1.
Financial incentives for hypertension control: rationale and study design.
Zheng, L, Wang, Y, Liu, S, Zheng, R, Pei, D, Sun, Y, Sun, Z
Trials. 2020;(1):134
Abstract
BACKGROUND Even though the effectiveness of lifestyle modifications and antihypertensive pharmaceutical treatment for the prevention of hypertension and its complications have been demonstrated in randomized controlled trials, the benefits of adhering to these treatments have not been popularized among the general public. Studies suggest that incentive approaches based on behavioral economic concepts can improve patients' adherence to treatment. Therefore, we aimed to test whether financial incentives will reduce the blood pressure (BP) of hypertensive patients in China. METHODS/DESIGN This is a multicenter, randomized controlled trial with two parallel arms. A total of 400 participants from six cities in the Liaoning and Shanxi provinces of China are block-randomized into intervention and control group with a 1:1 ratio. Patients in the control group will receive interactive management of mobile devices, including patient education and communication. Patients in the intervention group will receive financial incentives in addition to interactive management of mobile devices, conditional on them achieving their antihypertensive goals or hypertension control. Masking the arm allocation will be precluded by the behavioral nature of the intervention and investigators of BP measurement and statistics are masked to clinic assignment. The primary outcome is net change in systolic BP (SBP) from baseline to month 12 between the intervention and control groups. The secondary outcomes are net change in diastolic BP (DBP), BP control, change in medication adherence and lifestyle, and cost-effectiveness. DISCUSSION This trial will determine whether financial incentives will improve hypertension control and generate necessary data for controlling hypertension and concomitant cardiovascular diseases among hypertensive patients in China. TRIAL REGISTRATION ISRCTN13467677. Registered on 16 May 2019.
2.
E-counseling as an emerging preventive strategy for hypertension.
Nolan, RP, Liu, S, Payne, AY
Current opinion in cardiology. 2014;(4):319-23
Abstract
PURPOSE OF REVIEW Lifestyle counseling that includes exercise training, diet modification, and medication adherence is critical to hypertension management. This article summarizes the efficacy of lifestyle counseling interventions in face-to-face, telehealth, and e-counseling settings. It also discusses the therapeutic potential of e-counseling as a preventive strategy for hypertension. RECENT FINDINGS The recent proliferation of telehealth and e-counseling programs increases the reach of preventive counseling for patients with cardiovascular disorders. Blood pressure reduction following these interventions is comparable to face-to-face interventions. However, the effectiveness of e-counseling varies depending on the design features of the core protocol. An evidence-based guideline needs to be established that identifies e-counseling components which are independently associated with blood pressure reduction. As the Internet becomes more sophisticated, e-counseling is demonstrating a therapeutic advantage in comparison with other telehealth interventions. SUMMARY Current evidence supports further development of preventive e-counseling programs for hypertension. A pressing challenge for investigators is to specify key evidence-based components of e-counseling that are essential to the core protocol. In order to achieve this goal, it will be necessary to ensure that e-counseling programs are also clinically organized, in order to guide patients through the process of initiating and sustaining therapeutic behavior change.
3.
Molecular mechanisms of FK506-induced hypertension in solid organ transplantation patients.
Wang, J, Guo, R, Liu, S, Chen, Q, Zuo, S, Yang, M, Zuo, X
Chinese medical journal. 2014;(20):3645-50
Abstract
OBJECTIVE Tacrolimus (FK506) is an immunosuppressive drug, which is widely used to prevent rejection of transplanted organs. However, chronic administration of FK506 leads to hypertension in solid organ transplantation patients, and its molecular mechanisms are much more complicated. In this review, we will discuss the above-mentioned molecular mechanisms of FK506-induced hypertension in solid organ transplantation subjects. DATA SOURCES The data analyzed in this review were mainly from relevant articles without restriction on the publication date reported in PubMed. The terms "FK506" or "tacrolimus" and "hypertension" were used for the literature search. STUDY SELECTION Original articles with no limitation of research design and critical reviews containing data relevant to FK506-induced hypertension and its molecular mechanisms were retrieved, reviewed and analyzed. RESULTS There are several molecular mechanisms attributed to FK506-induced hypertension in solid organ transplantation subjects. First, FK506 binds FK506 binding protein 12 and its related isoform 12.6 (FKBP12/12.6) and removes them from intracellular ryanodine receptors that induce a calcium ion leakage from the endoplasmic/sarcoplasmic reticulum. The conventional protein kinase C beta II (cPKCβII)-mediated phosphorylation of endothelial nitric oxide (NO) synthase at Thr495, which reduces the production of NO, was activated by calcium ion leakage. Second, transforming growth factor receptor/SMAD2/3 signaling activation plays an important role in Treg/Th17 cell imbalance in T cells which toget converge to cause inflammation, endothelial dysfunction, and hypertension following tacrolimus treatment. Third, the activation of with-no-K(Lys) kinases/STE20/SPS1-related proline/alanine-rich kinase/thiazide-sensitive sodium chloride co-transporter (WNKs/SPAK/NCC) pathway has a central role in tacrolimus-induced hypertension. Finally, the enhanced activity of renal renin-angiotensin-aldosterone system seems to play a crucial role in the pathophysiology of FK506-induced hypertension. CONCLUSION FK506 plays a predominant role in the pathophysiology of hypertension in solid organ transplantation subjects.