[Possibilities of Predicting Peak Oxygen Consumption in Patients With Chronic Heart Failure According to the 6­Minute Walk Test].

AIM: To determine the correlation between the results of the 6-minute walk test (6MWT) and peak oxygen consumption (VO2peak) for populations of patients with chronic heart failure with pronounced clinical and demographic differences; to study a possibility of indirect measurement of VO2peak based on the results of 6MWT using the formulas available from the literature. MATERIAL AND METHODS: Two databases were analyzed: 50 patients included in the AEROFIT study (group A), and 31 patients from the Almazov National Medical Research Center (group B). The inclusion criteria were the availability of data from the cardiopulmonary stress test and the 6MWT. The possibility of predicting VO2peak was calculated based on the results of 6MWT using the formulas reported in the literature (L. P. Cahalin et al., 1996; R. M. Ross et al., 2010; R. A. Adedoyin et al., 2010). The predictive accuracy of the models was assessed using the coefficient of determination (R2). The relationship between functional and clinical-demographic indicators was assessed using the Pearson or Spearman correlation analysis. RESULTS: The study groups differed significantly in all parameters, except for the proportion of men and the mean VO2peak. Group B patients were 20 years younger than group A patients, had a lower left ventricular ejection fraction (24.06±7.75 and 41.52±10.48 %, respectively; p<0.001), and covered a 130 m shorter distance in the 6MWT. Despite the absence of a significant difference in VO2peak between groups A and B (13.6 and 13.1 ml / kg / min, respectively; p=0.6581), 61 % of group B patients and 20% of group A belonged to Weber functional class IV. In group A, the 6MWT distance correlated closely with VO2peak (R=0.78; p<0.01) and weakly with age (R=0.4) and body mass index (R=0.3). In group B, the 6MWT distance correlated only with VO2peak (R=0.77; p<0.01). For group A, the R.M. Ross et al. model demonstrated high accuracy in determining the mean VO2peak value with a 0.06% prediction error normalized to measured VO2peak. For group B, none of the models showed satisfactory predictive accuracy. The Ross and Cahalin models showed the best coefficients of determination for groups A and B: Group A, Ross et al. (R2=0.58) and Cahalin et al. (R2=0.59); Group B, Ross et al. (R2=0.59) and Cahalin et al. (R2=0.6). CONCLUSION: In two groups of patients with a statistically insignificant difference in the mean values of VO2peak, the mean values of 6MWT distance were significantly different, although these indicators correlated closely. The VO2peak prediction models showed satisfactory accuracy for estimation of mean VO2, but poor accuracy for estimation of individual values. A better predictive accuracy is determined by similar clinical and demographic characteristics between the training and testing populations, and likely also by models based on larger, more diversified populations.

Tolerability of an Individualized Physical Rehabilitation Program in Patients Dependent on Inotropic Support With End-Stage Chronic Heart Failure.

Aim      To assess the tolerability of an individualized physical rehabilitation program (PRP) in inotrope-dependent patients with end-stage chronic heart failure (CHF).Material and methods  This prospective randomized study included 120 men aged 18-65 years with left ventricular ejection fraction ≤30 % and blood pressure ≥90 / 60 mm Hg. Patients who have received dobutamine or dopamine for ≥2 weeks were randomized into two groups: group 1, 40 patients who participated in the PRP and group 2, 40 patients who did not participate in the PRP. Group 3 included 40 patients without inotropic support who participated in the PRP.Results Patients of groups 1 and 3 attended >80 % of the scheduled classes without developing life-threatening adverse events (AEs) associated with exercise (E). After 6 months of the study, the exercising patients achieved a comparable (average) E intensity: 44 [35; 50]% and 45 [40;52]% of heart rate reserve and Borg scale scores 14 [12; 14] and 13 [11; 14] in groups 1 and 3, respectively (p>0.05). Initially, after 3 and 6 months at the peak of physical activity in groups 1 and 3, there was no decrease in arterial blood oxygen saturation according to pulse oximetry (SpO2) <93 %. At baseline, lactate levels in central venous blood at rest were normal in all groups. After 6 months, the lactate concentration was 1.1 mmol / l in group 1, 2.3 mmol / l in group 2, and 1.4 mmol / l in group 3 (р1-2=0.005; p2-3=0.008, respectively). At the E peak at baseline, after 3 and 6 months, comparable increases in lactate not exceeding 3 mmol / l were detected in groups 1 and 3.Conclusion      The study allowed assessment of the tolerability of individualized PRP performed at the aerobic level of energy supply, in inotropic-dependent patients with CHF. Individualized 6-month PRP in inotropic-dependent patients with end-stage CHF, provided safety criteria are met, is well tolerated and does not increase the number of AEs associated with CHF and physical rehabilitation (PR). Continued inotropic support with dopamine or dobutamine should not be considered as a contraindication to PR in patients with CHF in the absence of E intolerance or life-threatening AEs.

[Arterial hypertension after heart transplantation].

Aim To evaluate incidence of arterial hypertension (AH) in the posttransplantation period and to identify risk factors for this complication.Materials and methods From January, 2010 through December, 2017, 96 heart transplantations (HT) (70 men and 26 women aged 46.5±13.9 years) were performed. During the first month following HT, 8 recipients died and were excluded from the analysis. The retrospective evaluation of results included 88 patients followed up for more than one year.Results For the entire post-HT period (maximum 92 months), AH was observed in 75 of 88 (85%) recipients. Post-HT AH was correlated with male gender (r=0.24; p=0.031), history of smoking before HT (r=0.45; p<0.001), history of ischemic heart disease (IHD) (r=0.28; p=0.01), older age (r=0.35; p=0.001), higher body weight index (r=0.37; p=0.0005), creatinine level (r=0.37; p=0.001), and low-density lipoprotein cholesterol level (r=0.27; p=0.04). Interrelations with other AH risk factors were not found. Most patients developed AH within the first two years after HT. During the first year, AH was diagnosed in 60% (53 of 88) of patients (relapse, 85% (n=29); newly diagnosed, 45% (n=24), p=0.0003). At two years, AH was detected in 79% (46 of 58) of patients (relapse, 53% (n=18); newly diagnosed, 53% (n=28), p=0.9). All recipients received an adequate antihypertensive therapy. 40-63% of patients required a single-drug therapy at different points of follow-up; from 29 to 45% of patients required a two-drug therapy, and 5-15% of patients required three or more drugs. During all 5 years of treatment, most patients used angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) (70-87%) and slow calcium channel blockers (SCCB) (48-53%). The presence of AH following HT was associated with development of all cardiovascular events (CVE; r=0.31; p=0.012) whereas persistent AH, which required a combination antihypertensive treatment, was associated with a high mortality (r=0.61; p=0.015).Conclusion AH is a frequent complication of HT (85%), which is newly diagnosed in most patients during the first two years. AH incidence was higher for male recipients with a history of IHD, hypertension, and smoking. Approximately half of patients required only a single-drug antihypertensive therapy. After HT, the most frequently prescribed drugs included ACE inhibitors or ARBs and SCCBs (70-87% and 48-53%, respectively, depending on the time elapsed after HT). Persistent AH requiring a treatment with two or more antihypertensive drugs was associated with development of all CVEs and a higher long-term mortality.

Skeletal Muscle Resident Progenitor Cells Coexpress Mesenchymal and Myogenic Markers and Are Not Affected by Chronic Heart Failure-Induced Dysregulations.

BACKGROUND AND PURPOSE: In heart failure (HF), metabolic alterations induce skeletal muscle wasting and decrease of exercise capacity and quality of life. The activation of skeletal muscle regeneration potential is a prospective strategy to reduce muscle wasting; therefore, the aim of this project was to determine if functional properties of skeletal muscle mesenchymal progenitor cells (SM-MPC) were affected by HF-induced functional and metabolic dysregulations. METHODS: Gastrocnemius muscle biopsy samples were obtained from 3 healthy donors (HD) and 12 HF patients to purify mRNA for further analysis and to isolate SM-MPC. Cells were expanded in vitro and characterized by immunocytochemistry and flow cytometry for expression of mesenchymal (CD105/CD73/CD166/CD146/CD140b/CD140a/VIM) and myogenic (Myf5/CD56/MyoG) markers. Cells were induced to differentiate and were then analyzed by immunostaining and Q-PCR to verify the efficiency of differentiation. The expression of genes that control muscle metabolism and development was compared for HD/HF patients in both muscle biopsy and in vitro-differentiated myotubes. RESULTS: The upregulation of MYH3/MYH8/Myf6 detected in HF skeletal muscle along with metabolic alterations indicates chronic pathological activation of the muscle developmental program. SM-MPC isolated from HD and HF patients represented a mixed population that coexpresses both mesenchymal and myogenic markers and differs from AD-MMSC, BM-MMSC, and IMF-MSC. The functional properties of SM-MPC did not differ between HD and HF patients. CONCLUSION: In the present work, we demonstrate that the metabolic and functional alterations we detected in skeletal muscle from HF patients do not dramatically affect the functional properties of purified and expanded in vitro SM-MPC. We speculate that skeletal muscle progenitor cells are protected by their niche and under beneficial circumstances could contribute to muscle restoration and prevention and treatment of muscle wasting. The potential new therapeutic strategies of HF-induced skeletal muscle wasting should be targeted on both activation of SM-MPC regeneration potential and improvement of skeletal muscle metabolic status to provide a favorable environment for SM-MPC-driven muscle restoration.