Cardiac dysrhythmias and autonomic dysfunction in chronic spinal cord injury: A 24-hour Holter monitoring and heart rate variability study

Abstract

The purpose of this study is to evaluate chronic spinal cord injury (SCI) patients for the incidence of cardiac dysrhythmias and the level of autonomic nervous system (ANS) dysfunction using 24-hour Holter recordings and long term time-domain and frequency domain heart rare variability (HRV) analysis. There was no difference between groups for the frequency of ventricular or supraventricular ectopics, minimal and mean heart rate, and the longest RR intervals. Maximum heart rate was lower in the quadriplegic group compared with controls (124.1 +/- 11.2 vs. 139.4 +/- 10.9, p < 0.05). Frequency-domain spectral analysis of high, low, total frequency powers, and ratio LF/HF showed no significant difference between groups. On time-domain analysis SDANN (94.5 +/- 26.4 vs. 131.1 +/- 15.1, p < 0.01) and SDNN (110.1 +/- 29.2 vs. 143.6 +/- 19.1, p < 0.05) were significantly lower in quadriplegics compared with controls. SDANN (74.0 +/- 17.9 vs. 115.0 +/- 14.2 p < 0.01) and SDNN ( 90.2 +/- 21.1 vs. 130.0 +/- 22.0 p < 0.05) were significantly lower in complete quadriplegics compared with incomplete quadriplegics. When the effect of wake (07-22)-sleep (23-07) cycle on frequency-domain parameters were assessed, HF (12.38 +/- 5.1 vs. 21.18 +/- 8.05, p = 0.001) and TP (35.93 +/- 10.5 vs. 45.68 +/- 12.68, p = 0.004) showed the physiologic increase during sleep in controls, but was unchanged in quadriplegics (10.48 +/- 5.39 vs. 13.35 +/- 8.03, p = 0.205 and 30.67 +/- 10.61 vs. 37.01 +/- 17.59, p = 0.208, respectively). In paraplegics a blunted increase in HF (14.61 +/- 7.69 vs. 19.85 +/- 14.13, p = 0.09) and TP (38.5 +/- 12.77 vs. 47.13 +/- 23.08, p = 0.08) was observed. LF showed no significant change in the three groups. Heart rate circadian rhythm was preserved in all three groups (p < 0.01). We concluded that chronic complete cervical SCI may disrupt modulatory sympathetic flow and downregulates parasympathetic activity but causes no major arrhythmias needing treatment.