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Acute effects of aldosterone on intracardiac monophasic action potentials
Hanns-Christian Tillmann1, Burghard Schumacher, Oleksiy Yasenyev
1Faculty of Clinical Medicine Mannheim, Institute of Clinical Pharmacology, Heidelberg University, Theodor-Kutzer-Ufer, 68135, Mannheim, Germany.
Insights
Aldosterone, a hormone linked to heart failure mortality, was found to prolong cardiac action potential duration in humans. This rapid effect suggests a non-genomic mechanism, potentially contributing to adverse cardiac events.
Area of Science:
- Cardiology
- Electrophysiology
- Endocrinology
Background:
- Elevated plasma aldosterone is an independent risk factor for mortality in congestive heart failure.
- Aldosterone is implicated in sudden cardiac death and atrial fibrillation, a major cause of stroke.
- The electrophysiological effects of aldosterone in humans remain incompletely understood.
Purpose of the Study:
- To investigate the acute effects of aldosterone on intracardiac monophasic action potentials in humans.
- To characterize the electrophysiological properties of aldosterone in the context of cardiac function.
Main Methods:
- Monophasic action potentials were recorded in six patients with supraventricular arrhythmias.
- Patients received an intravenous injection of either placebo (0.9% NaCl) or aldosterone (0.5 mg).
- Action potential duration at 90% repolarization (MAPd90) was measured and compared between treatments.
Main Results:
- Aldosterone administration significantly increased mean MAPd90 from 287+/-22 ms to 299+/-25 ms (P<0.02).
- This prolongation of action potential duration remained statistically significant after heart rate adjustment (P<0.01).
- The maximal effect of aldosterone was observed within 4-6 minutes post-injection.
Conclusions:
- Aldosterone rapidly increases myocardial action potential duration following intravenous administration.
- The rapid onset suggests a non-genomic mechanism of action for aldosterone's electrophysiological effects.
- Aldosterone may exert unfavorable cardiac effects by altering myocardial repolarization.
Background:
Elevated plasma aldosterone levels represent an independent risk factor for increased mortality in congestive heart failure. Sudden cardiac deaths contribute substantially to the excessive mortality in congestive heart failure and so does atrial fibrillation as one of the major causes of stroke in elderly persons. So far, the electrophysiological properties of aldosterone have not been thoroughly characterized. In the present study, the effects of aldosterone on intracardiac monophasic action potentials were investigated in humans.
Methods And Results:
Monophasic action potentials were recorded in six patients with supraventricular arrhythmias. Eleven ml of 0.9% NaCl (placebo) were injected intravenously, and monophasic action potentials recorded for 10 min. Thereafter, aldosterone (0.5 mg in 0.9% NaCl) was injected and recording of monophasic action potentials continued as previously. The mean action potential duration at 90% repolarization was calculated for the entire 10-min period of each treatment. All patients were in sinus rhythm and had normal electrolyte status. In the placebo period, mean MAPd90 was 287+/-22 ms (mean+/-S.D.), and 299+/-25 ms following aldosterone (P<0.02). After adjustment for heart rate, the difference remained statistically significant (P<0.01). The maximal effect of aldosterone was seen 4-6 min after injection.
Conclusion:
Aldosterone increases monophasic action potential duration within minutes after intravenous application. Therefore, this effect is likely to be mediated nongenomically. It may be hypothesized that aldosterone exerts its unfavorable effects partly via altering myocardial repolarization.