OBJECTIVES To evaluate the day-night variation of acute myocardial infarction (MI) in patients with obstructive sleep apnea (OSA). BACKGROUND OSA has a high prevalence and is characterized by acute nocturnal hemodynamic and neurohormonal abnormalities that may increase the risk of MI during the night. METHODS AND RESULTS We prospectively studied 92 patients with MI, for which the time of onset of chest pain was clearly identified. The presence of OSA was determined by overnight polysomnography. For patients with and without OSA we compared the frequency of MI during different intervals of the day based on the onset time of chest pain. The groups had similar prevalence of comorbidities. MI occurred between midnight and 6am in 32% of OSA patients and 7% of non-OSA patients (P=0.01). The odds of having OSA in those patients whose MI occurred between midnight and 6am was six-fold higher than in the remaining 18 hours of the day (95% C.I: 1.3 −27.3, P=0.01). Of all patients having an MI between midnight and 6am, 91% had OSA. CONCLUSIONS The diurnal variation in the onset of MI in OSA patients is strikingly different from the diurnal variation in non-OSA patients. Patients with nocturnal onset of MI have a high likelihood of having OSA. These findings suggest that OSA may be a trigger for MI. Patients having nocturnal onset of MI should be evaluated for OSA, and future research should address the effects of OSA therapy for prevention of nocturnal cardiac events. CONDENSEND ABSTRACT We studied 92 patients with MI, for whom the time of onset of chest pain was clearly identified. MI occurred between midnight and 6am in 32% of OSA patients and 7% of non-OSA patients (P=0.01). The odds of having OSA in those patients whose MI occurred between midnight and 6am was 6 fold higher than in the remaining 18 hours of the day (95% C.I: 1.3 −27.3, P=0.01). The diurnal variation in the onset of MI in patients with OSA is strikingly different; patients with nocturnal onset of MI have a high likelihood of having OSA.

Background: Epidemiologic studies link short sleep duration to obesity and weight gain. Insufficient sleep appears to alter circulating levels of the hormones leptin and ghrelin, which may promote appetite, although the effects of sleep restriction on caloric intake and energy expenditure are unclear. We sought to determine the effect of 8 days/8 nights of sleep restriction on caloric intake, activity energy expenditure, and circulating levels of leptin and ghrelin.

Obesity has been associated with increased cardiac sympathetic activation during wakefulness, but the effect on sleep-related sympathetic modulation is not known. The aim of this study was to investigate the effect of fat gain on cardiac autonomic control during wakefulness and sleep in humans. We performed a randomized controlled study to assess the effects of fat gain on heart rate variability (HRV). We recruited 36 healthy volunteers, who were randomized to either a standardized diet to gain approximately 4 kg over 8 weeks followed by an 8 week weight loss period (n=20), or to serve as a weight-maintainer control (n=16). An overnight polysomnogram with power spectral analysis of HRV was performed at baseline, after weight gain, and after weight loss to determine the ratio of low frequency (LF) to high frequency (HF) power, and to examine the relationship between changes in HRV and changes in insulin, leptin and adiponectin levels. Mean weight gain was 3.9 kg in the fat gain group versus 0.1 kg in the maintainer group. LF/HF increased both during wakefulness and sleep after fat gain and returned to baseline after fat loss in the fat gain group, and did not change in the control group. Insulin, leptin and adiponectin also increased after fat gain and fell after fat loss, but no clear pattern of changes were seen that correlated consistently with changes in HRV. Short-term fat gain in healthy subjects is associated with increased cardiac sympathetic activation during wakefulness and sleep but the mechanisms remain unclear.

Obstructive sleep apnea (OSA) is highly prevalent in patients with established coronary artery disease. 1 We have reported that OSA is also a common comorbidity, affecting approximately two-thirds of patients who had a recent myocardial infarction (MI). 2 However, the prognostic implications of OSA after an MI remain unknown.Endothelial dysfunction is an early marker of vascular function impairment and is also predictive of future cardiovascular events. 3 Measurement of fl owmediated dilation (FMD ) is recognized as a measure of endothelial dysfunction and has been used to determine risk factors for cardiovascular disease in several clinical studies. 4 Moreover, FMD is closely related to coronary endothelial function. 5 Prior studies have shown diffuse endothelial dysfunction in patients with long-term 6 and short-term coronary syndromes. 7 Epidemiologic and experimental data suggest that patients with OSA have impaired endothelial function, a mechanism that may help explain the association between OSA and cardiovascular diseases. 8,9 However, to our knowledge, there Background: Impaired brachial fl ow-mediated dilation (FMD) is associated with risk for subsequent cardiovascular events in patients after myocardial infarction (MI). These patients often have obstructive sleep apnea (OSA). We tested the hypothesis that patients with OSA post MI will exhibit more severe impairment in FMD. Methods: We studied 64 patients with MI admitted to our hospital. OSA was determined using polysomnography. FMD was measured using high-resolution ultrasonography, with researchers blind to the OSA diagnosis.