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Editorials
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(NETs) in promoting cancer-associated arterial thrombo- sis has been reported in patients with ischemic stroke and cancer.4
According to Trousseau’s first observations, traditional- ly the association between thrombosis and malignancy has been focused on the occurrence of venous throm- boembolism (VTE). Overall, cancer has been reported to account for 17-29% of all VTE cases;5 on the other hand, in the prospective Vienna Cancer and Thrombosis Study (CATS), 7.7% of the cancer patients developed VTE with- in one year after diagnosis or progression of the disease.6
The epidemiology of arterial thrombosis in cancer patients has received much less attention. Indeed, throm- bosis in arteries has long been recognized in cancer patients.7 In this issue of the Journal, Grilz et al. report the up-dated results of the CATS study, aimed to investigate the incidence of arterial thromboembolism (ATE), the related risk factors, and the impact on mortality in a cohort of 1880 patients with active newly diagnosed or relapsed cancer.8
The global burden of arterial thrombosis in the general population for the two common artery acute diseases (i.e. acute myocardial infarction and ischemic stroke) has been estimated to be 139.3 and 114.3 per 100,000 people, accounting for an overall incidence rate of 0.25% of indi- viduals.9 In the CATS cohort, the frequency of ATE was 2.6% during a median prospective observation time of two years. In agreement with previous reports, the rate of VTE was 8.4%.8 It is difficult to compare this with earlier reports due to the considerable heterogeneity in the design, inclusion criteria, and source of information (Table 1).10-15 In the paper of Grilz et al., the multivariable analysis demonstrated among the types of cancer a signif- icant association only with kidney cancer [Hazard Ratio
Figure 1. Interaction of multiple fac- tors involved in the pathogenesis of arterial thromboembolism in cancer patients. IMIDs: immunomodulatory drugs; TKI: tyrosine kinase inhibitors; VEGF: vascular endothelial growth factor.
(HR) 1.6];8 this association had already been reported in some cohorts12,13 but not in others.10 Lung cancer was found to be significantly associated with ATE in most reports;10,12-15 this was confirmed in the CATS cohort but only under univariable analysis.8 Cancer stage has been reported to be associated with the risk of ATE,12-15 but this increase in risk has not been found in the CATS cohort,8 in agreement with a report on hospitalized patients under chemotherapy.10
Grilz et al. addressed the role of cardiovascular risk fac- tors in the CATS cohort as determinants of ATE in cancer; age, male sex, and smoking were independent risk factors for ATE. Moreover, history of cardiovascular disease, hypertension, and medical conditions needing treatment with lipid-lowering agents or antiplatelet agents were all associated with a 2.2-3.7-fold increase in risk of ATE.8 This was aligned with the findings obtained in the RIETE cohort of cancer patients with VTE, in which history of arterial thrombosis, hypertension, diabetes, and use of statins were over-represented in the patients with subse- quent ATE compared with those without.15 The role of previous ATE as a predictor of a novel ATE is indirectly confirmed by the low rate of ATE in the study of Di Nisio et al.,11 in which patients with a history of cardiovascular events were excluded. The median age of the patients recruited in the CATS cohort was 61 years, explaining the relatively lower rate of ATE with respect to the study based on the SEER-Medicare dataset, which collected data from patients over 65 years of age (Table 1).14
Notably, the presence of two or more cardiovascular risk factors (hypertension, diabetes, known arterial car- diovascular disease, and dyslipidemia) resulted in an as high as 5.6-12.5% higher risk of ATE at two years from diagnosis in comparison with patients with none or a sin-
haematologica | 2018; 103(9)