Pathophysiological mechanisms of bradycardia in patients with anorexia nervosa.

BACKGROUND

The purpose of this investigation was to examine heart rate variability (HRV), interbeat interval (IBI), and their interrelationship in healthy controls, bradycardic hyperpolarization-activated cyclic nucleotide-gated channel 4 () mutation carriers, and patients with anorexia nervosa (AN). We tested the hypothesis that neural mechanisms cause bradycardia in patients with AN. Therefore, we assumed that saturation of the HRV/IBI relationship as a consequence of sustained parasympathetic control of the sinus node is exclusively detectable in patients with AN.

METHODS

Patients with AN between the ages of 12 and 16 years admitted to our hospital due to malnutrition were grouped and included in the present investigation (N = 20). A matched-pair group with healthy children and adolescents was created. Groups were matched for age and sex. A 24-hour Holter electrocardiography (ECG) was performed in controls and patients. More specifically, all patients underwent two 24-hour Holter ECG examinations (admission; refeeding treatment). Additionally, the IBI was recorded during the night in mutation carriers (N = 4). HRV parameters were analyzed in 5-minute sequences during the night and plotted against mean corresponding IBI length. HRV, IBI, and their interrelationship were examined using Spearman's rank correlation analyses, Mann-Whitney tests, and Wilcoxon signed-rank tests.

RESULTS

The relationship between IBI and HRV showed signs of saturation in patients with AN. Furthermore, signs of HRV saturation were present in two mutation carriers. In contrast, signs of HRV saturation were not present in controls.

CONCLUSIONS

The existence of HRV saturation does not support the existence of parasympathetically mediated bradycardia. Nonneural mechanisms, such as downregulation, may be responsible for bradycardia and HRV saturation in patients with AN.