Purpose: Blood pressure telemonitoring and remote counselling (BPTM) improves blood pressure (BP) control in patients with hypertension (HTN). Studies assessing the efficacy of BPTM from a value-based perspective are lacking. We investigated whether BPTM fits all principles of the value-based approach (clinical and economic effectiveness, improvement in patient-reported outcome/experience measures (PROM/PREM)). Materials and methods: Two hundred and forty ambulatory patients with uncontrolled HTN were randomised in a 2: 1 manner to BPTM (n ¼ 160, mean age 47 y.o.) and usual care (UC, n ¼ 80; 49 y.o.) with baseline and 3-month follow-up clinic visits. BPTM employed a mobile application (for patients) and a desktop version (for clinician), which allowed communication and exchange of medical data. The main outcomes were changes in office and ambulatory systolic (S) BPs, rate of BP control. The incremental cost-effectiveness ratio (ICER) and incremental costutility ratio (ICUR) were evaluated in economic analysis. The MOS SF-36 score was taken as a PROM, and the PEQ score was used as a PREM. Results: Larger decreases in office and ambulatory SBPs (-16.8 and À8.9 mm Hg, respectively; p < .05) was achieved in BPTM group while the treatment intensity was equal (2.4 drugs). The ICER 11.1 EUR/-1 mm Hg 24-hour SBP/1 year was 75% effective as per willingness-to-pay threshold. BPTM improved PROM (þ2.1 in mean MOS SF-36; p ¼ .04), reduced long-term mortality (þ0.11 life years gained), leading to þ0.49 quality-adjusted life years (QALYs) gained as compared with UC. The ICUR was 4 169.4 EUR/QALY gained. Patient-reported experience was higher in the BPTM (þ10 PEQ, p ¼ .01). The UC group showed minor changes in MOS SF-36 and PEQ (þ1.3; þ6, respectively; p n.s.). Conclusions: Being cost-effective, BPTM incorporates both clinical benefits and patient-perceived value. Larger randomised studies are needed to confirm our findings.

<b><i>Background:</i></b> Brugada syndrome (BrS) is a rare inherited cardiac arrhythmia with increased risk of sudden cardiac death. Mutations in gene <i>SCN5A</i>, which encodes the α-subunit of cardiac voltage-gated sodium channel Na_V1.5, have been identified in over 20% of patients with BrS. However, only a small fraction of Na_V1.5 variants, which are associated with BrS, are characterized in electrophysiological experiments. <b><i>Results:</i></b> Here we explored variants V281A and L1582P, which were found in our patients with BrS, and variants F543L and K1419E, which are reportedly associated with BrS. Heterologous expression of the variants in CHO-K1 cells and the Western blot analysis demonstrated that each variant appeared at the cell surface. We further measured sodium current in the whole-cell voltage clamp configuration. Variant F543L produced robust sodium current with a hyperpolarizing shift in the voltage dependence of steady-state fast inactivation. Other variants did not produce detectable sodium currents, indicating a complete loss of function. In a recent cryoEM structure of the hNa_V1.5 channel, residues V281, K1419, and L1582 are in close contacts with residues whose mutations are reportedly associated with BrS, indicating functional importance of respective contacts. <b><i>Conclusions:</i></b> Our results support the notion that loss of function of Na_V1.5 or decrease of the channel activity is involved in the pathogenesis of BrS.

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