title: Evolution of heart rate control after transplantation: conduction versus autonomic innervation.
abstract: In cardiac transplantation, the donor organ is not initially innervated and demonstrates decreased heart rate variability (HRV). However, HRV may improve after several months. The mechanism for HRV improvement has not been elucidated; autonomic "reinnervation" of the donor heart has been proposed. The role of atrioatrial conduction from recipient to donor organ has not been evaluated. We prospectively evaluated cardiac transplant patients with a limited electrophysiology study at the time of their surveillance biopsies. Recordings were made of recipient and donor signals, observing conduction properties between recipient and donor atria. Holter recordings were analyzed and HRV was determined using spectral analysis techniques, recording mean RR interval, low-frequency power (LF), high-frequency power (HF), and the LF/HF ratio. These were compared to published norms. From November 1999 to May 2000, 21 patients (6 female) who underwent cardiac transplantation participated at a median age of 101 months (range, 4.1-217 months). Time posttransplant ranged from 26 days to 71 months. Holter data were available for 20 patients and demonstrated dissociated P waves in 13 (65%). The mean heart rate on Holter was 111 beats per minute (bpm) (range, 85-161 bpm). We were able to record distinct recipient atrial signals in 16 of 21 (76%) patients. The average recipient tissue heart rate was 55% that of the donor heart rate. We documented atrioatrial association in only 1 patient. HRV did not reach normal values for most patients and did not increase with time posttransplantation. The LF values were in the normal range for most patients, whereas 3 patients had normal HF values and 2 patients had values just below normal. Recipients of heart transplantation have a predominantly sympathetic influence of HRV. These preliminary data suggest that atrioatrial conduction does not play a role in reestablishing normal heart rate control following pediatric cardiac transplantation.
authors.affiliation: Division of Cardiology, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada.
authors.forename: S
authors.initials: S
authors.lastname: Sanatani
authors.forename: C
authors.initials: C
authors.lastname: Chiu
authors.forename: D
authors.initials: D
authors.lastname: Nykanen
authors.forename: J
authors.initials: J
authors.lastname: Coles
authors.forename: L
authors.initials: L
authors.lastname: West
authors.forename: R
authors.initials: R
authors.lastname: Hamilton
mesh_terms: D000293:Adolescent; D000714:Anastomosis, Surgical; D001341:Autonomic Nervous System / Q000503:physiopathology / Q000601:surgery; D002170:Canada; D009202:Cardiomyopathies / Q000401:mortality / Q000503:physiopathology / Q000601:surgery; D002648:Child; D002669:Child Welfare; D002675:Child, Preschool; D015716:Electrocardiography, Ambulatory; D004567:Electrodes, Implanted; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D006325:Heart Atria / Q000503:physiopathology / Q000601:surgery; D006329:Heart Conduction System / Q000503:physiopathology / Q000601:surgery; D006330:Heart Defects, Congenital / Q000401:mortality / Q000503:physiopathology / Q000601:surgery; D006339:Heart Rate / Q000502:physiology*; D016027:Heart Transplantation; D006801:Humans; D007223:Infant; D007229:Infant Welfare; D008297:Male; D011183:Postoperative Complications / Q000209:etiology / Q000401:mortality; D011446:Prospective Studies; D016019:Survival Analysis; D016896:Treatment Outcome