Pulmonary hypertension in the context of left heart disease is the most common form of pulmonary hypertension encountered in clinical practice and is associated with worse prognosis in patients being considered for cardiac transplantation. Therapies targeting left ventricular unloading, as well as pulmonary vascular remodeling, are being increasingly studied and used in daily practice.

In recent years, cancer treatment has evolved, and new therapies have been introduced with significant improvement in prognosis. The immunotherapies stand out owing to their efficacy and remission rate. Chimeric antigen receptor (CAR) T-cell therapy is a part of this new era of therapies. Chimeric antigen receptor T-cell therapy is a form of adoptive cellular therapy that uses a genetically encoded CAR in modified human T cells to target specific tumor antigens in a nonconventional, non-major histocompatibility complex (MHC) protein presentation. Chimeric antigen receptor T-cell therapy successfully identifies tumor antigens and through activation of T cells destroys tumoral cells. It has been found to efficiently induce remission in patients who have been previously treated for B-cell malignancies and have persistent disease. As the use of this novel therapy increases, its potential side effects also have become more evident, including major complications like cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). Cytokine release syndrome is a major systemic inflammatory process as a result of massive cytokine production by the proliferating and activated CAR T cells in which multiple interleukins and immune cells contribute to the inflammatory response. Cytokine release syndrome has been associated with cardiovascular life-threatening complications including hypotension, shock, tachycardia, arrhythmias, left ventricular dysfunction, heart failure, and cardiovascular death. Arrhythmias, among its major complications, vary from asymptomatic prolonged corrected QT interval (QTc) to supraventricular tachycardia, atrial fibrillation, flutter, and ventricular arrhythmias like Torsade de pointes. This article focuses on the cardiovascular complications and arrhythmias associated with CRS and CAR T-cell therapy.

Background This study assessed in-hospital outcomes of patients with chronic systolic, diastolic, or mixed heart failure (HF) undergoing transcatheter aortic valve replacement (TAVR) or surgical aortic valve replacement (SAVR). Methods The Nationwide Inpatient Sample database was used to identify patients with aortic stenosis and chronic HF who underwent TAVR or SAVR between 2012 and 2015. Propensity score matching and multivariate logistic regression were used to determine outcome risk. Results A cohort of 9,879 patients with systolic (27.2%), diastolic (52.2%), and mixed (20.6%) chronic HF were included. No statistically significant differences in hospital mortality were noted. Overall, patients with diastolic HF had the shortest hospital stays and lowest costs. Compared with patients with diastolic HF, the risk of acute myocardial infarction (TAVR odds ratio [OR], 1.95; 95% CI, 1.20–3.19; P = .008; SAVR OR, 1.38; 95% CI, 0.98–1.95; P = .067) and cardiogenic shock (TAVR OR, 2.15; 95% CI, 1.43–3.23; P < .001; SAVR OR, 1.89; 95% CI, 1.42–2.53; P ≤ .001) was higher in patients with systolic HF, whereas the risk of permanent pacemaker implantation (TAVR OR, 0.58; 95% CI, 0.45–0.76; P < .001; SAVR OR, 0.58; 95% CI, 0.40–0.84; P = .004) was lower following aortic valve procedures. In TAVR, the risk of acute deep vein thrombosis and kidney injury was higher, although not statistically significant, in patients with systolic HF than in those with diastolic HF. Conclusion These outcomes suggest that chronic HF types do not incur statistically significant hospital mortality risk in patients undergoing TAVR or SAVR.

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guanylate cyclase stimulator, riociguat, has also been used in place of PDE5i but the benefit of switching from PDE5 to this drug has not been established. We sought to investigate the clinical and hemodynamic effects of replacing PDE5i with riociguat. Methods: We retrospectively analyzed data from patients who had been switched from a PDE5i to riociguat for a clinical indication. Baseline (pre-PDE5i), on PDE-5i, and post-riociguat exchange hemodynamic and clinical data were analyzed to determine if any changes were associated with riociguat exchange. Covariate analysis was performed to correct for length of time on therapy and whether other PH specific therapies had been added or intensified. Results: 18 consecutive PDE5i to riociguat switch patients were screened for inclusion and, since 5 were found to have incomplete records, 13 were included for analysis. In comparing pre-PDE5i to post-PDE5i parameters, there were no significant hemodynamic or clinical differences between the groups after a mean of 172 weeks of follow-up despite 75% of patients having other PH therapies added or intensified. However, after PDE5i to riociguat exchange for a minimum of 12 weeks (mean 34 weeks), cardiac index (CI) by Fick increased by 0.41±0.16 L/min/m2 (p= 0.026), pulmonary vascular resistance (PVR) decreased by 1.56±0.67 WU (p= 0.037) and mean arterial pressure (MAP) decreased by 19±5 mmHg (p= 0.001). Further, covariate analysis showed no significant contribution from length of time on riociguat or whether PH therapies were intensified at the time of riociguat exchange. Conclusion: We conclude that PDE5i to riociguat exchange is a viable option for patients with worsening clinical status and, after 12 weeks, is associated with significantly increased CI, decreased PVR, and decreased MAP irrespective of intensifying other PH directed therapies or extended use of the drug beyond 12 weeks. Forthcoming data from the prospective RESPITE trial may aid in further delineating this relationship.