Plaque formations can grow large enough to significantly reduce the blood's flow through an artery. When a plaque formation becomes brittle or inflamed, it may rupture, triggering a blood clot to form. A clot may either further narrow the artery, or completely block it. Medicines Medicines can disrupt the body's normal blood clotting process. Other Factors Many other factors can lead to excessive blood clotting: Smoking raises the risk of unwanted blood clots and makes it more likely that platelets will stick together.
Smoking also damages the lining of the blood vessels, which can cause clots to form. Increased homocysteine levels , linked to a high risk of vascular disease. Increased levels of this substance may damage the inner lining of the arteries. Women are more likely to develop blood clots when they're pregnant due to an increase in platelets and clotting factors. The uterus can also compresses the veins slowing blood flow, which can lead to blood clots.
Prolonged bed rest. Several days or weeks in bed from surgery or illness can increase risk of excessive blood clotting. Use of birth control pills or hormone replacement therapy.
These can slow blood flow and cause clotting. Some types of cancer increase the proteins that clot your blood. The risk of blood clots is highest in HIV patients who have infections, are taking certain medicines, have been hospitalized, or are older than Share this article. Explore other support options There are a range of support options available to help you quit. Free Quit Support Calling the Quitline increases your chance of quitting successfully.
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Not what you were looking for? Analysis of only studies that adjusted for body mass index a measure of body fat and a known risk factor for conditions that affect the heart and circulation yielded a slightly higher RR 1. For ever smokers, the population attributable fraction the proportional reduction in VTE that would accrue in the population if no one smoked was 8. Notably, the risk of VTE increased by Thus, an individual who smoked one pack of cigarettes per day for 40 years had a Finally, smoking was associated with an absolute risk increase of These findings indicate that cigarette smoking is associated with a statistically significant, slightly increased risk for VTE among the general population and reveal a dose-relationship between smoking and VTE risk.
They cannot prove that smoking causes VTE—people who smoke may share other unknown characteristics confounding factors that are actually responsible for their increased risk of VTE. Indeed, these findings identify body mass index as a potential confounding factor that might affect the accuracy of estimates of the association between smoking and VTE risk.
Although the risk of VTE associated with smoking is smaller than the risk associated with some well-established VTE risk factors, smoking is more common globally, there are 1. Thus, smoking behavior should be considered when screening individuals for VTE and in the prevention of first and subsequent VTE events. PLoS Med 10 9 : e This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist. Although cigarette smoking has been responsible for approximately 5 million deaths every year, there are still an estimated 1.
The magnitude of this public health challenge is growing, and estimates suggest that as many as 8 million people may die from smoking-related diseases by [2]. Venous thromboembolism VTE is a serious medical event and associated with a substantial risk of mortality [3]. Smoking is a well-established risk factor for atherosclerotic disease, but its role as an independent risk factor or effect modifier for VTE remains controversial.
Several prospective studies reported smoking to be an independent risk factor [7] , [8] , whereas others failed to detect a significant relationship between smoking and VTE [9] , [10]. However, the meta-analysis involving a total of ten studies included only about one-third of the data currently available. In addition, six of the ten studies included were clinical trials of oral contraceptives, in which the samples may not be representative of the general population.
Furthermore, the VTE risk may be underestimated due to lack of distinction between former and current smokers and no adjustment for cardiovascular risk factors.
Smoking can be potentially reduced by individual and population-related measures; therefore, demonstrating the link between smoking and the risk of VTE may help reduce the burden of this disease. Therefore, we conducted a meta-analysis with the following aims: 1 to estimate the link between smoking and risk of VTE in the general population; 2 to measure the smoking-VTE relationship according to different degrees of adjustment for confounding factors, study designs, study populations, sex category, and type of VTE; and 3 to study dose-response patterns of tobacco exposure on the risk of VTE.
We searched articles published in any language and scrutinized references from these studies to identify other relevant studies. To minimize differences between studies, we imposed the following methodological restrictions for the inclusion criteria: 1 Studies that contained the minimum information necessary to estimate the relative risk RR associated with smoking, including case-control and cohort studies published as original articles; 2 Studies in which populations were representative of the general population and not those with selected participants on the basis of risk factor for VTE, such as tumor, surgery, or use of oral contraceptives.
In instances of multiple publications, the most up-to-date or comprehensive information was used. Because there is no standardized quality scoring system for observational studies, we selected a priori several important design characteristics that may affect study quality, including method of case confirmation, percentage of patients completing planned follow-up, smoking as the primary analysis of interest, selection criteria for control participants, matching criteria, and control for confounding.
Any disagreements were resolved by consensus. Data on the following characteristics were independently extracted: study size, number of patients who developed VTE, total person-years of follow-up, study population, publication year, study design, sampling framework, study location defined as Europe, North America, or Asia ; gender category, site of VTE studied deep vein thrombosis [DVT] or PE , type of VTE studied unprovoked or provoked , ascertainment of VTE validated or not validated , smoking category ever, current, or former , and reported adjustment for potential confounders.
When available, we used the most comprehensively adjusted risk estimates. RR was used as a measure of the relationship between smoking and the risk of VTE. For case-control studies, the OR was used as a surrogate measure of the corresponding RR. On the basis of population-based cohort studies, the average prevalence of three categories of smoking was estimated by weighting by the sample size of each study. Subgroup analyses and meta-regression models were carried out to investigate potential sources of between-study heterogeneity.
When several risk estimates were present in a single study i. In the dose-response analysis, we considered cigarettes per day and pack-years as explanatory variables. Because for many studies continuous exposures were reported as categorical data with a range, we assigned the mid-point in each category to the corresponding RR for each study. We used generalized least squares GLST regression models to assess the pooled dose-response relation between smoking and risk of VTE across studies that had heterogeneous categorizations of smoking [16].
Linear models were fitted and evaluated on the logarithm of the RRs. To enable the total person-years of observation to be calculated, we included data from reports that specified one or more of the following: total person-time of follow-up; sample size and mean or median follow-up per patient; or sample size and cumulative incidence rate.
The principal summary measure was event rate expressed per , patient-years of follow-up. Weighted meta-analytic prevalence estimates for outcomes were calculated with the variance-stabilizing Freeman-Tukey double-arcsine transformation with an inverse-variance random-effects model [17].
Small study bias, consistent with publication bias, was assessed with funnel plot, by Begg's adjusted rank correlation test and by Egger's regression asymmetry test [18].
With the search strategy, 1, unique citations were initially retrieved. Of these, articles were considered of interest and full text was retrieved for detailed evaluation. One hundred ninety-nine of these articles were subsequently excluded and finally 32 articles were included in the meta-analysis Figure 1.
Thirty-two independent observational studies reporting 3,, individuals and 35, incident cases were identified [7] , [8] , [19] — [48]. Fifteen studies were based in Europe, eight in North America, and nine in Asia. No studies were based in Africa or South America.
Studies were published between January and March Thirteen studies were prospective cohort studies and 19 were case-control studies. The methodological quality of the included studies was generally good.
Average follow-up duration ranged from 5. Patients were followed up for an average of over 10 y in a majority of studies The proportion of patients with complete follow-up to the end of the study was given for 11 studies and ranged from The sizes of the cohorts ranged from to 2,, in total 3,, , with the two largest studies recruiting participants over 1 million Table 1 [26] , [29].
Nineteen case-control studies were designed to evaluate risk factors for VTE, and eight of them used either hospital discharge data or data from registries. Of all the studies, two included only patients with DVT [36] , [44] and four investigated only patients with PE [19] , [31] , [35] , [40]. Four cohort studies [8] , [22] , [27] , [28] and four case-control studies [33] , [38] , [39] , [48] compared the prevalence of smoking between patients with unprovoked VTE and provoked VTE.
Eight studies investigated only women [19] , [23] , [25] , [29] , [30] , [32] , [34] , [48] and three studies included only men [20] , [22] , [24]. The association between smoking and VTE was the primary outcome of interest for 20 studies, whereas it was a secondary question in 12 studies. The ascertainment of VTE varied across studies; 24 studies based on medical record, radiology or autopsy validated , and eight confirmed by questionnaire or patient registry not validated Tables 1 and 2.
Adjusted RRs could be determined for all cohort studies and nine of the case-control studies. Most risk estimates were adjusted for age 19 studies and sex 11 studies. Eighteen studies Detailed information on adjustments is reported in Tables 1 and 2.
Figures 2 , S1 , and S2 showed the results from the random-effects model parallel analysis with fixed-effects model combining the RRs for VTE. Overall, the ever smokers compared with the reference group experienced a significantly increased risk for developing VTE RR: 1. Oral contraceptives cause significant increases in fibrinogen levels in smokers and nonsmokers, but only the latter appear to have a compensatory increase in antithrombin III activity.
Factor XIII, which stabilizes fibrin clots, is increased in smokers. Quantitative exposure to passive smoke has been positively correlated with blood coagulation activity.
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