Sleep Apnea Syndrome: Insights into Neurocardiogenic Interactions
Abstracts & Commentary
Sources: Garrigue S, et al. N Engl J Med. 2002;346:404-412; Gottlieb DJ. N Engl J Med. 2002;346:444-445.
Sleep apnea syndrome (SAS) is a disorder with wide ranging physiological and social consequences. In the obstructive, "Pickwickian" type, obesity and a shortened, floppy upper airway result in severe snoring and impaired air flow. In the central type, there is a loss of medullary respiratory drive, resulting in prolonged periods of arrested respiratory effort. In either type, poor sleep hygiene results in frustrated bed partners, daytime sleepiness with impaired productivity, and even an increased incidence in vehicular accidents. Nocturnal hypoxia contributes to hypertension, right-sided heart failure, and increased cardiac mortality. Treatment with continuous positive airway pressure (CPAP) is effective, but often uncomfortable and always cumbersome.
The data of Garrigue and colleagues provide fascinating new insight into this disorder. They studied 15 patients with SAS, all of whom had a programmable dual chamber sequential pacemaker. These patients somewhat serendipitously had both conduction system (sinus node) disease requiring the pacemaker and SAS, 2 disorders not believed to be directly related. Although most of the patients had mild left ventricular dysfunction, heart failure was not thought to cause their noctural breathing problems.
Patients were roughly equally divided between obstructive and central types of SAS, which does represent a skewed population. More than 90% of SAS in the community have the obstructive type. Each patient was treated with atrial overdrive pacing at a rate of 15 beats per minute faster than their baseline. Episodes of apnea and hypopnea during polysomnography were measured according to strict accepted criteria. Obstructive or central events were distinguished by the presence or absence of diaphragmatic effort. The overall duration of sleep was not affected by treatment, indicating that any benefit of pacing was not merely a consequence of arousal. The hypopnea index (total number of episodes divided by the number of hours of sleep) was reduced with pacing from 9 ± 4 to 3 ± 3 (P < 0.001). For both apnea and hypopnea, the reduction was 28 ± 22 to 11 ± 14 (P < 0.001). Patients with both obstructive and central SAS benefited from treatment. Central apnea events, however, were more significantly reduced (P < 0.007) than those of an obstructive type (P < 0.03).
Garrigue et al speculate that atrial pacing maintains sympathetic activity and counteracts an excess of vagal tone in these patients. This vagolytic effect may then influence central respiratory drive. Such a reflex loop, they argue, which is known to exist for pulmonary afferents, may also be affected by sensory inputs from the heart.
Commentary
In the editorial accompanying Garrigue et al’s report, Gottlieb further speculates on the possible mechanisms that may explain this apparently potent heart-lung-brain interaction. It is likely that cardiac vagal afferents directly affect respiration. These neurons form synapses in the nucleus of the tractus solitarius, which directly influences medullary respiratory control. It is more difficult, however, to explain how atrial pacing might effect obstructive SAS, a purely mechanical pharyngeal problem. As Gottlieb indicates, the activity of upper airway muscles, such as the genioglossus, appear to parallel diaphragmatic activity in a cyclical fashion. It is, therefore, possible that central factors guiding the respiratory process may have a powerful influence on neck muscle tone. It is also possible that the autonomic balance between sympathetic and parasympathetic activity may be important, as epinepherine has been shown to have an excitatory effect on respiratory neurons, including the pharyngeal muscles.
Although it is improbable that pacemaker insertion will become a standard therapy for SAS, these data provide a novel approach to a disorder with previously limited treatment. Perhaps these data can be generalized to patients without intrinsic cardiac disease. Interdisciplinary approaches to sleep medicine involving neurology, pulmonology, and cardiology will be needed to further explore this multisystem problem. —Alan Z. Segal
Dr. Segal, Assistant Professor, Department of Neurology, Weill-Cornell Medical College, Attending Neurologist, New York Presbyterian Hospital, is Assistant Editor of Neurology Alert.
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