Head to Head Comparison of Suppression of Tumorogenicity 2 and Copeptin Significance for Prognosis of Patients After Acute Heart Failure Decompensation.

PURPOSE: To assess the suppression of tumorogenicity 2 (ST2) and copeptin significance for risk stratification of patient (pts) with acute decompensated heart failure (ADHF) during long-term follow-up compared with traditional risk factors. METHODS: We included in a prospective study 159 pts with ADHF. Blood samples to determine copeptin, sST2, NT-proBNP and hsTnT concentration were collected at admission and at discharge from the hospital. Serial determination of biomarker concentration was performed at 3, 6 and 12 months of follow-up. The combined primary end point of the trial included cardiovascular (CV) death, hospitalization due to HF, episodes of HF deterioration requiring additional intravenous diuretics and CV death with successful resuscitation. RESULTS: During 1-year follow-up (295.3±113.2 days) 56 pts (35.2%) had 78 (49.1%) cardiovascular events. Biomarker concentrations in low risk pts (without CV events) were significantly lower compared with high risk pts (with CV events). Discharge copeptin and NT-proBNP values were comparable for pts risk stratification: AUC=0.727 (95% CI 0.637-0.816), р.

[Soluble Suppression of Tumorogenicity 2 Increases Opportunities for Risk Stratification After Acute Heart Failure Decompensation].

PURPOSE: to evaluate the significance of soluble ST2-receptor (sST2) concentrations in patient (pts) risk stratification in with acute decompensated heart failure (ADHF) during long-term follow-up period. METHODS: In the prospective single-center study were included 159 pts with ADHF III-IV FC NYHA. Blood samples to determine NT-proBNP, sST2, hsTnT concentration were collected at the admission and at discharge from the hospital, and after 3, 6 and 12 months of follow-up. The combined primary end point of the trial included cardiovascular (CV) death, hospitalization due to HF, episodes of HF deterioration needed additional i/v diuretics and CV death with successful resuscitation. RESULTS: At admission all pts had elevated biomarker concentrations: NT-proBNP - 3615.5 (1578.0; 6289.3)pg/ml, sST2 - 60,49 (41.95; 92.87) ng/ml, hsTnT - 29.95 (21.85; 49.63) pg/ml; and at discharge: NT-proBNP - 2165.5 (982.7; 4221,2) pg/ml (%=-38,27 (-49.7; -24.34)%, p<0.0001), sST2 - 38.43 (24.67; 63.72) ng/ml (%=-30,13 (-42,07; -17,64)%, p<0,0001), and hsTnT - 28,37(21.29; 46.6) pg/ml. During 1-year follow-up 56 pts (35.2 %) had 78 (49.1%) cardiovascular events. Biomarker concentrations in low risk pts (without CV events) were significantly lower compared with high risk pts (who have CV events). At the discharge NT-proBNP and sST2 concentrations had the most predictive capacity relatively the primary end point during 1-year follow-up: AUC=0.727 (95% CI 0.637-0.816), <0,0001, and AUC=0,768 (95% CI 0.682-0.854), <0.0001, respectively. Maximally sST2 values were predictive for 180 days period of follow-up: AUC=0,809 (95% CI 0.726-0.921; <0,0001). Lack of NT-proBNP and sST2 concentrations decrease below 1696 pg/ml and 37.8 ng/ml respectively were associated with the highest risk of CV events (HR 4.41 [95% CI 1.41-9.624], p<0,0001 and HR 6.755 [95% CI 3.026- 15.082], p<0.0001, respectively). Changes of sST2 concentration during the period of pts hospitalization were also prognostically important, AUC=0.696 (0.596-0.796); p<0.0001. And pts with insufficient degree of sST2 concentrations reduction during the period of hospitalization (% <-28,3%) had the worst short-term and long-term prognosis [HR 3.68 (95% CI 2.05-6.64), p<0.0001]. Values of sST2 at the discharge were the most significant independent predictor of CV events in long-term follow-up (=0.519, p<0.0001). 91,8% of pts without CV events in the study had sST2 and NT-proBNP levels below 37.8 ng/ml and 1696 pg/ml respectively after 3, 6 and 12 months of follow-up. CONCLUSION: The values of soluble ST2-receptor over 37.8 ng/ml and NT-proBNP over 1696 pg/ml at the discharge from the hospital reflects the adverse prognosis in patients with ADHF. Serial determination of sST2 and NT-proBNP concentrations after discharge from the hospital indicates the necessity of reduction the levels of these biomarkers below the cut-off values (<37.8ng/mL and <1696pg/ml respectively) in pts with ADHF in long-term follow-up period.

[Head to Head Comparison of Suppression of Tumorogenicity 2 and Copeptin Significance for Prognosis of Patients After Acute Heart Failure Decompensation].

PURPOSE: To assess the suppression of tumorogenicity 2 (ST2) and copeptin significance for risk stratification of patient (pts) with acute decompensated heart failure (ADHF) during long-term follow-up compared with traditional risk factors. METHODS: We included in a prospective study 159 pts with ADHF. Blood samples to determine copeptin, sST2, NT-proBNP and hsTnT concentration were collected at admission and at discharge from the hospital. Serial determination of biomarker concentration was performed at 3, 6 and 12 months of follow-up. The combined primary end point of the trial included cardiovascular (CV) death, hospitalization due to HF, episodes of HF deterioration requiring additional intravenous diuretics and CV death with successful resuscitation. RESULTS: During 1-year follow-up (295.3±113.2 days) 56 pts (35.2%) had 78 (49.1%) cardiovascular events. Biomarker concentrations in low risk pts (without CV events) were significantly lower compared with high risk pts (with CV events). Discharge copeptin and NT-proBNP values were comparable for pts risk stratification: AUC=0.727 (95% CI 0.637-0.816), р.

[Therapy of High Risk Patients After Decompensation of Heart Failure Under NT-proBNP Control. Main Results].

AIM: to compare efficacy of treatment of high risk patients after acute decompensation (AD) of chronic heart failure (CHF) based on monitoring of NT-proBNP concentration and standard treatment. MATERIAL AND METHODS: Patients (n=100) with class III-IV CHF and left ventricular ejection fraction (LV EF) <40% due to ischemic heart disease (IHD), dilated cardiomyopathy (DCMP), or arterial hypertension (AH) after compensation of HF before discharge were distributed into groups of low (NT-proBNP <1400 picog/ml, n=30) or high (NT-proBNP more or equal 1400 picog/ml, n=70) risk. High risk patients were randomized into 2 treatment groups: NT-proBNP based (group I, n=35) and standard (group II, n=35) therapy. At study closure we formed another group consisting of group I and II participants noncomplaint with study protocol (group NC, n=10). Groups practically did not differ by main clinical functional characteristics. Aim of treatment was lowering of NT-proBNP level below 1000 picog/ml or more or equal 50% from baseline. At discharge median NT-proBNP concentration was 3750.0 (2224.0; 6613.0), 2783.0 (2021.5; 4827.5), and 2162.0 (1684.5; 5750.0) picog/ml in groups I, II, and NC, respectively (=0.315). RESULTS: At study entry all group I and II patients received combination of angiotensin converting enzyme inhibitors or angiotensin receptor blockers, -adrenoblockers, antagonists of mineralocorticoid receptors. After 6 months changes of doses of neuro-hormonal modulators in group I were more pronounced than in group II. NT-proBNP concentration decreased by 53% down to 1585.5 (976,6; 2742,5) picog/ml, =0.001, and by 10.2% in groups I and II, respectively (between group =0.001). In group I compared with II we observed more pronounced improvement of clinical functional indicators, quality of life, and parameters of systolic and diastolic LV function (<0.05), fewer cardiovascular deaths (4 vs. 10, =0.033) and repeat decompensations and rehospitalizations because CHF (4 vs. 14, =0.007). CONCLUSION: Compared with standard therapy long-term NT-proBNP guided treatment of high risk patients significantly significantly decreased rate of CV deaths and repeat decompensations and rehospitalizations because CHF, and more effectively influenced clinical and functional state, quality of life and main echocardiographical parameters of LV systolic and diastolic function.

[The Role of Markers of Organ Damage in Patients With Chronic Heart Failure].

This review is devoted to the studies of the role of modern markers of myocardial and renal damage (high sensitivity troponin T [hsTnT] and urinary neutrophil gelatinase-associated lipocain [NGAL/lipocalin-2] in patients with chronic heart failure (CHF). It contains description.

[Treatment of patients with chronic heart failure based on monitoring of concentrations of natriuretic peptides--to what extent it is justified in clinical practice?].

The review is devoted to consideration of novel pathways of treatment of patients with chronic heart failure (CHF) in particular of the high risk group. All main studies of the problem of treatment of patients with CHF based on monitoring of concentration of natriuretic peptides (MCNUP) BNP or NT-proBNP have been analyzed. The use of MCNUP with the aim of optimizing treatment of patients with CHF is completely justified biologically. Nevertheless results of available studies gave no 100% evidence of efficacy of such therapy mostly because of insufficient statistical power of these studies to obtain such a proof. In most of positive studies effect of MCNUP controlled therapy was assessed with the use of composite end points and main contribution in achievement of success was made not by effect on mortality but on stabilization of clinical state with lowering of number of hospitalizations due to CHF. This fact was confirmed in most of the protocols--both positive and neutral--in patients younger than 75 years with systolic left ventricular dysfunction. Taking into consideration pronounced effect of MCNUP controlled therapy on development of repeat decompensations and CHF related hospitalizations this variant of therapy can be justified especially in high risk patients requiring intensified control and optimization of therapy after discharge from hospital.