Thrombosis is one of the leading causes of death in cancer. Cancer-induced hypercoagulable state contributes to thrombosis and is often overlooked. Prostate cancer may not be of high thrombogenic potential compared with other cancers, but its high prevalence brings it into focus. Pathological evidence for venous thromboembolisms (VTEs) in prostate cancer exists. Factors such as age, comorbidities, and therapies increase the VTE risk further. There is a need to systematically identify the risk of VTE in regard to patient-, cancer-, and treatment-related factors to risk stratify patients for better-targeted and individualized strategies to prevent VTE. Sensitive tests to enable such risk assessment are urgently required. There is sufficient evidence for the utility of thromboelastography (TEG) in cancer, but it is not yet part of the clinic and there is only limited data on the use of TEG in prostate cancer. One study revealed that compared with age-matched controls, 68.8% of prostate cancer patients demonstrated hypercoagulable TEG parameters. The absence of clinical guidelines is a limiting factor in TEG use in the cancer population. Cancer heterogeneity and the unique cancer-specific microenvironment in each patient, as well as determining the hypercoagulable state in each patient, are added limitations. The way forward is to combine efforts to design large multicenter studies to investigate the utility and clinical effectiveness of TEG in cancer and establish longitudinal studies to understand the link between hypercoagulable state and development of thrombosis. There is also a need to study low thrombogenic cancers as well as high thrombogenic ones. Awareness among clinicians and understanding of test applicability and interpretation are needed. Finally, expert discussion is critical to identify the investigation priorities.

Introduction: Female patients are significantly more likely than male patients to experience symptoms of depression and anxiety post-acute coronary syndrome (ACS), correlated with higher rates of cardiovascular morbidity and mortality. Yet, it is unclear if all female patients are impacted broadly or if specific subgroups of female patients are at elevated risk. We aimed to identify the cardiovascular and psychosocial variables correlated with increased depression and anxiety symptoms immediately post-ACS as well as at 3 and 6-month follow-up. Hypothesis: There is a combination of cardiovascular and psychosocial factors associated with elevated depressive/anxious symptoms (Hospital Anxiety and Depression Scale (HADS) score ≥8 on the depression/anxiety subscales) in female patients post-ACS. Methods: This was a prospective multi-center questionnaire-based clinical research study featuring data from 6 sites across Canada using a logistic regression model to delineate multivariate strength of association. Baseline visit (within 72 hours of ACS) included HADS and a sociodemographic questionnaire. Follow-up visits (3 and 6-months) include HADS, Cardiac Anxiety Questionnaire, new health events, mortality, Short Form-12 Health Survey, and Somatic Symptom Scale-8. Results: A total of 245 patients were included in analysis (Table 1). HADS-A≥8 was associated with increased health anxiety at baseline (OR6.56; p<0.001). Conversely, HADS-D≥8 was associated with low social support at baseline (OR3.35; p=0.005) and 3-month follow-up (OR22.65; p<0.001) as well as previous diagnosis of depression at 3-month (OR22.73; p<0.001) and 6-month (OR5.50; p=0.02) follow-up. Conclusion: We identify key factors associated with symptoms of depression and anxiety post-ACS in female patients. Developing a deeper understanding of the relationship between mental health and ACS will benefit patients by informing intervention and prevention strategies.

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