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Effects of propranolol on ventricular repolarization in man
1Medical Department B, Rikshospitalet, Oslo, Norway.
European Journal of Clinical Pharmacology
|January 1, 1990
Summary
Propranolol, a beta-blocker, slightly shortened action potential duration in patients with coronary artery disease. This medication did not alter the ventricle effective refractory period, impacting electrical restitution curves.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Coronary artery disease (CAD) poses significant cardiovascular risks.
- Understanding the electrophysiological effects of beta-blockers like propranolol is crucial for managing cardiac conditions.
- Monophasic action potentials (MAP), QT interval, and effective refractory period (ERP) are key indicators of cardiac electrical activity.
Purpose of the Study:
- To investigate the acute electrophysiological effects of propranolol on MAP, QT interval, and right ventricle effective refractory period (V-ERP) in patients with CAD.
- To assess how propranolol influences electrical restitution properties.
- To evaluate the combined effects of propranolol and isometric handgrip stress on cardiac electrophysiology.
Main Methods:
- Acute administration of propranolol (0.2 mg/kg) to 10 patients with coronary artery disease.
- Measurement of monophasic action potential duration at 90% repolarization (MAP90) and V-ERP at a paced heart rate of 100 beats/min.
- Analysis of electrical restitution curves before and after propranolol administration.
- Assessment of the impact of isometric handgrip stress on MAP90, both with and without propranolol.
Main Results:
- Propranolol significantly shortened the median MAP90 from 238 ms to 228 ms (p<0.05).
- The V-ERP remained unchanged after propranolol administration.
- The ratio of V-ERP to MAP90 increased from 1.00 to 1.03, indicating altered repolarization dynamics.
- Electrical restitution curves became more horizontal post-propranolol, suggesting reduced rate-dependence of action potential duration.
- Isometric handgrip induced a similar, slight shortening of MAP90 before and after propranolol.
Conclusions:
- Propranolol exerts acute electrophysiological effects in patients with CAD, primarily by shortening action potential duration without affecting ventricular refractoriness.
- The observed changes in electrical restitution suggest a potential modulation of arrhythmogenic substrate.
- These findings contribute to understanding the electrophysiological profile of propranolol in the context of ischemic heart disease.