Key result
In male patients with acute myocardial infarction, systemic hypertension, older age, and higher BMI, but not obstructive sleep apnea, were independent predictors of increased thoracic aortic size.
Why the study?
Does obstructive sleep apnea or hypertension independently determine thoracic aortic dilatation in male patients with acute myocardial infarction?
Observational (n=94)
Single-blind
No
Does obstructive sleep apnea or hypertension independently determine thoracic aortic dilatation in male patients with acute myocardial infarction?
Effect estimate: Standardized coefficient 0.133 (for OSA) (95% CI -0.381-2.281)
p-value: p=NS
In male patients with AMI, systemic hypertension, age, and BMI—rather than obstructive sleep apnea—are the primary determinants of thoracic aortic dilatation and functional abnormalities.
Hypertension, age, and BMI may drive thoracic aortic size in male AMI more than OSA; supports risk stratification but leaves OSA's role open.
BACKGROUND: Recent studies suggest that obstructive sleep apnea (OSA) causes thoracic aortic dilatation; but it is well accepted that hypertension can cause aortic dilatation, and hypertension is a common finding in patients with OSA. We aimed to investigate the relative impact of OSA and hypertension on the structural and functional changes of the thoracic aorta. METHODS: This was an echocardiography substudy of our prospective OSA study in patients with acute myocardial infarction (AMI). Ninety-four male patients who completed both echocardiography and polysomnography were recruited. OSA was defined as an apnea-hypopnea index (AHI) > or = 15/hour. RESULTS: The patients' mean age was 53 +/- 10 years, and mean body mass index (BMI) was 24.6 +/- 3 kg/m2. Sixty-four (68.1%) patients had OSA; of these, 39 (41.5%) had severe OSA. Thirty-three (52.6%) of the OSA cohort had hypertension. There was no correlation between any of the echocardiographic parameters and thoracic aortic size. Stepwise multivariate regression showed that BMI (P = 0.024), older age (P = 0.044), and hypertension (P = 0.025) were the only determinants. There was no significant independent relationship between OSA/AHI and thoracic aortic size. Systolic blood pressure but notAHI correlated significantly with aortic distensibility and compliance (r = -0.40 and -0.26, P < 0.001 and 0.022, respectively). CONCLUSIONS: Hypertension is a common finding in male AMI patients with OSA. In these patients, increased afterload from systemic hypertension rather than mechanical stress on the aortic wall determines the thoracic aortic size and abnormalities in aortic functional indices. BMI and age were also independent predictors of thoracic aortic dilatation.
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Li-Ching et al. (2010) conducted an observational in Acute myocardial infarction (n=94). Obstructive sleep apnea and hypertension vs. Patients without obstructive sleep apnea or hypertension was evaluated on Thoracic aortic size (aortic root diameter) independent predictors (Standardized coefficient 0.133 (for OSA), 95% CI -0.381-2.281, p=NS). In male patients with acute myocardial infarction, systemic hypertension, older age, and higher BMI, but not obstructive sleep apnea, were independent predictors of increased thoracic aortic size.
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