1. Induce acute stress in healthy volunteers and study whether changes occur in some of the main ECG indicators of ANS control of cardiac electrophysiology.2. Visualize and quantify the neurochemical effects in the brain (including amygdala and…
ID
Source
Brief title
Condition
- Other condition
- Heart failures
Synonym
Health condition
stress and the brain
Research involving
Sponsors and support
Intervention
Outcome measures
Primary outcome
o ECG markers of ANS control: heart rate (HR), heart rate variability (HRV)
o Concentrations of GABA and glutamate in amygdala and hippocampus
Secondary outcome
o Stress markers: The State-Trait Anxiety Inventory (STAI), Perceived Stress
Reactivity Scale (PRSR), Barratt Impulsiveness Scale (BIS), life event
questionnaire, saliva biomarkers of stress (cortisol) and catecholamines
(alpha-amylase10), blood pressure
o Amygdala and hippocampus connectivity after the SECPT and control condition
(fMRI).
Background summary
Stress can strongly affect health and, among others, has an impact on
cardiovascular outcomes, including sudden cardiac death (SCD) (Lampert, 2016).
SCD is mostly due to cardiac arrhythmia (ventricular fibrillation, VF). Similar
to other heart diseases with a sudden onset (e.g., acute myocardial infarction,
AMI), SCD may be triggered by a disrupted autonomic nervous system (ANS)
control of the heart. Indeed, SCD has been associated with stress, including
increased cortisol levels. However, the mechanisms whereby a disruption of ANS
control affects cardiac physiology is incompletely understood. This project
aims to fill this gap by studying whether acute changes in gamma-aminobutyric
acid (GABA) and glutamate levels in the brain induced by acute stress impacts
on electrocardiogram (ECG) indicators of ANS control of cardiac physiology.
We focus on the GABAergic system and amygdala and hippocampus, as GABA is the
main inhibitory neurotransmitter in the brain (its concentration in the brain
is 200-1000 times greater than that of the monoamines or acetylcholine).
Neurosteroids, such as cortisol, that potentiate the inhibitory actions of GABA
by, among others, modulation of the GABA-A receptor produce anxiolytic effects
by the action on the amygdala, and GABA antagonists induce anxiogenic effects
(Davis & Whalen, 2001). Furthermore, Takotsubo cardiomyopathy has been reported
during withdrawal from multiple GABA agonists (e.g., benzodiazepine), which is
thought to follow a sudden decrease in GABA signaling (Penget et al., 2016). We
will also study glutamate, the main (mostly stimulatory) neurotransmitter in
the brain.
Study objective
1. Induce acute stress in healthy volunteers and study whether changes occur in
some of the main ECG indicators of ANS control of cardiac electrophysiology.
2. Visualize and quantify the neurochemical effects in the brain (including
amygdala and hippocampus GABA and glutamate levels) induced by acute stress.
3. Associate ANS and GABA/glutamate levels with stress markers and brain
activity.
Study design
Within-subject design
Intervention
The socially evaluated cold-pressor test (SECPT)
Study burden and risks
Risk assessment:
- MRI is a non-invasive imaging modality. All volunteers will receive extensive
information about the MRI procedures beforehand. Volunteers suffering from
claustrophobia will be excluded.
- SECPT is an evaluated stress test without any risks for participants.
Meibergdreef 9
Amsterdam 1105AZ
NL
Meibergdreef 9
Amsterdam 1105AZ
NL
Listed location countries
Age
Inclusion criteria
- Male
- Age 20-35 years
- no heart and vascular disease history
- no psychiatric disorder history
Exclusion criteria
- General contraindications for MRI (such as claustrophobia)
- heart and vascular disease history
- psychiatric disorder history
Design
Recruitment
Followed up by the following (possibly more current) registration
No registrations found.
Other (possibly less up-to-date) registrations in this register
No registrations found.
In other registers
| Register | ID |
|---|---|
| CCMO | NL64376.018.17 |