Effect of Smoking Status on Monocyte Tissue Factor Activity, Carotid Atherosclerosis and Long-Term Prognosis in Metabolic Syndrome

Kohashi, Keiichi; Nakagomi, Akihiro; Morisawa, Taichirou; Endoh, Ikuko; Kawaguchi, Naomi; Kusama, Yoshiki; Shimizu, Wataru

doi:10.1253/circj.cj-17-0644

Cited by 13 publications

(11 citation statements)

References 34 publications

(36 reference statements)

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“… 8 , 9 Few studies examined the effects of acute CSE on clotting, but circulating tissue factor activity increased levels have been demonstrated after short-term of cigarette smoking. 9 , 10 So, CSE shows increasing prothrombotic biomarkers and might directly promote thrombosis.…”

mentioning

confidence: 99%

Effects of cigarette smoking on coagulation screening tests and platelet counts in a Sudanese male adults population

Elkhalifa

2018

SMJ

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Objectives:To study the effects of heavy cigarette smoking on coagulation (CGG) screening tests and platelet counts (PLTs) in a Sudanese male adults population.Methods:A case control study was conducted at both Kosti and Gabalein towns, Sudan, during October 2016 to May 2017. A 100 adult cigarette smokers were selected and another 100 matched non-smokers were selected as healthy controls. Blood samples were collected in trisodium citrate anti-coagulant for prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR), analyzed using standard methods (co-agulometer machine) and Ethylenediaminetetraacetic acid for the platelet counts, using an automated haematology analyzer (Sysmex, Tokoyo, Japan).Results:The results showed that the mean platelet counts were significantly lower in the smokers (183x103/cmm±64x103/cmm) versus (244x103/cmm±38x103/cmm) in non-smokers, (p<0.000). Pearson correlation analysis suggested a weak negative correlation between platelet counts with the duration of smoking (r= -0.289, p<0.004) and the age of the smokers (r= -0.238, p<0.017). The mean PT and INR were also significantly lower in smokers (12.9±1.2 seconds) compared with the non-smokers (13.7±1.04 seconds, p<0.000), for PT and (0.95±0.09 versus 1.01±0.08, p<0.000) for INR. In contrast, PTT had no significant variation in smokers (30.5±3.8 seconds) and the non-smokers (37.9±4.6 seconds). A p-value>0.05 was considered significant.Conclusion:Cigarette smokers tend to have lower platelet counts, shorter PT, and INR values, compared to non-smokers. Therefore, smoking might be associated with bleeding disorders but further investigations are needed.

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confidence: 99%

Effects of cigarette smoking on coagulation screening tests and platelet counts in a Sudanese male adults population

Elkhalifa

2018

SMJ

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“…In a small group of patients with metabolic syndrome (n=301), four groups were identified according to smoking status at entry and at 12 months: never smokers, past smokers, quitters, and persistent smokers. After 12 months of follow-up even a C-IMT regression was observed in never smokers, past smokers and quitters (by -2.78%, -0.33%, and -1.16%, respectively), whereas persistent smokers showed a progression of 33.3% from baseline [12]. Current or even past smoking emerged by multivariate analyses as independent predictors of C-IMTp in many other population-based cohort studies [4,7,8,[13][14][15][16][17][18][19], as well as in patients with hypercholesterolemia [20], type 1 diabetes (T1DM) [21], or cardiovascular disease (CVD) [22].…”

Section: Methodsmentioning

confidence: 91%

Traditional Risk Factors are Causally Related to Carotid Intima-Media Thickness Progression: Inferences from Observational Cohort Studies and Interventional Trials

Frigerio

Werba

Amato

et al. 2020

CPD

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In the present review, associations between traditional vascular risk factors (VRFs) and carotid intimamedial thickness progression (C-IMTp) as well as the effects of therapies for VRFs control on C-IMTp were appraised to infer causality between each VRF and C-IMTp. Cohort studies indicate that smoking, binge drinking, fatness, diabetes, hypertension and hypercholesterolemia are associated with accelerated C-IMTp. An exception is physical activity, with mixed data. Interventions for the control of obesity, diabetes, hypertension and hypercholesterolemia decelerate C-IMTp. Conversely, scarce information is available regarding the effect of smoking cessation, stop of excessive alcohol intake and management of the metabolic syndrome. Altogether, these data support a causative role of several traditional VRFs on C-IMTp. Shortcomings in study design and/or ultrasonographic protocols may account for most negative studies, which underlines the importance of careful consideration of methodological aspects in investigations using C-IMTp as the outcome.

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“…Smoking influences all stages of atherosclerotic plaque formation [55,56]. Cigarette smoking is associated with vascular endothelial dysfunction, increased expression of monocyte tissue factor, and oxidative stress due to the increased ROS production and decreased antioxidant defense systems [57,58]. These changes have an important effect on monocyte recruitment.…”

Section: Macrophagesmentioning

confidence: 99%

Macrophage origin, phenotypic diversity, and modulatory signaling pathways in the atherosclerotic plaque microenvironment

Liu¹,

Zhang²,

Sun³

et al. 2021

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Effect of Smoking Status on Monocyte Tissue Factor Activity, Carotid Atherosclerosis and Long-Term Prognosis in Metabolic Syndrome

Cited by 13 publications

References 34 publications

Effects of cigarette smoking on coagulation screening tests and platelet counts in a Sudanese male adults population

Effects of cigarette smoking on coagulation screening tests and platelet counts in a Sudanese male adults population

Traditional Risk Factors are Causally Related to Carotid Intima-Media Thickness Progression: Inferences from Observational Cohort Studies and Interventional Trials

Macrophage origin, phenotypic diversity, and modulatory signaling pathways in the atherosclerotic plaque microenvironment

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