Association Between Parasympathetic Activity and Late Potentials at Low Noise Level

Abstract

Background: Late potentials (LP) in the signal‐averaged ECG represent activation of myocardial areas with slow conduction and predicts re‐entrant malignant ventricular arrhythmias in coronary artery disease. Low heart rate variability, which reflects low vagal and concomitantly elevated sympathetic activation also predicts ventricular arrhythmia. This autonomic profile is associated with the presence of LP (detected at noise level 0.4 μ;V) early after myocardial infarction. In contrast, sympathetic stimulation and diminution of vagal tone influence LP parameters (detected at noise level 0.2 μ;V) in the opposite direction in healthy subjects. The aim of this study was to estimate the possible association between measures of cardiac autonomic function and LP (detected at 0.4 and 0.2 μ;V) in patients with chronic coronary artery disease.Methods: ECGs of 174 consecutive patients with angiographically documented coronary artery disease and without myocardial infarction during the last 3 months were signal‐averaged to noise level 0.2 and 0.4 μ;V. LP were considered to be present if any two of the following criteria were present: signal‐averaged QRS duration > 120 ms, root‐mean‐square voltage of the terminal 40 ms of the averaged QRS complex < 25 μ;V, and late potential duration > 40 ms. Heart rate variability was measured at rest in 5‐minute ECG recordings as: the standard deviation (SD) of all RR intervals, SD corrected for RR (SD/mean RR), and the power of high frequency (HF) component (0.15–0.40 Hz).Results: One hundred seven (61%) of the patients had LP at noise level 0.2 μ;V. LPs were more frequently observed in patients with slow heart rate, high heart rate variability, and high levels of vagal activity (mean RR >; 1000 ms, SD >; 60 ms, and HF >; 100 ms2) than in patients with higher heart rate, low heart rate variability and attenuated vagal activity: 73% vs 54% (P = 0.02), 71% vs 53% (P = 0.02), 72% vs 51% (P = 0.005) for mean RR, SD, and HF power, respectively. Adjustment for possible confounding from mean RR level, gender, previous acute myocardial infarction, treatment with betablocker, and left ventricular ejection fraction did not significantly alter these associations. At noise level 0.4 μ;V 26% (45/174) had LP and the diagnosis of LP was not significantly associated with heart rate variability.Conclusions: At low noise level (0.2 μ;V) higher parasympathetic activity is associated with the diagnosis of LP. The predictive power of presence of LP diagnosed at low noise level for development of sudden cardiac death may be reduced by this association. In order to increase the predictive accuracy of LP we recommend either the use of noise level 0.4 μ;V, or identification of high arrhythmia‐risk patients by a combination of the presence LP and impaired heart rate variability. However, a prognostic study is needed to further clarify this.