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AimsLake Louise Criteria (LLC) are time-dependent and some acute myocarditis (AM) with preserved left ventricular ejection fraction (LVEF) could be missed, due to the limited accessibility of Cardiac Magnetic Resonance (CMR). We aimed to assess the potential value of cardiac strain measured by feature tracking (FT) imaging in this population.Methods and resultsEighty-three patients with clinically suspected AM and normal LVEF were divided into 39 “confirmed AM” (positive LLC) and 44 “suspected AM” (negative LLC). An age and gender-matched sample of 42 normal subjects underwent CMR. In all groups, FT-derived biventricular strains and STE- global longitudinal strain (GLS) were assessed, being regularly measurable. Strain values < 5th percentile of the control group were considered abnormal. “Suspected” and “confirmed” AM were similar, except for medium time of CMR evaluation (5.2 vs 1 months from presentation, respectively; p = 0.004). Compared to healthy controls, both “suspected” and “confirmed” AM showed significantly impaired strain values. LV-global circumferential strain (GCS), right ventricular GCS and LV-GLS were abnormal in 15.4% and 15.9%, 20.5% and 15.9%, 7.7% and 9.1% in “confirmed” and “suspected” AM, respectively. STE analysis confirmed the results on LV-GLS, however a weak correlation emerged between STE and CMR-FT LV-GLS (p = 0.08).ConclusionsCompared to STE, CMR-FT analysis provided a more comprehensive and complementary biventricular strain evaluation that resulted similar in “confirmed” and “suspected” AM with normal LVEF. Conversely, mostly biventricular GCS was significantly reduced in up to 20% of patients, compared to healthy controls.Graphic abstract

Left ventricular ejection fraction (EF) remains the major parameter for diagnosis, phenotyping, prognosis and treatment decisions in heart failure. The 2016 ESC heart failure guidelines introduced a third EF category for an EF of 40–49%, defined as heart failure with mid-range EF (HFmrEF). This category has been largely unexplored compared with heart failure with reduced EF (HFrEF; defined as EF <40% in this Review) and heart failure with preserved EF (HFpEF; defined as EF ≥50%). The prevalence of HFmrEF within the overall population of patients with HF is 10–25%. HFmrEF seems to be an intermediate clinical entity between HFrEF and HFpEF in some respects, but more similar to HFrEF in others, in particular with regard to the high prevalence of ischaemic heart disease in these patients. HFmrEF is milder than HFrEF, and the risk of cardiovascular events is lower in patients with HFmrEF or HFpEF than in those with HFrEF. By contrast, the risk of non-cardiovascular adverse events is similar or greater in patients with HFmrEF or HFpEF than in those with HFrEF. Evidence from post hoc and subgroup analyses of randomized clinical trials and a trial of an SGLT1–SGLT2 inhibitor suggests that drugs that are effective in patients with HFrEF might also be effective in patients with HFmrEF. Although the EF is a continuous measure with considerable variability, in this comprehensive Review we suggest that HFmrEF is a useful categorization of patients with HF and shares the most important clinical features with HFrEF, which supports the renaming of HFmrEF to HF with mildly reduced EF.Heart failure with mid-range or mildly reduced ejection fraction (HFmrEF) accounts for up to 25% of patients with heart failure. In this Review, Lund and colleagues provide a comprehensive overview of the epidemiology, clinical profile, prognosis and potential treatment of patients with HFmrEF.

Dilated cardiomyopathy (DCM) is a complex disease with multiple causes and various pathogenic mechanisms. Despite improvements in the prognosis of patients with DCM in the past decade, this condition remains a leading cause of heart failure and premature death. Conventional treatment for DCM is based on the foundational therapies for heart failure with reduced ejection fraction. However, increasingly, attention is being directed towards individualized treatments and precision medicine. The ability to confirm genetic causality is gradually being complemented by an increased understanding of genotype–phenotype correlations. Non-genetic factors also influence the onset of DCM, and growing evidence links genetic background with concomitant non-genetic triggers or precipitating factors, increasing the extreme complexity of the pathophysiology of DCM. This Review covers the spectrum of pathophysiological mechanisms in DCM, from monogenic causes to the coexistence of genetic abnormalities and triggering environmental factors (the ‘two-hit’ hypothesis). The roles of common genetic variants in the general population and of gene modifiers in disease onset and progression are also discussed. Finally, areas for future research are highlighted, particularly novel therapies, such as small molecules, RNA and gene therapy, and measures for the prevention of arrhythmic death. In this Review, Mestroni and colleagues provide an overview of the pathophysiological mechanisms underlying dilated cardiomyopathy, including both genetic and non-genetic causes, and discuss the development of novel therapies, such as small molecules and gene therapy. Key points Dilated cardiomyopathy (DCM) is a heterogeneous disease with multiple causes and high variability in phenotype presentation and outcomes. Genetic testing has been recommended in guidelines as a fundamental step in the clinical decision-making process; the results can guide not only family screening but also aetiological characterization and risk stratification. Genotype–phenotype correlations can aid clinicians in prioritizing genetic testing in patients with a higher likelihood of identifying a disease-causing variant, particularly for genes associated with major arrhythmic events. A strong interaction exists between the genetic background and environmental exposures, which can lead to different phenotypic manifestations of the disease (that is, the two-hit hypothesis). Advances in the management of DCM are moving towards a precision medicine approach to the diagnostic work-up and treatment. Future research and resource allocation will focus on the identification of disease-modifying treatments for DCM, which include molecular targeted and gene therapies.

Extracorporeal cardiopulmonary resuscitation (E-CPR) may improve survival with favorable neurological outcome in patients with refractory out-of-hospital cardiac arrest (OHCA). Unfortunately, recent results from randomized controlled trials were inconclusive. We performed a meta-analysis to investigate the impact of E-CPR on neurological outcome compared to conventional cardiopulmonary resuscitation (C-CPR). A systematic research for articles assessing outcomes of adult patients with OHCA either treated with E-CPR or C-CPR up to April 27, 2023 was performed. Primary outcome was survival with favorable neurological outcome at discharge or 30 days. Overall survival was also assessed. Eighteen studies were included. E-CPR was associated with better survival with favorable neurological status at discharge or 30 days (14% vs 7%, OR 2.35, 95% CI 1.61–3.43, I2 = 80%, p < 0.001, NNT = 17) than C-CPR. Results were consistent if the analysis was restricted to RCTs. Overall survival to discharge or 30 days was also positively affected by treatment with E-CPR (OR = 1.71, 95% CI = 1.18–2.46, I2 = 81%, p = 0.004, NNT = 11). In this meta-analysis, E-CPR had a positive effect on survival with favorable neurological outcome and, to a smaller extent, on overall mortality in patients with refractory OHCA. •Evidence on E-CPR benefit in out-of-hospital cardiac arrest is inconclusive•This updated meta-analysis included 15 observational studies and 3 RCTs•E-CPR patients showed better short-term survival with good neurological status•The superiority of E-CPR on C-CPR persisted at 180 days outcome analysis•This meta-analysis supports the use of E-CPR in out-of-hospital cardiac arrest

Abstract Dilated cardiomyopathy (DCM) is a primary heart muscle disease characterized by left or biventricular systolic impairment. Historically, most of the clinical attention has been devoted to the evaluation of left ventricular function and morphology, while right ventricle (RV) has been for many years the forgotten chamber. Recently, progresses in cardiac imaging gave clinicians precious tools for the evaluation of RV, raising the awareness of the importance of biventricular assessment in DCM. Indeed, RV involvement is far from being uncommon in DCM, and the presence of right ventricular dysfunction (RVD) is one of the major negative prognostic determinants in DCM patients. However, some aspects such as the possible role of specific genetic mutations in determining the biventricular phenotype in DCM, or the lack of specific treatments able to primarily counteract RVD, still need research. In this review, we summarized the current knowledge on RV involvement in DCM, giving an overview on the epidemiology and pathogenetic mechanisms implicated in determining RVD. Furthermore, we discussed the imaging techniques to evaluate RV function and the role of RV failure in advanced heart failure.

Background:T-lymphocyte activation within atherosclerotic plaque, and widespread to the myocardium, has been shown in patients with acute coronary syndromes.Objective:To investigate the presence of T-lymphocyte infiltrate at different stages of acute coronary syndromes by studying patients with sudden coronary death, acute myocardial infarction (AMI) and healed infarction, in comparison with patients with myocarditis and patients with non-ischaemic heart failure.Methods:72 cases were studied at autopsy: 12 dying of sudden coronary death (group 1), 12 dying <4 weeks (group 2) and 12 dying >4 months after AMI (group 3), 12 with active lymphocytic myocarditis (group 4), 12 with hypertensive heart disease (group 5), and 12 control subjects (group 6). Light microscopy was performed to measure the number of activated T-lymphocytes (CD3+/DR+) in the myocardium and coronary artery wall, and intercellular adhesion molecule-1 (ICAM-1) expression in the myocardium.Results:Activated T-lymphocyte infiltrates and ICAM-1 myocardial expression in both remote and peri-infarction regions and activated T-lymphocytes within the epicardial coronary artery wall of both the infarct- and non-infarct-related arteries were found in groups 1, 2 and 3, whereas myocardial, but not coronary, infiltrates were found in groups 4 (p<0.001 vs groups 1, 2 and 3 for coronary infiltrates). Groups 5 and 6 had no evidence of myocardial or coronary inflammation (p<0.001 vs groups 1, 2 and 3).Conclusions:The study shows the presence of a lymphocytic infiltrate in both coronary arteries and myocardium and a proinflammatory phenotype shift in the myocardium associated with acute coronary thrombosis in patients dying suddenly, shortly, or even late after coronary thrombosis.