Article

Carotid plaque, a subclinical precursor of vascular events - The Northern Manhattan Study

Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Neurology (Impact Factor: 8.3). 05/2008; 70(14):1200-7. DOI: 10.1212/01.wnl.0000303969.63165.34
Source: PubMed

ABSTRACT Carotid atherosclerosis is a known biomarker associated with future vascular disease. The risk associated with small, nonstenotic carotid plaques is less clear. The objective of this study was to examine the association between maximum carotid plaque thickness and risk of vascular events in an urban multiethnic cohort.
As part of the population-based Northern Manhattan Study, carotid plaque was analyzed among 2,189 subjects. Maximum carotid plaque thickness was evaluated at the cutoff level of 1.9 mm, a prespecified value of the 75th percentile of the plaque thickness distribution. The primary outcome measure was combined vascular events (ischemic stroke, myocardial infarction, or vascular death).
Carotid plaque was present in 1,263 (58%) subjects. After a mean follow-up of 6.9 years, vascular events occurred among 319 subjects; 121 had fatal or nonfatal ischemic stroke, 118 had fatal or nonfatal myocardial infarction, and 166 died of vascular causes. Subjects with maximum carotid plaque thickness greater than 1.9 mm had a 2.8-fold increased risk of combined vascular events in comparison to the subjects without carotid plaque (hazard ratio, 2.80; 95% CI, 2.04-3.84). In fully adjusted models, this association was significant only among Hispanics. Approximately 44% of the low-risk individuals by Framingham risk score had a 10-year vascular risk of 18.3% if having carotid plaque.
Maximum carotid plaque thickness is a simple and noninvasive marker of subclinical atherosclerosis associated with increased risk of vascular outcomes in a multiethnic cohort. Maximum carotid plaque thickness may be a simple and nonexpensive tool to assist with vascular risk stratification in preventive strategies and a surrogate endpoint in clinical trials.

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Available from: Tatjana Rundek, Jan 26, 2015
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    • "All these carotid segments were examined for presence of atherosclerotic plaque. Plaque was defined as an area of focal wall thickening >50% greater than surrounding wall thickness [4] "
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    ABSTRACT: Recent cohort studies suggested that serum levels of soluble Receptor for Advanced Glycation End-products (sRAGE) are associated with the risk of cardiovascular disease. We hypothesized that sRAGE levels are associated with subclinical atherosclerosis in a racially and ethnically diverse population. 828 stroke-free participants from the Northern Manhattan Study (mean age 71.1 ± 8.7yrs; 64% Hispanic, 19% black, and 17% white) underwent high-resolution carotid B-mode ultrasound to measure carotid plaque (present in 62% of subjects) and intima-media thickness (IMT) (mean Total = 0.96 ± 0.10 mm). Serum sRAGE was measured by ELISA and associations tested between sRAGE with IMT and plaque presence. Soluble RAGE levels were not associated with plaque presence or IMT after adjusting for sociodemographic, vascular risk factors and medication use. Stratification by race-ethnicity did not reveal any associations with carotid IMT or plaque. In the present study, sRAGE levels were not associated with carotid atherosclerosis. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    Atherosclerosis 02/2015; 240(1):17-20. DOI:10.1016/j.atherosclerosis.2015.02.015 · 3.97 Impact Factor
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    • "Maximum plaque thickness was measured for each plaque in an individual at the highest plaque prominence between the lumeneintima and mediaeadventitia boundaries. The maximum value of maximal thickness measured in all plaques within an individual was used in the analyses [22] "
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    ABSTRACT: Objective The objective of this cross-sectional analysis was to investigate the relation between two major high-density lipoprotein cholesterol (HDL-C) subfractions (HDL2-C and HDL3-C) and carotid plaque in a population based cohort. Methods We evaluated 988 stroke-free participants (mean age 66 ± 8 years; 40% men; 66% Hispanic and 34% Non-Hispanic) with available data on HDL subfractions using precipitation method and carotid plaque area and thickness assessed by a high-resolution 2D ultrasound. The associations between HDL-C subfractions and plaque measurements were analyzed by quantile regression. Results Plaque was present in 56% of the study population. Among those with plaque, the mean ± SD plaque area was 19.40 ± 20.46 mm² and thickness 2.30 ± 4.45 mm. The mean ± SD total HDL-C was 46 ± 14 mg/dl, HDL2-C 14 ± 8 mg/dl, and HDL3-C 32 ± 8 mg/dl. After adjusting for demographics and vascular risk factors, there was an inverse association between HDL3-C and plaque area (per mg/dl: beta = −0.26 at the 75th percentile, p = 0.001 and beta = −0.32 at the 90th percentile, p = 0.02). A positive association was observed between HDL2-C and plaque thickness (per mg/dl; beta = 0.02 at the 90% percentile, p = 0.003). HDL-C was associated with plaque area (per mg/dl: beta = −0.18 at the 90th percentile, p = 0.01), but only among Hispanics. Conclusion In our cohort we observed an inverse association between HDL3-C and plaque area and a positive association between HDL2-C and plaque thickness. HDL-C subfractions may have different contributions to the risk of vascular disease. More studies are needed to fully elucidate HDL-C anti-atherosclerotic functions in order to improve HDL-based treatments in prevention of vascular disease and stroke.
    Atherosclerosis 11/2014; 237(1):163–168. · 3.97 Impact Factor
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    • "High-resolution B-mode 2-dimensional ultrasound was performed for the examination of carotid plaque according to the standard scanning and reading protocols [3]. Carotid bifurcation and internal and common carotid arteries were examined for plaque defined as an area of focal wall thickening N 50% greater than surrounding wall thickness in millimeters. "
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    ABSTRACT: Background and purpose: Smoking greatly increases the risk of atherosclerotic plaque and the effect may vary from individual to individual. A genome-wide scan was performed for smoking x single nucleotide polymorphism (SNP) interactions on carotid plaque burden (CPB) to identify the potential genetic moderators in Hispanics. Methods: Carotid B-mode ultrasonography and genotyping by the Affymetrix 6.0 chip were performed in a discovery sample of 665 Caribbean Hispanics, followed by replication analyses in 264 Caribbean Hispanics. CPB was expressed as the sum of plaque areas over the segments in common and internal carotid arteries and bifurcation. Smoking was classified as 0, <20, and >= 20 cigarette pack-years. Assuming an additive genetic model, regression analysis was conducted to test for smoking x SNP interaction on the cube root transformed CPB while controlling for age, sex, and the top 3 principal components of ancestry. Results:Two SNPs showed a significant interaction with smoking on CPB with the similar effects in both discovery (P < 1.0E - 5) and replication (P < 0.05) populations. Specifically, for SNP rs10205487 within MXD1, more smoking was significantly associated with greater CPB in A allele carriers (beta +/- SE: 0.24 +/- 0.08, P = 0.005 in AG carriers; beta +/- SE: 0.48 +/- 0.12, P = 0.0002 in AA carriers) but not in GG (P = 0.06). For SNP rs7001413 within LY96 and JPH1, more smoking was significantly associated with greater CPB in GG carriers (beta +/- SE: 0.24 +/- 0.06, P = 6.8E - 5) but not in T carriers (P = 0.06). Conclusions: Our study suggests that genetic variants may modulate the effect of smoking on CPB and highlights several genes for further investigation of their role in atherosclerosis, especially in smoking population.
    Journal of the Neurological Sciences 09/2014; 344(1-2):27-31. DOI:10.1016/j.jns.2014.06.006 · 2.26 Impact Factor
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