Effect of Autonomic Dysfunction on P-Wave Dispersion in Patients with Chronic Spinal Cord Injury

Yasar E, Yilmaz B, Yasar AS, Goktepe AS, Alaca R, Mohur H: Effect of autonomic dysfunction on P-wave dispersion in patients with chronic spinal cord injury. Am J Phys Med Rehabil 2010; 89: 824-830. Objective: To provide information about the effect of autonomic dysfunction on P-wave dispersion, as a predictor of atrial fibrillation, in patients with spinal cord injury. Design: Thirty patients with chronic traumatic spinal cord injury and 27 healthy controls were included in this study. The initial assessment of the patients included routine physical examination and evaluation of 12-lead electrocardiography. In the patient group, blood pressure and electrocardiography recordings were obtained during urodynamic assessment. The measurements of the P-wave duration were performed manually by two blinded investigators. P-wave dispersion was calculated as the difference between maximum P-wave duration and minimum P-wave duration. P-wave dispersion values of resting electrocardiography recordings in control and study groups were compared. In the patient group, subgroup analyses were also performed according to the injury level and severity and existence of autonomic dysfunction in examinations. Results: P-wave dispersion values were greater in patients with spinal cord injury than in healthy controls. There was statistically significant difference between P-wave dispersion values of the patients with and without autonomic dysfunction. P-wave dispersion values at initial sensation of vesical filling were greater than those of the resting state in the patients without autonomic dysfunction. Conclusions: Our findings indicate that P-wave dispersion increases significantly in chronic spinal cord injured patients with autonomic dysfunction. This finding suggests a tendency for atrial fibrillation occurrence in patients with spinal cord injury, which may cause further cerebrovascular complications in this special subset of patients by creating a thromboembolic milieu.