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Nighttime acute coronary syndrome (ACS) occurred significantly more often in patients with visceral fat accumulation and sleep-disordered breathing, investigators reported.

Among 25 patients with nighttime onset of ACS, two-thirds of those with ≥100 cm² of visceral fat accumulation also had sleep-disordered breathing as compared with a fourth of patients with less visceral fat.

In contrast, sleep-disordered breathing occurred in a similar proportion of patients with and without visceral fat and daytime-onset ACS.

Patients with sleep-disordered breathing, visceral fat accumulation, and nighttime-onset ACS also had hypoadiponectinemia and nocturnal dysregulation of circulating adiponectin levels, as reported online in the American Journal of Cardiology.

"These results suggest that an association of sleep-disordered breathing and excess visceral fat with nocturnal dysregulation of adiponectin may play some role in the development of nighttime-onset ACS," Ken Kishida, MD, PhD, of Osaka University in Japan, and co-authors wrote in summation.

"Sleep-disordered breathing and excess visceral fat are treatable risk factors," they added. "Decrease of excess visceral fat and treatment of sleep-disordered breathing could be beneficial in preventing nocturnal cardiac events."

ACS during sleep occurs infrequently, and predisposing factors remain unclear but could include disordered sleep and obstructive sleep apnea (OSA). Patients with OSA have an increased risk of sudden cardiac death with nighttime onset, the authors noted in their introduction.

Kishida and colleagues recently reported dysregulation of adipocytokines during sleep in obese patients with OSA (Am J Physiol Endocrinol Metab 2008; 294: E778-E784, J Atheroscler Thromb 2011; 18: 240-247).

They hypothesized that the combination of sleep-disordered breathing, visceral fat accumulation, and nocturnal dysregulation of adipocytokines might play a role in the occurrence of ACS during sleep.

To test the hypothesis, the authors studied 109 consecutive Japanese patients from a single center who had revascularization procedures for ACS and overnight cardiorespiratory monitoring before discharge. The study population consisted of 66 patients with ST-segment elevation myocardial infarction, 27 with non-ST elevation MI, and 16 with high-risk angina.

The patients had a mean age of 66, mean body mass index of 23.8, total fat area of 239 cm², visceral fat area of 127 cm², and an apnea-hypopnea index that averaged 11 events per hour.

Investigators defined excess visceral fat as ≥100 cm², apnea as cessation of airflow >10 seconds, hypopnea as a decrease in the airflow signal to <70 of the preceding level associated with >4% desaturation, and sleep-disordered breathing as an apnea-hypopnea index ≥5.

Adiponectin levels were measured shortly before sleep onset and after waking. Onset of chest pain from midnight to 7 a.m. was considered nighttime ACS, and onset any other time was considered daytime ACS.

ACS had a nighttime onset in 25 patients and daytime onset in 84. Sleep monitoring results showed that 63 (58%) of the patients had sleep-disordered breathing, and 64 (59%) had visceral fat accumulation ≥100 cm².

Among patients with nighttime onset of ACS, 12 of 17 with excess visceral fat also had sleep-disordered breathing as compared with two of eight patients who had visceral fat accumulation <100 cm² (P<0.05).

In patients with daytime ACS, the prevalence of sleep-disordered breathing did not differ between patients with (26 of 47) and without (22 of 37) excess visceral fat.

Circulating adiponectin levels were significantly lower before and after sleep among patients with excess visceral fat, regardless of the time of ACS onset.

Patients with nighttime-onset ACS and excess visceral fat had mean adiponectin levels 6.3 and 6.2 µg/mL, respectively, before and after sleep versus 16.9 and 18.0 µg/mL in patients with visceral fat <100 cm² (P<0.05, P<0.01).

Among patients with daytime ACS, those with excess visceral fat had mean adiponectin levels of 6.8 and 6.7 µg/mL before and after sleep versus 11.6 and 11.7 µg/mL for patients with <100 cm² visceral fat accumulation (P<0.01 for both).

Excess visceral fat was associated with a significantly higher apnea-hypopnea index in patients with nighttime ACS (14 versus three events per hour, P<0.05), but not in the group with daytime ACS.

Patients with nighttime ACS and excess visceral fat also had higher levels of plasminogen activator inhibitor-1 and CD40 ligand.

Calling polysomnography the gold standard for diagnosing OSA, the authors acknowledged that they had used other methods for monitoring sleep, noting that polysomnography might not be cost-effective or convenient for identifying sleep-disordered breathing in patients with ACS.

The study was also limited because there were no controls without ACS, the potential bias inherent in a single-center study, and the potential for medical therapy to affect laboratory parameters, which were taken a week after onset of ACS.

From the American Heart Association:

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