[Nocturnal ventricular arrhythmia in patients with sleep apnea and suspected coronary heart disease]. / Nächtliche ventrikuläre Arrhythmien bei Patienten mit Schlafapnoe und Verdacht auf koronare Herzerkrankung.

BACKGROUND: Patients with sleep apnea and nocturnal brady- and tachyarrhythmia are considered to be patients at especially high risk within the group of all apnea patients. PATIENTS AND METHODS: 13 patients with sleep apnea (apnea-index > 10 events/h), suspected coronary heart disease and known increased frequency of nocturnal premature ventricular contractions (PVC) were studied. Polysomnography, long-term ECG and six-lead ECG were performed. RESULTS: Within the period studied (1.00 to 6.00 o'clock), an average of 47 PVC per hour was recorded (range 4 to 337/h). In two patients 24 episodes of nocturnal myocardial ischemia were observed, but were not accompanied by PVC. Interestingly only 387 of 1371 premature ventricular contractions (28.2%) were associated to apnea/hyperventilation episodes. Arrhythmia occurred mainly during sleep stages I/II and REM (n.s.). There was a tendency towards more frequent PVC with more pronounced oxygen desaturations. CONCLUSION: Patients with coronary heart disease, obstructive sleep apnea and severe hyoxemia are at higher risk of developing nocturnal PVC because reduced hypoxic tolerance of the heart may lead to electrical instability.

[Nocturnal hypoxia--its relevance with reference to sleep structure in patients with coronary heart disease]. / Nächtliche Hypoxie--Ihre Relevanz bezüglich der Schlafstruktur bei Patienten mit koronarer Herzerkrankung.

A disorder in the physiological structure of the sleep cycles (macrostructure) is known to occur both in patients with sleep apnoea (SA) and coronary heart disease (CHD). The study presented here was concerned with the problem whether the sleep structure in patients suffering from CHD and apnoea-conditioned hypoxia is greatly disturbed e.g. by myocardial ischaemia. Polysomnographic recordings including EEG, EOG, EMG and 6-channel ECG were performed for 6 nights in 30 patients suffering from sleep apnoea (AI > 10/h) and/without CHD. The average age of the patients was 57.9 years (range 47-68 yrs). The 2nd, 4th and 6th nights were subjected to fine analysis. In 6 patients it was possible to detect a total of 144 episodes with nocturnal myocardial ischaemia, 123 of these during cumulative apnoea and oxygen desaturation. The 30 patients spent on the average 67.1% in sleep stages I and II, 14.9% in deep sleep (stages III and IV) and 18% in REM sleep. 77.8% of the ischemie, episodes occurred during REM sleep and only 1.4% during the deep sleep stages. Sleep during myocardial ischaemia showed significantly more arousals than to control periods without ischaemia. There was furthermore a dependence of the degree of arousal on the degree of oxygen desakivations during apnoea. I. Patients suffering from CHD and sleep apnoea are endangered by nocturnal hypoxia-conditioned myocardial ischaemia which in turn can lead to increased electrical instability. II. The macrostructure of the sleep of patients suffering from CHD and sleep apnoea is comparatively as disturbed as that of patients with apnoea without CHD.(ABSTRACT TRUNCATED AT 250 WORDS)

Nocturnal myocardial ischemia and cardiac arrhythmia in patients with sleep apnea with and without coronary heart disease.

To study the effect of apnea and hypoventilation-induced hypoxemia on the heart, we carried out polysomnographic recordings over 4 nights with electrocardiographic tracings in 30 patients with and without coronary heart disease. Evaluations of the data were based on the 2nd and 4th nights. In six subjects, five with coronary heart disease, we found 85 episodes of nocturnal ischemia, mainly during REM sleep (83.5%), high apnea activity, and sustained and progressive hypoxemia. Complex ventricular ectopy was observed in 14/13 patients (nights 2/4) and repetitive ventricular ectopy in 5/3. There was no significant difference in the quality and quantity of ventricular ectopy during wake and sleep states between the CHD group and the control group. In one patient ventricular bigeminy was observed only at a threshold of SaO2 below 60%. Bradyarrhythmia was made evident in four subjects from the CHD group and correlated mainly with apnea activity. We suppose that patients with sleep apnea and CHD are at cardiac risk because coronary heart disease can be aggravated by insufficient arterial oxygen supply due to cumulative phase of apnea and hypoventilation. The reduced hypoxic tolerance of the heart may lead to myocardial ischemia and increased electrical instability.