Long QT Syndrome
Conditions
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.
Interventions
None listed
Sponsors
University of Copenhagen
Study design
Observational model
CASE_CONTROL
Time perspective
CROSS_SECTIONAL
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
Yes
Inclusion criteria
LQTS Gain of function Matched healthy controls
Exclusion criteria
none
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| glucose homeostasis | 6 hours | measured by glucose, insulin, glucagon, GLP-1 and GIP response to glucose (OGTT) |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| QT | 6 hours | cardiac repolarisation |
Outcome results
None listed