Aortic Expansion Assessed by Imaging Follow-up after Acute Aortic Syndrome: Effect of Sleep Apnea.

After surgical treatment of type A acute aortic syndrome (AAS), some patients exhibit aneurysmal aorta expansion (AAE) either upstream or downstream of the prosthetic tube. The mechanisms promoting AAE are not fully understood. It is recognized that intermediary mechanisms involved in obstructive sleep apnea (OSA) pathophysiology affect thoracic aorta expansion. The thoracic aorta of a patient with OSA is continuously strained by repetitive surges in blood pressure, transmural stretching resulting from huge variations in intrathoracic pressure, and intermittent hypoxiarelated vascular remodeling (1–4). To date, there are no data available on the effect of OSA on AAE after surgery for type A AAS. We retrospectively analyzed 62 patients initially surgically treated for type A AAS who were prospectively followed up by computed tomography or magnetic resonance imaging at 3 and 6 months postsurgery, and annually thereafter. At the 3-year median-term follow-up visit, the maximum rate of aortic diameter expansion (V : maxAo) was calculated to detect patients with stable aortic aneurysm or AAE. Patients with surgical or radiologic intervention on downstream aorta and Marfan syndrome were excluded. Independent observers, blinded to the clinical data, analyzed aortic images. V : maxAo was calculated as follows: (D22D1)/T, with D1 being the initial diameter and D2 the final diameter (maximum increase at the same anatomical level) between the first and the most recent postoperative measurements. The normal aortic expansion rate is 1 to 2 mm/yr (5). We classified patients into two groups: group 1, with no abnormal increase in aortic diameter (V : maxAo, 2 mm/yr), and group 2, for whom V : maxAo> 2 mm/yr. At the 3-year visit, all patients underwent 24-hour blood pressure monitoring (ABPM), biological assays, carotid-to-femoral pulse wave velocity measurement, and full polysomnography and answered the Epworth sleepiness scale questionnaire. SA was defined by an apnea–hypopnea index above 5 per hour of sleep and was considered central when more than 50% of apneas and hypopneas were central. All patients gave informed consent to participate in this institutional review board–approved study. The patients had undergone the following operations: replacement of the ascending aorta with an interposition tube graft (35 patients), of the ascending aorta and the aortic arch (5 patients), and of the ascending aorta and aortic valve by a composite graft (Bentall technique, 21 patients), and one patient had an interposition graft with separate aortic valve replacement. Table 1 summarizes the general characteristics of the study population that were similar for the two groups with the exception of the polysomnographic parameters. The prevalence of OSA was 72% throughout the population, and 18% of the patients presented with central SA. The prevalence of central SA and OSA was similar in patients with or without AAE (15% vs. 19% and 70% vs. 74% [P = 0.6], respectively). However, hypoxia during sleep was worse in patients with AAE, who had a significantly lower mean nocturnal SpO2 than those without AAE (92.56 1.9 vs. 93.66 1.7; P, 0.04) (Figure 1). The Epworth sleepiness score was 5.66 4.9 in patients without AAE and 7.16 5.6 in patients with AAE (P = 0.39). The prevalence of office hypertension (BP values. 135/80 mm Hg) was 77%, with 40% of patients exhibiting resistant hypertension. Using ABPM, 44% of patients had 24-hour hypertension, 42% had daytime hypertension, and 57% had nighttime hypertension. The prevalence of office and 24-hour ABPM hypertension was similar in both groups. The baseline aortic dimensions did not influence secondary dilatation (r = 0.11; P = 0.6). In patients with increasing aortic diameter, V : maxAo was significantly correlated with 24-hour systolic BP (r = 0.374; P = 0.013) and mean nocturnal SpO2 (r =20.381; P = 0.02). On multivariate analysis, the V : maxAo was independently (adjusted for age, body mass index, creatinine level) and positively correlated with mean nocturnal SpO2 (b =20.479; P = 0.01). In multivariate logistic regression analysis, only mean nocturnal SpO2 was independently (adjusted for the same parameters) and significantly predictive of absence of AAE (odds ratio = 0.549; 95% confidence interval, 0.35–0.862; P = 0.009). Figure E1 in the online supplement shows images in a patient who presented with severe OSA and AAE. Our original data set demonstrates the high prevalence of SA in patients with surgical procedures for type A AAS. Our study demonstrates a positive association between AAE and SA severity, as assessed by the degree of intermittent hypoxia. To date, only one study has reported the prevalence of OSA in patients who presented AAS. Sampol and colleagues compared 19 patients with a history of operated type A or medically treated type B aortic dissection with 19 hypertensive patients without aortic disease (6). They found that patients with aortic disease more frequently suffered from severe OSA than patients with hypertension. However, this case–control study did not permit us to clarify whether SA is a risk factor for AAE and was not designed to evaluate deterioration in patients with aortic disease. Here we used a retrospective study that included, by design, some limitations. We show the deleterious role of SA-linked intermittent hypoxia on the evolution of aortic diameters. We have previously described the deleterious role of hypoxia that increases carotid (7) and aortic (8) root diameters in patients with OSA. Nocturnal hypoxia increases sympathetic activity. Supported by the French Society of Hypertension and the Clinical Research Department at Grenoble University Hospital.