Ischemic Chronic Heart Failure Patients Research Articles

Pre-existing type 2 diabetes is associated with increased all-cause death independently of echocardiographic predictors of poor prognosis only in ischemic heart disease

Background and aimsIt is unknown whether the prognostic role of diabetes (T2DM) in outpatients with chronic heart failure (CHF) is independent of the most important echocardiographic markers of poor prognosis. The aims of this analysis were to evaluate whether T2DM modifies the risk of mortality in CHF patients stratified by etiology of disease or by right-ventricular to pulmonary arterial coupling at echocardiography and to evaluate how T2DM interacts with the prognostic role of cardiac plasma biomarkers. Methods and resultsThis is a retrospective analysis of 1627 CHF outpatients who underwent a complete echocardiographic examination. During a median follow-up period of 63 months 255 patients died. Poor right-ventricular to pulmonary arterial coupling and reduced left ventricular ejection fraction were independent predictors of outcome, whereas ischemic etiology and T2DM were not. T2DM interacted with etiology increasing the risk of mortality by 32% among patients with ischemic disease (p = 0.003). Elevated hsTNI plasma levels were associated with poor survival in T2DM but not in non-diabetic patients. ConclusionT2DM signals a worse outcome in ischemic CHF patients regardless of the echocardiographic phenotype. High plasma levels of hsTNI are stronger predictors of mortality in CHF patients with T2DM than in patients without diabetes.

REMODELING OF THE HEART AND VESSELS IN ATRIAL FIBRILLATION PATIENTS WITH CHRONIC HEART FAILURE ACCORDING TO CYSTATIN C-RELATED GLOMERULAR FILTRATION RATE

Aim. To investigate on structural and functional specifics of the left cardiac chambers and arteries in patients with permanent atrial fibrillation (AF) comorbid with chronic heart failure (CHF) of ischemic origin, with relation to cystatin C-dependent glomerular filtration rate (GFR). Material and methods. Sixty patients, age 35-60 y. o., with permanent AF of ischemic origin. All patients underwent echocardiography for the dysfunction verification: systolic function was assessed by ejection fraction of the left ventricle by Simpson, diastolic function was assessed via the velocity of transmitral currents and visualization of tissues of the mitral valve; Holter ECG monitoring was done, as volumetric sphygmopletysmography of peripheral arteries, assessment of kidney function by Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) by creatinine and cystatin C, evaluation of the status of collagen production by the tissue inhibitor of matrix metalloproteases type 1 (TIMP-1), measurement of NT-proBNP. In the first part of the study, patients were selected to 3 groups: by GFR 60 mL/min/1,73 m 2 . In the second — by cystatin C levels below or higher than the referent. Results. In the permanent AF with ischemic CHF patients, concentration of cystatin C in the blood correlates strongly depending on the NT-proBNP (r=0,60; р=0,003), left ventricle myocardial mass index (r=0,68; р=0,005), mean E/e’ (r=0,73; p<0,001), isovolumetric relaxation time (r=0,53; р=0,012), mean daily heart rate (r=0,51; р=0,016); correlates weakly with TIMP-1 (r=0,26, p=0,002); correlates negatively strongly with SDNN (r=-0,59; р<0,001). The GFR (CKD-EPIcys) correlates negatively strongly with the septal e’ (r=-0,51; р=0,041), with R-AI (r=-0,74; p<0,001), with CAVI1 (r=-0,53; р=0,008), and directly moderately with SDNN (r=0,42; р<0,001). Conclusion. Assessment of cystatin C in the blood and cystatin C-dependent GFR in permanent AF and ischemic CHF are not only the early markers of CKD, but are the risk factors of development and progression of target organs (heart, vessels).

IMMUNE RESPONSE IN DECOMPENSATED CHRONIC HEART FAILURE OF ISCHEMIC ORIGIN

Recently, a significance has been established, for the role of inflammation in the pathology of chronic heart failure (CHF). It is well known that raised level of circulating pro-inflammatory cytokines in ischemic CHF patients correlate with the severity and prognosis of the disease. Monocytes play key role in an inflammatory cascade and are the main source of pro-, as contra-inflammatory cytokines. Disbalance of physiological inflammation in alteration and healing of the myocardium might lead to formation of pathological chronic inflammation. In the article, the role of monocytes discussed, and of inflammation, in CHF and its decompensation. The kinds of cytokines observed with their role in inflammation. Also, the analysis presented, of the drugs used for modulation of immune response in CHF.

High Fibrinogen Levels Promote Erythrocyte-Erythrocyte Adhesion: A Cardiovascular Risk Factor in Heart Failure and Arterial Hypertension Patients

Erythrocyte aggregation is an indicator of cardiovascular risk, which is influenced by plasma fibrinogen concentration. Fibrinogen levels are elevated during cardiovascular diseases. Our main goals were to understand how fibrinogen-erythrocyte binding influences erythrocyte aggregation and how it constitutes a cardiovascular risk factor in essential arterial hypertension (EAH) and chronic heart failure (CHF). Fibrinogen-erythrocyte and erythrocyte-erythrocyte adhesion measurements were conducted by atomic force microscopy (AFM)-based force spectroscopy. Upon increasing fibrinogen concentration, there was an increase in the work and force necessary for cell-cell detachment, both for healthy donors and EAH patients. Nevertheless, higher values were obtained for the EAH patients at each fibrinogen concentration. Fibrinogen-erythrocyte (un)binding forces were higher in EAH and CHF patients, when compared with the control group, despite a lower binding frequency. Ischemic CHF patients showed increased binding forces compared to non-ischemic patients. Differences between CHF patients and healthy donors, in terms of erythrocyte elasticity (Young's modulus) and AFM tip penetration depth into the cells were also assessed. Erythrocytes from non-ischemic patients presented higher stiffness than those from the other two groups. Nevertheless, a significantly higher cell penetration depth at the same applied force was observed for ischemic heart failure patients. Erythrocyte deformability (assessed as elongation index) results show that heart failure patients presented higher erythrocyte deformability than the control group at lower shear stresses, and lower deformability at higher shear stresses. This indicates that patients’ erythrocytes are more deformable than those from healthy donors in blood vessels with larger internal diameters; however, in smaller-diameter vessels the opposite trend exists. Finally, a 12-month clinical follow-up shows that CHF patients with higher fibrinogen-erythrocyte binding forces, probed by AFM at the beginning of the assessment, had a significantly higher probability of being hospitalized due to cardiovascular complications on the subsequent year. Our results show that AFM can be a promising tool for clinical prognosis, pinpointing those patients with increased risk for cardiovascular diseases.Guedes et al. (2016) Nature Nanotechnology, 11:687-92.

The relationship between serum uric acid level and concentration of proangiogenic mononuclear progenitor cells in patients with chronic heart failure

Objective: Serum uric acid (UA) is considered as a marker of natural progression of chronic heart failure (CHF). Progression of CHF associates with declining of circulating mononuclear progenitor cells (MPCs) in the blood. The objective of this study was to evaluate the interrelationship between SUA concentrations and proangiogenic MPCs in ischemic CHF patients. Methods: The study was structured retrospectively after determining the coronary artery disease (CAD) by contrast-enhanced spiral computed tomography angiography in 126 subjects (54 male), aged 48 to 62 years, with CHF. Serum UA level was measured by enzymatic method and N-terminal proBNP (NT-pro-BNP) level was examined by immunoelectrochemiluminesence method. All biomarkers were measured at baseline. Results: Concentrations of SUA were distributed by quartiles (Me; IQR): QI=20.11 (19.06; 22.33) mmol/l; QII=27.53 (23.2; 31.10) mmol/l; QIII=35.80 (32.0; 39.0) mmol/l; and QIV=44.9 (40.00; 49.60) mmol/l. Cox proportional adjusted Odds Ratios analyses for CD14+CD309+ and CD14+CD309+Tie2+ MPCs by SUA Quartiles (Q) has showed that high Q (Q3 and Q4) of SUA versus low Q (Q1 and Q2) associated with increased risk of depletion of both CD14+CD309+ and CD14+CD309+Tie2+ MPCs. The ROC analysis has been showed that there was the cut-off point for the SUA level with the best prognostic potential on the risk of decreasing MPCs in both models equal 31.5 mmol/l. Conclusion: Circulated level of proangiogenic MPCs is declined progressively depended on quartiles of serum UA level in CHF subjects. We suggest that mild elevation of serum UA might be considered as a predictor of low proangiogenic MPCs in CHF patients. J Clin Exp Invest 2014; 5 (4): 511-520

Brain natriuretic peptide, structural and functional cardiac remodeling in chronic heart failure with overweight and obesity

Aim. The presence of obesity in patients with coronary heart disease contributes to its progression and increased mortality. In order to study the relationship between brain natriuretic peptide and the structural and functional cardiac parameters 69 patients with ischemic chronic heart failure associated with overweight and obesity were examined.Methods and results. Doppler echocardiography, immunoassay study of the structural and functional features of left ventricular myocardial remodeling and the level of N-terminal fragment brain natriuretic peptide were done. It was found that CHF patients with obesity in comparison with groups with normal weight lower levels of NT-proBNP were detected, regardless of functional class.Conclusion. Level of NT-proBNP in ischemic chronic heart failure patients with obesity had a significant correlation relationship with structural heart geometric parameters that characterize the remodeling of the left ventricular myocardium, mainly concentric type, and the type of diastolic dysfunction disorders relaxation.

Serum uric Acid predicts declining of circulating proangiogenic mononuclear progenitor cells in chronic heart failure patients.

Introduction: Serum uric acid (SUA) is considered a marker for natural progression of chronic heart failure (CHF) mediated cardiovascular remodelling. CHF associates with declining of circulating mononuclear progenitor cells (MPCs). The objective of this study was to evaluate the interrelationship between SUA concentrations and proangiogenic MPCs in ischemic CHF patients. Methods: The study population was structured retrospectively after determining the coronary artery disease (CAD) by contrast-enhanced spiral computed tomography angiography in 126 subjects with symptomatic ischemic mild-to-severe CHF and 128 CAD subjects without CHF. Baseline biomarkers were measured in all patients. Cox proportional multivariate hazard ratio was calculated for predictors of MPCs declining in both CHF and non-CHF patient population predictors of MPCs declining in CHF subjects were examined in stepwise logistic regression. C-statistics, integrated discrimination indices (IDI) and net-reclassification improvement were utilized for prediction performance analyses. Results: Cox proportional adjusted hazard ratio analyses for CD14+CD309+ and CD14+CD309+Tie2+ MPCs by SUA has shown that the higher quartiles (Q3 and Q4) of SUA compared to the lower quartiles (Q1 and Q2) are associated with increased risks of depletion of both CD14+CD309+ and CD14+CD309+Tie2+ MPCs. The addition of Q4 SUA to the ABC model improved the relative IDI by 13.8% for depletion of CD14+CD309+ MPCs and by 14.5% for depletion of CD14+CD309+Tie2+ MPCs. Conclusion: Circulating levels of proangiogenic MPCs are declined progressively depending on the levels of SUA in the HF subjects with CHF. We suggest that even mild elevations of SUA might be used to predict of relative depletion of proangiogenic MPCs among chronic HF patients.

Effect of enhanced external counterpulsation treatment on mean platelet volume in patients affected by ischemic chronic heart failure

Mean platelet volume (MPV) is increased in chronic heart failure (CHF) and is an independent predictor of mortality in CHF patients. It is not known whether enhanced external counterpulsation (EECP) therapy leads to decreased MPV values or not. The purpose of this study was to examine the effects of EECP on platelet count and MPV values and to assess the influence of MPV on the risk of death and recurrent ischemic events in ischemic CHF patients. A total of 68 ischemic heart failure patients with CHF symptoms and refractory angina pectoris were included in the study, 47 consecutive patients (39 males and eight females) aged 44-82 years. Although follow-up period started after completion of EECP in treated patients, control group follow-up started at the end of 7-week treatment without EECP. All patients were monitored for a mean duration of 13 ± 8 months (range, 1-36 months). The primary endpoints of the study were effects of EECP treatment on platelets after treatment period (7 weeks) and the recurrence of ischemic events. Secondary endpoint was cardiovascular death during the follow-up period. We observed a significant increase in platelet count and decrease in MPV levels (P = 0.044 and P = 0.004, respectively) in the control group. There were no significant differences in platelet count and MPV levels in the EECP group (P > 0.05). After the treatment period, New York Heart Association functional classification (2.60 ± 0.75 vs. 1.72 ± 0.68, P < 0.001) and Canadian Cardiovascular Society functional classification of angina (2.50 ± 0.90 vs. 1.60 ± 0.74, P < 0.001) improved in patients with EECP treatment. In our study, we found that EECP therapy had a neutral effect on MPV values and platelet count.

Symptoms of fatigue and depression in ischemic heart disease are driven by personality characteristics rather than disease stage: a comparison of CAD and CHF patients

Symptoms of fatigue and depression are prevalent across stages of ischemic heart disease (IHD). We examined (i) the effect of both the IHD stage and type-D personality on fatigue and depressive symptoms at 12-month follow-up, and (ii) whether the effect of type-D personality on these symptoms is moderated by IHD stage. Two different samples of patients were included to represent IHD stage: 401 percutaneous coronary intervention patients (early-stage IHD) and 105 ischemic chronic heart failure patients (end-stage IHD) completed the DS14 Type-D Scale at baseline. Logistic regression analysis was used to examine the impact of IHD stage and type-D personality on fatigue and depression at follow-up. Disease stage was neither associated with symptoms of fatigue (P=0.99) nor depression (P=0.29) at 12 months. In contrast, type-D personality was shown to predict both symptoms of fatigue [odds ratio (OR)=2.96; 95% confidence interval (CI): 1.92-4.58, P<0.001] and depression (OR=4.91; 95% CI: 3.16-7.65, P<0.001) at follow-up; the effect of type-D personality on these symptoms was not moderated by disease stage. In multivariable analysis, type-D remained a significant predictor of symptoms of fatigue (OR=3.14; 95% CI: 1.98-4.99, P<0.001) and depression (OR=5.90; 95% CI: 3.60-9.67, P<0.001), also after controlling for symptom levels at baseline. Type-D personality but not disease stage predicted symptoms of fatigue and depression at 12-month follow-up.

Reverse remodelling through exercise training is more pronounced in non-ischemic heart failure

Most training studies in patients with chronic heart failure (CHF) do not consider CHF aetiology in the interpretation of the results. About 60% of the patients in those studies have ischemic CHF (IHF) and 40% non-ischemic CHF (NHF). Recently, we conducted a randomized controlled trial to study three different training modalities in 60 patients with severe CHF, with a similar distribution of IHF and NHF patients. In the present post hoc analysis we compared the differences in training results between ischemic and non-ischemic patients. Left ventricular ejection fraction (EF), end diastolic volume (EDV), end systolic volume (ESV), measured with radionuclide ventriculography (RNV) and echocardiography, NT-pro BNP, peak oxygen uptake (peak V(O)(2)), working capacity and muscular volume were analyzed before and after training in 45 patients training for 40 sessions, 3 times per week. Fifteen patients served as control group. The outcome was analyzed considering the aetiology of CHF, either ischemic or non-ischemic. There were no significant differences in improvements of peak V(O)(2), working capacity and muscular volume between IHF and NHF patients. In NHF patients, EF increased while EDV and ESV decreased after training. These parameters remained unchanged in IHF patients after training. NT-pro BNP decreased significantly in NHF patients and increased in IHF patients after training. In the control group, patients showed a mild improvement of EF and a decrease of NT-pro BNP. This post hoc analysis shows that training intervention is associated with significant reverse remodelling in NHF, but not in IHF patients, whereas V(O)(2) peak and muscle volume improve regardless of CHF aetiology. Future prospective studies are needed to confirm our findings.

Physical training in patients with chronic heart failure of ischemic origin: effect on exercise capacity and left ventricular remodeling

Physical training is a well-known complementary treatment for chronic heart failure (CHF); however, many aspects require further studies. One of them is the impact on remodeling of the left ventricle (LV). The purpose of this study was to evaluate the effect of 6 months of training on LV, exercise capacity and safety issues in patients with ischemic CHF. Fifty patients (mean age 60.1+/-9.2 years) with ischemic CHF, New York Heart Association (NYHA) classification class II and III and left ventricular ejection fraction (LVEF) <or=35% were randomized into groups: undergoing 6-month training (25 patients) and not trained (25 patients). In both groups at baseline and at 6 months a cardiopulmonary exercise test and magnetic resonance imaging (MRI) with evaluation of LV were performed. Training was limited by the achievement of 80% of the predicted heart rate at VO2peak achieved at the baseline cardiopulmonary exercise test. All patients completed the 6-month observation. No serious adverse events were found in either group. Exercise capacity improved only in the trained group (VO2peak increased by 31%). At 6 months in the trained group there was a tendency towards an improvement in some LV parameters: ejection fraction, end-diastolic volume and wall motion score index (WMSI), whereas an opposite trend was seen in the controls (P<0.05, P<0.05 and P<0.01 for comparison of LVEFs, end-diastolic volumes and WMSIs, respectively). Six-month training in ischemic CHF patients is a safe modality. Training improves exercise capacity. There was no negative impact on LV morphology, and a trend towards improvement of functional parameters on MRI may suggest an anti-remodeling effect of training in patients with ischemic CHF.