Evaluation of the impact of cigarette smoking on platelet parameters

Swaminathan, Anandhalakshmi; Amitkumar, Kalaivani; Ganapathy, Shivasekar; Ayyavoo, Saravanan

doi:10.5455/njppp.2015.5.1009201570

Cited by 15 publications

(18 citation statements)

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“…Platelet activation and aggregability are more augmented in smokers than in non-smokers (5,6,26–29). A previous report found that chronic exposure to cigarette smoke sustains the activation of the endothelial-coagulative system, such as by increasing vWF antigen, D-dimer, prothrombin fragment F1+2, platelet factor-4 and beta-thromboglobulin, and smoking abstinence may result in the improvement of several endothelial-coagulative system abnormalities (30).…”

Section: Discussionmentioning

confidence: 99%

“…vWF activity decreases as early as 2 months after starting smoking abstinence, and other circulating endothelial-coagulative activation markers are substantially modified at 6 and 12 months after smoking abstinence in regular smokers (30). The mean platelet volume, which is known to be a simple and convenient indicator for platelet activation, is significantly higher in regular smokers than in non-smokers (6,28) and decreases significantly at three months after smoking cessation (28). In contrast, Morita et al (14) reported that only two weeks of smoking cessation in long-term smokers was able to ameliorate the enhanced platelet aggregability and intraplatelet redox imbalance.…”

Section: Discussionmentioning

confidence: 99%

“…Concerning the platelet function, the number of small aggregates of platelets in smokers' plasma is significantly higher than in non-smokers in the absence of chemical stimulants (5). Furthermore, acute smoking exposure in habitual smokers increases the platelet aggregation and induces greater resistance to thrombolysis than in non-smokers (5), and the mean platelet volume and platelet distribution width, which are indicators of platelet activation, are significantly higher in smokers than in non-smokers (6). However, there are no significant differences between smokers and non-smokers in platelet aggregation induced by ADP (7).…”

Section: Introductionmentioning

confidence: 99%

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Smoking cessation affects human platelet activation induced by collagen

et al. 2019

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It is firmly established that smoking is a risk factor of cardiovascular disease, stroke and peripheral vascular disease. Although smoking alters the hemostatic process, the influence of smoking on human platelet activation remains controversial. For patients undergoing surgery, cessation of smoking prior to the procedure is recommended as it increases the risk of postoperative morbidity or mortality. The presented study investigated the effects of smoking cessation on human platelet activation induced via collagen (n=19 patients). Blood samples were taken on four occasions: Before smoking cessation, and at 4, 8 and 12 weeks after smoking cessation. Platelet aggregation using citrated platelet-rich plasma (PRP) was monitored using a PA-200 aggregometer, which determined the size of platelet aggregates using laser scattering methods. A low dose of collagen (1 µg/ml) accelerated platelet aggregation at 4 or 8 weeks after smoking cessation when compared with results before cessation. After 12 weeks, levels of platelet aggregation induced by collagen were almost equal to those recorded prior to smoking cessation. The secretion levels of collagen-induced platelet-derived growth factor (PDGF)-AB at 4 or 8 weeks after smoking cessation were significantly higher than those before smoking was stopped. Furthermore, smoking cessation markedly strengthened the collagen-induced phosphorylation of p38 mitogen-activated protein (MAP) kinase after 4 weeks. The results of the current study indicated that smoking cessation causes temporary short-term human platelet hyper-activation. The further suggest that the incidence of complications due to human platelet hyper-reactivity may be lowered by considering the period of smoking abstinence.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Smoking cessation affects human platelet activation induced by collagen

et al. 2019

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“… 7 , 8 Smoking, however, augments platelet activation/aggregation and supports activation of the endothelial-coagulative system. 10 – 13 This special risk group of current smokers therefore might especially benefit from DPI, but the preferred way would be simply to quit smoking life long, thereby favourably shifting cost-effectiveness evaluations.…”

Section: Cost-effectiveness Of Dpi and Clinical All Day Care Realitymentioning

confidence: 99%

Cost-effectiveness of rivaroxaban plus aspirin (dual pathway inhibition) for prevention of ischaemic events in patients with cardiovascular disease: on top optimisation of secondary prevention medication in the context of COVID-19 pandemia

Rauch

2020

Eur J Prev Cardiolog

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“…Quitting smoking is also recommended for patients who are scheduled to undergo surgery because of the increased risk of the postoperative complications, such as pneumonia, wound-healing distress and even mortality (10)(11)(12)(13)(14)(15). With regard to the relationship between cigarette smoking and human platelets, it has been reported that platelets from habitual smokers exhibit increased spontaneous aggregation compared with those of non-smokers (16), and the activity of platelets in smokers is said to be much higher than in nonsmokers (17). Collagen is well recognized as a strong stimulator for human platelet activation, leading to the release of other stimulators, such as thromboxane A 2 and ADP (18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

Cigarette Smoking Cessation Temporarily Enhances the Release of Phosphorylated-HSP27 from Human Platelets

et al. 2020

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Objective Cigarette smoking is a risk factor for arteriopathy, including acute coronary syndrome, stroke and peripheral vascular disease. Thus, cessation is strongly recommended in order to reduce these risks. We recently demonstrated that smoking cessation causes temporary hyper-aggregability of human platelets. We previously showed that heat shock protein 27 (HSP27) is released from human platelets stimulated by collagen, accompanied by its phosphorylation. Accumulating evidence indicates potent roles of extracellular HSP27 as a modulator of inflammation. In the present study, using the stored samples obtained in the previous study, we investigated the effect of cigarette smoking cessation on the release of phosphorylated-HSP27 from collagen-activated human platelets (n=15 patients). Methods We enrolled patients who visited smoking cessation outpatient services between January 2012 and November 2014. Platelet-rich plasma, chronologically obtained before and after the cessation, was stimulated by collagen using a PA-200 aggregometer in the previous study. The levels of phosphorylated-HSP27 released from platelets were determined by an enzyme-linked immunosorbent assay. The phosphorylation of HSP27 in platelets was evaluated by a Western blot analysis. Results Cessation of cigarette smoking significantly upregulated the levels of collagen-stimulated release of phosphorylated-HSP27 at four and eight weeks after quitting smoking compared to before cessation. However, there was no significant difference between the levels before cessation and those at 12 weeks after cessation. The levels of phosphorylated-HSP27 stimulated by collagen in the platelets at four weeks after smoking cessation were remarkably enhanced compared to before cessation. Conclusion Cigarette smoking cessation temporarily enhances the collagen-stimulated release of phosphorylated-HSP27 from human platelets in the short term.

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Evaluation of the impact of cigarette smoking on platelet parameters

Cited by 15 publications

References 0 publications

Smoking cessation affects human platelet activation induced by collagen

Smoking cessation affects human platelet activation induced by collagen

Cost-effectiveness of rivaroxaban plus aspirin (dual pathway inhibition) for prevention of ischaemic events in patients with cardiovascular disease: on top optimisation of secondary prevention medication in the context of COVID-19 pandemia

Cigarette Smoking Cessation Temporarily Enhances the Release of Phosphorylated-HSP27 from Human Platelets

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