Transatrial Cannulation of the Left Ventricle for Acute Type A Aortic Dissection: A 5-Year Experience.

BACKGROUND: Acute type A aortic dissection (AAD) is a life-threatening disorder with a high rate of mortality and complications. All cannulation techniques currently used to establish arterial flow for cardiopulmonary bypass are associated with a considerable risk of organ malperfusion, stroke, or access site trauma. Here, we report the impact of transatrial cannulation of the left ventricle on patient outcome after surgical treatment of AAD. METHODS: Between 2010 and 2013, 46 patients underwent emergency surgery for AAD using transatrial cannulation of the left ventricle. Their outcome was retrospectively compared with that of 73 age- and sex-matched patients operated on for AAD between 2006 and 2010 before introduction of the new technique. RESULTS: No differences concerning preoperative details were found. Arterial flow before 2010 was established after preparation of the femoral artery in 46 patients (63.0%) or by direct cannulation of the ascending aorta in 27 patients (37.0%). Operation times were significantly lower in the transatrial cannulation group (271.2 ± 75.4 versus 308.3 ± 78.2; p = 0.02). Postoperatively, we observed a significantly reduced stroke rate in the group with transatrial cannulation (6.5% versus 26.5%; p = 0.007) and a decreased rate of acute renal failure (20.0% versus 32.4%; p = 0.003). Intraoperative mortality (0% versus 6.8%; p = 0.16), 30-day mortality (8.9% versus 10.3%; p = 1.00), and mortality during follow-up (9.8% versus 34.4%; p = 0.08) did not differ. However, overall mortality was significantly lower in the group after transatrial cannulation (17.7% versus 45.2%; p = 0.003). CONCLUSIONS: In patients undergoing surgery for AAD, transatrial cannulation of the left ventricle proved to be a safe and easy cannulation method that significantly reduced postoperative complications.

Aromatase activity induction in human adipose fibroblasts by retinoic acids via retinoic acid receptor α.

Estrogen synthesis in adipose tissue is associated with the development of breast cancer. Tumors are preferentially found in breast quadrants with strongest expression of the cytochrome P450 aromatase (encoded by the gene CYP19A1). Several promoters regulated by various hormonal factors drive aromatase expression in human breast adipose fibroblasts (BAFs). As adipose tissue is a major source of retinoids, in this study, we investigated their role in the regulation of aromatase expression. The retinoids all-trans-retinoic acid (at-RA) and 9-cis-RA induce aromatase activity in human BAFs. In BAFs, at-RA induces aromatase gene expression via promoter I.4. In 3T3-L1 cells, both retinoids specifically drive luciferase reporter gene expression under the control of aromatase promoter I.4, whereas other promoters active in human adipose tissue are insensitive. Activation by retinoids depends on a 467 bp fragment (-256/+211) of promoter I.4 containing four putative retinoic acid response elements (RAREs). Site-directed mutagenesis revealed that only RARE2 (+91/+105) mediates the retinoid-dependent induction of reporter gene activity. In 3T3-L1 preadipocytes and human BAFs, RA receptor α (RARα (RARA)) expression is predominant, whereas RARß (RARB) or RARγ (RARG) expression is low. Electrophoretic mobility shift assays with nuclear extracts obtained from human BAFs and 3T3-L1 cells identified a specific RARE2-binding complex. Retinoids enhanced complex formation, whereas pre-incubation with anti-RARα antibodies prohibited the binding of RARα to RARE2. Chromatin immunoprecipitation showed RA-dependent binding of RARα to the RARE2-containing promoter region in vivo. Furthermore, we provide evidence that RARE2 is also necessary for the basal activation of promoter I.4 in these cells. Taken together, these findings indicate a novel retinoid-dependent mechanism of aromatase activity induction in adipose tissue.