Heart failure (HF) is a significant disease affecting 1–2% of the general population. Despite its general aspects, HF, like other cardiovascular diseases, presents various gender-specific aspects in terms of etiology, hemodynamics, clinical characteristics, therapy, and outcomes. As is well known, HF with preserved ejection fraction more frequently affects females, with diabetes and arterial hypertension representing the most critical determinants of HF. On the other hand, women are traditionally underrepresented in clinical trials and are often considered undertreated. However, it is not clear whether such differences reflect cultural behaviors and clinical inertia or if they indicate different clinical profiles and the impact of sex on hard clinical outcomes. We aimed to review the sex-related differences in patients affected by HF.

Antiblastic drugs-induced cardiomyopathy remains a relevant cause of morbidity and mortality, during and after chemotherapy, despite the progression in protective therapy against cardiovascular diseases and myocardial function. In the last few decades, many groups of researchers have focused their attention on studying the metabolic profile, first in animals, and, subsequently, in humans, looking for profiles which could be able to predict drug-induced cardiotoxicity and cardiovascular damage. In clinical practice, patients identified as being at risk of developing cardiotoxicity undergo a close follow-up and more tailored therapies. Injury to the heart can be a consequence of both new targeted therapies, such as tyrosine kinase inhibitors, and conventional chemotherapeutic agents, such as anthracyclines. This review aims to describe all of the studies carried on this topic of growing interest.

Emerging evidence indicates that specific genetic variants are associated with an increased risk of toxicity from anticancer treatments and cancer-related cardiovascular complications. These genetic factors influence drug metabolism, efficacy, and susceptibility to adverse effects. For cancer patients, the genetic background can have two major cardiovascular implications, namely therapy-related cardiotoxicity and cancer-related cardiovascular complications. Baseline risk stratification is essential to identify higher-risk individuals and ensure they receive appropriate preventive and therapeutic interventions and more frequent follow-up. Current guidelines recommend stratification based on cardiovascular risk factors, but these factors alone cannot accurately define individual risk. Genetic background has been shown to enhance risk stratification. Beyond rare genetic variants, recent genome-wide association studies have identified single nucleotide polymorphisms implicated in cancer therapy toxicity. Despite their current limitations, polygenic risk scores are expected to play a significant role in risk stratification. This review aims to summarize the current evidence on the role of the genetic background of patients with cancer treated with potentially cardiotoxic drugs who develop cardiotoxicity, aiming to provide insights to refine risk stratification further and tailor the management of these patients.