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Abstract Aims The Iron Intravenous Therapy in Reducing the burden of Severe Arrhythmias in HFrEF (RESAFE‐HF) registry study aims to provide real‐word evidence on the impact of intravenous ferric carboxymaltose (FCM) on the arrhythmic burden of patients with heart failure with reduced ejection fraction (HFrEF), iron deficiency (ID), and implanted cardiac implantable electronic devices (CIEDs). Methods and results The RESAFE‐HF (NCT04974021) study was designed as a prospective, single‐centre, and open‐label registry study with baseline, 3, 6, and 12 month visits. Adult patients with HFrEF and CIEDs scheduled to receive IV FCM as treatment for ID as part of clinical practice were eligible to participate. The primary endpoint is the composite iron‐related endpoint of haemoglobin ≥ 12 g/dL, ferritin ≥ 50 ng/L, and transferrin saturation > 20%. Secondary endpoints include unplanned HF‐related hospitalizations, ventricular tachyarrhythmias detected by CIEDs and Holter monitors, echocardiographic markers, functional status (VO2 max and 6 min walk test), blood biomarkers, and quality of life. In total, 106 patients with a median age of 72 years (14.4) were included. The majority were male (84.9%), whereas 92.5% of patients were categorized to New York Heart Association II/III. Patients' arrhythmic burden prior to FCM administration was significant—19 patients (17.9%) received appropriate CIED therapy for termination of ventricular tachyarrhythmia in the preceding 12 months, and 75.5% of patients have frequent, repetitive multiform premature ventricular contractions. Conclusions The RESAFE‐HF trial is expected to provide evidence on the effect of treating ID with FCM in HFrEF based on real‐world data. Special focus will be given on the arrhythmic burden post‐FCM administration.

AimWe aimed to investigate the main anthropometric, cardiorespiratory and haematological factors that can determine marathon race performance in marathon runners.MethodsForty-five marathon runners (36 males, age: 42 ± 10 years) were examined during the training period for a marathon race. Assessment of training characteristics, anthropometric measurements, including height, body weight (n = 45) and body fat percentage (BF%) (n = 33), echocardiographic study (n = 45), cardiopulmonary exercise testing using treadmill ergometer (n = 33) and blood test (n = 24) were performed. We evaluated the relationships of these measurements with the personal best marathon race time (MRT) within a time frame of one year before or after the evaluation of each athlete.ResultsThe training age regarding long-distance running was 9 ± 7 years. Training volume was 70 (50–175) km/week. MRT was 4:02:53 ± 00:50:20 h. The MRT was positively associated with BF% (r = 0.587, p = 0.001). Among echocardiographic parameters, MRT correlated negatively with right ventricular end-diastolic area (RVEDA) (r = −0.716, p < 0.001). RVEDA was the only independent echocardiographic predictor of MRT. With regard to respiratory parameters, MRT correlated negatively with maximum minute ventilation indexed to body surface area (VEmax/BSA) (r = −0.509, p = 0.003). Among parameters of blood test, MRT correlated negatively with haemoglobin concentration (r = −0.471, p = 0.027) and estimated haemoglobin mass (Hbmass) (r = −0.680, p = 0.002). After performing multivariate linear regression analysis with MRT as dependent variable and BF% (standardised β = 0.501, p = 0.021), RVEDA (standardised β = −0.633, p = 0.003), VEmax/BSA (standardised β = 0.266, p = 0.303) and Hbmass (standardised β = −0.308, p = 0.066) as independent variables, only BF% and RVEDA were significant independent predictors of MRT (adjusted R2 = 0.796, p < 0.001 for the model).ConclusionsThe main physiological determinants of better marathon performance appear to be low BF% and RV enlargement. Upregulation of both maximum minute ventilation during exercise and haemoglobin mass may have a weaker effect to enhance marathon performance.Clinical Trial Registrationwww.ClinicalTrials.gov, identifier NCT04738877.

Hypertrophic cardiomyopathy (HCM), the most variable cardiac disease in terms of phenotypic presentation and clinical outcome, represents the most common inherited cardiomyopathic process with an autosomal dominant trait of inheritance. To date, more than 1400 mutations of myofilament proteins associated with the disease have been identified, most of them "private" ones. This striking allelic and locus heterogeneity of the disease certainly complicates the establishment of phenotype-genotype correlations. Additionally, topics pertaining to patients' everyday lives, such as sudden cardiac death (SCD) risk stratification and prevention, along with disease prognosis, are grossly related to the genetic variation of HCM. This review incorporates contemporary research findings and addresses major aspects of HCM, including preclinical diagnosis, genetic analysis, left ventricular outflow tract obstruction and SCD. More specifically, the spectrum of genetic analysis, the selection of the best method for obstruction alleviation and the need for a unique and accurate factor for SCD risk stratification are only some of the controversial HCM issues discussed. Additionally, future perspectives concerning HCM and myocardial ischemia, as well as atrial fibrillation, are discussed. Rather than enumerating clinical studies and guidelines, challenging problems concerning the disease are critically appraised by this review, highlighting current speculations and recommending future directions.