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Solution to post MV repair aortic regurgitation
 
Published on 2014-02-09 by Walid Gharzuddine
 
 
History and Findings
 

Reminder: This patient presented about ten weeks after his initial mitral valve surgery with shortness of breath and was found to have significant aortic regurgitation. Early postoperative studies had failed to show any regurgitation.

 Transthoracic echocardiography was done with the plan to proceed to transesophageal echocardiography. The only explanations were 1) infective endocarditis and 2)… ascending aortic dissection.  Technically it was not possible to visualize the ascending aorta very well from the parasternal window but while performing imaging from the subcostal window the sonographer accidentally noted a flap in the abdominal aorta (video 1). CT angiography was requested and confirmed a type A aortic dissection (images 1,2,3). Maximal aortic diameter was 43 mm. The patient subsequently underwent successful surgical repair with grafting of the ascending aorta and re-suspension of the aortic valve with trivial residual regurgitation. The surgeon reported the intimal tear to be present posteriorly above the non-coronary sinus of Valsalva.  Histopathology showed significant medial degeneration in the excised ascending aorta.

Upon further questioning the patient reported having experienced acute severe abdominal pain while on a trip abroad. He was seen in an emergency department with no diagnosis reached.

 
 
 
video 1 flap in abdominal aorta
 
 
     
 
 
Discussion
 

Discussion: Reports suggest that acute type A aorta dissection (AAD) occurs in 0.12% to 0.16% of patients with a history of cardiac surgery and cardiopulmonary bypass (CPB), and, specifically, AAD may occur in 0.6% of patients who have had previous aortic valve replacement surgery (ref. 1).

Stanger et al. (ref. 2) report on a large retrospective review in 9 university institutions in Europe of about 60,000 adult cardiac surgical patients who underwent cardiac surgery with CPB between January 1, 1990 and December 31, 2012. A total of 103 patients (0.15%) with AAD and a history of previous cardiac surgery were identified. Patients with previous aortic surgery for aneurysm or dissection including Marfan syndrome and other connective tissue disorders were not included.

AAD was defined as intraoperative when the dissection occurred and was recognized during the primary cardiac surgery (before leaving the operating room) and was treated at the time of recognition. Acute AAD within 2 to 4 weeks after cardiac surgery is thought to have a particularly high risk of rupture and operative mortality that can be expected to change later when adhesions have formed and inflammation has resolved.  The early postoperative period was therefore defined as AAD within 30 days of primary surgery. Late acute dissection was defined as occurring >30 days after primary surgery, with surgical repair within 2 weeks after the onset of specific symptoms leading to the diagnosis of aortic dissection. Late chronic AAD cases were most often incidental findings with no acute or specific symptoms. These AADs had presumably occurred >30 days after the initial cardiac surgery, and the patients underwent elective surgery.

Most cases of intraoperative AAD were diagnosed visually after dilatation and bluish discoloration of the aorta (n=14), or immediately after aortotomy (n=2) and puncture of graft holes (n=1). AAD was suspected when arterial line pressures suddenly increased or when unexplained no-flow on bypass grafts was noticed (n=3). Transesophageal echocardiography was used in all cases to diagnose or confirm the clinical suspicion of AAD.

Patients with early postoperative AAD presented with sudden onset of severe chest pain, central neurological deficit, or signs of impending pericardial tamponade. Of 67 patients with late AAD, typical presentation with a sudden onset of sharp pain in the chest was noted in 50% of acute cases. There was only a single case of late acute AAD with rupture and severe tamponade. All other patients were hemodynamically stable on arrival in the operating room and without evidence of impending or severe tamponade.

 

Histology and Entry of Dissection:

The proximal graft anastomosis and aortotomy sites were identified as entries in approximately two-thirds of cases with previous isolated AVR (67.5%) and CABG (65.8%). Other dissection entry locations were sites of cannulation (n=8), cross-clamping and side-biting clamping (n=7), and cardioplegia (n=5). The entry was either not identified or not documented in 9 cases. With the exception of 4 cases, all other histology reports documented pathologies of the aortic wall: medial degeneration (MD, n=24), atherosclerosis (n=18), a combination thereof (n=6), and giant-cell arteritis (n=2).

In this study it was observed that AAD occurred mainly in patients with preexisting aortic wall pathology and hypertension at sites of iatrogenic mechanical trauma. The aortic wall was described at the initial surgery as thin or fragile in nearly all cases. Furthermore, the aortic diameter was 46±3 mm in all available imaging (CT/MRI) reports. According to convention and guidelines,2 this diameter per se does not necessitate aortic replacement at the time of AVR or CABG, but it is suggestive of aortic wall pathology.

A thin, fragile, and dilated aorta is typically associated with histopathologic changes such as medial degeneration (MD). Nearly all histological examinations of excised aortic tissues in this study showed evidence of MD, atherosclerosis, or both. MD is characterized by an accumulation of basophilic ground substance (mucopolysaccharides) in the media with cyst-like lesions, disruptions of collagen, elastic fragmentation, and apoptosis or necrosis of smooth muscle cells that results in weakening of the aortic tissue and higher wall stress. The presence of MD is typical of connective tissue diseases, but it was shown to precede aortic dissection in non-Marfan aortas as well (ref. 3).

Although it is no longer recommended to perform coronary angiography in patients with acute aortic dissection because the risks may outweigh the benefits and that angioplasty may be performed later (hybrid procedures); preoperative coronary angiography and operative management of native coronary and graft disease were significantly associated with better outcome in patients with previous CABG. In the group who developed AAD late after the initial operation, operative mortality was highest in patients without preoperative coronary angiography and appropriate management of their native coronary artery disease and graft disease (OR, 5.36; 95% CI, 1.68–17.0; P=0.002). All patients with previous CABG who underwent preoperative coronary angiography and received new bypass grafts survived. It is worth mentioning that some were too sick and had to be rushed to the operating room and hence suffered a bad outcome (ref. 2).

Conclusion: Non-aortic cardiac surgery is associated with a low but significant incidence of AAD and must be expected at any time. Preexisting aortic wall pathology and hypertension are associated with AAD occurring at sites of iatrogenic surgical trauma. In patients with previous coronary bypass surgery coronary angiography and dealing with coronary stenoses greatly improved outcomes.

 

References:

1). Collins JS, Evangelista A, Nienaber CA, Bossone E, Fang J, Cooper JV, Smith DE, O’Gara PT, Myrmel T, Gilon D, Isselbacher EM, Penn M, Pape LA, Eagle KA, Mehta RH; International Registry of Acute Aortic Dissection (IRAD). Differences in clinical presentation, management, and outcomes of acute type a aortic dissection in patients with and without previous cardiac surgery. Circulation. 2004;110(11 suppl 1):II237–II242.

 

2). Stanger O, Schachner T, Gahl B, Oberwalder P, Englberger L, Thalmann M, Harrington D, Wiedemann D, Südkamp M, Sheppard MN, Field M, Rylski B, Petrou M, Carrel T, Bonatti J, Pepper J. Type A aortic dissection after non-aortic cardiac surgery. Circulation. 2013, 128:1602–1611.

 

3). Luk A, Leong S, Soor G, Borger M, Butany J. Histological analysis of aortic dissections following previous cardiovascular surgery. Cardiovasc Pathol. 2008;17:199–205.

 
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