Aortic valve replacement in a bicuspid aortic valve patient followed by reoperation for ascending aorta rupture: a case report

Abstract

Bicuspid aortic valve (BAV), the most common congenital cardiac anomaly, predisposes individuals to aortic stenosis and regurgitation due to valve degeneration. Abnormal hemodynamics, arterial wall characteristics, and genetic factors contribute to ascending aorta dilatation, potentially leading to severe complications like aortic dissection. Presently, the most recent guidelines propose that individuals with BAV requiring valve replacement due to valve dysfunction should undergo simultaneous replacement of the ascending aorta when the diameter of aortic dilatation exceeds 4.5 cm. A 60-year-old female patient previously underwent mechanical aortic valve replacement and ascending aortoplasty at our center due to aortic stenosis and a 4.3 cm diameter ascending aorta. In the sixth postoperative year, she was readmitted due to ascending aorta rupture, resulting in blood entering the right atrium and causing acute right heart failure. We performed repair of the rupture and concomitant ascending aorta replacement to prevent further exacerbation of the patient's condition.

Keywords: aortic rupture; aortic valve replacement; ascending aortic dilatation; bicuspid aortic valve; cardiac reoperation.

Figure 1

The imaging tests conducted on patients after admission to the hospital. Preoperative computed tomography angiography of the thoracic and abdominal aorta in both transverse (a) and longitudinal (b) sections showed a significant rupture at the ascending aorta, with the rupture connecting to the right atrium as indicated by the red arrow. Three-dimensional CTA with red arrows also shows a significant rupture in the ascending aorta (c).

Figure 2

The postoperative patients’ aorta underwent pathological section staining. Hematoxylin-eosin staining (a), Masson's trichrome staining (b), and Verhoeff-van Gieson elastic staining (c) collectively revealed histological features indicative of smooth muscle cell disorganization, accompanied by a discernible decrease in elastin and collagen fiber density.