Heart failure pharmacotherapy and cancer: pathways and pre-clinical/clinical evidence

Abstract

Heart failure (HF) patients have a significantly higher risk of new-onset cancer and cancer-associated mortality, compared to subjects free of HF. While both the prevention and treatment of new-onset HF in patients with cancer have been investigated extensively, less is known about the prevention and treatment of new-onset cancer in patients with HF, and whether and how guideline-directed medical therapy (GDMT) for HF should be modified when cancer is diagnosed in HF patients. The purpose of this review is to elaborate and discuss the effects of pillar HF pharmacotherapies, as well as digoxin and diuretics on cancer, and to identify areas for further research and novel therapeutic strategies. To this end, in this review, (i) proposed effects and mechanisms of action of guideline-directed HF drugs on cancer derived from pre-clinical data will be described, (ii) the evidence from both observational studies and randomized controlled trials on the effects of guideline-directed medical therapy on cancer incidence and cancer-related outcomes, as synthetized by meta-analyses will be reviewed, and (iii) considerations for future pre-clinical and clinical investigations will be provided.

Early microvascular coronary endothelial dysfunction precedes pembrolizumab-induced cardiotoxicity. Preventive role of high dose of atorvastatin

“…There is an imperative need to understand the pivotal biological crosstalk between cardiovascular morbidities and malignancies, as on the one hand they may enable the development of novel therapeutic and preventive modalities for both diseases [52], whereas on the other hand they may reveal novel challenges for cardioprotection [28]. Despite the fact that prophylactic therapies against new-onset HF in cancer patients have been extensively investigated, studies and indications on cancer management in patients with preexisting HF and data on whether guideline-directed medical therapy for HF should be modified upon cancer diagnosis are still obscure and need further investigation [73]. It is described that endothelial dysfunction and cancer might share common confounders, namely activation of the Wnt signaling pathway and depression of peroxisome proliferator-activated receptor gamma (PPAR gamma) signaling [53], which might link endothelial microvascular dysfunction and cancer.…”