Stanford type A aortic dissection after urgent prosthetic valve replacement: case reports

The patient was a 57-year-old Asian male who underwent treatment for dental caries in March 2004. Two months later, he developed high fever and visited a nearby hospital. He had only a history of hypertension and no contributory family history, including of Marfan syndrome. Echocardiography revealed moderate aortic and mitral valve insufficiency with obvious vegetations. The ascending aorta was enlarged in width to 44 mm. Blood culture failed to isolate any bacteria. Roth’s spots were detected in the eyes, and Osler’s nodes in the fingers of the right hand. Under the clinical diagnosis of infective endocarditis, the patient was initiated on intravenous antibiotic therapy with Penicillin G and gentamicin. However, he failed to show satisfactory response to the medical therapy, the symptoms of heart failure deteriorated, and he developed several distal embolic episodes. Urgent double valve replacement (Aortic valve: ATS #25 mm, Mitral valve: ATS #31 mm) was performed. The native aortic valve was tricuspid. The ascending aorta was left untouched at this time-point. Examination of the operative samples from the mitral and aortic valves revealed bacterium and eumycetes. Therefore, administration of Fosfluconazole, meropenem, and vancomysin was started. The postoperative course was uneventful and the infection was well-controlled. The patient was discharged and followed up at the outpatient clinic thereafter. Four years later, in January, 2008, the patient presented with chest pain of sudden onset, and computed tomography angiography (CTA) showed dissection of the ascending aorta (Stanford A) (Figure 1). A re-do sternotomy was undertaken immediately, and cardiopulmonary bypass was established with arterial perfusion from the femoral artery and bicaval drainage. The entry was located in the ascending aorta, away from the previous cannulation and aortotomy sites. The mechanical valve at the aortic position was preserved. Aortic root and ascending aortic replacement with retrograde cerebral perfusion in deep hypothermia (18°C) and reconstruction of the right and left coronary arteries was performed. Histopathological examination did not show any evidence of inflammation caused by bacteria, but only atherosclerotic changes of the vessel wall without medial necrosis. At present, 5 years later, the patient is doing well.

The second patient was a 62-year-old Asian male, who complained of fever and dyspnea on exertion in January 2000. He had no significant past medical history or any contributory family history. He went to a nearby hospital and echocardiography revealed moderate aortic valve insufficiency with vegetations on the valve and dilatation of the ascending aorta to 46 mm. The patient was initiated on antibiotic therapy and during the course of the hospitalization for the therapy. However, because of repeated embolic episodes, urgent aortic valve replacement (Carpentier-Edwards tissue valve: #25 mm) was performed. The native aortic valve was tricuspid. Nine years later, in March 2009, the patient presented with severe right leg pain, and was admitted to the hospital. The right femoral arterial pulse was not palpable on arrival. A CTA showed dissection of the ascending aorta continuing to the iliac bifurcation and obstruction of the right common iliac artery (Stanford A) (Figure 2). Initially, we performed surgical fenestration and cross-over femoral bypass grafting with an 8-mm PTFE graft for the right leg ischemia, since the patient and his family refused consent for open heart surgery. Fortunately, there was no pericardial effusion and no evidence of aortic bioprosthetic valve insufficiency. The postoperative course was uneventful. However, one month later, a repeat CTA showed gradual enlargement of the ascending aortic width to 80-mm (Figure 3). Therefore, we persuaded the patient and his family to provide consent for surgery on the ascending aortic aneurysm. Cardiopulmonary bypass was established with arterial perfusion from the femoral bypass graft and bicaval drainage after re-sternotomy. The entry was located in the ascending aorta, away from the previous cannulation and aortotomy sites. The false lumen extended to the right coronary ostium and just above the annulus. A re-do aortic valve replacement was not considered necessary as there was no prosthetic valve deterioration. Ascending aortic replacement with retrograde cerebral perfusion in deep hypothermia (18°C) and right coronary artery reconstruction were performed. Similar to the findings in case 1, histopathological examination did not show any evidence of inflammation caused by bacteria, but only atherosclerotic changes of the vessel wall without medial necrosis. The immediate postoperative course was uneventful and the patient was discharged three weeks after the second surgery. At present, 4 years since the surgery, the patient continues to do well.