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Echogenicity of the carotid arterial wall in active smokers.

ABSTRACT: This pilot study evaluated associations between carotid wall echogenicity, cardiovascular disease (CVD) risk factors, and three markers of smoking heaviness in a cohort of active smokers. Common carotid artery (CCA) grayscale median (GSM) values were measured from sonographic images. Univariable correlations and exploratory multivariable models were used to determine associations between CCA GSM, CVD risk factors, and measures of smoking heaviness. CCA GSM was measured in 162 smokers and was correlated inversely with cigarettes smoked/day (r=-0.16, p=0.048), pack-years (r=-0.204, p=0.009), CVD risk factors such as age, male sex, waist circumference, and low-density lipoprotein cholesterol (all p?0.03) and positively with high-density lipoprotein cholesterol (p<0.001). Associations between CCA GSM and smoking heaviness markers were not statistically significant after adjustment for traditional risk factors. The results from this pilot study demonstrate the feasibility of measuring the GSM value of the CCA far wall and its association with measures of smoking heaviness and traditional CVD risk factors among current smokers.

SUBMITTER: Mitchell C

PROVIDER: S-EPMC6051703 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature

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Echogenicity of the carotid arterial wall in active smokers.

Mitchell Carol C Piper Megan E ME Korcarz Claudia E CE Hansen Kristin K Weber JoAnne J Fiore Michael C MC Baker Timothy B TB Stein James H JH

Journal of diagnostic medical sonography : JDMS 20171219 3

This pilot study evaluated associations between carotid wall echogenicity, cardiovascular disease (CVD) risk factors, and three markers of smoking heaviness in a cohort of active smokers. Common carotid artery (CCA) grayscale median (GSM) values were measured from sonographic images. Univariable correlations and exploratory multivariable models were used to determine associations between CCA GSM, CVD risk factors, and measures of smoking heaviness. CCA GSM was measured in 162 smokers and was cor ...[more]

PMID: 30035269

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Project description:ObjectivesAlthough carotid artery intima media thickness (CIMT) is a widely used determinant of subclinical atherosclerosis, gray-scale median of the intima-media complex (IM-GSM) of the common carotid artery is a relatively novel measure of echogenicity reflecting composition of the arterial wall. It is important to compare cardiovascular disease (CVD) risk factor correlates across CIMT and IM-GSM to determine whether these measures reflect distinct aspects of atherosclerosis.MethodsBaseline information from a completed randomized clinical trial of 643 healthy postmenopausal women without clinically apparent CVD was included in this cross-sectional study. The women were on average ± SD 61 ± 7 years old, and predominantly non-Hispanic White. CIMT and IM-GSM were measured by high-resolution B-mode ultrasonogram in the far wall of the right common carotid artery. CVD risk factors including age, race, body mass index (BMI), smoking, weekly hours of physical activity, systolic (SBP) and diastolic blood pressure (DBP), lipids, glucose, and inflammatory markers were measured at baseline. Linear regression models were used to assess associations of CVD risk factors with CIMT and IM-GSM. Multivariable models included groups of risk factors added one at a time with and withoutbasic demographic factors (age, race, BMI, physical activity) with model R2 values compared between CIMT and IM-GSM.ResultsIn multivariable analysis, age, Black race, BMI, SBP, and DBP were associated with CIMT (all P < .05), whereas age, Hispanic race, BMI, SBP, physical activity, LDL-cholesterol, and leptin were correlates of IM-GSM (all P < .05). Adjusted for age, race, BMI, and physical activity, the R2 value for SBP was greater for CIMT association, whereas R2 values for lipids, glucose, inflammatory markers, and adipokines were greater for IM-GSM associations.ConclusionsCIMT and IM-GSM assess different attributes of subclinical atherosclerosis. Integrating both measures may provide improved assessment of atherosclerosis in asymptomatic individuals.

Project description:Arterial wall dynamics arise from the synergy of passive mechano-elastic properties of the vascular tissue and the active contractile behaviour of smooth muscle cells (SMCs) that form the media layer of vessels. We have developed a computational framework that incorporates both these components to account for vascular responses to mechanical and pharmacological stimuli. To validate the proposed framework and demonstrate its potential for testing hypotheses on the pathogenesis of vascular disease, we have employed a number of pharmacological probes that modulate the arterial wall contractile machinery by selectively inhibiting a range of intracellular signalling pathways. Experimental probes used on ring segments from the rabbit central ear artery are: phenylephrine, a selective α1-adrenergic receptor agonist that induces vasoconstriction; cyclopiazonic acid (CPA), a specific inhibitor of sarcoplasmic/endoplasmic reticulum Ca2+-ATPase; and ryanodine, a diterpenoid that modulates Ca2+ release from the sarcoplasmic reticulum. These interventions were able to delineate the role of membrane versus intracellular signalling, previously identified as main factors in smooth muscle contraction and the generation of vessel tone. Each SMC was modelled by a system of nonlinear differential equations that account for intracellular ionic signalling, and in particular Ca2+ dynamics. Cytosolic Ca2+ concentrations formed the catalytic input to a cross-bridge kinetics model. Contractile output from these cellular components forms the input to the finite-element model of the arterial rings under isometric conditions that reproduces the experimental conditions. The model does not account for the role of the endothelium, as the nitric oxide production was suppressed by the action of L-NAME, and also due to the absence of shear stress on the arterial ring, as the experimental set-up did not involve flow. Simulations generated by the integrated model closely matched experimental observations qualitatively, as well as quantitatively within a range of physiological parametric values. The model also illustrated how increased intercellular coupling led to smooth muscle coordination and the genesis of vascular tone.

Project description:The arterial system in diabetic patients is characterized by generalized non-atherosclerotic alterations in the vascular extracellular matrix causing increased arterial stiffness compared with subjects without diabetes. The underlying pathophysiology remains elusive. The elastin-associated extracellular matrix protein, fibulin-1, was recently found in higher concentrations in the arterial wall and in plasma in patients with long duration type 2 diabetes. Furthermore, plasma fibulin-1 independently predicted total mortality and was associated with pulse pressure, an indirect measure of arterial stiffness. Whether plasma fibulin-1 is associated with arterial stiffness at earlier phases of type 2 diabetes has not been determined.In this cross-sectional study, we examined 90 patients with recently diagnosed type 2 diabetes (< 5 years) and 90 gender- and age-matched controls. Plasma fibulin-1 was measured immunochemically. Arterial stiffness was assessed by carotid-femoral Pulse Wave Velocity (PWV). Differences in means were assessed by t-tests. Associations were assessed by multivariate regression analyses.Plasma fibulin-1 levels were lower in the diabetic group compared with the control group, 93?±?28 vs 106?±?30 ?g/mL, p?=?0.005. In unadjusted analysis of the total study sample, plasma fibulin-1 was not associated with PWV, p?=?0.46. However, with adjustment for the confounders age, gender, mean blood pressure, heart rate, body mass index, diabetes and glomerular filtration rate, a 10 ?g/mL increase in plasma fibulin was associated with 0.09?±?0.04 m/s increase in PWV, p?<?0.05. In subgroup analysis, plasma fibulin-1 was associated with PWV in the diabetes group, (0.16?±?0.07 m/s increase in PWV per 10 ?g/mL increase in plasma fibulin-1, p<0.05), but not controls, ??=?0.021?±?0.057 m/s per 10 ?g/mL, p?=?0.70. The association remained significant in the diabetes group after adjustment for covariates, p < 0.05.Plasma fibulin-1 is independently associated with PWV. Yet, as the plasma level of fibulin-1 was lower in patients with recently diagnosed type 2 diabetes than in healthy controls, plasma fibulin-1 levels are not a simple marker of the degree of arterial stiffening. Further studies are needed to determine the exact role of fibulin-1 in arterial stiffness and cardiovascular risk in patients with type 2 diabetes.

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Echogenicity of the carotid arterial wall in active smokers.

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Echogenicity of the carotid arterial wall in active smokers.

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