The benefits of rehabilitation in heart failure (HF) patients are well established. Little is known about Nordic walking (NW) training in HF patients especially in those with cardiovascular implantable electronic devices (CIEDs). The purpose of this study was to assess safety, effectiveness, adherence to and acceptance of home-based telemonitored NW in HF patients, including those with CIEDs (i.e. cardiac resynchronisation therapy, implantable cardioverter-defibrillator). The study design was a single-centre, prospective, parallel-group, randomised (2:1), controlled trial among 111 HF patients, New York Heart Association (NYHA) II–III; left ventricular ejection fraction (EF) ≤ 40%. The intervention was a home-based telemonitored eight-week NW (training group (TG) n = 77) five times weekly vs usual care alone (control group (CG) n = 34). Outcome measures included a primary end point of functional capacity assessed by peak oxygen consumption (VO₂peak). Secondary end points included: workload duration (t) in cardiopulmonary exercise test (CPET), six-minute walking test (6-MWT) distance and quality of life (QoL), Medical Outcome Survey Short Form 36 (SF-36); safety; adherence to and acceptance of NW. Measurements were made before and after intervention. NW resulted in significant improvement in: VO₂peak (16.1 ± 4.0 vs 18.4 ± 4.1(ml/kg/min), p = 0.0001), t (471 ± 141 vs 577 ± 158 (s), p = 0.0001), 6-MWT(428 ± 93 vs 480 ± 87 (m), p = 0.0001) and QoL (79.0 ± 31.3 vs 70.8 ± 30.3 (score), p = 0.0001). We did not observe favourable results in the CG. The differences between the TG and CG were significant in: ΔVO₂peak (Δ2.0 ± 2.4 vs Δ−0.2 ± 2.1, p = 0.0004); Δt (Δ108 ± 108 vs Δ0.94 ± 109, p = 0.0031); Δ6-MWT (Δ53.8 ± 63.9 vs Δ22.0 ± 68.7, p = 0.0483). In neither group were there deaths nor necessity for hospitalisation. We did not observe any intervention from CIEDs during NW. All patients in the TG completed rehabilitation and accepted it well. In HF patients, including those with CIEDs, home-based telemonitored NW is safe and effective. NW was well accepted by patients and adherence was high and promising.

Objective The Multicentre Olmesartan atherosclerosis Regression Evaluation (MORE) study was a double-blind trial in patients with hypertension at increased cardiovascular risk with carotid wall thickening and a defined atherosclerotic plaque that used non-invasive 2- and 3-dimensionaL (D) ultrasound (US), to compare the effects of a 2-year treatment based on either olmesartan medoxomil or atenolol on common carotid (CC) intima-media thickness (IMT) and plaque volume (PV).

TTN gene truncating variants are common in dilated cardiomyopathy (DCM), although data on their clinical significance is still limited. We sought to examine the frequency of truncating variants in TTN in patients with DCM, including familial DCM (FDCM), and to look for genotype-phenotype correlations. Clinical cardiovascular data, family histories and blood samples were collected from 72 DCM probands, mean age of 34 years, 45.8% FDCM. DNA samples were examined by next generation sequencing (NGS) with a focus on the TTN gene. Truncating mutations were followed up by segregation study among family members. We identified 16 TTN truncating variants (TTN trunc) in 17 probands (23.6% of all cases, 30.3% of FDCM, 17.9% of sporadic DCM). During mean 63 months from diagnosis, there was no difference in adverse cardiac events between probands with and without TTN truncating mutations. Among relatives 29 mutation carriers were identified, nine were definitely affected (31%), eight probably affected (27.6%) one possibly affected (3.4%) and eleven were not affected (37.9%). When relatives with all affected statuses were combined, disease penetrance was still incomplete (62.1%) even after exclusion of unaffected relatives under 40 (82%) and was higher in males versus females. In all mutation carriers, during follow-up, 17.4% had major adverse cardiac events, and prognosis was significantly worse in men than in women. In conclusion, TTN truncating variants were observed in nearly one fourth of young DCM patient population, in vast majority without conduction system disease. Incomplete penetrance suggests possible influence of other genetic and/or environmental factors on the course of cardiotitinopathy. Counseling should take into account sex and incomplete penetrance.

BAG3 gene mutations have been recently implicated as a novel cause of dilated cardiomyopathy (DCM). Our aim was to evaluate the prevalence of BAG3 mutations in Polish patients with DCM and to search for genotype-phenotype correlations.

Aims This study was designed to evaluate the safety, tolerability and haemodynamic effects of BMS‐986231, a novel second‐generation nitroxyl donor with potential inotropic, lusitropic and vasodilatory effects in patients hospitalized with decompensated heart failure and reduced ejection fraction (HFrEF). Methods and results Forty‐six patients hospitalized with decompensated HFrEF were enrolled into four sequential dose‐escalation cohorts in this double‐blind, randomized, placebo‐controlled Phase 2a study. Patients with baseline pulmonary capillary wedge pressure (PCWP) of ≥20 mmHg and a cardiac index of ≤2.5 L/min/m² received one 6‐h i.v. infusion of BMS‐986231 (at 3, 5, 7 or 12 µg/kg/min) or placebo. BMS‐986231 produced rapid and sustained reductions in PCWP, as well as consistent reductions in time‐averaged pulmonary arterial systolic pressure, pulmonary arterial diastolic pressure and right atrial pressure. BMS‐986231 increased non‐invasively measured time‐averaged stroke volume index, cardiac index and cardiac power index values, and decreased total peripheral vascular resistance. There was no evidence of increased heart rate, drug‐related arrhythmia or symptomatic hypotension with BMS‐986231. Analyses of adverse events throughout the 30‐day follow‐up did not identify any toxicities specific to BMS‐986231, with the potential exception of infrequent mild‐to‐moderate headaches during infusion. There were no treatment‐related serious adverse events. Conclusions BMS‐986231 demonstrated a favourable safety and haemodynamic profile in patients hospitalized with advanced heart failure. Based on preclinical data and these study's findings, it is possible that the haemodynamic benefits may be mediated by inotropic and/or lusitropic as well as vasodilatory effects. The therapeutic potential of BMS‐986231 should be further assessed in patients with heart failure.

The aim of this study was to examine the significance of ultrasound-measured carotid intima-media thickness (CIMT) in high-risk patients with hypertension and coronary artery disease (CAD), as an independent prognostic factor in determining the risk of all-cause death or future cardiovascular events. The study included 297 consecutive patients (mean age +/- SD, 57 +/- 9.4 years) with diagnosed hypertension and CAD, referred for coronary angiography. The mean of maximal CIMT in two arterial segments bilaterally was calculated. The primary endpoint was a patient's death from all causes. Death, stroke, or myocardial infarction comprised the secondary, composite endpoint. There was a follow-up of 1 to 79 (mean, 41) months. The predictors of death in a multivariate Cox proportional hazards model were the number of stenosed coronary arteries (P = .007) and CIMT (P = .001). The risk of the secondary, composite endpoint (death, stroke, or myocardial infarction) was determined by diabetes (P = .008) and CIMT (P = .010). Nearly 99% of patients with "low CIMT" (< or =1.13 mm) survived for 5 years, versus 78% with "high CIMT" >1.13 mm (log-rank test; P < .001). For the secondary, composite endpoint (death, stroke, or myocardial infarction), the event-free survival rate was 95% (low CIMT), versus 74% after 5 years (high CIMT) (P < .008). Intima-media thickness of the carotid arteries is a strong and independent predictor of death and serious cardiovascular events in hypertensive patients with CAD referred for coronary angiography.