May 1, 1975Cardiovascular Research
Stress-induced and sympathetically-mediated electrocardiographic and circulatory variations in the primary hyperkinetic heart syndrome
Key result
Mental stimulation or isoproterenol caused ST depression and deep T-wave inversion, whereas pain or beta blockade normalized the repolarization phase in primary hyperkinetic heart syndrome.
Why the study?
How do different stressful factors and sympathetic modulation affect the electrocardiographic repolarization phase in patients with primary hyperkinetic heart syndrome?
Population
Patients with primary hyperkinetic heart syndrome
Comparison
Mental stimulation, isoproterenol, pain, or beta… vs Steady state
Design
Other
Authors
Discussion
Loading...
Member takes
Overview
Sympathetic repolarization changes in selectit syndrome may respond to beta blockade; leaves open validation in prospective cohorts.
Study Design
Type
Observational
Structured PICO
How do different stressful factors and sympathetic modulation affect the electrocardiographic repolarization phase in patients with primary hyperkinetic heart syndrome?
P
Population
Patients with primary hyperkinetic heart syndrome
E
Exposure
Mental stimulation, isoproterenol, pain, or beta blockade
C
Comparator
Steady state
O
Outcome
Electrocardiographic repolarization phase changessurrogate
In primary hyperkinetic heart syndrome, the electrical activity of the heart is directly influenced by adrenergic drive, with different stressors altering repolarization in opposite ways.
Cite This Study
Guazzi et al. (1975) conducted an observational in Primary hyperkinetic heart syndrome. Mental stimulation, isoproterenol, pain, or beta blockade vs. Steady state was evaluated on Electrocardiographic repolarization phase changes. Mental stimulation or isoproterenol caused ST depression and deep T-wave inversion, whereas pain or beta blockade normalized the repolarization phase in primary hyperkinetic heart syndrome.