Purpose of review Contemporary anticancer immunotherapy, particularly immune checkpoint inhibitors (ICI) and chimeric antigen receptor (CAR) T cell therapy, has changed the landscape of treatment for patients with a variety of malignancies who historically had a poor prognosis. However, both immune checkpoint inhibitors and CAR T cell therapy are associated with serious cardiovascular adverse effects. As immunotherapy evolves to include high-risk patients with preexisting cardiovascular risk factors and disease, the risk and relevance of its associated cardiotoxicity will be even higher. Recent findings ICI can cause myocarditis, which usually occurs early after initiation, can be fulminant, and prompt treatment with high-dose corticosteroids is crucial. CAR T cell therapy frequently leads to cytokine release syndrome, which is associated with cardiomyopathy or arrhythmia development and may also result in circulatory collapse. Supportive treatment, as well as tocilizumab, an anti-interleukin-6 receptor antibody, is the cornerstone of treatment. Recent findings suggest that preexisting cardiovascular risk factors and disease may increase the risk of such cardiotoxicity, and prompt recognition, as well as treatment, may favorably alter the outcomes. Summary ICI and CAR T cell therapy have improved cancer-related outcomes; however, they both are associated with potentially therapy-limiting cardiotoxicity. Cardio-oncologists are required to play an important role in patient selection, pretherapy cardiovascular optimization, and prompt recognition and treatment of cardiotoxicity.

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Background: We aim to assess the heterogeneity of demographics, gender variability and outcomes reporting for subjects enrolled in RCTs studying the role of statins and PCSK9 inhibitors in primary and secondary prevention of CAD. Methods: RCTs and metanalyses were searched for the use of statins and PCSK9 inhibitors published in journals with impact factor > 4 between 1995 and 2020. RCT data was analyzed for gender, race and geographic location. Metanalyses were searched for the outcomes-level heterogeneity. Results: A total 31 statin-based RCTs for primary and secondary prevention of CAD were found, of which 29 were included with a total 172,871 patients (71.4% males vs. 28.6% females). In WOSCOPS trial, all 6595 subjects were males. Though most of these trials included global patient populations, 10% of the trials included exclusively North Americans. Fifteen of the RCTs (52%) did not have race data. Of the 14 RCTs which reported race: 67% White, 4% Black. The mean number of White and non-White patients were 3950 and 1768 respectively. For PCSK9 inhibitors with a total of 13 RCTs included in our study there were cumulative 85,806 patients with globally enrolled patient population and predominantly male 71% vs 29% females. Ten RCTs (77%) reported race: 82% White, 0.3% Black. The mean number of White and non-White patients were 4671 and 1058 respectively. The eleven statin metanalyses included 823,936 patients. Ten of the eleven metanalyses reported statistical heterogeneity via I 2 % (mean 53%) for different outcomes. Five of the eleven metanalyses included primary outcomes of all-cause mortality, and the rest included onset/progression of different types of cardiovascular disease. The seven PCSK9 inhibitor metanalyses pooled 376,885 patients. All 7 metanalyses reported heterogeneity via I 2 % (mean 48%) for different outcomes, of which 2 included primary outcomes of all-cause mortality. Conclusions: Significant gender and racial disparities exist in RCTs for primary and secondary prevention lipid lowering therapies. Enrollment in PCSK9 inhibitor trials was global and significant treatment effect heterogeneity existed in metanalyses. Inequalities in female and non-White participation may hamper generalizability of these crucial medications.