Discussion
The concept of venous and arterial thrombosis as two separate entities has been challenged over the last years (1).  First, elements from the Virchow triad are involved in the genesis of both types of thrombosis. I have shown evidence from basic studies demostrating shared pathological pathways such as endothelial dysfunction, increased coagulation factor levels, platelet activation, microparticles and inflammation (2-4); all of which had provided reasonable evidence of a link between venous and arterial thrombosis. From a clinical standpoint, both entities recognize common clinical risk factors, increasing age being one of the most important. Finally, antiplatelet and anticoagulant drugs have proved efficacy in primary and secondary prophylaxis as well as treatment of venous and arterial thrombosis (6). 
However, both entities are multifactorial so the identification of only one and clear pathway to both seems unlikely. The hypothesis of atherosclerosis and/or inflammation as the connection between the two types of thrombosis are valid and logical, though none have offered irrefutable evidence and the investigation of the "common link" is still ongoing. 
In addition, clinically neither arterial nor venous thrombosis have only one manifestation. Myocardial infaction and stroke are the most prevalent and devastating presentations of arterial disease. Venous thrombosis of the legs and pulmonary embolism, which can be fatal, are the main expression of venous thrombosis. Even though, VT is a highly preventable complication; 30% of venous thrombosis are unprovoked which means that no triggering condition is identified (Puurunen et al. 2016).  This is the group of patients in whom distinguishing risk factors might have clinical impact, since it would lead to specific preventive measures. 
Many epidemiological studies have focused on the associaton of arterial disease as a risk factor for VT, specially unprovoked VT. As discussed in earlier chapters, the results of such studies have been conflicting but most of them observed an increased risk of VT during the 6 months after an arterial event (12, 17-19). However, none of the previous studies evaluated the risk of VT in the elderly, a high-risk population. This study is the first to investigate the risk of VT, both provoked and unprovoked, after a symptomatic cardiovascular event in an exclusively elderly population aged over 70 years old, a high-risk group.
My primary objective was to evaluate whether the risk of VT was increased in elderly patients with a history of MI or IS. I observed that a prior cardiovascular event per se was not a risk factor for VT in this population. The subgroup analysis according to the type of prior arterial disease showed no association between stroke and the risk of VT, which would suggest that immovilization or paralysis did not play a main role in the venous event, or that thromboprophylaxis was effective and done according to the guidelines. This speculation is further substantiated by the observation that several years passed between the stroke and the VT.
However, a prior MI was associated with 1.6 risk of PE, which increased to 2 fold if the diagnosis was PE without DVT. In agreement with other authors, a prior MI did not increase the risk of DVT in this study. The interval between the MI and the VT was over a decade in the majority of the cases, and only 10% of the VT occurred duing the first 6 months after the MI. The interpretation of such observations is that the VT was not triggered by the acute arterial event but it was probably due to hemostatic changes of ageing or other risk factors. The observation of an increased risk of VT in patients older than 80 years compared to those younger in our population would also support the role of ageing itself as a risk factor.  
Unlike the study by Sørensen et al. (20), heart failure was not associated with an increased risk of VT in our population, which demosntrates that not any cardiovascular disease increases the risk of VT. In summary, these observations would support the hypothesis that atherosclerosis might play a role in the genesis of VT, particularly in the elderly.  
Most of the venous event in our population were unprovoked, so we analyzed risk factors associated with this type of clinical presentation in the elderly. Unfortunately, and similarly to the previous studies in younger populations, I was not able to identify specific risk factors for unprovoked VT. 
Finally, male sex and age greater than 80 years were associated with an increased risk of VT in our population but not other common cardiovascular risk factors such as diabetes, obesity and smoking.
Even though the increase in the risk given by each risk factor in our study is small, if we take into consideration that the elderly are by definition a high-risk population with an incidence of VT of 1/100 in persons older than 80; these findings  care clinically relevant.
Despite the fact that no conclusions regarding therapy can be drawn from a non-interventional study, an interesting observation in our study was that the use of antiplatelet agents reduced the risk of VT in this elderly population regardless of the history of CVD. Aspirin has shown to be useful for secondary prevention of VT (6) and there is evidence that it might be used as thrombo-prophylaxis in the surgical setting as well (22). Our findings suggest that aspirin might have a role in primary prevention of VT in the elderly; however, whether aspirin is appropriate for this indication or which patients would benefit from this therapy, requires further investigation.
Similarly, as observed in prior studies (23-24), the use of lipid lowering drugs was associated with a decreased risk of VT in our population as well. An observation that further substantiates the hypothesis that atherosclerosis or chronic inflammation as potential risk factors for VT.
In conclusion, there was no increased risk of a future VT above age 70 in patients with a prior cardiovascular disease in general; however, a history of a prior MI was associated with a two-fold increased risk of PE. We were able to identify male sex and age older than 80 years as risk factors for VT in an aged population.
Our observations suggest that antiplatelet therapy might have a beneficial effect as primary and as secondary prophylaxis. Since most of VT in this high-risk population were unprovoked, assessing the efficacy and safety of aspirin in this setting might have clinical impact.