Obstructive sleep apnea and major depressive disorder in cardiovascular disease

摘要: In a recent editorial, Ehrmann et al. (1) proposed that comorbid obstructive sleep apnea (OSA) may help to explain the association between major depressive disorder (MDD) and cardiovascular disease (CVD). MDD OSA are highly comorbid, both risk factors for incident CVD cardiac events in established heart disease, they share many of same (2, 3). As al note, intermittent hypoxia secondary leads an increase inflammatory cytokines, nitric oxide synthase inhibition, sympathetic predominance, endothelial dysfunction, all which thought contribute development progression CVD. is also associated with these markers (2), it possible have additive or even synergistic effects on risks recurrent events. We propose two additional ways conditions interact further risk. First, patients blunted ventilatory response hypercapnia. Findings from our study depression consistent this possibility. Second, vasodilatory rising levels CO2 be MDD. Other studies support possibility. We recruited 53 medically stable MDD, 43 nondepressed (ND), 36 subclinical symptoms, undergo nights polysomnography order estimate prevalence undetected (4). All participants had preserved left ventricular function no known suspected disorders at time study. Polysomnography showed nearly least few apneic episodes per hour sleep. However, only 10% 8% ND was severe enough warrant initiation continuous positive airway pressure (CPAP) therapy. The mean number did not differ (6.1 ± 0.8) those who were depressed (4.4 0.9; p>0.05). duration longer (23.30 1.1 seconds) than (20.3 1.3), after adjusting age, gender, body mass index, history failure, hypertension, diabetes, current smoking Mixed events, is, central features, significantly (27.8 1.5 sec) (22.8 1.0 sec; p=0.01), as purely (MDD, 21.8±1.0 ND, 16.9 p=0.03). Although most more mild-to-moderate OSA, prolonged cumulatively exposes them substantially experience. clinically significant could lead greater events. Why should comparable patients? Obstructive terminate when chemoreceptors detect arterial (hypercapnia) signal respiratory centers brain clear resume inspiration. There evidence well psychiatric blunt delay cortical arousal hypercapnia (5–8). A fMRI documented found lesions frontal cortex, insula, cingulate, areas proximal amygdala hippocampus compared (9). hippocampus, deep cerebellar nuclei respond humans (10), suggests chemoreceptive modulatory functions dysregulated patients. There due harmful patients. When rise healthy individuals, there compensatory dilation cerebral arterioles downstream vascular beds increases blood flow. This helps mitigate negative neuronal functioning during cessation breathing (11). declines but adults show decline vasomotor reactivity inhalation do controlling ischemic white matter hyperintensities Thus, damaging patients. Our results require replication Future will then needed elucidate specific mechanisms underlying prolongation MDD; determine whether extended increased inflammatory, coagulant, responses; investigate event durations can shortened by treating depression. especially important whose CPAP yet still high meantime, we agree colleagues combination greatly