Induction of heart rate and blood pressure turbulence in the electrophysiologic laboratory

Abstract

Heart rate turbulence (HRT) is a transient tachycardia and/or bradycardia that follows ventricular premature complexes (VPCs). Absent or blunted HRT is associated with a poor prognosis in patients with heart disease, but its physiology is unknown. We hypothesized that HRT might be mediated by baroreflexes following early depolarizations. We sought to induce and characterize HRT in the electrophysiologic laboratory by introducing 1 ventricular extrastimulus every 60 seconds in 23 patients who underwent invasive electrophysiologic studies. On average, HRT was characterized by an initial RR interval decrease of 38 ms occurring 3.4 seconds after early depolarization. This was followed by a transient RR interval increase of 88 ms occurring 5.4 seconds later. HRT was preceded by similar hypotensive and/or hypertensive blood pressure turbulence. Baroreflex sensitivity estimates from post-VPCs and sinus sequences were similar (12.3 ± 10.3 vs 10.2 ± 8.9 ms/mm Hg, p = 0.51). The failure to induce HRT was associated with a limited initial hypotensive phase of blood pressure turbulence (−7.9 vs −12.1 mm Hg, p = 0.037). Patients with structural heart disease had reduced turbulence onset and reduced turbulence slope relative to those with structurally normal hearts, although blood pressure response was similar in both groups. HRT is an inducible, transient tachycardia and/or bradycardia that likely arises from a baroreflex response to transient hypotension following VPCs. Patients with structural heart disease have blunted HRT.