Paradoxical increase in heart rate before conversion to sinus rhythm in patients with recent-onset atrial fibrillation

Abstract

patients during vasodepressor syncope. It reached a value previously reported only in patients with septic shock.2 The pathophysiology of vasodepressor syncope is very complex. In the early phase, primary peripheral vasodilation probably predominates; subsequently, other mechanisms may be involved, such as lack of compensatory increase in cardiac rate and output, impairment of venous constriction and reflex-mediated vasodilation of skeletal muscle bed.’ Inhibition of the neuroadrenergic system may be an important factor. In fact, vasodepressor syncope can be experimentally induced by sudden interruption of sympathetic discharge.5 Moreover, norepinephrine activity does not increase during vasodepressor syncope3 Endogenous opioid peptides may inhibit the sympathetic system either centrally or peripherally.2-4~7*8 Moreover, endorphins may have a negative inotropic and chronotropic cardiac influence, reduce reflex discharge of cardiac or peripheral receptors, and exaggerate the response of J pulmonary receptors.214$7,8 In our study, no independent measure of sympathetic activity was obtained. We also did not examine the effect of administration of naloxone or other opioid antagonists on the occurrence of syncope. However, the fact that hunger, fatigue and painful stimulation may induce vasodepressor syncope,’ as well as modify plasma fi endorphin activity,9,10 suggests some link between opioid peptides and vasodepressor syncope. This is supported by our data. Whether increase of plasma @ endorphins during vasodepressor syncope is a primary etiologic event or a secondary phenomenon warrants further investigation.