Impact of Incident Venous Thromboembolism on Risk of Arterial Thrombotic Diseases

Abstract

Background-Growing evidence supports an association between venous thromboembolism (VTE) and arterial thrombotic diseases (ie, myocardial infarction and ischemic stroke). We aimed to study the association between VTE and future arterial events and to determine the population attributable risk of arterial events by VTE in a large prospective cohort recruited from the general population. Methods and Results-In 1994 to 1995 and 1993 to 1997, 81 687 subjects were included in the Tromsø Study and in the Diet, Cancer and Health Study and followed up to the date of incident venous and arterial events (myocardial infarction or ischemic stroke), death or migration, or to the end of the study period (2010 and 2008, respectively). There were 1208 cases of VTE and 90 subsequent arterial events during a median follow-up of 12.2 years. An association between VTE and future arterial events was found in all women and men aged <65 years but not in men aged >65 years. Women <65 years old with VTE had 3.3-fold higher risk of arterial disease (adjusted hazard ratio, 3.28; 95% confidence interval, 1.69-6.35) compared with women of the same age without VTE. The corresponding hazard ratio in men aged <65 years was 2.06 (95% confidence interval, 1.32-3.20). Only 0.9% of the arterial events were attributed to VTE, and the VTE explained 63.8% of the risk of arterial events among VTE patients. Conclusions-Our findings imply that women and young men with VTE have higher risk of arterial thrombotic disease than those without VTE. However, only 1% of the arterial thrombotic events in the population are attributed to VTE. (Circulation. 2014;129:855-863.)

Family History of Myocardial Infarction and Cause-Specific Risk of Myocardial Infarction and Venous Thromboembolism

“…37,38 Numerous observational studies have shown an independent association between arterial and venous thrombotic diseases. [10][11][12][13][14][15][16][17][18] However, the risk estimates for MI and VTE by FHMI in our study were similar in the traditional Cox model and in the cause-specific Cox model, implying that the associations between FHMI and MI and VTE were not affected by a direct interaction between VTE and MI. From a public health perspective, we found FHMI to be a considerable risk factor for VTE with a predictive value comparable with family history of VTE, 39 explaining 13% of the VTE events in the study population.…”

“…[10][11][12][13][14][15][16][17][18] However, growing evidence supports the notion that atherosclerotic risk factors, including diabetes mellitus, hypertension, and dyslipidemia, are not associated with VTE. [19][20][21][22][23] Obesity and advancing age were the only shared risk factors for arterial and venous thrombosis in cohort studies, investigating the influence of atherosclerotic risk factors on risk of MI and VTE within the same population.…”

Acute pulmonary embolism concomitant with ST-elevation myocardial infarction in a patient with pancreatic cancer

“…Women and young men with venous thromboembolism have higher risk of arterial thrombotic disease than those without venous thromboembolism in Tromsø's study. [13] Some cases with gastro-intestinal, hematological, and germinal system malignancy have been reported as having AMI. [12] Dieckmann, et al demonstrated that a majority patients diagnosed with testicular cancer and AMI did not have traditional atherosclerotic risk factors and coronary plaque.…”

“…The causes of venous and arterial thrombotic diseases underlie traditional atherosclerotic risk factors such as advanced aged, obesity, hypertension, dyslipidemia, and diabetes. [13] The possible mechanism of both venous and arterial embolism may result from direct cancer vascular invasion, mucin-mediated thrombosis, intra-cardiac or intra-vascular embolization, activation of coagulation cascade by tissue factor, thrombin, inflammatory cytokines, and endothelial and platelet adhesion molecules. [12][13][14]17] Other non-traditional risk factors for venous and arterial thrombosis were increased level of homocysteine, coagulation factors VIII, IX, XI, and von Willebrand factor.…”

“…[13] The possible mechanism of both venous and arterial embolism may result from direct cancer vascular invasion, mucin-mediated thrombosis, intra-cardiac or intra-vascular embolization, activation of coagulation cascade by tissue factor, thrombin, inflammatory cytokines, and endothelial and platelet adhesion molecules. [12][13][14]17] Other non-traditional risk factors for venous and arterial thrombosis were increased level of homocysteine, coagulation factors VIII, IX, XI, and von Willebrand factor. [12][13][14] Our presenting patient had high level of collating factor VIII but did not have an obvious intra-cardiac shunting from transthoracic echocardiography.…”