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Abstract

Surgical repair of aortic dissection in previously operated patients is quite challenging. The Cleveland Clinic reports superb results in this quite infrequent population: early mortality rate is minimal and long-term survival remarkable. The relatively small number of patients in a very unstable situation does not by itself explain these rewarding results. However, the low mortality reflects the quality of patient management both in the preoperative period (proper stabilization of the clinical condition and thorough evaluation) and during surgery (adequate arterial perfusion, fine surgical techniques, and adequate medical management). The major limitation of the paper is that it does not address the mechanism of aortic dissection following cardiac surgery. Every patient category is pooled and the study population includes patients operated for very different pathological lesions: coronary artery disease, aortic valve disease, or ascending aorta pathology, including chronic aneurysms and acute aortic dissections. The mechanism of the aortic dissection developing during long-term follow-up of these operations may be the consequence of a surgical problem during the first operation (eg, abnormality either on the suture line in saphenous vein bypass surgery or on the aortic suture after valve replacement; or weakening of the media at the site of the aortic cross clamping). The mechanism may also relate to the use of “tricks”, like application of gelatin-resorcin-formalin glue to the tissues [1Kirsch M. Ginat M. Lecerf L. Houël R. Loisance D. Aortic wall alterations after use of gelatin-resorcinol-formalin glue.Ann Thorac Surg. 2002; 73: 642-644Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar], to minimize the risk of tears and bleeding. Finally, the mechanism may relate to some biological abnormalities of the aortic wall, which are responsible for extreme weakness of the mural structure. These abnormalities sometimes may be present at the time of the first operation, like in a bicuspid aortic valve, ascending aorta enlargement, or a previous acute aortic dissection; or sometimes may develop after cardiac surgery in poorly managed patients who continue to smoke or who have uncontrolled hypertension. The aortic wall structure results from a balance between proteolytic activity mainly controlled by proteolytic enzymes and metalloproteinases-tissue inhibitors of MPs (MMP-TIMPs) interactions and permanent synthesis of new structural proteins, partly controlled by tissue growth factors [2Allaire E. Muscatelli-Groux B. Guinault A. et al.Vascular smooth muscle cell endovascular therapy stabilizes already developed aneurysms in a model of aortic injury elicited by inflammation and proteolysis.Ann Surg. 2004; 239: 417-427Crossref PubMed Scopus (70) Google Scholar]. Loss of this balance, either genetically controlled or as the consequence of an abnormal inflammatory process, will increase the risk of intramural hemorrhage and/or intimal fracture. Recognition of this situation at the time of the first operation should have an impact on the initial repair itself (eg, aortic root replacement in a bicuspid orifice, extensive surgery of the aorta in aortic dissection, etc). In the mean time the more liberal use of modern imaging techniques like magnetic resonance and helicoidal scanners should permit earlier detection of an abnormal risk of aortic dissection. Aortic Dissection After Previous Cardiovascular SurgeryThe Annals of Thoracic SurgeryVol. 78Issue 6PreviewRisk of repairing aortic dissection after previous cardiovascular surgery has not been described clearly. This study assesses early and late outcomes of such reoperations. Full-Text PDF