Biglycan expression in current cigarette smokers: A possible link between active smoking and atherogenesis

Mandraffino, Giuseppe; Imbalzano, Egidio; Mamone, F.; Aragona, Caterina Oriana; Gullo, Alberto Lo; D’Ascola, Angela; Alibrandi, Angela; Cinquegrani, Antonella; Mormina, Enricomaria; Versace, Antonio Giovanni; Basile, Giorgio; Sardo, M.A.; Cinquegrani, Maria; Carerj, Scipione; Saitta, Antonino

doi:10.1016/j.atherosclerosis.2014.10.024

Cited by 15 publications

(10 citation statements)

References 39 publications

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“…In 10 studies (10 of 63 studies), stiffness was assessed locally (termed "single-point" onward) by measuring local vessel diameter and distension by ultrasound or MRI and estimating the corresponding local pulse pressure driving the cyclic distension (9,28,64,80,81,87,113,125,138,143). Conventionally, pressure-diameter or pressure-area data are used to calculate local distensibility (DC) or compliance (CC) coefficients, which are linear approximations over the observed diastolic/systolic range.…”

Section: Content Analysis Of Selected Papersmentioning

confidence: 99%

Constitutive interpretation of arterial stiffness in clinical studies: a methodological review

Reesink

Spronck

2019

American Journal of Physiology-Heart and Circulatory Physiology

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Clinical assessment of arterial stiffness relies on noninvasive measurements of regional pulse wave velocity or local distensibility. However, arterial stiffness measures do not discriminate underlying changes in arterial wall constituent properties (e.g., in collagen, elastin, or smooth muscle), which is highly relevant for development and monitoring of treatment. In arterial stiffness in recent clinical-epidemiological studies, we systematically review clinical-epidemiological studies (2012–) that interpreted arterial stiffness changes in terms of changes in arterial wall constituent properties (63 studies included of 514 studies found). Most studies that did so were association studies (52 of 63 studies) providing limited causal evidence. Intervention studies (11 of 63 studies) addressed changes in arterial stiffness through the modulation of extracellular matrix integrity (5 of 11 studies) or smooth muscle tone (6 of 11 studies). A handful of studies (3 of 63 studies) used mathematical modeling to discriminate between extracellular matrix components. Overall, there exists a notable gap in the mechanistic interpretation of stiffness findings. In constitutive model-based interpretation, we first introduce constitutive-based modeling and use it to illustrate the relationship between constituent properties and stiffness measurements (“forward” approach). We then review all literature on modeling approaches for the constitutive interpretation of clinical arterial stiffness data (“inverse” approach), which are aimed at estimation of constitutive properties from arterial stiffness measurements to benefit treatment development and monitoring. Importantly, any modeling approach requires a tradeoff between model complexity and measurable data. Therefore, the feasibility of changing in vivo the biaxial mechanics and/or vascular smooth muscle tone should be explored. The effectiveness of modeling approaches should be confirmed using uncertainty quantification and sensitivity analysis. Taken together, constitutive modeling can significantly improve clinical interpretation of arterial stiffness findings.

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Section: Content Analysis Of Selected Papersmentioning

confidence: 99%

Constitutive interpretation of arterial stiffness in clinical studies: a methodological review

Reesink

Spronck

2019

American Journal of Physiology-Heart and Circulatory Physiology

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“…Arterial hypertension and hyperlipidemia predicted cardiovascular complications such as myocardial infarction and stroke. The effect of total cholesterol (TCH) and low-density lipoprotein cholesterol (LDL-C) levels on carotid intimamedia thickness was studied in previous works and the differences in the dependence on smoking status were confirmed [3]. It was expected that different mechanisms were involved in atherogenesis in LDL according to smoking status [4,5].…”

Section: Introductionmentioning

confidence: 99%

Features of the Lipid Profile in Patients with Arterial Hypertension and Cardiovascular Diseases According to Smoking Status

Gaisenok¹,

Martsevich²,

Леонова³

2018

TOHYPERJ

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Introduction: Smoking is a risk factor for cardiovascular diseases. The direct influence of smoking status on the lipid profile was highlighted in patients with arterial hypertension and associated cardiovascular disease. Objective: We aimed to evaluate lipid profile among patients related to smoking status in a registry-based cohort study. Methods: The data of registry of National Research Сenter of Preventive Medicine were conducted. Patients filled in the special questionnaire in order to identify their smoking status, statins therapy. Results: 274 patients were included; main nosologic disease was arterial hypertension (230 patients), 14.8% were smokers, 62.9% non-smokers, and 22.2% past-smokers. The rank analysis of variations by Kruskal-Wallis (H) test for multiple comparisons between groups revealed significant differences in lipid levels for patients according to smoking status: total cholesterol H (2, n=234) =9.119, p=0.0105; LDL-cholesterol H (2, n=225) =6.2615, p=0.0437; triglycerides H (2, n=216) =9.8485, p=0.0073; these indicators of lipid profile among non-smoking patients were lower than among smokers, these indices among past-smokers were lower than among smokers. The absence of statistically significant differences between groups was confirmed in statin therapy (χ2 =3.169, df=4, p=0.529). Logistic regression analysis was conducted to identify factors that influence achievement target lipid levels. Only 2 statistically significant signs were identified in this model: smoking (OR 0.1; 95%CI [0.13;4.87]; p=0.03) and statin therapy (OR 8.2;95%CI [-3.6; -,078]; p=0.002). Conclusion: Significantly higher lipid levels have been observed in smokers compared to non-smokers in patients with arterial hypertension and associated cardiovascular disease. Smoking is a great factor disincentive to achieve target lipid levels.

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“…In this issue of Atherosclerosis, Mandraffino and colleagues analysed a large number (n > 250) of healthy young current smokers and found increased monocytic BGN expression, which highly correlated with arterial stiffness and c-IMT [7]. Their findings are of special relevance regarding CVDs as they provide strong evidence for the early onset and accelerated atherogenesis in young cigarette smokers.…”

mentioning

confidence: 97%

Biglycan: Unpuzzling the causal links between tobacco-smoking and atherosclerosis?

Baumgartner

2014

Atherosclerosis

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Biglycan expression in current cigarette smokers: A possible link between active smoking and atherogenesis

Cited by 15 publications

References 39 publications

Constitutive interpretation of arterial stiffness in clinical studies: a methodological review

Constitutive interpretation of arterial stiffness in clinical studies: a methodological review

Features of the Lipid Profile in Patients with Arterial Hypertension and Cardiovascular Diseases According to Smoking Status

Biglycan: Unpuzzling the causal links between tobacco-smoking and atherosclerosis?

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