| 1. |
- Nessler, Jadwiga, et al.
(författare)
-
Concentration of BNP, endothelin 1, pro-inflammatory cytokines (TNF-alpha, IL-6) and exercise capacity in patients with heart failure treated with carvedilol
- 2008
-
Ingår i: Kardiologia Polska. - 1897-4279. ; 66:2, s. 144-153
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Recent studies on the pathophysiology of heart failure indicate the role of neurohormones and immune and inflammatory processes as potential mechanisms involved in the pathogenesis and clinical course of chronic heart failure (CHF). Aim: To analyse the relationship between concentrations of brain natriuretic peptide (BNP), endothelin-1 (ET-1), inflammatory cytokines (TNF-alpha, IL-6) and cardiopulmonary stress test parameters, and to evaluate their changes during carvedilol treatment. Methods: The study included 86 patients (81 men and 5 women) aged from 35 to 70 years (56.8 +/- 9.19) with symptomatic heart failure and left ventricular ejection fraction < 40%, receiving an inhibitor of angiotensin II converting enzyme, diuretic and/or digoxin but not beta-blockers. All patients at baseline, and then at 3 and 12 months after treatment, underwent a panel of studies to assess functional capacity according to NYHA, echocardiographic and cardiopulmonary stress test (CPX) parameters, and serum concentrations of BNP, ET-1, TNF-alpha and IL-6. Before introducing carvedilol we found a weak relationship between concentrations of BNP, ET-1, IL-6 and decreased VO2 (peak). Results: At 12 months exercise tolerance was significantly improved (exercise stress testing prolonged by 143.9 s, p=0.001) and an increase in metabolic equivalent (MET) by 1.41 (p=0.001) was observed. The VO2 (peak) was nonsignificantly increased by a mean of 0.9 ml/kg/min. In patients with baseline VO2 (peak) < 14 ml/kg/min the concentrations of ET-1 and TNF-alpha were significantly higher than in the remaining ones, and after treatment they were significantly reduced. In these patients VO2 (peak)%N was also significantly increased (39.5 +/- 7.5 vs. 50.1 +/- 15,0; p=0.013). The number of patients with VO2 (peak) < 14 ml/kg/min also significantly decreased from 39 to 21 (p=0.013). Conclusions: In patients with HF decreased value of VO2 (peak) is associated with LV systolic function disorders and increased levels of BNP, ET-1, TNF-alpha and IL-6. Chronic treatment with carvedilol improves LV systolic function, exercise tolerance and peak oxygen consumption and is associated with significant decrease of BNP, ET-1, TNF-alpha and IL-6 concentrations.
|
|
| 2. |
- Nessler, Jadwiga, et al.
(författare)
-
Sudden cardiac death risk factors in patients with heart failure treated with carvedilol
- 2007
-
Ingår i: Kardiologia Polska. - 1897-4279. ; 65:12, s. 1417-1424
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Chronic heart failure (CHF) is associated with a high risk of sudden cardiac death (SCID). Most frequently SCID occurs in patients with NYHA class II and III. Aim: To evaluate the influence of prolonged carvedilol therapy on SCID risk in CHF patients. Methods: The study included 86 patients (81 men and 5 women) aged 56.8 +/- 9.19 (35-70) years with CHF in NYHA class II and III receiving an ACE inhibitor and diuretics but not beta-blockers. At baseline and after 12 months of carvedilol therapy the following risk factors for SCID were analysed: in angiography - occluded infarct-related artery; in echocardiography - left ventricular ejection fraction (LVEF) < 30%, volume of the left ventricle (LVEDV) > 140 ml; in ECG at rest - sinus heart rate (HRs) > 75/min, sustained atrial fibrillation, increased QTc; in 24-hour ECG recording - complex arrhythmia, blunted heart rate variability (SDNN < 100 ms) and abnormal turbulence parameters (TO and TS or one of them); in signal-averaged ECG - late ventricular potentials and prolonged QRS > 114 ms. The analysis of SCD risk factors in basic examination in patients who suddenly died was also performed. Results: During one-year carvedilol therapy heart transplantation was performed in 2 patients; 5 patients died. At 12 months the following risk factors for SCID were significantly changed: HRs > 75/min (50 vs. 16 patients, p=0.006), LVEF < 30% (37 vs. 14 patients, p=0.01), SDNN < 100 ms (19 vs. 9 patients, p=0.04). At 12 months the number of risk factors for SCD in each patient was significantly reduced (p=0.001). In patients who suddenly died we found a greater amount of SCID risk factors in basic examination (7 vs. 5) as compared to alive patients. Conclusions: Prolonged beta-adrenergic blockade reduces risk of sudden cardiac death through significant LVEF increase, reduction of HR at rest and improvement of HRV.
|
|
