Cardiovascular disease in transgender people: a systematic review and meta-analysis.

OBJECTIVE: Hormone therapy in transgender people might be associated with an increased risk of cardiovascular disease (CVD). We aimed to investigate whether the risk of CVD is increased in transgender people compared with people of the same birth sex. DESIGN AND METHODS: PubMed, Cochrane, Embase, and Google Scholar were searched until July 2022. Studies evaluating cardiovascular events in transgender women or men were included. Primary outcomes were stroke, myocardial infarction (MI), and venous thromboembolism (VTE). The risk for transgender women versus cisgender men and for transgender men versus cisgender women was analysed through random-effects meta-analysis. RESULTS: Twenty-two studies involving 19 893 transgender women, 14 840 transgender men, 371 547 cisgender men, and 434 700 cisgender women were included. The meta-analysis included 10 studies (79% of transgender women and 76% of transgender men). In transgender women, incidence of stroke was 1.8%, which is 1.3 (95% confidence interval [CI], 1.0-1.8) times higher than in cisgender men. Incidence of MI was 1.2%, with a pooled relative risk of 1.0 (95% CI, 0.8-1.2). Venous thromboembolism incidence was 1.6%, which is 2.2 (95% CI, 1.1-4.5) times higher. Stroke occurred in 0.8% of transgender men, which is 1.3 (95% CI, 1.0-1.6) times higher compared with cisgender women. Incidence of MI was 0.6%, with a pooled relative risk of 1.7 (95% CI, 0.8-3.6). For VTE, this was 0.7%, being 1.4 (95% CI, 1.0-2.0) times higher. CONCLUSIONS: Transgender people have a 40% higher risk of CVD compared with cisgender people of the same birth sex. This emphasizes the importance of cardiovascular risk management. Future studies should assess the potential influence of socio-economic and lifestyle factors.

The efficacy of aspirin to inhibit platelet aggregation in patients hospitalised with a severe infection: a multicentre, open-label, randomised controlled trial.

Patients with severe infection have an increased risk of cardiovascular events. A possible underlying mechanism is inflammation-induced platelet aggregation. We investigated whether hyperaggregation occurs during infection, and whether aspirin inhibits this. In this multicentre, open-label, randomised controlled trial, patients hospitalised due to acute infection were randomised to receive 10 days of aspirin treatment (80 mg 1dd or 40 mg 2dd) or no intervention (1:1:1 allocation). Measurements were performed during infection (T1; days 1-3), after intervention (T2; day 14) and without infection (T3; day > 90). The primary endpoint was platelet aggregation measured by the Platelet Function Analyzer® closure time (CT), and the secondary outcomes were serum and plasma thromboxane B2 (sTxB2 and pTxB2). Fifty-four patients (28 females) were included between January 2018 and December 2020. CT was 18% (95%CI 6;32) higher at T3 compared with T1 in the control group (n = 16), whereas sTxB2 and pTxB2 did not differ. Aspirin prolonged CT with 100% (95%CI 77; 127) from T1 to T2 in the intervention group (n = 38), while it increased with only 12% (95%CI 1;25) in controls. sTxB2 decreased with 95% (95%CI - 97; - 92) from T1 to T2, while it increased in the control group. pTxB2 was not affected compared with controls. Platelet aggregation is increased during severe infection, and this can be inhibited by aspirin. Optimisation of the treatment regimen may further diminish the persisting pTxB2 levels that point towards remaining platelet activity. This trial was registered on 13 April 2017 at EudraCT (2016-004303-32).