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Purpose of reviewHistologic evidence of myocardial inflammatory infiltrate not secondary to an ischemic injury is required by current diagnostic criteria to reach a definite diagnosis of myocarditis. Endomyocardial biopsy (EMB) is therefore often indicated for the diagnosis of myocarditis, although it may lack sufficient sensitivity considering the limited possibility of myocardial sampling. Improving the diagnostic yield and utility of EMB is of high priority in the fields of heart failure cardiology and myocarditis in particular. The aim of the present review is to highlight indications, strengths, and shortcomings of current EMB techniques, and discuss innovations currently being tested in ongoing clinical studies, especially in the setting of acute myocarditis and chronic inflammatory cardiomyopathy.Recent findingsEMB provides unique diagnostic elements and prognostic information which can effectively guide the treatment of myocarditis. Issues affecting the diagnostic performance in the setting of acute myocarditis and chronic inflammatory cardiomyopathies will be discussed in this review in the light of recent expert consensus documents on the management of these conditions and on indication to EMB. Recent innovations using electroanatomic mapping (EAM)-guided EMB and fluoroscopic-guided EMB during temporary mechanical circulatory support have improved the utility of the procedure. EMB remains an important diagnostic test whose results need to be interpreted in the context of (1) clinical pre-test probability, (2) timing of sampling, (3) quality of sampling (4) site of sampling, (5) histologic type of myocarditis, and (6) analytic methods that are applied. Herein we will review these caveats as well as perspectives and innovations related to the use of this diagnostic tool.

Most acquired and inherited cardiomyopathies are characterized by regional left ventricular involvement and nonischemic myocardial scars, often with a disease-specific pattern. Irrespective of the etiology and pathophysiological mechanisms, myocardial disorders are invariably associated with cardiac fibrosis, which contributes to dysfunction and electrical instability. Accordingly, cardiac magnetic resonance plays a central role in the diagnostic work-up and prognostic risk stratification of cardiomyopathies, particularly with the increasing correlation between genetic background and specific disease phenotype. Starting from pattern and distribution of myocardial fibrosis at cardiac magnetic resonance, we provide a practical regional atlas of nonischemic myocardial scar to guide the diagnostic approach to nonischemic cardiomyopathies., Competing Interests: Dr Olivotto was supported by the European Union's 10.13039/100010661Horizon 2020 Research and Innovation Programme under Grant Agreement number: 777204: “SILICOFCM - In Silico trials for drug tracing the effects of sarcomeric protein mutations leading to familial cardiomyopathy”; by the Italian Ministry of Health (Left ventricular hypertrophy in aortic valve disease and hypertrophic cardiomyopathy: genetic basis, biophysical correlates and viral therapy models” (RF-2013-02356787); and by the EnteCassa di Risparmio di Firenze (bando 2016) “juvenile sudden cardiac death: just know and treat.” The authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2024 The Authors.)

Dilated cardiomyopathy (DCM) is defined by the presence of left ventricular dilation and systolic dysfunction in the absence of coronary artery disease, valvular disease, congenital heart disease, or altered haemodynamic conditions. Dilated cardiomyopathy can recognize multiple aetiologies, including infectious processes, effect of toxic substances, immunological mechanisms, and genetic causes. In recent years, many genes coding for proteins involved in the structure and function of the cardiomyocytes have been associated with the development of DCM, making the identification of familial forms increasingly frequent. At the same time, an ever-increasing use of cardiac magnetic resonance imaging has made it possible to identify early morpho-functional alterations in subjects with initial forms of the disease, or carriers of pathogenic genetic variants. The increasingly in-depth understanding of the genetic and molecular mechanisms operating in DCM has also favoured the development of new therapeutic strategies including drugs with molecular targets and gene therapies. In this panorama, screening of family members of patients affected by DCM represents an important tool for early diagnosis, treatment, and prognostic stratification. In relation to its clinical relevance and its complexity, it is important that family screening and follow-up of identified patients are carried out in units dedicated to the treatment and study of cardiomyopathies., Competing Interests: Conflict of interest: none declared., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Aims: In the EXPLORER-HCM trial, mavacamten reduced left ventricular outflow tract obstruction (LVOTO) and improved functional capacity of symptomatic hypertrophic obstructive cardiomyopathy (HOCM) patients. We sought to define the potential use of mavacamten by comparing real-world HOCM patients with those enrolled in EXPLORER-HCM and assessing their eligibility to treatment., Methods and Results: We collected information on HOCM patients followed up at 25 Italian HCM outpatient clinics and with significant LVOTO (i.e. gradient ≥30 mmHg at rest or ≥50 mmHg after Valsalva manoeuvre or exercise) despite pharmacological or non-pharmacological therapy. Pharmacological or non-pharmacological therapy resolved LVOTO in 1044 (61.2%) of the 1706 HOCM patients under active follow-up, whereas 662 patients (38.8%) had persistent LVOTO. Compared to the EXPLORER-HCM trial population, these real-world HOCM patients were older (62.1 ± 14.3 vs. 58.5 ± 12.2 years, p = 0.02), had a lower body mass index (26.8 ± 5.3 vs. 29.7 ± 4.9 kg/m 2 , p < 0.0001) and a more frequent history of atrial fibrillation (21.5% vs. 9.8%, p = 0.027). At echocardiography, they had lower left ventricular ejection fraction (LVEF, 66 ± 7% vs. 74 ± 6%, p < 0.0001), higher left ventricular outflow tract gradients at rest (60 ± 27 vs. 52 ± 29 mmHg, p = 0.003), and larger left atrial volume index (49 ± 16 vs. 40 ± 12 ml/m 2 , p < 0.0001). Overall, 324 (48.9%) would have been eligible for enrolment in the EXPLORER-HCM trial and 339 (51.2%) for treatment with mavacamten according to European guidelines., Conclusions: Real-world HOCM patients differ from the EXPLORER-HCM population for their older age, lower LVEF and larger atrial volume, potentially reflecting a more advanced stage of the disease. About half of real-world HOCM patients were found eligible to mavacamten., (© 2023 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Introduction: It is not clear if differences exist about treating left main bifurcation (LMB) and non-left main bifurcation (non-LMB) lesions by means of percutaneous coronary intervention (PCI)., Methods: We prospectively analyzed all consecutive patients treated at our center for bifurcation lesions from January 1, 2011 to December 31, 2015, including acute myocardial infarction (MI) and cardiogenic shock, and compared the angiographic and clinical outcomes of patients with LMB and non-LMB lesions treated with PCI and second-generation drug-eluting stent (2G-DES) implantation. The primary endpoint was the major adverse cardiac event (MACE) composite, including MI, clinically indicated target-vessel revascularization (TVR), and cardiac death (CD) at 2-year follow-up. We also compared the angiographic patency of the vessel, which was a composite of the restenosis-reocclusion (RR) rate., Results: Out of 1081 patients (1368 bifurcations), a total of 320 patients had LMB (29%). Overall, procedural success was 98.4%. Clinical follow-up rate was 100%. Angiographic follow-up rate was 83.7%. No differences were seen regarding the primary endpoint of all MACE (17.8% in LMB vs 18.0% in non-LMB; P>.99), MI rate (4.3% in LMB vs 2.9% in non-LMB; P=.20), and CD (8.7% in LMB vs 5.8% in non-LMB; P=.08). The overall RR rate was 11.8%, with 5% RR rate in the LMB group (16/320 lesions) and 9.7% RR rate in the non-LMB group (102/1048 lesions); P<.01. The LMB group had a better TVR rate (5.0% vs 9.4% in the non-LMB group; P=.01)., Conclusion: PCI with 2G-DES for LMB has better target-vessel patency and TVR rates when compared with non-LMB lesions, without clinical differences in terms of 2-year clinical outcomes.