Ventricular arrhythmic disturbances and autonomic modulation after beating-heart revascularization in patients with pulmonary normotension.

BACKGROUND

De-novo ventricular arrhythmias are potentially life-threatening complications after beating-heart revascularization (off-pump CABG). Whether pulmonary hypertension can influence initiation of ventricular arrhythmias through increased sympathetic activity is controversial. In order to determine the influence of pulmonary hypertension on its relative contribution to ventricular arrhythmia, we first had to define the role of cardiac autonomic modulation in patients with pulmonary normotension. We aimed to observe how parameters of linear and nonlinear heart rate variability are changed pre- and postoperatively in patients with pulmonary normotension undergoing off-pump CABG.

METHODS

Fifteen-minute ECG recordings were collected before and after off-pump CABG in 54 patients with multivessel coronary artery disease and pulmonary normotension to determine linear (TP, HF, LF, LF:HF ratio) and nonlinear detrended fluctuation analysis (alpha1, alpha2) and fractal dimension (average, high and low) parameters of heart rate variability. Arrhythmia was monitored preoperatively in 24-hour Holter recordings and postoperatively by continuous monitoring and clinical assessment.

RESULTS

Deterioration from simple (Lown I-II) to complex (Lown III-V) ventricular arrhythmia was observed in 19 patients, and improvement from complex to simple arrhythmia in five patients (P = 0.022). Patients with postoperative deterioration of ventricular arrhythmia had preoperatively significantly lower values of TP, HF and LF (P = 0.024-0.043) and postoperatively significantly higher values on the low fractal dimension index (P = 0.031) than patients with postoperative improvement of arrhythmia.

CONCLUSION

Patients experiencing postoperative deterioration of ventricular arrhythmia already have impaired autonomic regulation before surgery. Higher postoperative values on the low fractal dimension index indicate that sympathetic predominance with or without concomitant vagal withdrawal is the underlying neurogenic mechanism contributing to ventricular arrhythmia.