Metabolism of Patients With Genetically Caused Cardiac Arrhythmia

University of Copenhagen50 enrolled

Overview

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.

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 Type

OBSERVATIONAL

Enrollment

Conditions

Long QT Syndrome

Eligibility

Sex: ALLMin age: 18 YearsHealthy volunteers:

Medical Language ↔ Plain English

Inclusion Criteria: LQTS Gain of function Matched healthy controls Exclusion criteria: none

Outcomes

Primary Outcomes

glucose homeostasis

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

Time frame: 6 hours

Secondary Outcomes

cardiac repolarisation

Time frame: 6 hours

Data from ClinicalTrials.gov

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