Passive Smoking Severely Decreases Platelet Sensitivity to Antiaggregatory Prostaglandins

Sinzinger, H.; Kefalides, A

doi:10.1016/s0140-6736(82)90588-8

Cited by 52 publications

(18 citation statements)

References 4 publications

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“…Importantly, these results are also “similar” to those observed with traditional tobacco smoke, which heightens platelet activation (eg, aggregation)17, 94 and renders platelets less sensitive to PGI 2. 95 On the other hand, we observed no difference in the activation state of leukocytes between e‐cigarettes and clean air. This finding suggests that leukocytes do not contribute to the observed e‐cigarette phenotype; at least under the present experimental conditions.…”

Section: Discussionmentioning

confidence: 53%

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Qasim

Karim

Silva‐Espinoza

et al. 2018

JAHA

100

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BackgroundCardiovascular disease is the main cause of death in the United States, with smoking being the primary preventable cause of premature death, and thrombosis being the main mechanism of cardiovascular mortality in smokers. Due to the perception that electronic/e‐cigarettes are “safer/less harmful” than conventional cigarettes, their usage—among a variety of ages—has increased tremendously during the past decade. Notably, there are limited studies regarding the negative effects of e‐cigarettes on the cardiovascular system, which is also the subject of significant debate.Methods and ResultsWe employed a passive e‐VapeTM vapor inhalation system and developed an in vivo whole‐body e‐cigarette mouse exposure protocol that mimics real‐life human exposure scenarios/conditions and investigated the effects of e‐cigarettes and clean air on platelet function and thrombogenesis. Our results show that platelets from e‐cigarette–exposed mice are hyperactive, with enhanced aggregation, dense and α granule secretion, activation of the αIIbβ3 integrin, phosphatidylserine expression, and Akt and ERK activation, when compared with clean air–exposed platelets. E‐cigarette–exposed platelets were also found to be resistant to inhibition by prostacyclin, relative to clean air. Furthermore, the e‐cigarette–exposed mice exhibited a shortened thrombosis occlusion and bleeding times.ConclusionsTaken together, our data demonstrate for the first time that e‐cigarettes alter physiological hemostasis and increase the risk of thrombogenic events. This is attributable, at least in part, to the hyperactive state of platelets. Thus, the negative health consequences of e‐cigarette exposure should not be underestimated and warrant further investigation.

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Section: Discussionmentioning

confidence: 53%

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Qasim

Karim

Silva‐Espinoza

et al. 2018

JAHA

100

View full text Add to dashboard Cite

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“…85 These findings are consistent with experimental data showing a nonlinear effect on platelet activation and aggregation. 82,[86][87][88] Public smoking bans in multiple countries were associated with rapid and significant reductions in thrombotic cardiovascular events. [9][10][11] In a study in France, it was reported that smoke-free legislation led to a 40% reduction in fibrin-rich clot stiffness coupled with a drop in clotting time and fiber density among exposed subjects.…”

Section: Passive Smoking and Thrombosismentioning

confidence: 99%

Mechanisms of Coronary Thrombosis in Cigarette Smoke Exposure

Barua

Ambrose

2013

ATVB

207

126

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Abstract-Acute rupture or erosion of a coronary atheromatous plaque and subsequent coronary artery thrombosis cause the majority of sudden cardiac deaths and myocardial infarctions. Cigarette smoking is a major risk factor for acute coronary thrombosis. Indeed, a majority of sudden cardiac deaths attributable to acute thrombosis are in cigarette smokers. Both active and passive cigarette smoke exposure seem to increase the risk of coronary thrombosis and myocardial infarctions. Cigarette smoke exposure seems to alter the hemostatic process via multiple mechanisms, which include alteration of the function of endothelial cells, platelets, fibrinogen, and coagulation factors. This creates an imbalance of antithrombotic/ prothrombotic factors and profibrinolytic/antifibrinolytic factors that support the initiation and propagation of thrombosis.

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“…For example, Kritz and Sinzinger (30) observed an increase in markers of platelet activation and a decrease in platelet sensitivity to PGI2 among 12 nonsmokers exposed for 20-min in an 18 m3 room in which 30 Gitanes had recently been smoked. The hypercoagulable state demonstrated among nonsmokers acutely exposed to ETS (30)(31)(32)(33)(34) resembles the acute changes in smokers who consume one or two cigarettes after a period of abstinence (35)(36)(37)(38)(39)(40)(41)(42)(43). Schmid et al (31) found that, prior to ETS exposure, the platelets of nonsmokers were significantly less activated than those of smokers, whereas after 20 min exposure to ETS, platelet activation increased among the nonsmokers exposed to ETS (p < 0.01) but remained constant among the active smokers (p > 0.05).…”

Section: Experimental Studies Ofets Exposurementioning

confidence: 99%

Why Is Environmental Tobacco Smoke More Strongly Associated with Coronary Heart Disease Than Expected? A Review of Potential Biases and Experimental Data

Howard¹,

Thun²

1999

Environmental Health Perspectives

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Despite exposure levels estimated to be equivalent to smoking only 0.1-1.0 cigarettes per day, exposure to environmental tobacco smoke (ETS) is estimated to increase the risk of death from coronary heart disease (CHD) between 25 and 35% above the risk of nonexposed persons. This surprisingly large risk associated with a seemingly small exposure has raised doubts about the validity of attributing the increased CHD risk to ETS exposure. This paper reviews various biases that have been hypothesized to account for the increased CHD risk associated with ETS in the epidemiologic studies and characterizes the adverse effects of ETS on thrombosis, vascular endothelium, and exercise tolerance observed in experimental studies of humans and laboratory animals. None of the identified factors that has been proposed to introduce a spurious association between ETS and heart disease seem to invalidate the epidemiologic findings, either separately or in combination. In addition, experimental studies of ETS and heart disease demonstrate that acute exposure of humans and other species to ETS affects platelet function, vascular endothelium, and myocardial exercise tolerance at exposure concentrations widely prevalent in the workplace. Because exposure to ETS affects multiple physiologic pathways, it appears biologically plausible that ETS could cause the substantial increase in CHD risk that has been observed in epidemiologic studies. Key words: atherosclerosis, cardiovascular disease, risk factor, smoking. -Environ Health Perspect 1 07(suppl 6): 853-858 (1999). http.//ehpnet 1. niehs. nih.gov/docs/1999/suppl-6/853-858howard/abstract. html

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Passive Smoking Severely Decreases Platelet Sensitivity to Antiaggregatory Prostaglandins

Cited by 52 publications

References 4 publications

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Mechanisms of Coronary Thrombosis in Cigarette Smoke Exposure

Why Is Environmental Tobacco Smoke More Strongly Associated with Coronary Heart Disease Than Expected? A Review of Potential Biases and Experimental Data

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