AIMS Severe deficiency of the essential trace element selenium can cause myocardial dysfunction although the mechanism at cellular level is uncertain. Whether, in clinical practice, moderate selenium deficiency is associated with worse symptoms and outcome in patients with heart failure is unknown. METHODS AND RESULTS BIOSTAT-CHF is a multinational, prospective, observational cohort study that enrolled patients with worsening heart failure. Serum concentrations of selenium were measured by inductively coupled plasma mass spectrometry. Primary endpoint was a composite of all-cause mortality and hospitalization for heart failure; secondary endpoint was all-cause mortality. To investigate potential mechanisms by which selenium deficiency might affect prognosis, human cardiomyocytes were cultured in absence of selenium, and mitochondrial function and oxidative stress were assessed. Serum selenium concentration (deficiency) was <70 μg/L in 485 (20.4%) patients, who were older, more often women, had worse New York Heart Association class, more severe signs and symptoms of heart failure and poorer exercise capacity (6-min walking test) and quality of life (Kansas City Cardiomyopathy Questionnaire). Selenium deficiency was associated with higher rates of the primary endpoint [hazard ratio (HR) 1.23; 95% confidence interval (CI) 1.06-1.42] and all-cause mortality (HR 1.52; 95% CI 1.26-1.86). In cultured human cardiomyocytes, selenium deprivation impaired mitochondrial function and oxidative phosphorylation, and increased intracellular reactive oxygen species levels. CONCLUSIONS Selenium deficiency in heart failure patients is independently associated with impaired exercise tolerance and a 50% higher mortality rate, and impaired mitochondrial function in vitro, in human cardiomyocytes. Clinical trials are needed to investigate the effect of selenium supplements in patients with heart failure, especially if they have low plasma concentrations of selenium.

中文翻译：

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硒和心力衰竭的预后。

尽管在细胞水平上的机制尚不确定，但基本微量元素硒的严重缺乏会导致心肌功能障碍。在临床实践中，中度硒缺乏与心衰患者的不良症状和预后是否相关尚不清楚。方法和结果BIOSTAT-CHF是一项多国性，前瞻性，观察性队列研究，纳入了心力衰竭加重的患者。血清硒浓度通过电感耦合等离子体质谱法测定。主要终点指标是全因死亡率和心衰住院治疗的综合指标。次要终点是全因死亡率。为了研究硒缺乏可能影响预后的潜在机制，在缺硒的情况下培养了人类心肌细胞，评估线粒体功能和氧化应激。485名（20.4％）患者的血清硒浓度（缺乏）<70μg/ L，这些患者年龄较大，女性较多，纽约心脏协会等级较差，心力衰竭的症状和体征更严重，运动能力较差（6分钟步行测试）和生活质量（堪萨斯城心肌病问卷）。硒缺乏与主要终点发生率升高相关[危险比（HR）1.23；95％置信区间（CI）1.06-1.42]和全因死亡率（HR 1.52； 95％CI 1.26-1.86）。在培养的人心肌细胞中，硒缺乏会损害线粒体功能和氧化磷酸化，并增加细胞内活性氧的含量。结论心力衰竭患者中的​​硒缺乏与人的心肌细胞的运动耐量降低，死亡率高50％以及体外线粒体功能受损独立相关。需要进行临床试验来研究补充硒对心力衰竭患者的影响，尤其是血浆中硒浓度低的患者。