Nonstenotic Plaques Research Articles

Carotid Artery Plaques, Carotid Intima-Media Thickness, and Risk of Cardiovascular Events and All-Cause Death in Older Adults: A 5-Year Prospective, Community-Based Study.

We assessed the effect of asymptomatic carotid atherosclerosis (CAS) on the development of cardiovascular diseases (CVDs) in a community-based population aged ≥55 years in China. A total of 1376 residents underwent CAS assessment by ultrasonography in July 2009. New CVD events, including stroke and coronary heart events, were collected at the follow-up survey at the end of 2014. After adjusting for baseline demographic characteristics and traditional CVD risk factors, the risk of CVD in patients with minimal CAS (mean common carotid artery intima-media thickness [CCA-IMT] ≥1 mm and no plaques), nonstenotic plaques (carotid stenosis <50%), and stenotic plaques (carotid stenosis ≥50%) was 0.8 (hazard ratio [HR]: 0.75, 95% confidence interval [CI]: 0.33-1.69), 2.0 (HR: 2.01, 95% CI: 1.24-3.25), and 3.1 (HR: 3.05, 95% CI: 1.62-5.74) times greater, respectively, than that of patients without CAS (CCA-IMT <1 mm and no plaques). Our findings provide direct evidence of the independent predictive value of the severity of asymptomatic CAS for the development of CVD in older Chinese adults.

Carotid artery web and ischemic stroke: A case-control study.

To determine whether there is an association between carotid artery web and ischemic stroke. This was a single-center, age- and sex-matched, case-control study. Cases were consecutive patients with anterior circulation ischemic stroke of undetermined etiology (Trial of Org 10172 in Acute Stroke Treatment [TOAST] classification). Controls were consecutive patients with cerebral aneurysms, arteriovenous malformations, or primary intracerebral hemorrhages. Additional inclusion criteria were age <60 years and CT angiography of the neck. Two neuroradiologists diagnosed webs according to previously published criteria. One neuroradiologist also assessed for nonstenotic atherosclerotic plaque (carotid wall thickness ≥3 mm or intramural calcification). We used conditional logistic regression to estimate the odds ratio between carotid web and ischemic stroke and its 95% confidence interval. Fifty-three of 62 cases (85%) were matched by age (within 1 year) and by sex to 102 controls. There was a carotid web in 4 of 53 cases (9.4%) vs 1 of 102 controls (1.0%, odds ratio = 8.0, 95% confidence interval = 1.2-67, p = 0.032). There was no significant difference in the prevalence of nonstenotic carotid atherosclerotic plaque between the case and control groups. There was agreement on diagnosis of web for 163 of 164 patients (99%) and 7 of 8 webs (88%), and the Cohen κ for interobserver agreement was 0.93. There is an association between carotid artery web and ischemic stroke in patients who lack an alternative cause of stroke. Carotid web may be an underappreciated risk factor for stroke.

OS 18-02 ANTIHYPERTENSIVE TREATMENT AND RISK OF BRAIN ISCHEMIA DUE TO CAROTID STENOSIS IN A SURVEY OF HOSPITALISED PATIENTS AGED 90 YEARS AND OLDER

Objective: In elderly hypertensive patients, systolic blood pressure (sBP) goals recommended by US and European guidelines (ESH) for the initiation of treatment are more liberal than in younger patients because of an increased risk of treatment-associated side-effects and hypotension. Carotid stenosis increases with age and poses a risk of brain ischemia if hypotension occurs. Its relevance for the routine care of elderly hypertensives, however, remains unclear. We analyzed data on precerebral artery morphology and BP evolution from a survey of aged hospitalized patients. Design and Method: All patients ≥ 90 years admitted to the medical ward of a primary care hospital were prospectively included over 15 months. Ultrasound exams of the precerebral arteries were performed for routine evaluation of cardiovascular risk. Intima-media thickness (IMD) of the common carotid arteries (CCA) and internal and external carotid artery (I/ECC) stenosis were analyzed together with BPs (admission and discharge). Patients who died, with circulatory shock and readmissions were excluded (n = 9). Results: Sixty-three patients aged 92 ± 3 years (mean ± SD; range 90–101) with a median hospital stay of 11 days were analyzed (78% female, 35% diabetics, 24% atrial fibrillation, 41% coronary heart disease). On admission, 76% were on antihypertensive drugs and 43% had their number changed. Mean BP was 149/88 mmHg (36% sBP < 140 mmHg) vs. 129/72 mmHg at discharge (64% sBP <140 mmHg; p<0.05). Mean IMD (right/left) was 8.7/9.4 mm. Frequencies of non-stenotic plaque were: CCA 13/16%, ICC 13/16%, ECC 19/29%, bulb 62/70%; of ICC stenosis (≥ 60%) 5/5%, ECC stenosis (≥ 60%) 10/19%, ICC occlusion 2/2%, bilateral ICC stenosis 2% (1/63); none with bilateral ICC occlusion. Conclusions: In very old treated hypertensive patients, the risk of carotid stenosis-associated brain ischemia appears to be very low compared to stroke risk by the global burden of atrial fibrillation. Concerning carotid stenosis, sBP targets < 140 mmHg should be safe for the majority of nonagenarians.

Nonstenotic carotid plaque on CT angiography in patients with cryptogenic stroke.

To determine whether large (≥3 mm thick) but nonstenotic (<50%) carotid artery atherosclerotic plaque predominantly occurs ipsilateral rather than contralateral to cryptogenic stroke. This was a cross-sectional observational study. Using a stroke registry, we identified consecutive patients with anterior circulation embolic stroke of undetermined source (ESUS). Using CT angiography, we measured carotid plaque size (thickness, mm) and carotid artery stenosis (North American Symptomatic Carotid Endarterectomy Trial method) for each patient. We dichotomized plaque size at several predefined thresholds and calculated the frequency of plaque size above each threshold ipsilateral vs contralateral to stroke. We included 85 patients with ESUS. Plaque with thickness ≥5 mm was present ipsilateral to stroke in 11% of patients, and contralateral in 1% (9/85 vs 1/85; p = 0.008). Plaque with thickness ≥4 mm was present ipsilateral to stroke in 19% of patients, and contralateral in 5% (16/85 vs 4/85; p = 0.002). Plaque with thickness ≥3 mm was present ipsilateral to stroke in 35% of patients, and contralateral in 15% (30/85 vs 13/85; p = 0.001). There was no difference in percentage stenosis ipsilateral vs contralateral to stroke (p = 0.98), and weak correlation between plaque size and stenosis (R(2) = 0.26, p < 0.001). Large but nonstenotic carotid artery plaque is considerably more common ipsilateral than contralateral to cryptogenic stroke, suggesting that nonstenotic plaque is an underrecognized cause of stroke. We measured plaque size using CT angiography, a method that could be easily implemented in clinical practice.

Abstract TMP46: Computed Tomography of Non-Stenotic Carotid Plaque in Patients with Embolic Stroke of Undetermined Source (ESUS)

Introduction: In up to 25% of patients with an ischemic stroke, the standard investigations fail to identify a cause. Many of these cryptogenic strokes are thromboembolic, but without an established source, so called “embolic strokes of undetermined source” (ESUS). Non-stenotic carotid plaque is a potential source. Hypothesis: We hypothesized that among patients with ESUS, there is an association between non-stenotic carotid atherosclerotic plaque diagnosed using CT angiography and ipsilateral ischemic stroke. Methods: From a prospectively maintained stroke registry, we identified consecutive patients between January 2012 and March 2015 with a carotid territory ischemic stroke, who fulfilled the diagnostic criteria for ESUS. Two radiologists, blinded to clinical information, independently measured carotid plaque thickness ipsilateral and contralateral to the ischemic stroke using CT angiography. Results: Eighty-five of 1038 ischemic stroke patients were included in the analysis. There was no difference in the degree of carotid artery stenosis ipsilateral versus contralateral to ischemic stroke (median 0% versus 0%, p=0.98). There was a weak correlation between degree of carotid artery stenosis and carotid plaque thickness (R2 = 0.26, p&lt;0.001). Plaque thickness ≥ 5 mm (9/85 versus 1/85, p=0.008), ≥ 4 mm (16/85 versus 4/85, p=0.002), and ≥ 3 mm (30/85 versus 13/85, p=0.001) were each more common ipsilateral than contralateral to ischemic stroke. Plaque thickness ≥ 2 mm had the same frequency ipsilateral and contralateral to ischemic stroke. Conclusions: Our data suggest that large, non-stenotic carotid plaque may be an important source of embolism in patients with ESUS. We evaluated non-stenotic plaque using routine CT angiography, a method that could be easily translated into clinical practice.

Nonstenotic Culprit Plaque: The Utility of High-Resolution Vessel Wall MRI of Intracranial Vessels after Ischemic Stroke.

Intracranial atherosclerotic disease (ICAD) accounts for 9–15% of ischemic stroke in the United States. Although highly stenotic ICAD accounts for most of the strokes, it is assumed that nonstenotic ICAD (nICAD) can result in stroke, despite being missed on standard luminal imaging modalities. We describe a patient with nICAD who suffered recurrent thromboembolic stroke and TIA but had a negative conventional stroke workup. As a result, they were referred for high-resolution magnetic resonance imaging (HR-MRI) of the arterial vessel wall, which identified a nonstenotic plaque with multiple high-risk features, identifying it as the etiology of the patient's thromboembolic events. The diagnosis resulted in a transition from anticoagulation to antiplatelet therapy, after which the patient's clinical events resolved. HR-MRI is an imaging technique that has the potential to guide medical management for patients with ischemic stroke, particularly in cryptogenic stroke.

Free-floating thrombus in stroke patients with nonstenotic internal carotid artery-an ultrasonographic study.

There are multiple causes of free-floating thrombus (FFT) formation in carotid arteries. The purpose of this study was to evaluate the incidence and natural history of FFT in nonstenotic internal carotid arteries of patients with acute ischemic stroke. During a 50-month period, 3,200 consecutive patients with acute ischemic stroke were evaluated for internal carotid artery stenosis and the presence of FFT by color-coded duplex ultrasonography. Diagnostic workup included brain CT, transthoracic echocardiography, Holter electrocardiogram, and hypercoagulability state evaluation. We found an FFT in 5 (0.18%) of 2,757 patients with acute stroke and nonstenotic internal carotid artery (mean age 44 years). The underlying pathology was hypercoagulable state in active pulmonary tuberculosis (n = 1), essential thrombocythemia (n = 1), thrombotic complications of nonstenotic plaques (n = 1), unknown (n = 2). All patients clinically improved under antiplatelet therapy. Follow-up color-coded duplex ultrasonography showed complete dissolution of FFT in all cases. There was no stroke recurrence. Internal carotid artery FFT could be found in young stroke patients without identifiable arterial disease and could be resolved with antithrombotic treatment.

Prevalence of stenoses and occlusions of brain-supplying arteries in young stroke patients

Atherosclerosis is believed to be a minor cause of TIA and stroke in younger and middle-aged patients. However, data from large cohorts are limited. This study investigates the prevalence of extracranial and intracranial atherosclerosis in stroke and TIA patients aged 18-55 years in the multinational sifap1 study. From the sifap1 cohort (n = 5,023), we analyzed a subset of patients with complete data from carotid ultrasound studies. Patients with arterial dissections, vasculitis, and mobile thrombi were excluded. Among the remaining 2,187 patients (men: n = 1,319; 18-44 years: n = 744), intracranial arteries were additionally examined with ultrasonography in 1,612 patients (73.7%). Patients were stratified by sex and age groups (younger: 18-44 years; middle-aged: 45-55 years). In patients with ischemic stroke, the overall prevalence of carotid artery stenoses and occlusions was 8.9% (younger: 4.9%; middle-aged: 11.0%), of which 81% were symptomatic. Nonstenotic carotid plaques were more common in men than in women (15.8% vs. 7.7%; p < 0.001), and in middle-aged than in younger patients (17.0% vs. 4.9%; p < 0.001). Supratentorial intracranial artery stenoses and occlusions amounted to 11.8%. Supratentorial stenoses occurred more frequently in middle-aged patients (13.0% vs. 7.8%; p < 0.001), whereas occlusions were equally common (both 3.2%; not significant). We observed a substantial proportion of atherosclerotic carotid artery stenoses and occlusions in younger stroke patients. Intracranial stenoses and occlusions were even more prevalent than extracranial carotid artery disease. Together with nonstenotic plaques, one-fifth of patients (21.2%) had symptomatic or asymptomatic large-artery atherosclerosis, which should encourage future stroke prevention campaigns to target risk factor modification in young people.

Endothelial shear stress in the evolution of coronary atherosclerotic plaque and vascular remodelling: current understanding and remaining questions

The heterogeneity of plaque formation, the vascular remodelling response to plaque formation, and the consequent phenotype of plaque instability attest to the extraordinarily complex pathobiology of plaque development and progression, culminating in different clinical coronary syndromes. Atherosclerotic plaques predominantly form in regions of low endothelial shear stress (ESS), whereas regions of moderate/physiological and high ESS are generally protected. Low ESS-induced compensatory expansive remodelling plays an important role in preserving lumen dimensions during plaque progression, but when the expansive remodelling becomes excessive promotes continued influx of lipids into the vessel wall, vulnerable plaque formation and potential precipitation of an acute coronary syndrome. Advanced plaques which start to encroach into the lumen experience high ESS at their most stenotic region, which appears to promote plaque destabilization. This review describes the role of ESS from early atherogenesis to early plaque formation, plaque progression to advanced high-risk stenotic or non-stenotic plaque, and plaque destabilization. The critical implication of the vascular remodelling response to plaque growth is also discussed. Current developments in technology to characterize local ESS and vascular remodelling in vivo may provide a rationale for innovative diagnostic and therapeutic strategies for coronary patients that aim to prevent clinical coronary syndromes.

Utility of High-Spatial-Resolution Gray-Scale US in Characterizing Nonstenotic Plaque

Utility of High-Spatial-Resolution Gray-Scale US in Characterizing Nonstenotic Plaque

Determining patient prognosis using computed tomography coronary angiography

In addition to demonstrating luminal narrowings, cardiac computed tomography angiography (CTA) has the ability to detect nonstenotic plaque, vessel wall calcification and can assess left ventricular function. CTA prognostic studies have considered these components individually and in combination to produce novel risk factor scores to help predict clinical outcomes. In this article, we will consider the utility of CTA to predict clinical risk by considering the evidence for luminal stenosis, plaque scores, plaque descriptors and models combining these elements. We will also discuss some of the emerging applications of CTA that will likely provide future prognostic data in coronary artery disease patients. Although initially described as an anatomical investigation to determine the presence of coronary disease, CTA is being explored as a tool for functional imaging and may soon provide a noninvasive technique of anatomical and functional assessment previously only possible by invasive methods.

Optical molecular imaging of atherosclerosis using nanoparticles: shedding new light on the darkness

The application of optical nanoparticles in cardiovascular research is increasing because of the high spatiotemporal resolution and high sensitivity of optical techniques as compared with other imaging platforms. The major cause of cardiovascular events is atherosclerosis, which is a chronic inflammation of the arterial wall. Interestingly, the composition rather than the size of nonstenotic atherosclerotic plaques and severe plaques with >90% stenosis are indicators for high-risk vulnerability to rupture and acute cardiovascular events. Optical techniques may be highly suitable for discriminating, at subcellular resolution, the different stages of plaque progression by targeting bright and nontoxic optical nanoparticles toward distinct molecular epitopes in order to distinguish vulnerable from stable atherosclerotic plaques. Several optical techniques including two-photon laser scanning microscopy (TPLSM), optical coherence tomography (OCT), and photoacoustic imaging (PAI) have been applied for (in vivo) characterization of atherosclerotic plaques, in addition to investigate their feasibility in the clinical setting. Optical nanoparticles, however, have predominantly been used in optical molecular imaging of tumors, but their application in cardiovascular research is increasing. In this review, we first describe shortly the basics of the mentioned optical techniques. Then, we detail on the most-extensively studied optical nanoparticles and relatively new optical nanoparticles that hold promise for in vivo applications in atherosclerosis research.

Prognostic Value of Coronary Computed Tomographic Angiography in Diabetic Patients Without Known Coronary Artery Disease

OBJECTIVEDiabetic patients have a high prevalence of coronary artery disease (CAD), but timely diagnosis of CAD remains challenging. We assessed the ability of coronary computed tomography angiography (CCTA) to detect CAD in diabetic patients and to predict subsequent cardiac events.RESEARCH DESIGN AND METHODSWe analyzed 140 diabetic patients without known CAD undergoing CCTA; 1,782 patients without diabetes were used as a control group. Besides calcium scoring and the degree of the most severe stenosis, the atherosclerotic burden score counting the number of segments having either a nonstenotic plaque or a stenosis was recorded. The primary end point was a composite of hard cardiac events defined as all-cause death, nonfatal myocardial infarction, or unstable angina requiring hospitalization.RESULTSDuring a mean follow-up of 33 months, there were seven events in the diabetic group and 24 events in the control group. The best predictor in diabetic patients was the atherosclerotic burden score: the annual event rate ranged from 0.5% for patients with <5 lesions to 9.6% for patients with >9 lesions, resulting in a hazard ratio (HR) of 1.3 (95% CI 1.1–1.7) for each additional lesion (P = 0.005). For comparison, in nondiabetic patients the annual event rate ranged from 0.3 to 2.2%, respectively, resulting in an HR of 1.2 (95% CI 1.1–1.3, P < 0.001). The atherosclerotic burden score improved the prognostic value of conventional risk factors significantly (P < 0.001).CONCLUSIONSIn diabetic patients without known CAD, CCTA can identify a patient group at particularly high risk for subsequent hard cardiac events.

Segmental Heterogeneity of Vasa Vasorum Neovascularization in Human Coronary Atherosclerosis

Our aim was to investigate the role of coronary vasa vasorum (VV) neovascularization in the progression and complications of human coronary atherosclerotic plaques. Accumulating evidence supports an important role of VV neovascularization in atherogenesis and lesion location determination in coronary artery disease. VV neovascularization can lead to intraplaque hemorrhage, which has been identified as a promoter of plaque progression and complications like plaque rupture. We hypothesized that distinctive patterns of VV neovascularization and associated plaque complications can be found in different stages of human coronary atherosclerosis. Hearts from 15 patients (age 52+/-5 years, mean+/-SEM) were obtained at autopsy, perfused with Microfil (Flow Tech, Inc., Carver, Massachusetts), and subsequently scanned with micro-computed tomography (CT). The 2-cm segments (n=50) were histologically classified as either normal (n=12), nonstenotic plaque (<50% stenosis, n=18), calcified (n=10) or noncalcified (n=10) stenotic plaque. Micro-CT images were analyzed for VV density (number/mm2), VV vascular area fraction (mm2/mm2), and VV endothelial surface fraction (mm2/mm3). Histological sections were stained for Mallory's (iron), von Kossa (calcium), and glycophorin-A (erythrocyte fragments) as well as endothelial nitric oxide synthase, vascular endothelial growth factor, and tumor necrosis factor-alpha. VV density was higher in segments with nonstenotic and noncalcified stenotic plaques as compared with normal segments (3.36+/-0.45, 3.72+/-1.03 vs. 1.16+/-0.21, p<0.01). In calcified stenotic plaques, VV spatial density was lowest (0.95+/-0.21, p<0.05 vs. nonstenotic and noncalcified stenotic plaque). The amount of iron and glycophorin A was significantly higher in nonstenotic and stenotic plaques as compared with normal segments, and correlated with VV density (Kendall-Tau correlation coefficient 0.65 and 0.58, respectively, p<0.01). Moreover, relatively high amounts of iron and glycophorin A were found in calcified plaques. Further immunohistochemical characterization of VV revealed positive staining for endothelial nitric oxide synthase and tumor necrosis factor-alpha but not vascular endothelial growth factor. Our results support a possible role of VV neovascularization, VV rupture, and intraplaque hemorrhage in the progression and complications of human coronary atherosclerosis.

Percentage White: A New Feature for Ultrasound Classification of Plaque Echogenicity in Carotid Artery Atherosclerosis

Atherosclerotic stenotic and nonstenotic plaques of the carotid artery with low echogenicity have been shown to be associated with cardiovascular disease. The aim was to develop a new method for semiautomated ultrasound image analysis to classify nonstenotic carotid plaques, evaluate cases with multiple plaques and examine the association between a new image analysis feature of echogenicity and predictors of cardiovascular disease. The new image analysis feature, percentage white (PW), represents the fraction of bright structures inside a plaque and is integrated in an objective semiautomated method to evaluate echogenicity (SAMEE) in carotid plaques. PW was constructed to take into account overall echogenicity of the image as well as noise surrounding the plaque. Consecutive ultrasound examinations of carotid plaques from a population-based screening of 64-year-old women with varying risk for cardiovascular disease were selected for the present project; 92 far-wall and 47 near-wall plaques were used as a training dataset to develop the SAMEE algorithm with visual classification according to Gray-Weale as reference; 273 plaques were used to validate the method. All plaques were included in an analysis relating predictors of cardiovascular to average PW in all plaques, PW in the biggest plaque and to the plaque with lowest PW in each subject, respectively. In the training dataset the intermethodological variability between SAMEE and visual classification showed a κ of 0.78 and a sensitivity and specificity of 96% and 81%, respectively. In the validation set, SAMEE and visual classification showed a κ of 0.77, a sensitivity of 96% and a specificity of 80%. The reproducibility of PW was high, evidenced by r = 0.96 and CV = 9.85% at repeated examinations. Average PW values were associated with several predictors of cardiovascular risk: lipoprotein (a), HbA1c, blood glucose, apolipoproteinB/apolipoproteinA-I; and associated negatively with the levels of adiponectin and apolipoprotein A-I. In conclusion, PW integrated within a SAMEE is a new feature for assessment of echogenicity in carotid plaques and shows excellent reproducibility and agreement with visual assessment. (E-mail: ulrica.prahl@wlab.gu.se).

Association of pericardial fat accumulation rather than abdominal obesity with coronary atherosclerotic plaque formation in patients with suspected coronary artery disease

Objectives The purpose of this study was to examine the association of pericardial fat with the presence of coronary plaques. Background Waist circumference, reflecting abdominal obesity, is a risk factor of metabolic syndrome and coronary artery disease (CAD). Adipose tissue secretes many factors implicated in atherogenesis, however, the role of pericardial fat (ectopic visceral fat around coronary arteries) in the pathogenesis of CAD is not clear. Methods We measured total pericardial fat volume (PFV) and determined presence and characteristics of coronary plaques using 64-slice computed tomography in 171 consecutive patients suspected of CAD (101 men; mean age, 66 ± 11 years, ±SD). Results PFV correlated with age ( p < 0.05), body mass index ( p < 0.05), waist circumference ( p < 0.01), and high-density lipoprotein cholesterol ( p < 0.01) by multivariate regression analysis. PFV was significantly larger in patients with coronary plaques, even nonstenotic or noncalcified ones, than those without plaques (any plaques, n = 123; 201 ± 71 cm 3, nonstenotic plaques, n = 51; 192 ± 63, noncalcified plaques, n = 32; 196 ± 56 vs. no plaque, n = 48; 144 ± 45, p < 0.001, respectively). Multivariate backward logistic regression analysis demonstrated that PFV, but not waist circumference, significantly associated with the presence of any coronary plaques (odds ratio [OR]; 2.876, 95% confidence interval [95% CI]; 1.614–5.125, p < 0.001), nonstenotic plaques confirmed by coronary angiography (OR; 3.423, 95% CI; 1.764–6.642, p < 0.001), and noncalcified plaques (OR; 3.316, 95% CI; 1.435–7.661, p < 0.01). Conclusions PFV correlated significantly with the presence of nonstenotic and noncalcified coronary plaques assessed by multislice computed tomography. Pericardial fat is more highly associated with early development of CAD than simple anthropometric measures of abdominal obesity.

Prevalence and correlation factors of carotid atherosclerosis among the middle and old aged workers in an iron and steel corporation, Chongqing

To investigate the prevalence and correlation factors of carotid atherosclerosis (CAS) among workers of Chongqing Iron and Steel Corporation, and to offer information for the development of prevention program for cerebro-vascular disease. 512 asymptomatic individuals (mean age 56.8 years, ranged from 45 to 80) from the subsidiary workshop of Chongqing Iron and Steel Corporation were recruited. Demographic data and serum were collected and the internal-media thickness (IMT) of the CAS and the extent of plaque formation were evaluated by B-mode ultrasound. Logistic regression analysis was used to estimate the correlation factors of CAS. Results (1) The overall prevalence of carotid atherosclerosis among the iron and steel workers was 37.6%. IMT was found as 10.2% , with the prevalence rates of nonstenotic plaque and stenotic plaque were 25.0% and 2.4% respectively. (2) It was shown by logistic regression analysis that age (OR = 1.289, 95% CI: 1.014-1.568, P < 0.001), smoking (OR = 1.420, 95% CI: 0.802-3.872, P < 0.001), hypertension (OR= 4.530, 95% CI: 3.952-6.753, P < 0.001) , diabetes mellitus (OR = 2.285, 95% CI: 1.008-5.057, P < 0.001), HsCRP (OR = 1.273, 95% CI: 0.479-2.889, P = 0.037), TC (OR = 1.032, 95% CI: 0.320-1.882, P = 0.047) and LDL-C (OR = 2.313, 95% CI: 1.237-4.331, P = 0.008) were significantly associated with the severity of CAS. (3) Prevalence of the CAS increased with the increasing number of correlation factors. The prevalence of CAS among the iron and steel workers was higher than those in ordinary people of the same age. Age, smoking, hypertension, diabetes mellitus, HsCRP, TC and LDL-C were independent risk factors related to CAS. The prevalence of CAS was increasing parallel to the number of correlation factors.

58-Year Old Men with Non-Stenotic Carotid Artery Plaques and the Relationship with Cardiovascular Risk Factors and Future Cardiovascular Events

58-Year Old Men with Non-Stenotic Carotid Artery Plaques and the Relationship with Cardiovascular Risk Factors and Future Cardiovascular Events

ARFI Imaging for Noninvasive Material Characterization of Atherosclerosis Part II: Toward In Vivo Characterization

Seventy percent of cardiovascular disease (CVD) deaths are attributed to atherosclerosis. Despite their clinical significance, nonstenotic atherosclerotic plaques are not effectively detected by conventional atherosclerosis imaging methods. Moreover, conventional imaging methods are insufficient for describing plaque composition, which is relevant to cardiovascular risk assessment. Atherosclerosis imaging technologies capable of improving plaque detection and stratifying cardiovascular risk are needed. Acoustic radiation force impulse (ARFI) ultrasound, a novel imaging method for noninvasively differentiating the mechanical properties of tissue, is demonstrated for in vivo detection of nonstenotic plaques and plaque material assessment in this pilot investigation. In vivo ARFI imaging was performed on four iliac arteries: (1) of a normocholesterolemic pig with no atherosclerosis as a control, (2) of a familial hypercholesterolemic pig with diffuse atherosclerosis, (3) of a normocholesterolemic pig fed a high-fat diet with early atherosclerotic plaques and (4) of a familial hypercholesterolemic pig with diffuse atherosclerosis and a small, minimally occlusive plaque. ARFI results were compared with spatially matched immunohistochemistry, showing correlations between elastin and collagen content and ARFI-derived peak displacement and recovery time parameters. Faster recoveries from ARFI-induced peak displacements and smaller peak displacements were observed in areas of higher elastin and collagen content. Importantly, spatial correlations between tissue content and ARFI results were consistent and observable in large and highly evolved as well as small plaques. ARFI imaging successfully distinguished nonstenotic plaques, while conventional B-mode ultrasound did not. This work validates the potential relevance of ARFI imaging as a noninvasive imaging technology for in vivo detection and material assessment of atherosclerotic plaques. (E-mail: russbehler@unc.edu)

Controlling Cardiac Transport and Plaque Formation

Macro-particles transported in the bloodstream, such as LDL particles and macrophages, are considered to be one of the initiating factors of atherosclerotic plaque development. LDL infiltration from the bloodstream into a blood vessel's wall, whether the coronary, peripheral, or carotid arteries, is considered a major inflammatory factor, recruiting macrophages from the blood flow and leading to the formation of vulnerable atherosclerotic plaques. Infiltration sites are influenced by patterns of blood flow, as regions of lower shear stresses and high oscillations may give rise to higher infiltration rates through the endothelium, exacerbating the growth of a plaque and its tendency to rupture. Previous studies demonstrated a high prevalence of rupture sites proximal to the minimum lumen area, which raised the question of whether the existence of two distinct adjacent plaques, in which the distal plaque is more severe, can give rise to hemodynamic forces that can push the non-stenotic plaque to rupture. Models of the coronary arteries with one and two eccentric and concentric stenotic narrowings were built into a closed flow loop. The single stenosis model had a 75% area reduction narrowing (representing the vunerable atherosclerotic plaque) with relevant elastic properties. The double stenosis model included an additional distal 84% area reduction narrowing. The flow in the area between the two stenoses was recorded and analyzed using continuous doppler particle image velocimetry (CDPIV), together with the hydrostatic pressure acting on the proximal plaque. Results indicated that the combined shear rates and pressure effects in a model with a significant distal stenosis can contribute to the increase in plaque instability by LDL and enhanced macrophage uptake. The highly oscillatory nature of the disturbed flow near the shoulder of the vulnerable atherosclerotic plaque enriches its lipid soft core, and the high hydrostatic pressures acting on the same lesion in this geometry induce high internal maximal stresses that can trigger the rupture of the plaque.