Metabolism of Patients With Genetically Caused Cardiac Arrhythmia
试验速览
- 阶段
- 不适用
- 入组人数
- 50
- 主要终点
- glucose homeostasis
研究概览
简要总结
Loss-of-function mutations in voltage-gated potassium channels cause long QT syndrome (LQTS) due to a prolonged cardiac repolarisation phase. Hypoteses: patients with loss-of-function mutations also exhibit altered hormone release upon glucose ingestion.
详细描述
Loss-of-function mutations in voltage-gated potassium channels cause long QT syndrome (LQTS) due to a prolonged cardiac repolarisation phase.
Voltage-gated potassium (Kv-) channels are known for their relation to malignant cardiac arrhythmias, but also play a role in pancreatic alpha- and beta cell hormone secretion, and possibly in incretin hormone secretion. We hypothesised that patients with loss-of-function mutations also exhibit altered hormone release upon glucose ingestion.
研究设计
- 研究类型
- Observational
- 观察模型
- Case Control
- 时间视角
- Cross Sectional
入排标准
- 年龄范围
- 18 Years 至 —（Adult, Older Adult）
- 性别
- All
- 接受健康志愿者
- 是
入选标准
- •LQTS Gain of function Matched healthy controls
- •Exclusion criteria:
排除标准
- 未提供
结局指标
主要结局
glucose homeostasis
时间窗: 6 hours
measured by glucose, insulin, glucagon, GLP-1 and GIP response to glucose (OGTT)
次要结局
- QT(6 hours)
研究者
Signe Torekov
Associate professor
University of Copenhagen