Risk Of Subsequent Venous Thromboembolism Research Articles

Association of scrub typhus with the risk of venous thromboembolism and long-term mortality: a population-based cohort study.

The existing literature lacks studies examining the epidemiological link between scrub typhus and deep vein thrombosis (DVT) or pulmonary embolism (PE), and the long-term outcomes. The objective of this study is to explore the potential association between scrub typhus and the subsequent risk of venous thromboembolism, and long-term mortality. This nationwide cohort study identified 10,121 patients who were newly diagnosed with scrub typhus. Patients with a prior DVT or PE diagnosis before the scrub typhus infection were excluded. A comparison cohort of 101,210 patients was established from the general population using a propensity score matching technique. The cumulative survival HRs for the two cohorts were calculated by the Cox proportional hazards model. After adjusting for sex, age, and comorbidities, the scrub typhus group had an adjusted HR (95% CI) of 1.02 (0.80-1.30) for DVT, 1.11 (0.63-1.93) for PE, and 1.16 (1.08-1.25) for mortality compared to the control group. The post hoc subgroup analysis revealed that individuals younger than 55 years with a prior scrub typhus infection had a significantly higher risk of DVT (HR: 1.59; 95% CI: 1.12-2.25) and long-term mortality (HR: 1.75; 95% CI, 1.54-1.99). The scrub typhus patients showed a 16% higher risk of long-term mortality. For those in scrub typhus cohort below 55 years of age, the risk of developing DVT was 1.59 times higher, and the risk of mortality was 1.75 times higher. Age acted as an effect modifier influencing the relationship between scrub typhus and risk of new-onset DVT and death.

Incidence and prognosis of superficial vein thrombosis during pregnancy and the post-partum period: a Danish nationwide cohort study

The incidence of superficial vein thrombosis (SVT) of the legs and the subsequent risk of venous thromboembolism during pregnancy and the post-partum period is unknown. To better understand the clinical course of SVT during these times, we aimed to estimate the incidence rate of SVT during pregnancy and in the post-partum period, as well as the risk of subsequent venous thromboembolism. In this nationwide cohort study, we collected data on all pregnant women who delivered between Jan 1, 1997, and Dec 31, 2017, in Denmark were extracted from the Danish Medical Birth Register, the Danish National Patient Registry, and the Danish National Prescription Registry. Data on ethnicity were not available. Incidence rates per 1000 person-years were calculated for each trimester and the antepartum and post-partum period. Among women with a pregnancy-related SVT, risk of subsequent venous thromboembolism within the same pregnancy or post-partum period were calculated and compared with a matched cohort of pregnant women without SVT using Cox proportional hazards analysis. During 1 276 046 deliveries, 710 diagnoses of lower extremity SVT occurred from conception up to 12 weeks postpartum (0·6 per 1000 person-years [95% CI 0·5-0·6]). The incidence rates of SVT per 1000 person-years were 0·1 (95% CI 0·1-0·2) during the during the first trimester, 0·2 (0·2-0·3) during the second trimester, and 0·5 (0·5-0·6) during the third trimester. The incidence rate was 1·6 per 1000 person-years (95% CI 1·4-1·7) during the post-partum period. Of the 211 women with antepartum SVT included in the analysis, 22 (10·4%) were diagnosed with venous thromboembolism, compared with 25 (0·1%) in women without SVT (hazard ratio 83·3 [95% CI 46·3-149·7]). The incidence rate of SVT during pregnancy and the post-partum period was low. However, if SVT during pregnancy was diagnosed, the risk of developing venous thromboembolism during the same pregnancy was high. These results might help physicians and patients to make decisions about anticoagulant management of pregnancy-related SVT. None.

Early Dynamics of C-Reactive Protein Predict Risk of Venous Thromboembolism in Patients with Cancer Treated with Immune Checkpoint Inhibitors

Background: Patients with cancer treated with immune checkpoint inhibitors (ICI) have a substantial risk of venous thromboembolism (VTE). Conventional prothrombotic risk factors seem inefficient in the prediction of VTE under ICI-therapy. Recently, C-reactive protein (CRP) trajectories were proposed as prognostic and predictive biomarker for survival and therapy response in patients treated with ICI. The aim of the present study was to explore early dynamics of systemic CRP-levels after initiation of ICI for the prediction of VTE. Methods: Adults patients with cancer treated with ICI at the Medical University of Vienna were included in this retrospective cohort study. Levels of CRP were obtained at study baseline within 4 weeks prior to and longitudinally at 1, 2, and 3 months after ICI-initiation. Patients were stratified according to their CRP-dynamics relative to baseline measurements, defining a CRP-flare as an increase by the factor of 2.5 relative to baseline measurements and a CRP-response as a 50% relative decrease in CRP-levels within the first 3 months after ICI-initiation, respectively. Patients were followed for the time of ICI therapy, the initiation of any subsequent anti-cancer therapy, death, or a maximum of 3 months after the last ICI-cycle. Risk of VTE was analysed in a competing-risk framework, accounting for all-cause mortality as competing outcome event. Results: Overall, 405 patients treated with ICI were included (median age: 63 years [interquartile range, IQR: 53-72]; 38% female). The most frequent tumour types were melanoma (33%) and lung cancer (26%), with 91% of patients diagnosed with stage IV cancer at ICI-initiation. Over a median follow-up of 7.9 months (IQR: 4-16), we observed 29 VTE (cumulative incidence: 12.7% [95% confidence interval, CI: 6.9-20.5]). In patients with a CRP-flare after ICI-initiation (n=296; 73%), an increased risk of VTE was observed (sub-distribution hazard ratio (SHR): 3.58 [95%CI: 1.07-11.94], p=0.038), which prevailed upon multivariable adjustment for tumour type, cancer stage, age, sex, Charlson comorbidity index, and ECOG-performance status. Cumulative VTE-incidences in patients with a CRP-flare were 17.5% (95%CI: 8.8-28.7), compared to 2.9% (95%CI: 0.8-7.7) in the remainder of patients (Figure 1). Further, in patients with a CRP-response within the first 3 months after therapy initiation (n=126; 31%), numerically lower VTE rates were observed compared to the remainder of patients (SHR: 0.41 [95%CI: 0.16-1.06], p=0.066), with the lowest VTE-rates in those with CRP-responses without a prior CRP-flare (n=62; 15%; cumulative VTE-incidence: 1.6% [95%CI: 0.1-7.6]). Conclusion: Early dynamics of systemic CRP-levels are associated with risk of VTE during ICI-therapy, with the highest rates observed in patients with an initial CRP-flare. These data suggest a potential link between the ICI-induced systemic inflammatory response and subsequent risk of VTE. Figure 1: Cumulative incidence of VTE according to early CRP-flare after ICI-initiation. Competing risk cumulative incidence, accounting for all-cause mortality as competing outcome event. CRP-flare was defined as increase in CRP-levels by the factor of 2.5 within 3 months after ICI-initiation relative to baseline, pretherapeutic measurements. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

Superficial Vein Thrombosis

A large German registry on superficial vein thrombosis (SVT) documents that risk profiles, clinical presentation and treatment patterns are highly variable in patients with SVT, including a large variation in anticoagulation treatment modalities, intensities and durations. Inspite of a high percentage of initial anticoagulation there is a substantial risk of subsequent venous thromboembolism (VTE), recurrences or extension after three months. Inspite of current guideline recommendations, one third of the patients receives heparins, oral anticoagulants or no anticoagulation at all. At initial presentation about one quarter of the patients with SVT have a concomitant, frequently asymptomatic VTE. Risk factors for this complication include prior hospitalization, immobilization, prior VTE, autoimmune disorders, higher age, cancer and SVT occurring in a non-varicose veins or SVT-extension into the perforator veins. These risk factors are also associated with thromboembolic complications during follow-up. Based on a large placebo-controlled trial with clinical endpoints (The CALISTO-Study), guidelines recommend Fondaparinux 2.5 mg once daily administered over 4 to 6 weeks. Alternatively, an intermediate dose of low molecular weight heparin can be considered. In high-risk patients, rivaroxaban 10 mg once daily was noninferior compared to Fondaparinux. A rebound of VTE recurrences was observed in both study arms after treatment had been discontinued after 45 days. Further studies are required to determine whether treatment needs to be extended beyond 45 days in high-risk patients.

Weight change over 9 years and subsequent risk of venous thromboembolism in the ARIC cohort.

Background/Objectives:Weight gain increases risk of cardiovascular disease, but has not been examined extensively in relationship to venous thromboembolism (VTE). The association between weight change over 9 years and subsequent VTE among participants in the Atherosclerosis Risk in Communities (ARIC) study was examined, with a hypothesis that excess weight gain is a risk factor for VTE, relative to no weight change.Subjects/Methods:Quintiles of 9-year weight change were calculated (visit 4 1996–1998 weight minus visit 1 1987–1989 weight in kg: Quintile 1: ≥ −1.81 kg; Quintile 2: <−1.81 to ≥ 1.36 kg; Quintile 3: >1.36 to ≤4.08 kg; Quintile 4: >4.08 to ≤7.71 kg; Quintile 5: > 7.71 kg). Incident VTEs from visit 4 (1996–1998) through 2015 were identified and adjudicated using medical records. Hazard ratios (HRs) were calculated using Cox models.Results:529 incident VTEs were identified during an average of 19 years of follow up. Compared to Quintile 2, participants in Quintile 5 of weight change had 1.46 times the rate of incident VTE (HR = 1.46 (95% CI 1.09, 1.95), adjusted for age, race, sex, income, physical activity, smoking and prevalent CVD). The HR for Quintile 5 was modestly attenuated to 1.38 (95% CI 1.03, 1.84) when visit 1 BMI was included in the model. When examined separately, results were significant for unprovoked VTE, but not for provoked VTE. Among those obese at visit 1, both weight gain (HR 1.86 95% CI 1.27,2.71) and weight loss (HR 2.11 95% CI 1.39, 3.19) were associated with incident VTE, compared with normal weight participants with no weight change.Conclusions:Weight gain later life was associated with increased risk for unprovoked VTE. Among those with obesity, both weight gain and weight loss were associated with increased risk for VTE.

Respiratory and Blood Stream Infections are Associated with Subsequent Venous Thromboembolism After Primary Intracerebral Hemorrhage.

BackgroundInfection and venous thromboembolism (VTE) are associated with worse outcomes after intracerebral hemorrhage (ICH). The relationship between infection and VTE in ICH patients is unclear. We hypothesized that infection would be associated with subsequent VTE after ICH.MethodsWe retrospectively studied consecutively admitted spontaneous primary ICH patients from 2009 to 2018 surviving beyond 24 h. The primary predictor variable was infection, diagnosed prior to VTE. The primary outcome was VTE. We used multivariable logistic regression models to estimate the odds ratios and 95% confidence intervals (OR, 95% CI) for VTE risk after infection of any type, after adjusting for ICH score, length of stay and days to deep venous thrombosis (DVT) prophylaxis. Similar analysis was done to estimate the association of infection subtypes, including respiratory and urinary and blood stream infections (BSI) with VTE.ResultsThere were 414 patients (mean age 65 years, 47% female) that met were analyzed. Infection was diagnosed in 181 (44%) patients. Incident VTE was diagnosed in 36 (9%) patients, largely comprised of DVT (n = 32; 89%). Infection overall was associated with increased risk of subsequent VTE (adjusted OR 4.5, 95% CI 1.6–12.6). Respiratory (adjusted OR 5.7, 95% CI 2.8–11.7) and BSI (adjusted OR 4.0, 95% CI 1.3–11.0) were associated with future VTE. Urinary and other infections were not associated with subsequent VTE.ConclusionsInfections are associated with subsequent risk of VTE among patients with ICH. Further investigation is required to elucidate mechanisms behind this association and to improve VTE prevention after ICH.

Effect of prothrombotic genotypes on the risk of venous thromboembolism in patients with and without ischemic stroke. The Tromsø Study

Essentials Prothrombotic genotypes may agument the risk of venous thromboembolism (VTE) after ischemic stroke. We studied this effect in a case-cohort study using a genetic risk score. In stroke patients, a one-category increase in the genetic risk score was associated with a 50% higher relative risk of VTE. The risk of VTE in stroke patients increased with an increasing number of risk alleles. SUMMARY: Background Patients with ischemic stroke have a transiently increased risk of subsequent venous thromboembolism (VTE). Prothrombotic genotypes may augment VTE risk under conditions of high thrombosis risk related to stroke. Aims To investigate the effect of prothrombotic genotypes in patients with ischemic stroke on the risk of VTE in a population-based case-cohort study. Methods Cases with incident VTE (n=664) and a randomly selected age-weighted subcohort (n=1817) were sampled from three surveys of the Tromsø Study (1994-2008). Participants were genotyped for ABO (rs8176719), F5 (rs6025), F2 (rs1799963), FGG (rs2066865) and F11 (rs2036914) single-nucleotide polymorphisms (SNPs). Cox regression models were used to calculate hazard ratios (HRs) for incident VTE according to individual SNPs and categories of risk alleles (5-SNP score; 0-1, 2, 3-4 and ≥5) in participants with and without ischemic stroke. Results There were 192 patients with incident stroke, of whom 43 developed VTE during a median of 15.2years of follow-up. The risk alleles of individual SNPs augmented the elevated VTE risk brought about by ischemic stroke. In stroke patients, a one-category increase in the genetic risk score was associated with a 50% higher relative risk of overall VTE (HR1.5, 95% confidence interval [CI]1.3-1.8) and an 80% higher relative risk of provoked VTE (HR1.8, 95%CI1.5-2.1). Stroke patients with ≥5 risk alleles had a 12-fold (HR11.7, 95%CI4.1-33.3) higher relative risk of VTE than stroke-free participantswith 0-1 risk alleles. Conclusions Prothrombotic genotypes increased the risk of VTE in stroke patients, and the risk increased with an increasing number of riskalleles.

The Role of Stroke as a Trigger for Incident Venous Thromboembolism: Results from a Population-based Case-Crossover Study.

Stroke is associated with a short-term increased risk of subsequent venous thromboembolism (VTE). It is unclear to what extent this association is mediated by stroke-related complications that are potential triggers for VTE, such as immobilization and infection. We aimed to investigate the role of acute stroke as a trigger for incident VTE while taking other concomitant VTE triggers into account. We conducted a population-based case-crossover study with 707 VTE patients. Triggers were registered during the 90 days before a VTE event (hazard period) and in four preceding 90-day control periods. Conditional logistic regression was used to estimate odds ratios with 95% confidence intervals (CIs) for VTE according to triggers. Stroke was registered in 30 of the 707 (4.2%) hazard periods and in 6 of the 2,828 (0.2%) control periods, resulting in a high risk of VTE, with odds ratios of 20.0 (95% CI: 8.3–48.1). After adjustments for immobilization and infection, odds ratios for VTE conferred by stroke were attenuated to 6.0 (95% CI: 1.6–22.1), and further to 4.0 (95% CI: 1.1–14.2) when other triggers (major surgery, red blood cell transfusion, trauma, and central venous catheter) were added to the regression model. A mediation analysis revealed that 67.8% of the total effect of stroke on VTE risk could be mediated through immobilization and infection. Analyses restricted to ischemic stroke yielded similar results. In conclusion, acute stroke was a trigger for VTE, and the association between stroke and VTE risk appeared to be largely mediated by immobilization and infection.

Oral anticoagulation therapy and subsequent risk of venous thromboembolism in atrial fibrillation patients

Objective: Oral anticoagulation (OAC) prescribed to AF patients for the prevention of cardioembolic complications likely has the added benefit of preventing venous thromboembolism (VTE). This study evaluated, among AF patients who are anticoagulated, whether type of OAC was associated with subsequent VTE risk.Methods: Non-valvular AF patients prescribed OACs between 2010 and September 2015 were identified via the MarketScan administrative claims databases. OACs included warfarin and direct OACs (DOACs: dabigatran, rivaroxaban, and apixaban). Incident VTE was defined by ICD-9-CM codes. Patients were matched on age, sex, CHA2DS2-VASc, and high-dimensional propensity scores. The final analysis included 117,912 AF patients.Results: In total, 1357 VTE events accrued over a mean follow-up of 484 days. In multivariable-adjusted, propensity score-matched Cox models, relative to new users of warfarin, risk of incident VTE was lower among new users of dabigatran [hazard ratio (95% confidence interval) = 0.55 (0.47–0.66)] and apixaban [0.51 (0.39–0.68)], but similar among new users of rivaroxaban [1.01 (0.87–1.19)]. In head-to-head DOAC comparisons, VTE risk was lower among users of dabigatran [0.48 (0.36–0.64)] and apixaban [0.61 (0.47–0.78)] vs rivaroxaban. Findings were mostly similar across patient sub-groups.Conclusions: In this large practice-based population of AF patients prescribed OACs for primary prevention of stroke and systemic embolization, subsequent risk of VTE was lowest among those prescribed apixaban and dabigatran, while risk was similar with prescriptions for warfarin and rivaroxaban. Among AF patients prescribed OACs, lowering the risk of VTE may be an additional benefit of apixaban and dabigatran, beyond the reduced bleeding risk observed in randomized clinical trials.

The Risk of Venous Thromboembolism in Patients with Lower Urinary Tract Symptoms

Objectives: Atherosclerosis may lead to chronic bladder ischemia, which eventually results in lower urinary tract symptoms (LUTS). Patients with venous thromboembolism (VTE) have a higher prevalence of atherosclerosis. Methods: A total of 31,559 patients had been diagnosed with or without LUTS between 2000 and 2010 in Taiwan National Health Insurance Research Database, each was enrolled in the LUTS and non-LUTS cohorts, respectively. The risk of VTE in LUTS and non-LUTS cohorts was calculated by Cox proportional hazards regression model. Results: After adjustment for age, sex, and comorbidities, the risk of subsequent VTE was 1.34-fold higher in the LUTS than in the non-LUTS cohort. The adjusted risk of VTE was highest in patients with LUTS with any comorbidity. The age-specific relative risk of VTE was significantly higher in patients aged ≥50 years, particularly in those aged 50–64 years, in the LUTS than in the non-LUTS cohort. Conclusions: LUTS is a risk factor for VTE. Physicians should consider the possibility of underlying VTE in patients aged ≥50 years having cardiovascular comorbidities.

Increased risk of deep vein thrombosis and pulmonary thromboembolism in patients with aortic aneurysms: A nationwide cohort study.

Studies on the association between aortic aneurysm (AA) and the subsequent risk of venous thromboembolism (VTE) are limited to a few case reports and investigations which only focused on surgical effects. Therefore, we used the National Health Insurance Research Database to clarify whether patients with AAs have a heightened risk of subsequent VTEs, including deep vein thrombosis (DVT) and pulmonary embolism (PE). Our retrospective cohort study comprised patients aged ≥ 18 years who received a diagnosis of an AA and were hospitalized at any point during 2000–2010 (n = 16,630). Each AA patient was frequency-matched to 4 non-AA hospitalized patients based on age, sex, and index year (n = 66,453). The Cox proportional hazard regressions model was used to estimate the adjusted effect of AAs on VTE risk. The overall incidence of DVT and PE was higher in the patients with AA than in the non-AA group patients (23.5 versus 13.2 and 13.5 versus 7.98/1,000 person-years). After adjustment for age, sex, duration of hospitalization in the study period, and comorbidities, patients with AAs were associated with a 1.88-fold higher risk of DVT and 1.90-fold higher risk of PE compared to the non-AA cohort. Patients with abdominal AAs were more likely to develop DVT, whereas thoracic AA patients were more likely to develop PE. A diagnosis of a ruptured AA was associated with a substantially increased risk of DVT. Surgical treatment of AAs was associated with a heightened risk of VTE within 6-months post-operation. Our study demonstrates that AAs are associated with an increased risk of subsequent VTE. Future investigations are encouraged to delineate the mechanisms underlying this association and to evaluate the cost-effectiveness of screening for VTEs in patients with AAs.

Abstract WP179: Rate of Pulmonary Embolism After Cerebral Venous Thrombosis

Introduction: Cerebral vein thrombosis (CVT) is associated with an increased risk of subsequent venous thromboembolism. It is unknown whether the risk of pulmonary embolism (PE) after CVT is similar to that of PE after deep venous thrombosis (DVT). Methods: We performed a retrospective cohort study using administrative claims data from all emergency department visits and hospitalizations in California from 2005-2011, New York from 2006-2013, and Florida from 2005-2013. We identified patients with CVT or DVT as well as the primary outcome of PE using previously validated International Classification of Diseases, Ninth Revision, Clinical Modification ( ICD-9-CM ) codes. In order to minimize misclassification error, patients with both CVT and DVT during the same index hospitalization were excluded and patients with CVT were censored at the time of development of DVT and vice versa. Kaplan-Meier survival statistics and Cox proportional hazards models were used to compare the risk of PE after CVT versus after DVT while adjusting for demographics, vascular risk factors, and the Elixhauser comorbidity index. Results: We identified 4,450 patients with CVT and 217,589 patients with DVT. During a mean follow-up of 2.0 (±1.7) years, 124 patients with DVT developed a PE and 18,698 patients with DVT developed a PE. Patients with CVT were younger (mean age 45 vs 63), more often female (71% vs 52%), more often pregnant, and had fewer vascular risk factors than patients with DVT. During the index hospitalization, the rate of PE was 1.5% (95% confidence interval [CI], 1.1-1.8%) in patients with CVT and 6.2% (95% CI, 6.1-6.3%, p&lt;0.001) in patients with DVT. By 5 years, the cumulative rate of PE after CVT was 3.7% (95% CI, 3.0-4.4%) compared to 10.5% (95% CI, 10.3-10.6%, p&lt;0.001) after DVT. After adjustment for demographics and comorbidities, CVT was associated with a significantly lower hazard of PE when compared to DVT (hazard ratio, 0.31; 95% CI, 0.26-0.38). Conclusion: In a large, heterogeneous population, we found that the risk of PE after CVT was significantly lower than that of PE after DVT. Among patients with CVT, the greatest risk for PE was apparent during the index hospitalization.

Depression and Risk of Venous Thromboembolism

This study investigated the relationship between depression and the risk of subsequent venous thromboembolism (VTE) development. We conducted a population-based retrospective cohort analysis by using data for the period of 2000 to 2011 from the Longitudinal Health Insurance Database 2000 of Taiwan. A depression cohort comprising 35,274 patients and a nondepression cohort comprising 70,548 patients matched according to sex, age, and index year with no history of VTE were evaluated. Cox proportional hazard regression analysis was used to assess the effects of depression and comorbidities, and the Kaplan-Meier method was applied to estimate the cumulative VTE incidence curves. Compared with individuals without depression, depressed patients had a 1.38-fold greater risk (95% confidence interval = 1.09-1.73) of developing VTE. This risk was significantly higher in male and younger (≤49 years) patients. In addition, patients with comorbidities such as hypertension, diabetes, heart failure, and cancer had a higher risk of depression-associated VTE that was attenuated, although nonsignificantly, by antidepressant use. The incidence of VTE in Taiwan is higher in depressed patients than in nondepressed patients. Moreover, men, people 49 years or younger, and patients with comorbidities have a significantly greater risk of VTE after depression.

Reactive thrombocytosis and risk of subsequent venous thromboembolism: a cohort study

It is uncertain whether reactive thrombocytosis is associated with an increased risk of venous thromboembolism. This study assessed the incidence of reactive thrombocytosis, defined as platelet count ≥ 500 × 10(9) L(-1) , at intensive care unit discharge and its association with subsequent venous thromboembolism. This cohort study involved linkage of routinely collected intensive care unit, laboratory, radiology and death registry data of critically ill patients admitted to the intensive care unit between January 2009 and March 2010. The census date for survival and radiologically confirmed venous thromboembolism was 31 October 2011. Of the 1446 patients who survived to intensive care unit discharge, 139 patients had reactive thrombocytosis (9.6%, 95% confidence interval [CI] 8.2-11.2%). Twenty-nine patients developed venous thromboembolism after discharge (2%, 95% CI 1.4-2.9%; 67 per 100 person-years, 95% CI 45-97) and the median time to develop venous thromboembolism was 25 days (interquartile range 8-148). Reactive thrombocytosis was associated with an increased risk of subsequent venous thromboembolism (hazard ratio 5.3, 95% CI 1.7-16.4), after adjusting for other covariates. Platelet counts explained about 34% of the variability in the risk of venous thromboembolism and had a relatively linear relationship with the risk of venous thromboembolism when the platelet counts were > 400 × 10(9) L(-1) . Venous thromboembolism after intensive care unit discharge was associated with an increased risk of mortality (hazard ratio 2.0, 95% CI 1.1-3.9), after adjusting for reactive thrombocytosis. Reactive thrombocytosis during the recovery phase of critical illness was associated with an increased risk of subsequent venous thromboembolism.

Peak thrombin generation and subsequent venous thromboembolism: the Longitudinal Investigation of Thromboembolism Etiology (LITE) study.

Thrombin is an enzyme that is essential for the acceleration of the coagulation cascade and the conversion of fibrinogen to clottable fibrin. We evaluated the relationship of basal peak thrombin generation with the risk of future venous thromboembolism (VTE), and determined whether associations were independent of other coagulation markers. The Longitudinal Investigation of Thromboembolism Etiology (LITE) study investigated VTE in two prospective population-based cohorts: the Atherosclerosis Risk in Communities (ARIC) study and the Cardiovascular Health Study (CHS). Peak thrombin generation was measured on stored plasma in a nested case-control sample (434 cases and 1004 controls). Logistic regression was used to estimate the relationship of peak thrombin generation with VTE, adjusted for age, sex, race, center, and body mass index. Mediation was evaluated by additionally adjusting for factor VIII and D-dimer. Relative to the first quartile of peak thrombin generation, the odds ratio (OR) of VTE for those above the median was 1.74 [95% confidence interval (CI) 1.28-2.37]. The association was modestly attenuated by adjustment for FVIII and D-dimer (OR 1.47, 95% CI 1.05-2.05). Associations appeared to be stronger for idiopathic than for secondary VTE. Elevated peak thrombin generation more than added to the VTE risk associated with FV Leiden or low activated partial thromboplastin time. In this prospective study of two independent cohorts, elevated basal peak thrombin generation was associated with subsequent risk of VTE, independently of established VTE risk factors.

Arterial cardiovascular events, statins, low-dose aspirin and subsequent risk of venous thromboembolism: a population-based case-control study.

Atherosclerotic disease has been associated with the risk of venous thromboembolism, but the available data are conflicting. There are similar confusions regarding the association of the use of aspirin and statins with venous thromboembolism. To determine whether arterial cardiovascular events, use of statins and low-dose aspirin were associated with the risk of venous thromboembolism. In this population-based case-control study, we identified 5824 patients with venous thromboembolism and 58 240 population controls with a complete hospital and prescription history. We used logistic regression to estimate the relative risk of venous thromboembolism, adjusted for potentially confounding factors. Patients with a history of arterial cardiovascular events had a clearly increased relative risk. An event within 3 months before the index date conferred large increases in risk [relative risk 4.22 (95% confidence interval (CI), 2.33-7.64) after myocardial infarction, 4.41 (95% CI, 2.92-6.65) after stroke]. Myocardial infarction more than 3 months before the index date was not significantly associated with risk, although there was a relative risk of 1.29 (95% CI, 1.05-1.57) for myocardial infarction more than 60 months previously. A history of stroke was associated with small increases in risk after 3 months. Current use of statins was associated with a reduced risk of venous thromboembolism [relative risk=0.74 (95% CI, 0.63-0.85)]. Aspirin use was not associated with risk. Patients with cardiovascular events are at a short-term increased risk of venous thromboembolism. Statins might prevent venous thromboembolism but aspirin does not. However, as the study is non-randomized residual confounding cannot be excluded.

Risk of subsequent thromboembolism for patients with pre-eclampsia

Inherited thrombophilias affect over 16% of people and predispose them to venous thromboembolism.1 Pre-eclampsia is associated with occlusion of the placental spiral arteries.2 Thrombophilias may cause thrombosis of placental vessels,3...