Russian Society of Cardiology (RSC).With the participation of Russian Scientific Society of Clinical Electrophysiology, Arrhythmology and Cardiac Pacing, Russian Association of Cardiovascular Surgeons.Approved by the Scientific and Practical Council of the Russian Ministry of Health.

Aim To develop an algorithm for optimization of rate‐adaptive pacing settings in heart failure patients with preserved ejection fraction (HFpEF) and permanent cardiac pacing. Methods This is a prospective randomized controlled study. A total of 54 patients with HFpEF, permanent atrial fibrillation (AF), and VVIR pacing were randomized to an intervention group with optimization of rate‐adaptation parameters by using cardiopulmonary exercise testing (CPET) and pacemaker stress echocardiography (PASE), and to a control group with conventional programming. CPET, 6‐min walk test (6‐mwt), echocardiography (echo), Duke Activity Status Index (DASI), and Minnesota questionnaire (MLHFQ) were performed at baseline and after 3 months. PASE was used to exclude exercise‐induced ischemia and to determine safe upper sensor rate. Pacing parameters were corrected to achieve optimal heart rate increments of 3‐6 bpm for 1 mL/min/kg of VO2 (oxygen uptake). Results After 3 months, the intervention group demonstrated significant improvement of VO2 peak by 1.64 ± 1.6 mL/min/kg, anaerobic threshold by 1.33 ± 1.3 mL/min/kg, exercise time by 170 ± 98 s, 6‐mwt distance by 75 ± 63 m (P < .0001 for all), DASI by 5.23 points (P = .009), MLHFQ‐score (reduction by 9 points, P < .0001), and echo parameters (decrease in LA volume from 108 (84; 132) to 95 (85; 130) mL, P = .026; E/e’ from 11.7 ± 3.2 to 10.4 ± 2.9, P = .025; systolic pulmonary artery pressure (SPAP) from 44 ± 14 to 39 ± 12 mm Hg, P = .001) compared to the control group. Conclusion An algorithm incorporating CPET and PASE for optimal programming of rate‐adaptation parameters is a valuable tool to improve exercise capacity in HFpEF patients with permanent AF and VVIR pacing who remain exercise intolerant after conventional programming.

Aims To evaluate safety and efficacy of moderate intensity interval exercise training early after heart failure decompensation on exercise tolerance and health-related quality of life (HRQoL). Methods and results This is a prospective randomized controlled study. We screened 234 consecutive patients admitted with decompensated heart failure; 46 patients (42 men/4 women; 61 ± 12 years of age) were randomized to a moderate intensity aerobic interval training ( n = 24) or to a control group ( n = 22). Patients underwent cardiopulmonary exercise testing, echocardiography and Minnesota Living with Heart Failure questionnaire (MLHFQ) at baseline, after three weeks and after three months. After three weeks, peak-VO increased by 17% in the training group ( p = 0.003) with further increase by 10% after three months ( p < 0.001) but did not change significantly in controls. MLHFQ score improved after three weeks, with better results in the training group (from 64.6 ± 15.6 to 30.8 ± 12.9, p < 0.001). After three months, MLHFQ further improved in the exercise training group, but not in controls. Left ventricular ejection fraction was not significantly different between the two groups at baseline and after three months. No serious adverse events related to exercise testing or training were observed. Conclusions Interval exercise training early after an episode of heart failure decompensation is safe and effective in improving exercise tolerance and health-related quality of life in selected patients after achievement of clinical stability. Positive effects remained sustained after three months. Further studies are needed to define role and indications for interval exercise training early after heart failure decompensation.

ObjectiveTo determine the impact of sodium-dependent glucose type 2 cotransporter inhibitors on the renal function in acute heart failure.MethodsIn a single-centre, controlled, randomised study, patients were prescribed dapagliflozin in addition to standard therapy, or were in receipt of standard therapy. The prespecified outcome was renal function deterioration; the secondary outcomes were the development of resistance to diuretics, weight loss, death during hospitalisation and the rehospitalisation or death for any reason within 30 days following discharge.Results102 patients were included (73.4±11.7 years, 57.8% men). The average left ventricular ejection fraction was 44.9%±14.7%, the average N-terminal prohormone of brain natriuretic peptide (NT-proBNP) was 4706 (1757; 11 244) pg/mL, the average estimated glomerular filtration rate (eGFR) was 51.6±19.5 mL/min. eGFR decreased 48 hours after randomisation in the dapagliflozin group (−4.2 (−11.03; 2.28) mL/min vs 0.3 (−6; 6) mL/min; p=0.04) but did not differ between the groups on discharge (54.71±19.18 mL/min and 58.92±24.65 mL/min; p=0.36). The incidence of worsening renal function did not differ (34.4% vs 15.2%; p=0.07). In the dapagliflozin group, there was less tendency to increase the dose of loop diuretics (14% vs 30%; p=0.048), lower average doses of loop diuretics (78.46±38.95 mg/day vs 102.82±31.26 mg/day; p=0.001) and more significant weight loss (4100 (2950; 5750) g vs 3000 (1380; 4650) g; p=0.02). In-hospital mortality was 7.8% (4(8%) in the dapagliflozin and 4 (7.7%) in the control group (p=0.95). The number of deaths within 30 days following discharge in the dapagliflozin group and in the control group was 9 (19%) and 12 (25%), p=0.55; the number of rehospitalisations was 14 (29%) and 17 (35%), respectively (p=0.51).ConclusionThe use of dapagliflozin was associated with a more pronounced weight loss and less need to increase diuretic therapy without significant deterioration of the renal function. Dapagliflozin did not improve the in-hospital and 30-day prognosis after discharge.Trial registration numberN04778787.

The aim of this study is to assess the influence of gene CYP2C19, CYP3A4, CYP3A5 and ABCB1 polymorphisms on clopidogrel antiplatelet activity, rivaroxaban concentration equilibrium, and clinical outcomes among patients with acute coronary syndrome and non-valvular atrial fibrillation. Methods: In the multicenter prospective registry study of the efficacy and safety of a combined antithrombotic therapy 103 patients with non-valvular atrial fibrillation both undergoing or not a percutaneous coronary intervention were enrolled. The trial assessed the primary outcomes (major bleeding, in-hospital death, cardiovascular death, stroke\transient ischaemic attack, death/renal insufficiency) and secondary outcomes (platelet reactivity units (PRU), rivaroxaban concentration). Results: For none of the clinical outcomes when combined with other covariates, the carriership of polymorphisms CYP3A5*3 rs776746, CYP2C19*2 rs4244285;*17 rs12248560, ABCB1 3435 C>T, ABCB1 rs4148738 was significant. None of the markers under study (CYP3A5*3 rs776746, CYP2C19*2 rs4244285, *17 rs12248560, ABCB1 3435 C>T, ABCB1 rs4148738) has proven to affect rivaroxaban equilibrium concentration in blood plasma among patients with atrial fibrillation and acute coronary syndrome. Conclusion: In situations of double or triple antithrombotic rivaroxaban and clopidogrel therapy among patients with atrial fibrillation and acute coronary syndrome, the genetic factors associated with bleeding complications risk (CYP2C19*17) may prove to be clinically relevant.