Cardiac electrophysiologic effects of mental stress

Abstract

Background: Mental stress may trigger serious arrhythmias. Mental stress tests cause significant increases in heart rate, blood pressure and cardiac output. When beta-adrenergic inhibition is considered for secondary antiarrhythmic prophylaxis beta1 selective agents are often preferred because of less adverse reactions. The importance of the different beta-adrenoceptors on the electrophysiologic function is incompletely known.

Methods: In all studies, healthy volunteers were investigated by means of standard electrophysiologic catheterization procedures. Electrophysiologic and hemodynamic variables were measured under different settings of autonomic modulation with the primary goal to characterize the effects of mental stress on cardiac conductive tissues and the importance of :1 and :2 adrenergic receptors in cardiac tissues. To this mean infusion of adrenergic agonists (using epinephrine, dobutamine and salbutamol), a mental stress test (Stroop s Colour Word Conflict Test, CWT) and selective and unselective autonomic tone inhibition, ATI, (using atenolol, propranolol and atropine) were used.

Study I investigated the electrophysiologic effects on the cardiac conduction system elicited by CWT and compared them with the effects of epinephrine. Mental stress produced significant electrophysiologic effects with shortening of all measured electrophysiologic variables except atrial, most markedly those of the sinus and the atrioventricular nodes. During infusion of epinephrine, corresponding effects could only be reproduced at a much higher plasma level than during CWT.

Study II investigated gender differences in the cardiac electrophysiologic effects elicited by CWT and by ATI. During CWT men had shorter QT and JT durations. Women had shorter refractoriness in the atrial tissue and in the AV node. After ATI no gender differences in sinus nodal properties were noted, whereas AV nodal refractoriness and conduction time were shorter in women. QT and JT duration, and the refractory period of the right ventricle, became shorter in men.

Study III assessed the overall electrophysiologic effects of infusion with the beta2-agonist salbutamol. To distinguish beta2-agonist effects a comparison was made with the beta1 selective agonist dobutamine. Salbutamol produced significant changes in electrophysiologic properties both in myocardial and nodal tissues, the effects being greater on nodal properties. The proportional decreases in the AV node parameters were more pronounced than in the sinus node. There was an increase in the duration of the QS interval, indicating slower depolarization of the ventricle. QT dispersion increased.

Study IV evaluated if the type of beta-blocker, beta1-selective or unselective, is of importance in inhibition of the electrophysiologic effects of CWT, which was also assessed with each beta-blocker combined with atropine. With propranolol as the beta-blocker in ATI the electrophysiologic effects of CWT were completely eliminated. ATI with atenolol, though, gives an incomplete inhibition of the effects of mental stress on sinus cycle length, sinus node recovery time, AV nodal and the ventricular refractoriness, and on QT-duration.

Conclusions: Mental stress produces pronounced electrophysiologic effects, most markedly in the sinus and AV nodes and less in the ventricle. Circulating epinephrine plays only a minor direct role as a mediator of mental stress effects on the heart. During mental stress, women exhibit a more pronounced effect on the AV node and on the sinus node, and men react with a more pronounced effect on ventricular EP properties. After ATI, women have higher heart rate, longer QT and JT intervals, faster AH conduction, shorter AV nodal effective refractory period, and longer ventricular effective refractory period. Beta2-stimulation with salbutamol results in significant effects on cardiac electrophysiology, most pronounced in sinus and AV nodes and less on atrial and ventricular parameters. A discordant effect on ventricular conduction, which slowed, and refractoriness of the ventricular myocardium, which shortened, was seen. QT dispersion increased. Inhibition with atenolol does not eliminate the effects of mental stress on the ventricular myocardium, effects that at least partly appears mediated through stimulation of :2 adrenoceptors. Vagal withdrawal is part of the reaction to mental stress also in the ventricular myocardium.