Key result
Metoprolol in stable CHF linked to a ~41% reduction in plasma sFas and improved LVEF.
Why the study?
Cardiac myocyte apoptosis contributes to CHF progression, and the effect of metoprolol with standard treatment on apoptotic mediators and LV function was investigated.
Does metoprolol added to standard therapy reduce apoptotic mediators and improve left ventricular function in patients with stable congestive heart failure?
Cohort (n=106)
Does metoprolol added to standard therapy reduce apoptotic mediators and improve left ventricular function in patients with stable congestive heart failure?
Metoprolol added to standard heart failure therapy significantly reduces plasma apoptotic mediators and improves left ventricular remodeling and functional capacity over 1 year.
Answers are grounded in this paper and cite their sources.
Metoprolol-associated sFas reduction may accompany LVEF gains in stable CHF; leaves open mechanistic role and need for RCTs before clinical adoption.
Recent studies suggest that cardiac myocyte apoptosis contributes to the progress of CHF (congestive heart failure). In the present study, we tested the hypothesis that metoprolol in conjunction with the standard treatment regime for CHF [an ACE (angiotensin-converting enzyme) inhibitor, diuretics and digoxin] may significantly reduce the plasma concentrations of the apoptotic mediators sFas (soluble Fas) and sFasL (soluble Fas ligand) in patients with CHF. An ELISA was used to determine the plasma concentrations of sFas and sFasL in 106 patients with stable CHF at recruitment. Echocardiography was performed at baseline and after 1 year of treatment with metoprolol in conjunction with the standard treatment regime for CHF (i.e. an ACE inhibitor, diuretics and digoxin). The dose of metoprolol was doubled on a biweekly basis up to 50 mg twice a day or maintained at the maximum tolerated dose. Data after 1 year were available for 92 patients and were analysed. The plasma concentrations of sFas and sFasL in patients with CHF decreased significantly (P<0.01) after 1 year of treatment with metoprolol in conjunction with the standard treatment regime compared with at baseline (5.4+/-0.2 compared with 3.2+/-0.1 ng/ml respectively for sFas, and 52.1+/-2.3 compared with 26.7+/-1.0 pg/ml respectively for sFasL). Compared with baseline, after 1 year of treatment with metoprolol in conjunction with the standard treatment regime there were significant improvements in LV (left ventricular) ejection fraction (from 32.6+/-0.9 to 51.5+/-0.8%; P<0.01), LV end-diastolic dimension (from 69.8+/-0.6 to 57.7+/-0.3 mm; P<0.01), LV end-systolic dimension (from 53.9+/-0.6 to 40.5+/-0.5 mm; P<0.01), LV end-diastolic volume (from 254.7+/-5.0 to 164.1+/-2.2 ml; P<0.01) and LV end-systolic volume (from 142.0+/-4.2 to 72.2+/-2.0 ml; P<0.01). In addition, the distance walked in a 6-min walk test increased markedly (P<0.01) from 260.3+/-5.2 m at baseline to 440.9+/-5.7 m after 1 year of treatment. In conclusion, we have demonstrated that metoprolol in conjunction with an ACE inhibitor, diuretics and digoxin in patients with CHF can lead to a reverse in LV remodelling potentially through its anti-apoptotic effects.
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Hou et al. (2007) conducted a cohort in Stable congestive heart failure (CHF) (n=106). Metoprolol in conjunction with standard treatment (ACE inhibitor, diuretics, and digoxin) vs. Baseline was evaluated on Plasma concentration of sFas (p=<0.01). One year of treatment with metoprolol and standard therapy in patients with stable CHF reduced plasma sFas concentrations from 5.4 to 3.2 ng/ml and improved LV ejection fraction.
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