The increasing efficacy of cancer therapies has significantly improved survival rates, but it has also highlighted the prevalence of cancer-therapy-related cardiac dysfunction (CTRCD). This review provides a comprehensive overview of the identification, monitoring, and management of CTRCD, a condition resulting from several treatments, such as anthracyclines, HER2-targeted therapies, target therapies, and radiotherapy. The paper includes a discussion of the mechanisms of CTRCD associated with various cancer treatments. Early detection through serum biomarkers and advanced imaging techniques is crucial for effective monitoring and risk stratification. Preventive strategies include pharmacological interventions such as ACE inhibitors/angiotensin receptor blockers, beta-blockers, and statins. Additionally, novel agents like sacubitril/valsartan, sodium-glucose co-transporter type 2 inhibitors, and vericiguat show promise in managing left ventricular dysfunction. Lifestyle modifications, including structured exercise programs and optimized nutritional strategies, further contribute to cardioprotection. The latest treatments for both asymptomatic and symptomatic CTRCD across its various stages are also discussed. Emerging technologies, including genomics, artificial intelligence, novel biomarkers, and gene therapy, are paving the way for personalized approaches to CTRCD prevention and treatment. These advancements hold great promise for improving long-term outcomes in cancer patients by minimizing cardiovascular complications.

Background: The normal limits of left ventricular (LV) hemodynamic forces (HDFs) are not exactly known. The aim of this study was to explore the full spectrum of HDF parameters in healthy subjects and determine their physiologic correlates. Methods: 269 healthy subjects were enrolled (mean age: 43 ± 14 years; 123 (45.7%) men). All participants underwent an echo-Doppler examination. Tri-plane tissue tracking from apical views was used to measure 2D global endocardial longitudinal strain (GLS), circumferential strain (GCS), and LV HDFs. HDFs were normalized with LV volume and divided by specific weight. Results: LV systolic longitudinal HDFs (%) were higher in men (20.8 ± 6.5 vs. 18.9 ± 5.6, p = 0.009; 22.0 ± 6.7 vs. 19.8 ± 5.6, p = 0.004, respectively). There was a significant correlation between GCS (increased) (r = −0.240, p < 0.001) and LV longitudinal HDFs (reduced) (r = −0.155, p = 0.01) with age. In a multivariable analysis age, BSA, pulse pressure, heart rate and GCS were the only independent variables associated with LV HDFs (β coefficient = −0.232, p < 0.001; 0.149, p = 0.003; 0.186, p < 0.001; 0.396, p < 0.001; −0.328, p < 0.001; respectively). Conclusion: We report on the physiologic range of LV HDFs. Knowledge of reference values of HDFs may prompt their implementation into clinical routine and allow a more comprehensive assessment of the LV function.

Background. Cardiac contractility modulation (CCM) is a novel device-based therapy for patients with heart failure with reduced and mild reduced ejection fraction (HFrEF/HFmrEF). CCM increases cardiac performance and produces reverse left ventricular remodeling, with improved symptoms, functional capacity, quality of life, and reduced HF-related hospitalizations. However, to date, little evidence is available on the effects of CCM on right ventricle (RV) function. Therefore, we analyzed the effects of CCM on RV systolic function and RV–pulmonary artery (PA) coupling. Methods. Twenty-one (65 ± 12.5 years) patients with NYHA class III, ejection fraction < 40% and QRS < 120 ms were assessed at baseline. During follow up, two patients had died, and so nineteen patients were evaluated six months after CCM therapy. Using echocardiography, tricuspid annular systolic excursion (TAPSE), myocardial systolic excursion velocity (RVs), and RV free-wall strain was measured. PA systolic pressure (PASP) was estimated from tricuspid regurgitation, adding the right atrial pressure estimation. The RV-PA coupling was calculated as TAPSE/PASP ratio. Results. After six months, patients who underwent CCM therapy showed a reduction in RV diameters and improved RV systolic function, as evidenced by the increase in both TAPSE (16.6 ± 4.2 mm vs. 18.5 ± 3.6 mm; p < 0.05), RVs (10.1 ± 1.8 cm/s vs. 11.3 ± 11.4 cm/s; p < 0.05), and RV strain (−13.7 ± 1.8% vs. −15.6 ± 2.3%; p < 0.05). CCM also determined a reduction in PASP (34.2 ± 9.8 mmHg vs. 28 ± 6.2 mmHg; p < 0.05) and an increase in the TAPSE/PASP ratio (0.52 ± 0.14 mm/mmHg vs. 0.66 ± 0.23 mm/mmHg; p < 0.05). Conclusions. At six months, CCM increases RV reverse remodeling and performance, reducing RV size and improving RV systolic function, PASP, and RV-PA coupling.

Cancer therapies have revolutionized patient survival rates, yet they come with the risk of cardiotoxicity, necessitating effective monitoring and management. The existing guidelines offer a limited empirical basis for practical approaches in various clinical scenarios. This article explores the intricate relationship between cancer therapy and the cardiovascular system, highlighting the role of advanced multimodality imaging in monitoring patients before, during, and after cancer treatment. This review outlines the cardiovascular effects of different cancer therapy classes, offering a comprehensive understanding of their dose- and time-dependent impacts. This paper delves into diverse imaging modalities such as echocardiography, cardiac magnetic resonance imaging, cardiac computed tomography, and nuclear imaging, detailing their strengths and limitations in various conditions due to cancer treatment, such as cardiac dysfunction, myocarditis, coronary artery disease, Takotsubo cardiomyopathy, pulmonary hypertension, arterial hypertension, valvular heart diseases, and heart failure with preserved ejection fraction. Moreover, it underscores the significance of long-term follow-up for cancer survivors and discusses future directions.

Background: Virtually all patients with heart failure with reduced ejection fraction have a reduction of myocardial mechano-energetic efficiency (MEE). Cardiac contractility modulation (CCM) is a novel therapy for the treatment of patients with HFrEF, in whom it improves the quality of life and functional capacity, reduces hospitalizations, and induces biventricular reverse remodeling. However, the effects of CCM on MEE and global longitudinal strain (GLS) are still unknown; therefore, this study aims to evaluate whether CCM therapy can improve the MEE of patients with HFrEF. Methods: We enrolled 25 patients with HFrEF who received an Optimizer Smart implant (the device that develops CCM therapy) between January 2018 and January 2021. Clinical and echocardiographic evaluations were performed in all patients 24 h before and six months after CCM therapy. Results: At six months, follow-up patients who underwent CCM therapy showed an increase of left ventricular ejection fraction (30.8 ± 7.1 vs. 36.1 ± 6.9%; p = 0.032) as well a rise of GLS 10.3 ± 2.7 vs. −12.9 ± 4.2; p = 0.018), of MEE (32.2 ± 10.1 vs. 38.6 ± 7.6 mL/s; p = 0.013) and of MEE index (18.4 ± 6.3 vs. 24.3 ± 6.7 mL/s/g; p = 0.022). Conclusions: CCM therapy increased left ventricular performance, improving left ventricular ejection fraction, GLS, as well as MEE and MEEi.