Effects of Cigarette Smoke Exposure on Clot Dynamics and Fibrin Structure

Barua, Rajat S.; Sy, Fridolin; Srikanth, Sundararajan; Huang, Grace Y.; Javed, Usman; Buhari, Cyrus F.; Margosan, Dennis A.; Ambrose, John A.

doi:10.1161/atvbaha.109.195024

Cited by 114 publications

(104 citation statements)

References 23 publications

(33 reference statements)

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“…In the case of CORM-2 exposure, both normal and factor XIII deficient PPP demonstrated a decrease in large fiber and increase in fine fiber formation as documented by transmission electron microscopy [50]. A similar increase in clot matrix density and fine fiber formation was observed in PPP obtained from smokers as determined by scanning electron microscopy (SEM) [83]. Using PRP, Pretorius and colleagues demonstrated by SEM the formation of not just finer fibers, but also sheet-like matting of thrombus ultrastructure in the settings of smoking [84], type II diabetes mellitus [85] and rheumatoid arthritis [86].…”

Section: Ultrastructural Findings Supporting a Procoagulant Role For Comentioning

confidence: 68%

“…Investigations of platelet poor plasma (PPP) or platelet rich plasma (PRP) obtained from samples exposed to CORM-2 [50], obtained from smokers [83,84], obtained from patients with type II diabetes mellitus [85], and rheumatoid arthritis [86] all display similar Nielsen et al 16 16 features that may be secondary to CO exposure compared to normal subject plasma.…”

Section: Ultrastructural Findings Supporting a Procoagulant Role For Comentioning

confidence: 98%

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Carbon monoxide: Anticoagulant or procoagulant?

Nielsen

Pretorius

2014

Thrombosis Research

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Within the past decade there have been several investigations attempting to define the impact of exogenous and endogenous carbon monoxide exposure on hemostasis.Critically, two bodies of literature have emerged, with carbon monoxide mediated platelet inhibition cited as a cause of in vitro human and in vitro/in vivo rodent anticoagulation. In contrast, interaction with heme groups associated with fibrinogen, α 2 -antiplasmin and plasmin by carbon monoxide has resulted in enhanced coagulation and decreased fibrinolysis in vitro in human and other species, and in vivo in rabbits. Of interest, the ultrastructure of platelet rich plasma thrombi demonstrates an abnormal increase in fine fiber formation and matting that are obtained from humans exposed to carbon monoxide.Further, thrombi obtained from humans and rabbits have very similar ultrastructures, whereas mice and rats have more fine fibers and matting present. In sum, there may be

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Section: Ultrastructural Findings Supporting a Procoagulant Role For Comentioning

confidence: 68%

Section: Ultrastructural Findings Supporting a Procoagulant Role For Comentioning

confidence: 98%

Carbon monoxide: Anticoagulant or procoagulant?

Nielsen

Pretorius

2014

Thrombosis Research

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“…However, this study neither mimicked real‐life conditions (eg, employed e‐cigarette extracts) nor used an in vivo whole‐body exposure model to investigate the effects of e‐cigarettes on platelets. It is noteworthy that thrombosis is the main mechanism of cardiovascular mortality in smokers17; smoking causes a prothrombotic state through altering fibrinolytic and thrombotic factors17, 18; smokers’ isolated platelets exhibited increased aggregation19, 20; and exposure to cigarette smoke alters the dynamics of clot formation, making them more resistant to thrombolysis as compared with clots of nonsmokers 21, 22, 23. However, whether e‐cigarettes exert similar effects is yet to be determined and warrants investigation.…”

Section: Introductionmentioning

confidence: 99%

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

Qasim

Karim

Silva‐Espinoza

et al. 2018

JAHA

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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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“…It is known that smoking leads to prothrombotic alterations, including endothelial dysfunction, increased platelet adhesiveness and aggregation, impaired fibrinolysis, and more compact fibrin clot networks. 30,31 This study provides additional evidence for a prothrombotic state in smokers. In contrast to recurrent DVT, 32 elevated D-dimer after anticoagulation withdrawal did not identify patients at risk of the LAA thrombus.…”

Section: Discussionmentioning

confidence: 66%

Prothrombotic State in Patients With a Left Atrial Appendage Thrombus of Unknown Origin and Cerebrovascular Events

Meus

Son

Sobczyk

et al. 2016

Stroke

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Background and Purpose— We hypothesized that formation of left atrial appendage (LAA) thrombi of unknown origin is associated with altered fibrin clot properties and blood hypercoagulability. Methods— In a case–control study, we investigated 32 patients with a history of LAA thrombus after successful anticoagulant treatment versus 32 control subjects matched for age, sex, and diabetes mellitus. All subjects had previous ischemic stroke, transient ischemic attack, or migraine associated with patent foramen ovale. Patients with documented atrial fibrillation were excluded. We determined plasma fibrin clot permeability, fibrinolytic efficiency, thrombin generation, platelet and endothelial markers. Stroke or transient ischemic attack were assessed during a median follow-up of 74 (range 19–98) months. Results— Compared with controls, patients with LAA thrombus more frequently were smokers (43.8% versus 18.8%) and had 20% prolonged clot lysis time, lower plasminogen (−14%), and higher plasminogen activator inhibitor-1 (+17%), thrombin–antithrombin complexes (+17%), CD40 ligand (+30%), P-selectin (+29%), and von Willebrand factor (+30%, all P <0.05). Occurrence of LAA thrombus was predicted by von Willebrand factor (β=0.038, P =0.004), plasminogen (β=−0.048, P =0.01), plasminogen activator inhibitor-1 (β=−0.161, P =0.03), and clot permeability (β=−1.076, P =0.03). During follow-up, cerebrovascular events occurred in 10 (33.33%) of the 30 available patients in the LAA thrombus group, including 7 (23.3%) with recurrent LAA thrombus and 4 (13.33%) with documented atrial fibrillation. Recurrent LAA thrombus was associated with lower baseline K s and higher thrombin generation, fibrinogen, plasminogen activator inhibitor-1, and soluble CD40 ligand (all P <0.05). Conclusions— Prothrombotic blood alterations could be involved in the LAA thrombus formation in patients without documented atrial fibrillation and are associated with increased risk of stroke or transient ischemic attack during follow-up.

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Effects of Cigarette Smoke Exposure on Clot Dynamics and Fibrin Structure

Cited by 114 publications

References 23 publications

Carbon monoxide: Anticoagulant or procoagulant?

Carbon monoxide: Anticoagulant or procoagulant?

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

Prothrombotic State in Patients With a Left Atrial Appendage Thrombus of Unknown Origin and Cerebrovascular Events

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