Sleep and ventricular arrhythmias

Sleep is usually associated with a reduction in the frequency of ventricular arrhythmias. We analyzed 1260 24-hour Holter recordings exhibiting ventricular ectopy and identified 50 patients who had significant increases in sleep-related ectopy. This study group was compared to an age, sex, and 24-hour ventricular ectopic frequency matched control group. There were 21 females and 29 males with a mean age of 64 years in each group. During sleep, the study patients had more frequency of ventricular ectopy per hour than did controls (mean ± SEM; 143.2 ± 30.7 vs 62.9 ± 16.3; p < 0.005). The study group had fewer daytime ventricular premature beats per hour than did the control patients (45.2 ± 13.6 vs 67.7 ± 13.8; p < 0.05). The study patients also exhibited a significant sleep-related increase in complexity of ventricular arrhythmlas (χ² = 22.1; p < 0.001) and the control group a decrease (χ² = 19.1; p < 0.001). Nocturnal heart rates were slower than daytime rates in both the study (69.4 ± 14.5 vs 79.2 ± 12.2 bpm; p < 0.005) and control groups (75.5 ± 15.8 vs 82.6 ± 16.4 bpm; p < 0.005), without significant differences between the two groups. No significant differences in clinical and ECG characteristics of the study and control groups were found regarding presence or type of organic heart disease, pulmonary disease, hypertension, medication use, intraventricular conduction delay, abnormal Q waves, ventricular hypertrophy, or QT prolongation. Neurologic abnormalities (60% vs 28%; χ² = 9.38 p < 0.005), in particular cerebrovascular disease (30% vs 14%; χ² = 7.56; p < 0.01), were significantly more common in the study group. We have identified a subgroup of individuals with ventricular ectopy who increase the frequency and complexity of premature ventricular beats during sleep. The higher prevalence of neurologic disease in these individuals suggests a neurologic or neurohumoral mediation of these arrhythmias.