Altered Cardiac Contractility in Sleep Apnea

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Abstract
Adrenergic regulation in sleep apnea is a complex process because adrenergic physiology is difficult to summarize with one measure. Furthermore, the role of the adrenergic system in sleep apnea is often confounded with hypertension, making interpretation difficult in hypertensive apneics. Sixty-six people with and without apnea and/or hypertension (all were off antihypertensive medication) participated in this study. Cardiac β-adrenergic drive, as assessed by systolic time intervals, was examined at rest and in response to a mild laboratory stressor. These measures of cardiac contractility included the pre-ejection period, electrical systole (QT) interval and the cardiac acceleration index. At rest, apneics showed elevated myocardial contractility on all measures (p = 0.001). In response to the laboratory stressor, non-apneics showed an increase in cardiac β-adrenergic drive (p = 0.001), whereas the contractility in apneics did not change or decreased relative to baseline. These findings suggest disrupted cardiac adrenergic regulation in people with sleep apnea. Apnea appears to increase resting sympathetic activity and down regulate β2-adrenergic receptors. The downregulation of cardiac β-adrenergic receptor activity may explain the inability of people with sleep apnea to respond with appropriate cardiac contractility to a mild perturbation.

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