AimsThe aim was to assess the effect of a telemonitoring programme vs. standard care (SC) in preventing all‐cause deaths or unplanned hospitalisations in heart failure (HF) at 18 months.Methods and resultsOSICAT was a randomised, multicentre, open‐label French study in 937 patients hospitalised for acute HF ≤12 months before inclusion. Patients were randomised to telemonitoring (daily body weight measurement, daily recording of HF symptoms, and personalised education) (n = 482) or to SC (n = 455). Mean ± standard deviation number of events for the primary outcome was 1.30 ± 1.85 for telemonitoring and 1.46 ± 1.98 for SC [rate ratio 0.97, 95% confidence interval (CI) 0.77–1.23; P = 0.80]. In New York Heart Association (NYHA) class III or IV HF, median time to all‐cause death or first unplanned hospitalisation was 82 days in the telemonitoring group and 67 days in the SC group (P = 0.03). After adjustment for known predictive factors, telemonitoring was associated with a 21% relative risk reduction in first unplanned hospitalisation for HF [hazard ratio (HR) 0.79, 95% CI 0.62–0.99; P = 0.044); the relative risk reduction was 29% in patients with NYHA class III or IV HF (HR 0.71, 95% CI 0.53–0.95; P = 0.02), 38% in socially isolated patients (HR 0.62, 95% CI 0.39–0.98; P = 0.043), and 37% in patients who were ≥70% adherent to body weight measurement (HR 0.63, 95% CI 0.45–0.88; P = 0.006).ConclusionTelemonitoring did not result in a significantly lower rate of all‐cause deaths or unplanned hospitalisations in HF patients. The pre‐specified subgroup results suggest the telemonitoring approach improves clinical outcomes in selected populations but need further confirmation.

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Mechanisms determining the benefit of beta blockade in patients with heart failure remain incompletely understood but are assumed consequent to prevention of deleterious effects of catecholamines. Recent studies have demonstrated that oxidative stress in congestive heart failure may be related to increased catecholamine levels. The aim of this study was to examine effects of long-term treatment with propranolol on progression of left ventricular (LV) dysfunction, remodeling and oxidative stress on an experimental model of chronic heart failure. Six weeks after myocardial infarction by coronary ligation, Wistar rats were randomized to two groups: 10 weeks of therapy with propranolol (50 mg/kg/day in drinking water) and no treatment (infarcted controls). A third group was sham-operated rats without treatment. Animals were anesthetized for hemodynamic measurements, and hearts were then removed for histologic analysis, papillary muscle contractility study, and oxidative stress measurements using thiobarbituric acid reactive substance (TBARS) determination. Control infarcted rats demonstrated significant alterations of hemodynamic parameters and remodeling with increase of heart weight/body weight, of right ventricular lateral wall thickness, of LV circumference, LV septal area/body weight, and LV papillary muscle weight/body weight as compared with sham. In propranolol-treated rats, hypertrophy of the LV septum, papillary muscle, and right ventricle were similar to those of the infarcted control. Myocardial oxidative stress was significantly increased in control infarcted rats compared with sham, and propranolol prevented such oxidative stress increase. Papillary muscle isometric tension parameters were not significantly different among groups. Propranolol treatment prevented isoprenaline-induced spontaneous papillary muscle activity in vitro. Oxidative stress is increased in the rat model of heart failure secondary to coronary ligation. Long-term treatment with propranolol in vivo does not modify the compensatory process of hypertrophy but completely abolishes the oxidative stress increase and reduces the increased cardiac sensitivity to catecholamine-induced arrhythmias observed in this experimental model of heart failure.