Treatment with β-blockers is the main strategy for managing patients with heart failure and reduced ejection fraction because of their ability to reverse the neurohumoral effects of the sympathetic nervous system, with consequent prognostic and symptomatic benefits. However, to date, they are underused, mainly because of the misconception that hypotension and bradycardia may worsen the haemodynamic status of patients with HFrEF and because of the presence of comorbidities falsely believed to be absolute contraindications to their use. To promote proper use of β-blockers in this article, we review the clinical pharmacology of β-blockers, the evidence of the beneficial effects of these drugs in heart failure with reduced ejection fraction, and the current guidelines for their use in clinical practice and in the presence of comorbidities (e.g., pulmonary disease, diabetes, atrial fibrillation, peripheral arterial disease, etc.). It is hoped that the practical approach discussed in this review will allow for a proper diffusion of knowledge about the correct use of β-blockers and the drug-disease interactions to achieve their increased use and titration, as well as for the selection of a specific agent with a view to a properly tailored approach for HFrEF patients.

Cardiac transplantation represents the gold standard of treatment for selected patients with advanced heart failure who have poor functional capacity and prognosis despite guideline-directed medical therapy and device-based therapy. Proper patient selection and appropriate referral of patients to centers for the treatment of advanced heart failure are the first but decisive steps for screening patients eligible for cardiac transplantation. The eligibility and the decision to list for cardiac transplantation, even for patients with relative contraindications, are based on a multidisciplinary evaluation of a transplant team. This review will discuss the practical indications, the process of patient eligibility for cardiac transplantation, the principle of donor selection, as well as the surgical technique.

Multimodality imaging is a comprehensive strategy to investigate left ventricular hypertrophy (LVH), providing morphologic, functional, and often clinical information to clinicians. Hypertrophic cardiomyopathy (HCM) is defined by an increased LV wall thickness not only explainable by abnormal loading conditions. In the context of HCM, multimodality imaging, by different imaging techniques, such as echocardiography, cardiac magnetic resonance, cardiac computer tomography, and cardiac nuclear imaging, provides essential information for diagnosis, sudden cardiac death stratification, and management. Furthermore, it is essential to uncover the specific cause of HCM, such as Fabry disease and cardiac amyloidosis, which can benefit of specific treatments. This review aims to elucidate the current role of multimodality imaging in adult patients with HCM.

In this report, an atypical case of Noonan syndrome (NS) associated with sarcomeric hypertrophic cardiomyopathy (HCM) in a 33-year-old patient was described. Genetic testing revealed two different disease-causing mutations: a mutation in the PTPN11 gene, explaining NS, and a mutation in the MYBPC3 gene, known to be associated with HCM. This case exemplifies the challenge in achieving a definite etiological diagnosis in patients with HCM and the need to exclude other diseases mimicking this condition (genocopies or phenocopies). Compound heterozygous mutations are rare but possible in HCM patients. In conclusion, this study highlights the important role of genetic testing as a necessary diagnostic tool for performing a definitive etiological diagnosis of HCM.

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.

We describe the case of a young man with an initial diagnosis of acute myocarditis that was finally recognized as a familial left-dominant arrhythmogenic cardiomyopathy. The diagnostic process was also based on demonstration, serial cardiac magnetic resonance imaging, and typical patterns of myocardial damage, including features of the disease’s inflammatory “hot phase”.