Metabolism of Patients With Genetically Caused Cardiac Arrhythmia

• Conditions: Long QT Syndrome

• Registration Number: NCT02775513
• Lead Sponsor: University of Copenhagen

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 Description

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.

Study Timeline

• Study Start: 2010-09
• Study First Submitted: 2016-03-16
• Status Verified: 2016-05
• Primary Completion: 2016-05
• Study First Submitted QC: 2016-05-13
• Last Update Submitted: 2016-05-13
• Study First Posted: 2016-05-17
• Last Update Posted: 2016-05-17

Recruitment & Eligibility

• Status: UNKNOWN
• Sex: All
• Target Recruitment: 50

Inclusion Criteria

LQTS Gain of function Matched healthy controls

Exclusion criteria:

none

Exclusion Criteria

Not provided

Study & Design

• Study Type: OBSERVATIONAL
• Study Design: Not specified

Primary Outcome Measures

Name	Time	Method
glucose homeostasis	6 hours	measured by glucose, insulin, glucagon, GLP-1 and GIP response to glucose (OGTT)

Secondary Outcome Measures

Name	Time	Method
QT	6 hours	cardiac repolarisation