Efficacy of Long-term Selenium Supplementation in the Treatment of Chronic Keshan Disease with Congestive Heart Failure.

Few effective treatments for chronic Keshan disease have been available till now. The efficacy of long-term selenium supplementation in the treatment of chronic Keshan disease with congestive heart failure is inconclusive. This study aimed to determine whether selenium supplementation is associated with a decreased risk of cardiac death in chronic Keshan disease with congestive heart failure by ten years of follow-up. A retrospective long-term follow-up analysis was performed on a monitored cohort consisting of 302 chronic Keshan disease patients with a mean age of 40.8±11.4 years. Of the 302 chronic Keshan disease patients, 170 (56.3%) were given selenium supplementation until the end point of follow-up. Cox proportional hazards regression models were used to identify the independent predictors of cardiac events. Our results showed that during the follow-up, there were 101 deaths of patients with chronic Keshan disease in the selenium supplementation group (101/170, 59.4%) and 98 in non-selenium supplementation group (98/132, 74.2%). Multivariate analyses suggested that selenium supplementation was associated with a decreased risk of cardiac death (HR 0.39, 95% CI 0.28-0.53) after adjustment for baseline age, sex, cigarette smoking, family history of Keshan disease, body mass index (BMI), heart rate, electrocardiogram (ECG) abnormalities, blood pressure, initial cardiothoracic ratio, left ventricular ejection fractions (LVEF) and whole-blood selenium concentration. Our ten-year follow-up analysis indicated that selenium supplementation, specifically combined with the use of angiotensin-converting enzyme inhibitor and beta blocker therapy, improved the survival of patients with chronic Keshan disease with congestive heart failure. BMI, selenium deficiency, male, combined ECG abnormalities, LVEF, and fast heart rate increased the risk of cardiac events.

[Progressive Risks of Latent Keshan Disease: a Long Term Follow-up Study].

OBJECTIVE: To observe ten-year prognosis of patients with latent Keshan disease (KD) and to determine its associated risk factors. METHODS: A total of 448 patients with newly diagnosed latent KD were monitored and followed up for 10 years. Their ECG abnormalities were classified as major or minor using the Minnesota Code. COX proportional hazards regression models were established to identify risk factors associated with the development of chronic KD. RESULTS: A final sample of 414 cases was included in analyses, with an average of (112.9 ± 17.5) months of follow-up. At the end of follow-up, 92 (22. 2%) patients developed chronic KD. Older age (> 15 years), male, family history of KD, smoking, lower level of blood selenium (< 60 µg/L), major ECG abnormalities, and 18.5 kg/m² ≤ body mass index (BMI) 23.9 kg/m² were associated with higher cumulative incidence of chronic KD. The COX regression models showed that major ECG abnormalities, BMI, selenium deficiency, hypertension, and ventricular premature complex (VPC) abnormalities contributed to increased risk of chronic KD. A positive linear correlation (r = 0.719, P < 0.01) between GPx activity and blood selenium concentration was found. CONCLUSION: Major ECG abnormalities, BMI, selenium deficiency, hypertension and VPC abnormalities are associated with the development of chronic KD.

Selenium deficiency is associated with endoplasmic reticulum stress in a rat model of cardiac malfunction.

The relationship between selenium (Se) deficiency-induced cardiac malfunction and endoplasmic reticulum (ER) stress is poorly understood. In the present study, 18 weaning Sprague Dawley rats were randomly fed with three different Se diets, and myocardial glutathione peroxidase (GPx) activity was measured by an enzyme activity assay. Cardiac function was evaluated by hemodynamic parameters. ER stress markers immunoglobulin-binding protein (BiP)/glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) were detected by western blotting. Our data showed that myocardial GPx activity and cardiac function were conspicuously impaired in Se-deficient rats. Expression of GRP78 and CHOP was significantly upregulated by treatment of Se deficiency. Improvements in myocardial GPx activity and cardiac function, as well as decreases in expression of GRP78 and CHOP, were observed after Se supplementation. Consequently, our data show that ER stress was involved in Se deficiency-induced cardiac dysfunction.