL and MMP-9/NGAL complex (p=.0003 and p=.0078, respectively). Grade VI plaques were primarily detected in patients with "soft" plaques (12 type VI plaques in 25 patients), but also in patients with mixed (four of 19) and calcified (three of 39) plaques according to ultrasound. Higher grade carotid artery stenosis (≥90%) was not associated with elevated NGAL levels. The receiver operating characteristic curve analysis detecting grade VI lesions yields an area under the curve (AUC)=0.85, with respect to soft plaque on ultrasound the AUC=0.86. There were no gender specific differences in levels of NGAL 80.9 (37.7) ng/mL in women vs. 76.7 (36.3) ng/mL in men, p=.607) nor of MMP-9/NGAL 33.0 (18.2-55.5) ng/mL in women vs. 36.7 (20.2-54.0) ng/mL in men, p=.969. Likewise, there were no gender associated differences in vulnerable plaque characteristics: either for grade VI plaques (17.9% vs. 27.3%, p=.582) or for the presence of soft plaques as evaluated by ultrasound (35.9% vs. 25%, p=.503). Circulating NGAL and MMP-9/NGAL are significantly increased in asymptomatic patients with vulnerable carotid atherosclerotic plaques independent of gender. Accordingly, serum NGAL may be proposed as a valuable biomarker for the detection of unstable carotid plaques in asymptomatic patients, who can then be selected for early carotid endarterectomy or stenting.

Altered brain volume and its relationship to characteristics of carotid plaques in asymptomatic patients.

Carotid plaque is an aggregate marker of exposure to vascular risk factors, which are linked to structural brain changes. We investigated prestroke global and regional changes in brain volume in a carotid plaque population of cognitively healthy individuals and the association between carotid plaque characteristics and these changes.A total of 76 participants were divided into healthy control (HC, n = 28), vulnerable plaque (n = 27) and stable plaque groups (n = 21). All subjects underwent carotid ultrasound and brain magnetic resonance imaging (MRI). Voxel-based morphometry (VBM) was used to examine differences in regional gray matter volumes (rGMVs) among the different groups.The plaque group had a significantly lower mean total cerebral brain volume (TCBV) than the HC group (P = .03). Carotid intima-media thickness (CIMT) was negatively correlated with TCBV (r = -0.311, P = .006) and rGMV in the right thalamus (r = -0.589, P = .001). The rGMVs of the right middle occipital gyrus and bilateral lingual gyrus were significantly different between the unstable and stable groups. The gray-scale median (GSM) of the plaque and the total plaque risk score (TPRS) were correlated with the volume of the right middle occipital gyrus (r=-0.478, P = .001; r = 0.541, P = .001) and bilateral lingual gyrus (r = -0.419, P = .003; r = 0.288, P = .04).Carotid plaque is related to the volume of the brain parenchyma and right thalamus. The rGMVs of the right middle occipital gyrus and bilateral lingual gyrus differed between the vulnerable plaque and stable plaque groups, and the characteristics of carotid plaques may serve as indexes that reflect these changes

A case-control study of the localisation and composition of coronary atherosclerotic plaques in patients with familial hypercholesterolaemia as assessed by cardiac CT scanning

Aim: To assess the _ompound_d_o and composition of coronary artery plaques in asymptomatic patients with and without genetically confirmed heterozygous familial hypercholesterolaemia (FH).

Plaque Distribution and Characteristics in Low-Grade Middle Cerebral Artery Stenosis and Its Clinical Relevance: A 3-Dimensional High-Resolution Magnetic Resonance Imaging Study

The significance of atherosclerotic plaques in the parental artery with low-grade stenosis remains undetermined. We used three-dimensional high-resolution magnetic resonance imaging (3D HR-MRI) to investigate plaque distribution and characteristics of low-grade middle cerebral artery (MCA) stenosis and its clinical relevance with stroke events. We retrospectively studied 22 symptomatic patients and 24 asymptomatic patients with low-grade MCA stenosis (<50%). By 3D HR-MRI, each identified plaque was classified as either culprit (plaque on the ipsilateral side of a stroke) or nonculprit (plaques in asymptomatic patients or not within the vascular territory of a stroke). Plaque enhancement grades and distribution were assessed and compared between the groups. The association between plaque enhancement and distribution and ischemic stroke was evaluated. We identified 22 culprit plaques and 31 nonculprit plaques. More culprit plaques showed contrast enhancement compared to the nonculprit plaques (95.5% versus 29.0%, P <.001). Culprit plaques were more frequently superiorly distributed than the nonculprit plaques (46.9% versus 17.5%, P <.01). Contrast enhancement (odds ratio [OR] 17.0, 95% confidence interval [CI] 3.7-77.4) and superior distribution (OR 4.2, 95% CI 1.4-12.1) of a plaque were associated with a recent ischemic stroke, of which single subcortical infarctions accounted for the largest percentage (50%). Contrast enhancement and superior distribution may serve as indicators of culprit plaques in low-grade MCA stenosis, and they were significantly related to a recent ischemic stroke.

Abstract 233: CHI3L1 and Its Role in Vascular Smooth Muscle Cell Proliferation and Migration in Advanced Atherosclerosis

Objectives: Stroke is one of the leading causes for death and disability worldwide. The underlying pathomechanism is most likely a thrombotic event caused by acute rupture or erosion of an unstable plaque in the carotid artery. Vascular smooth muscle cells (VSMCs) play an important role in both, development and rupture of atherosclerotic plaques. Thus, efforts have been devoted determining the characteristics of VSMCs in atherosclerotic plaques to develop novel diagnostic and therapeutic strategies to prevent unstable plaque rupture. Methods: Laser capture microdissections of the fibrous cap of ruptured plaques in symptomatic patients (n=20) and stable plaques in asymptomatic patients (n=20) were used to perform a GeneChip 2.0 Human Transcriptome Array. CHI3L1 could be detected as the most significantly upregulated transcript in ruptured plaques. Following, immunohistochemistry was performed to compare distribution of CHI3L1-positive cells, VSMCs and macrophages in ruptured and stable plaques. In-vitro MTT-assay, Boyden Chamber assay and TUNEL assay were performed to investigate the role of this gene in human VSMC proliferation, migration and apoptosis. Results: The MTT-assay revealed that silencing of CHI3L1 lead to a decreased proliferation of human VSMCs. Further, migration was reduced in absence of CHI3L1. Immunohistochemistry of human carotid plaques indicated that in stable plaques mainly macrophages were CHI3L1-postive, whereas in unstable plaques both macrophages and VSMCs were CHI3L1-positive. In-vitro knockdown of CHI3L1 in cultured human VSMCs significantly increased CD68 expression, suggesting a potential role in transformation of VSMCs to macrophages. CHI3L1/CD68-positive cells (putative macrophages) in unstable plaques appeared hyperproliferative (Ki-67 positive). Conclusion: In summary, CHI3L1 plays a role in VSMC-regulation in atherosclerotic plaques. Expression levels in unstable plaques are increased. Further, it seems to induce proliferation as well as migration in VSMCs. Results of CHI3L1-induced CD68 expression indicate a potential role in VSMC-macrophage transformation. &lt;!--EndFragment--&gt;

Relation between characteristics of carotid atherosclerotic plaques and brain white matter hyperintensities in asymptomatic patients

White matter hyperintensities (WMH) can be incidentally found in patients with carotid atherosclerosis on brain magnetic resonance imaging (MRI). We investigated the relationship between WMH and characteristics of carotid plaques in asymptomatic patients without indication for carotid revascularization. We prospectively screened 235 consecutive patients with carotid stenosis <70%. After excluding patients with confounding causes of cerebral damage, 67 asymptomatic patients underwent carotid computed tomography angiography (CTA), contrast-enhanced ultrasound and brain MRI. Number and quantitative measurement of volume of WMH were associated with history of resistant hypertension, degree of stenosis (Doppler) and presence of an ulcerated plaque at CTA (p < 0.05). At multivariate regression analysis, resistant hypertension was independently associated with both number and volume of WMH, presence of an ulcer with number of WMH and degree of stenosis with WMH volume (p < 0.05), although WMH were equally distributed in both hemispheres irrespectively of plaque side. In conclusion, in asymptomatic patients with carotid plaques <70%, a higher burden of WMHs is associated with history of resistant hypertension that could be the expression of microvascular damage. Stenosis severity and presence of plaque ulceration are also associated with WMH burden although their causative relation is not supported by the bilateral distribution of WMH.

High burden of coronary atherosclerosis in patients with a new diagnosis of type 2 diabetes.

The purposes of this study were to compare the presence, extent and composition of coronary plaques in asymptomatic patients with newly diagnosed type 2 diabetes to age- and sex-matched controls. Patients with newly diagnosed (<1 year) type 2 diabetes ( n = 44) and controls ( n = 44) underwent contrast-enhanced coronary computed tomography angiography. Advanced plaque analysis including total plaque volume and volumes of plaque components (calcified plaque and non-calcified plaque, including low-attenuation [low-density non-calcified plaque]) was performed using validated semi-automated software. Coronary artery calcification was more often seen in patients with type 2 diabetes (66%) versus controls (48%), p < 0.05. Both the absolute volume (median; interquartile range) of low-density non-calcified plaque (7.9 mm3; 0-50.5 mm3 vs 0; 0-34.3 mm3, p < 0.05) and the increase in low-density non-calcified plaque ratio in relation to total plaque volume ( τ = 0.5, p < 0.001) were significantly higher in patients with type 2 diabetes. More patients with type 2 diabetes had spotty calcification (31% vs 0%, p < 0.05). By multivariate analysis, the presence of any low-density non-calcified plaque was higher in males (odds ratio: 4.06, p < 0.05), who also demonstrated a larger low-density non-calcified plaque volume ( p < 0.001). The presence and extent of low-density non-calcified plaque increased with age, smoking, hypertension and hyperglycaemia, all p < 0.05. Asymptomatic patients with newly diagnosed type 2 diabetes had plaque features associated with increased vulnerability as compared with age- and sex-matched controls.

Carotid Plaque Morphology in Asymptomatic Patients with and without Metabolic Syndrome

The aim of this study was to determine the impact of metabolic syndrome (MetS) on the morphology of carotid plaques, as evaluated using duplex ultrasound (DUS) with computer-assisted analysis. In this cross-sectional observational study, we analyzed 148 carotid artery plaques in asymptomatic patients. Data were obtained via clinical and laboratory examinations, and DUS was performed by a single operator. All plaques were scanned in a longitudinal fashion, and the best segment was selected, recorded, and evaluated using dedicated software. The main software-based analyses included gray-scale median (GSM) measurements and carotid plaque morphology histograms. MetS was identified in 51.8% of patients. Comparisons of patients with MetS and patients without MetS indicated that the former patients used more classes of antihypertensive drugs (2.49 vs. 1.93; P=0.004) and were treated with statins for a longer period (71.08 vs. 49.17months; P=0.003). Most patients of both types exhibited moderate carotid artery stenosis ranging from 50% to 69% (n=62; 37.3%), and MetS was not associated with an increased prevalence of severe carotid artery stenosis. The mean GSM was greater in the MetS group than in the non-MetS group (74.18 vs. 61.63; P=0.012). The histogram analysis revealed that there were lower quantities of blood and fat (2.91 vs. 3.88; P=0.006; 10.21 vs. 15.08; P=0.004, respectively) and more fibrous tissue (19.93 vs. 14.55; P=0.015) in the carotid plaques of patients with MetS than in the carotid plaques of patients without MetS. The present study demonstrated that MetS did not affect the stenosis grade or did it lead to unstable carotid plaques.

The impact of identifying carotid plaque on addressing cardiovascular risk in psoriatic arthritis.

BackgroundPatients with psoriatic arthritis (PsA) are at an increased risk for cardiovascular (CV) disease. The aim of this study was to identify the frequency of carotid plaque in asymptomatic patients with psoriatic arthritis at baseline and follow-up screening, and to assess for the impact of demonstrating plaque on management of traditional cardiovascular risk factors.MethodsEighty-seven PsA patients underwent carotid duplex ultrasound screening. Repeat carotid duplex ultrasound was offered to all patients between 12 and 30 months. Preventive cardiology referrals were generated for all patients through the electronic health record. Traditional cardiovascular risk factors, medication use, and rates of utilization of preventive cardiology services were compared between patients with and without plaque.ResultsCarotid plaque was identified in 34/87 (39 %) of PsA patients. Age and triglyceride levels were predictors of plaque presence. Patients with plaque trended toward higher rates of smoking and diabetes, and higher low-density lipoprotein levels. Only 9/87 (10 %) patients completed at least one visit with preventive cardiology after enrollment despite referral. Low use of statin (21 %) and antiplatelet (27 %) medication was observed. Rates of biologic medication use for PsA were higher (75 %) than studies in similar cohorts of patients with carotid plaque. No association was seen between disease duration or activity and the presence of carotid plaque.ConclusionDespite demonstration of high cardiac risk by the presence of carotid plaque, implementation of preventive cardiovascular services and rates of statin and antiplatelet use remained low. Age and triglyceride levels were significant variables in predicting plaque presence. There is no evidence that demonstration of plaque resulted in further evaluation or changes in treatment regimens to address heightened cardiovascular risk.

Treatment of hypertension in patients with coronary artery disease: A scientific statement from the American Heart Association, American College of Cardiology, and American Society of Hypertension

Neutrophil gelatinase associated lipocalin (NGAL) and matrix metalloproteinase (MMP)-9/NGAL complex were investigated in asymptomatic patients with carotid artery stenosis including gender specific differences aiming at vulnerable plaques prone to embolisation.Serum NGAL and MMP-9/NGAL levels were analysed in 83 patients with asymptomatic carotid artery stenosis. Pre-operative ultrasound and post-endarterectomy histology of carotid atherosclerotic lesions were evaluated.Patients with vulnerable plaques, as determined by ultrasound (plaques with decreased echogenicity) and histological analysis (type VI according to the classification of the American Heart Association), displayed the highest levels of NGAL and MMP-9/NGAL complex (p = .0003 and p = .0078, respectively). Grade VI plaques were primarily detected in patients with “soft” plaques (12 type VI plaques in 25 patients), but also in patients with mixed (four of 19) and calcified (three of 39) plaques according to ultrasound. Higher grade carotid artery stenosis (≥90%) was not associated with elevated NGAL levels. The receiver operating characteristic curve analysis detecting grade VI lesions yields an area under the curve (AUC) = 0.85, with respect to soft plaque on ultrasound the AUC = 0.86. There were no gender specific differences in levels of NGAL 80.9 (37.7) ng/mL in women vs. 76.7 (36.3) ng/mL in men, p = .607) nor of MMP-9/NGAL 33.0 (18.2–55.5) ng/mL in women vs. 36.7 (20.2–54.0) ng/mL in men, p = .969. Likewise, there were no gender associated differences in vulnerable plaque characteristics: either for grade VI plaques (17.9% vs. 27.3%, p = .582) or for the presence of soft plaques as evaluated by ultrasound (35.9% vs. 25%, p = .503).Circulating NGAL and MMP-9/NGAL are significantly increased in asymptomatic patients with vulnerable carotid atherosclerotic plaques independent of gender. Accordingly, serum NGAL may be proposed as a valuable biomarker for the detection of unstable carotid plaques in asymptomatic patients, who can then be selected for early carotid endarterectomy or stenting.

Association between C-reactive Protein and Type of Coronary Arterial Plaque in Asymptomatic Patients: Assessment with Coronary CT Angiography

To determine whether C-reactive protein is associated with the type of coronary plaque seen at computed tomographic (CT) angiography. The institutional review board approved this retrospective study, and the need for informed consent was waived. C-reactive protein levels were measured in 2653 asymptomatic subjects (mean age ± standard deviation, 54.7 years ± 9.2; 1811 men) who underwent self-referred coronary CT angiography as part of a general health checkup. The presence of coronary plaque, plaque type (calcified, mixed calcified, or noncalcified), stenosis degree, and number of involved segments were evaluated. Subjects with one type of plaque (calcified plaque, mixed plaque, and noncalcified plaque groups) and two or more types of plaque (multiple lesions group) were analyzed separately. Multivariate logistic regression analysis was used to evaluate the association between increasing C-reactive protein levels and plaque type. Coronary plaque was found in 1150 of the 2653 subjects (43.3%): calcified plaque (n = 604, 22.8%), mixed plaque (n = 67, 2.5%), noncalcified plaque (n = 208, 7.8%), and multiple lesions (n = 271, 10.2%). The C-reactive protein cutoff value of the fourth quartile was 1.2 mg/L (11.4 nmol/L), and all types of coronary plaque were increased in the higher quartile of the C-reactive protein levels. Multivariate logistic regression analysis showed that a higher C-reactive protein level was an independent predictor for the presence of noncalcified plaque (fourth vs first quartile group, odds ratio = 1.70, P = .025) and significant (50% and higher) coronary stenosis (odds ratio = 1.76, P = .020) after adjustment for traditional risk factors for coronary artery disease. C-reactive protein is associated with noncalcified coronary arterial plaque, as seen at coronary CT angiography in asymptomatic patients after adjustment for traditional risk factors.