Relationship between Venous and Arterial Thrombosis: A Review of the Literature from a Causal Perspective

Lijfering, Willem M.; Flinterman, Linda E.; Vandenbroucke, Jan P.; Rosendaal, Frits R.; Cannegieter, Suzanne C.

doi:10.1055/s-0031-1297367

Cited by 84 publications

(69 citation statements)

References 58 publications

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“…Two recent large cohort studies found that cardiovascular risk factors obesity and smoking were also risk factors for VTE [15,16]. However, others suggested that this increased risk may be therapy related [17] or that a local inflammatory response, induced by VTE, may accelerate atherosclerosis [8]. In our study, patients without PE had somewhat higher amounts of CAC and TAC than did patients with PE (either unprovoked or all patients with PE).…”

Section: Resultsmentioning

confidence: 42%

Coronary or thoracic artery calcium score in provoked and unprovoked pulmonary embolism: a case‐control study

Bijl

Klok

Huisman

et al. 2016

Journal of Thrombosis and Haemostasis

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To cite this article: van der Bijl N, Klok FA, Huisman MV, Roos de A, Kroft LJM. Coronary or thoracic artery calcium score in provoked and unprovoked pulmonary embolism: a case-control study. J Thromb Haemost 2016; 14: 931-5. Essentials• Patients with unprovoked pulmonary embolism (PE) are at increased risk of arterial thromboembolism.• Coronary and thoracic aorta calcium were evaluated in patients with and without (unprovoked) PE.• No association was found between (unprovoked) PE and coronary or aortic calcification.• Assessment of both calcium scores on computed tomography pulmonary angiography was highly reproducible.Summary. Objective: To evaluate the potential association between (unprovoked) pulmonary embolism (PE) and the presence and extent of coronary artery calcium (CAC) and thoracic aorta calcium (TAC). Methods: CAC and TAC derived from computed tomography pulmonary angiography of 100 patients with PE were compared to that of 100 patients in whom PE was ruled out. Results: Intraobserver and interobserver agreements for both TAC and CAC were excellent (intraclass correlation > 0.95 for both). In patients with PE vs. patients without PE, no significant differences were found in the presence of CAC or TAC (CAC 64% vs. 67%, odds ratio [OR] 1.0, 95% confidence interval [CI] 0.67-1.6; TAC 46% vs. 59%, OR 1.2, 95% CI 0.80-2.1). Mean CAC and TAC scores were significantly lower in patients with PE than in patients without PE (CAC 3.4 vs. 4.9, absolute difference 1.5, 95% CI 0.2-2.8; TAC 1.1 vs. 1.8, absolute difference 0.9, 95% CI 0.2-1.2). No significant differences were found in the presence of CAC or TAC or in mean CAC and TAC scores between patients with unprovoked PE vs.patients with provoked PE, or between patients with unprovoked PE vs. no PE. Conclusion: No significant differences were found between the extent of CAC and TAC in patients with unprovoked PE compared to those with provoked PE or without PE. The observed difference in the extend of CAC and TAC between patients with and without PE was dependent on prevalent cardiovascular risk factors.

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Section: Resultsmentioning

confidence: 42%

Coronary or thoracic artery calcium score in provoked and unprovoked pulmonary embolism: a case‐control study

Bijl

Klok

Huisman

et al. 2016

Journal of Thrombosis and Haemostasis

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“…4,5 Whether VT is causally associated with CVD is under debate. 6 Two prospective population-based cohort studies, the Atherosclerosis Risk in Communities and the Cardiovascular Health Study, 7,8 failed to confirm the association found earlier between atherosclerosis and VT. Furthermore, the increased risk of CVD after VT could be confounded by shared risk factors.…”

Section: Introductionmentioning

confidence: 99%

“…Age, sex, an increased body mass index (BMI), smoking, chronic disease, malignancy, and (genetic) thrombophilia have all been found to increase the risk of both VT and CVD. 6,9,10 However, either because of a lack of information on classical cardiovascular risk factors (apart from age and sex) or because of a broad definition of CVD (eg, otherwise unexplained death, angina, transient ischemic attack, and angioplasty), no study has yet provided estimates of the risk of myocardial infarction and ischemic stroke after VT adjusted for shared risk factors. [3][4][5]11 In addition, other health determinants that may affect the risk of both VT and CVD, such as socioeconomic status, diet, and alcohol consumption, have not previously been taken into account.…”

Section: Introductionmentioning

confidence: 99%

Increased risk of CVD after VT is determined by common etiologic factors

Roach¹,

Lijfering²,

Flinterman³

et al. 2013

Blood

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Key Points• Patients with VT have an increased risk of subsequent CVD compared with control participants.• The increased risk of CVD in these patients can be explained by etiologic factors leading to both diseases.Patients with venous thrombosis (VT) have an increased risk of subsequent CVD (CVD), but the underlying pathophysiology is unclear. Using data from the Multiple Environmental and Genetic Assessment of risk factors for venous thrombosis follow-up study, 4480 patients with VT, 2926 partner control participants, and 2638 random digit dialing (RDD) control participants were followed-up between 1999 and 2008. Incidence rates and hazard ratios with 95% confidence intervals (95% CIs) of CVD (defined as myocardial infarction or ischemic stroke) were calculated for patients vs controls. Measurable confounders (age, sex, body mass index, smoking, chronic disease, malignancy, genetic thrombophilia, and procoagulant markers) were adjusted for when comparing patients with RDD controls. Unmeasured lifestyle-related factors were also considered by comparing patients with their partners. During a median follow-up time of 5 years, 124 CVD events occurred. Incidence of CVD per 1000 person-years was 3.2 (95% CI, 2.5-4.0) in patients, 2.2 (95% CI, 1.5-3.0) in partners, and 1.6 (95% CI, 0.9-2.6) in RDD controls. Crude hazard ratio was 2.2 (95% CI, 1.2-3.8) in patients compared with RDD controls and 1.5 (95% CI, 1.0-2.3) in patients compared with partners. After adjustment for all confounders, these risks attenuated to 1.8 (95% CI, 0.8-4.2) and 1.3 (95% CI, 0.7-2.5) for patients compared with RDD control participants and partners, respectively. In conclusion, individuals with VT had an increased risk of CVD. This could be explained by common etiologic factors. (Blood. 2013;121(24):4948-4954)

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“…Although venous and arterial thrombosishave traditionally been considered distinct pathophysiologic entities, the two disorders have many features in common, and there is evidence that persons with venous thrombosis may be at greater risk for arterial events 5 . On the other side, the association of peripheral venous disease with arterial endothelial dysfunction was recently found 6,7 .…”

Section: Introductionmentioning

confidence: 99%