The association between ascending aortic aneurysm (AA) and bicuspid aortic valve (BAV) has been well established. Different genetic, haemodynamic and cardiovascular risk factors have been implicated in the development and progression of AA. However, to date, definite conclusions cannot be drawn regarding the exact molecular, cellular and haemodynamic mechanisms causing BAV-associated aortopathy. For this study, we performed a thorough electronic systematic review of the literature using MEDLINE (1960-2012) and EMBASE databases. MeSH terms included: 'bicuspid aortic valve and ascending aorta', 'bicommissural aortic valve and aneurysm', 'bicuspid aortopathy', 'bicuspid aortic valve pathophysiology', 'bicuspid aortic valve and genetics' and 'bicuspid aortic valve and treatment'. We aim in this review to discuss the mechanisms, pathophysiology, genetics and modern drug therapy in the context of BAV-associated aortopathy.

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Objective Acute kidney injury (AKI) is a common complication after surgical aortic valve replacement and is associated with increased mortality. Transcatheter aortic valve implantation (TAVI) is now considered the criterion standard treatment of patients with severe symptomatic aortic stenosis ineligible for surgery. The aim of this study was to establish the incidence, risk factors, and prognostic consequences of AKI after TAVI and at 1-year follow-up in a single center. Methods Between December 2007 and March 2011, a total of 79 patients with severe aortic stenosis who underwent 81 TAVI procedures with the Medtronic CoreValve System or the Edwards SAPIEN heart valve were included. Baseline characteristics and procedural complications were recorded. Acute kidney injury was defined according to the Valve Academic Research Consortium criteria (modified risk, injury, failure, loss, and end-stage kidney disease criteria). Results The mean age was 84 (78–87) years; 49 were men. After TAVI, 10 patients (12.3%) developed AKI, which had completely resolved in 9 patients before hospital discharge. Nine patients (10%) had mild AKI (stage 1) and only one patient (10%) experienced moderate AKI (stage 2) according to Valve Academic Research Consortium definitions. The predictive factors of AKI were diabetes (odds ratio, 6.722; P = 0.004) and preoperative creatinine level greater than 104 μmol/L (odds ratio, 1.024; P = 0.02). Thirteen patients (16.4%) died within 1 year after TAVI. Three of the nonsurvivors (3.7%) developed AKI postoperatively. Acute kidney injury was, however, not a predictive factor of 1-year mortality after TAVI. Conclusions Acute kidney injury occurred in 12.3% of the patients after TAVI and persisted in only one patient before hospital discharge. Diabetes and preoperative creatinine level were found to be the main predictive factors of AKI after TAVI. Acute kidney injury was not associated with increased 1-year mortality.