Chemotherapy induced cardiotoxicity is becoming increasingly prevalent with several new agents being used recently. The incidence of Takotsubo cardiomyopathy due to 5-fluorouracil based chemotherapeutic regimens like FOLFOX is not uncommon. It is also seen with platinum based chemotherapy. Most of these patients have reversible cardiotoxicity and the cardiac function recovers within a short period with supportive treatment. Here we have a patient who presented with cardiogenic shock after 5 days of receiving FOLFOX regimen for colorectal adenocarcinoma. She was treated with a percutaneous left ventricular assist device, Impella CP, for hemodynamic support with excellent outcome.

Background: The use of induction immunosuppression for heart transplantation (HT) is debated given the uncertain benefit and potential risks of infection and malignancy.Methods: This is a retrospective single‐center analysis of 475 consecutive HT recipients from 2003 to 2020 grouped by use of induction with basiliximab group (BG) and the no basiliximab group (NBG). Subgroup analysis by era compared pre‐2016 standard‐basiliximab (BX) induction and 2016–2020 with selective‐BX use as part of a calcineurin‐inhibitor‐sparing regimen.Results: When adjusted for confounders (sex, age, PRA, eGFR), the BG was less likely to have acute cellular rejection (ACR) (OR.42, p < .001), but had more antibody mediated rejection (AMR) (OR 11.7, p < .001) and more cardiac allograft vasculopathy (CAV) (OR 3.8, p = .04). There was no difference between BG and NBG in the incidence of malignancies or infections. When stratified by era (pre‐2016 vs. 2016–2020), ACR remained less common in the BG than the NBG (36% vs. 50%, p = .045) groups, while AMR remained more common (9.7 vs. 0% p = .005). There was no significant difference in conditional survival comparing pre‐and post‐2016 NBG (HR 2.20 (95% CI.75–6.43); however, both pre‐2016 BG and post‐2016 BG have significantly higher mortality (HR 2.37 [95% CI 1.02–5.50) and HR 2.69 (95% CI 1.08–6.71), p = .045 and.03, respectively].Conclusion: Basiliximab reduces the incidence of ACR but increases the risk of AMR, CAV, and may be associated with increased mortality. Mechanistic studies are needed to describe a potential T‐cell‐escape mechanism with enhanced humoral immunity.

Heart transplantation is the gold standard in patients with end stage heart failure, offering vastly improved survival, mortality and quality of life. However, hypertension occurring after cardiac transplantation is a serious issue, with the incidence ranging from 50 to 80% of patients. The pathophysiology of the hypertension encompasses a more varied and unique set of causes than those identified in non-organ transplant patients, particularly related to the use of calcineurin inhibitors (CNIs) especially cyclosporine. An in-depth understanding of hypertension after heart transplantation remains a critical issue that necessitates further clarification, due to its deleterious long-term consequence such as impaired graft survival, cardiac allograft vasculopathy (CAV), and overall survival. This article provides a comprehensive review of the prevalence, risk factors, etiology, complications, and management of hypertension after heart transplantation.

Hypertension (HTN) is a widely prevalent disease across the globe.