Clinical Trial: Metabolism of Patients With Genetically Caused Cardiac Arrhythmia

Study Status: Active, not recruiting
Recruit Status: Active, not recruiting
Study Type: Observational

Official Title: Metabolism of Patients With Genetically Caused Cardiac Arrhythmia

Brief Summary: 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.

Detailed Summary:

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.


Sponsor: University of Copenhagen

Current Primary Outcome: glucose homeostasis [ Time Frame: 6 hours ]

measured by glucose, insulin, glucagon, GLP-1 and GIP response to glucose (OGTT)


Original Primary Outcome: Same as current

Current Secondary Outcome: QT [ Time Frame: 6 hours ]

cardiac repolarisation


Original Secondary Outcome: Same as current

Information By: University of Copenhagen

Dates:
Date Received: March 16, 2016
Date Started: September 2010
Date Completion:
Last Updated: May 13, 2016
Last Verified: May 2016