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Eur J Cardiothorac Surg 2002;21:453-458
© 2002 Elsevier Science NL
Division of Cardiac Surgery, Department of Cardiac Surgery, Karl-Franzens University School of Medicine, Auenbruggerplatz 29, A-8036 Graz, Austria
Received 5 October 2001; received in revised form 3 December 2001; accepted 5 December 2001.
* Corresponding author. Tel.: +43-662-44820; fax: +43-662-828318
e-mail: olaf.stanger{at}kfunigraz.ac.at
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Abstract |
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 Top Abstract 1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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50 mm in all 11 cases upon presentation. Dissections were treated with Bentall procedures (3), Cabrol procedure (1), supracoronary tube graft (6) including concomitant CABG (3) and AVR with local repair (1). Total in-hospital mortality was 54% (6/11), and 66% (4/6) in cases with acute dissection due to low cardiac output (3) and myocardial infarction (3). Conclusions: Type-A aortic dissection can follow cardiac operations at any time with no typical interval or associated histology and with high overall hospital mortality. Male patients with arterial hypertension are at increased risk. Clinical presentation may differ from primary dissection with implications for management and risk estimation.
Key Words: Aortic dissection • Valve replacement • Coronary artery bypass surgery
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1. Introduction |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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Predisposing factors for aortic dissection include aortic valve pathology [6,7], arterial hypertension and Marfan syndrome [8]. Potential locations of injury during cardiac operations include sites with cross-clamp injury [9], suture lines from coronary artery bypass grafts [10] and the cannulation site [11], potentially making the use of cardiopulmonary bypass (CPB) and manipulation of the ascending aorta a hazard for subsequent dissection, especially in the presence of concomitant vessel wall abnormalities.
Almost all published series on delayed dissection focused on AVR [12,13] and very few data are available on the incidence of aortic dissections late after cardiac surgery. As tremendous numbers of cardiac operations are performed every year, it is important to know about the risk, presentation and outcome of this distinct clinical entity, with potential implications for management.
The purpose of this study was (1) to review and identify the factors associated with the risk of developing aortic dissection late after previous cardiac surgery and (2) consequently to improve strategies for further management.
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2. Patients and methods |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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2.1. Presentation
Type A dissection was acute in six patients and chronic in five (Table 1). Eight of the eleven patients (72%) were male and eight (72%) were hypertensive. None had a bicuspid valve at the time of the first intervention. The mean age of the patients was 62.7 (range 48.8–74.3) years at the time of reoperation. The median interval between the initial cardiac operation and subsequent diagnosis of aortic dissection was 3.3 years (mean 5.1, range 0.2–17). Only one case presented with hemodynamic instability with pericardial hemorrhage and malperfusion of the lower extremities following perforation. All others were hemodynamically stable at the time of operation. All cases with acute dissections presented with thoracic chest pain, but this was the case only with one patient with chronic dissection. Aortic regurgitation grade 3 was present in three acute and two chronic cases. Aortic diameter was 50 mm (range 5.0–10.5 cm) in all cases, but importantly, a dilated aorta with a diameter 40 mm was described in the primary operation reports in five cases, and ‘fragile’, ‘sclerotic’ or ‘thinned’ quality of the vessel wall was mentioned in three other cases.
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3. Results |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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The chosen surgical techniques included Bentall procedure (n=2), Bentall procedure+CABGx1 (n=1), Cabrol procedure (n=1), AVR+local repair (n=1), supracoronary tube graft (n=3) and replacement of ascending aorta with tube graft and concomitant CABGx1 (n=3). Femoral vessels and the right atrium were routinely cannuled and deep hypothermic circulatory arrest was used in three, clamping of the aorta proximal to the brachiocephalic trunk in all other cases.
Six hospital deaths occurred including four patients lost intraoperatively (low cardiac output, n=2; myocardial infarction, n=2) and two deaths at day 1 (MCI) and day 2 (LCO) postoperatively. This makes an early overall mortality of 54, or 66% in the group with the acute dissections. Importantly, four of the six fatal cases had previously undergone CABG alone or in combination with AVR. All other patients were discharged from hospital without complications and remain asymptomatic with a follow-up of 23.3 cumulative patient years (mean 4.7 years). No neurological complications were observed in any of the survivors at any time. The six autopsy reports failed to document acute brain damage as the cause of death.
The entry site of the tear was identified in all cases and described in the operation report (Table 1). There was no pattern to the distribution and the tear was found distal to the native coronary ostium in three cases but within the aortic sinus and distal to the valve in eight cases, however, never at the previous cannulation site or close to the proximal anastomosis and only once near the site of previous aortotomy. Histology was also uncharacteristic, describing degeneration (n=4), atherosclerosis (n=4) and cystic medial necrosis (n=1).
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4. Discussion |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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The low incidence of perforation after previous cardiac surgery is in agreement with previously reported prevalences of 6 and 9% [4,16]. Apparently, postoperative pericardial scarring and adhesions may in part explain this condition. Although CT, magnetic resonance imaging and echocardiography are established, highly sensitive tools for diagnosis of aortic dissection [17], only coronary angiography can reliably determine presence and extent of additional coronary artery disease (CAD) and should be mandatory in cases with type A aortic dissection after previous cardiac surgery, especially with known CAD. This is supported by our finding that four of the six fatal cases had previous CABG and progression of the disease may have been underestimated, contributing substantially to intraoperative MCI and mortality. Only four patients (one acute and three chronic cases) underwent coronary angiography prior to surgery, all of them were later survivors. This low number most likely reflects the intention to safe time as preoperative angiography was shown to delay surgery, cause hemodynamic instability and increase mortality in primary acute aortic dissection [18]. However, safe feasibility even under acute conditions has been shown in selected patients [19]. As demonstrated, rupture and hemodynamic instability are rare in patients after previous operation, even in acute type A dissection. Thus the potential benefit for outcome may outweigh the extra time required for coronary angiography with little additional risk.
Aortic dissections were repeatedly reported as complications originating from cross-clamp injury [9], from intimal tears at the suture line of a coronary artery bypass graft [10] or from the site of cannulation [11]. Thus, intimal injury can result from direct laceration and mechanical compression, with increased risk with severe atherosclerosis and cystic medial necrosis [14]. Further independent predictors are aortic valve pathology [6,7], aortic wall fragility, dilation and thinning [20]. Histology, site of entry tears and intervals since first operation in our series of 11 cases were uncharacteristic and do not allow a conclusion on causality to be drawn. Except for hypertension and male gender, none of the traditional predictors was conclusive in our series of 11 cases. Thus, type A dissection in patients after previous cardiac surgery must be regarded as de-novo dissections with, however, a distinct clinical presentation and outcome.
Importantly, a dilated aorta with a diameter >40 mm was documented at the primary operation in all available reports. That raises the question of a more radical initial operation including preventive ascending aorta replacement. The decision is difficult when the ascending aorta is only moderately dilated, and must be made individually. A diameter of only 37 mm can precede type A dissection [21]; other authors have suggested diameters of 55 mm [22] or less [12], 50 mm [13,24] and even 43 mm [20] as threshold for preventive replacement. Additional predictive factors such as aortic regurgation, arterial hypertension, bicuspid valve and cystic media necrosis (fragility of aortic wall and aortic wall thinning) sharply raise the probability of late dissection up to 96% after AVR and thus justify aortic surgery at the time of AVR [19]. As a consequence, we suggest considering a more radical preventive aortic replacement, especially in male patients with known hypertension and obvious aortic wall alterations, even if the diameter is only 40–45 mm.
From our data, we cannot completely exclude that iatrogenic mechanical damage to the aortic wall contributes to the incidence of late dissection. The precise number of cardiac operations with use of CPB in Europe can currently only be estimated from individual data bases, of which the National Adult Cardiac Surgical Database serves as a good example [23], and may well exceed 300,000 per year. Although only less than 1% of cardiac operations may subsequently present with late type A aortic dissection [4,5], 13.2% of our patients with type A dissection had previously undergone cardiac surgery. Interestingly, reported intervals from primary intervention to subsequent type A aortic dissection seem to be in good accordance at approximately 3–5 years (Table 2). This clinical entity must thus be expected with increasing frequency. General preventive measures includes preoperative evaluation of the ascending aorta. Calcification or dilated aorta should alert the surgeon and lead him/her to select the site of the anastomosis carefully, manipulate the aorta gently and choose appropriate clamps. The cannulation site should be distant from palpable aortic plaque to avoid separation of the plaque from the aortic wall, and systolic pressure should be below 100 mmHg to prevent excessive stress to the aortic wall [3].
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In conclusion, our data demonstrate that type-A aortic dissection may follow cardiac operations at any time with no typical interval or associated histology. Early hospital mortality is high, exceeding primary type A dissections almost two-fold. Clinical presentation differs from primary dissection with implications for management and risk estimation. Male patients with arterial hypertension are at increased risk. Additional aortic wall pathology should lead to consideration of individual preventive aortic replacement even when the generally accepted diameter of 6 cm has not yet been reached. Careful preoperative assessment of coronary status through coronary angiography, especially in patients with prior CABG, is suggested as a fundamental measure to reduce mortality and can safely be performed even in acute type A dissections after previous cardiac surgery.
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Footnotes |
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Appendix A. Conference discussion |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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Dr Stanger: That is a good question. Acute cases do have an indication.
Mr Nashef: What is that indication?
Dr Stanger: Life-threatening. Acute Type A aortic aneurysm are always operated on, as number of fatal pericardial effusions, rupture into the pericardium, have been described in excess of 20%, and they should die very soon otherwise.
Mr Nashef: What I would like to put to you is that if it is a redo, the situation changes. There are three reasons for operating on Type A: one, to prevent intrapericardial rupture; two, to prevent death from massive aortic regurgitation; and three, to prevent death from dissection of the coronary arteries due to involvement of the coronary arteries in the dissection, leading to massive myocardial infarction.
Anonymous: And four, from extension of the dissection.
Mr Nashef: Well, I think that is debatable. But these first three, at any rate, are modified substantially by the fact that the patient had previous cardiac surgery. The aortic valve may be replaced; the proximal anastomoses may prevent the dissection coming proximally; and rupture into the pericardium may not be possible. So my argument is that the indications for operating in Type A need to be reviewed in redos.
Dr Stanger: Actually this is something that I wanted to focus on. This is our experience now after we have seen the cases over the past 10 years, when we were not aware of the risk and that scarring prevents most of the dangerous situations. We have now learned from this.
Dr R. Schistek (Salzburg, Austria): There is one danger of rupture also in redo cases, as a remark, rupture to the right atrium, and this can happen. We have seen this. But I don't know how frequent this is.
Mr Nashef: I think that there are 17 cases in the literature.
Dr C. Muneretto (Brescia, Italy): I was concerned about some comment on the indication in redo surgery for aortic dissection. We experienced more than 12 patients up to date that had aortic dissection following cardiac surgery, especially following aortic surgery, and one-half of those patients came in our department because of chronic dissection and false aneurysm later on. So I don't feel that the manner of dissection should be the indication, but we can discuss about the opportunity to consider this type of operation as an emergency procedure or not. But anyway, I think that all those patients will have indication for replacement, of course.
Dr Stanger: I agree.
Dr J. Pirk (Prague, Czech Republic): Your observation confirmed my clinical observation that the highest risk of this is aortic valve disease because of the turbulence. So I am almost sure that the origin of the dissection is in the cannulation site. So I think we should pay better attention to close it, not just to tie the stitches like we do in the CABG patient.
Dr Stanger: That could be a point. I was able to find in the operating protocols in 10 out of 11 cases the precise location of the entry tear that was described by the surgeon, but this was not indicative at all, the tear could have happened at any place, and I was not able to show that it was in the area of the cross-clamping site or anywhere precise. Also, other authors have not described a typical tear or site. But, of course, we should be less aggressive probably in handling the aorta.
Dr J.-F. Legare (Halifax, Canada): I am just a little worried about the general statement of stating that any aorta of more than 4.5 cm should be dealt with. A little more data on that is how many of those valves were true bicuspid valve versus tricuspid valve, how well was the hypertension managed postoperatively, and do you have any data on the original operation, how big that aorta was at the time of the original operation, and should we follow patients instead with CAT scans or things of this sort such as echo?
Dr Stanger: Well, if I understood you correct, you want to emphasize on the situation with bicuspid valves? They, of course, are posing a high risk for future dissection; that is well known. Also, the antihypertensive treatment should be mandatory, of course.
Dr Legare: How big the aorta was on the original operation, if you had any of that data.
Dr Stanger: No, they are not complete, because some of these cases were pure CABG cases and we did not expect any pathology on the aorta, so we didn't perform a CT scan routinely. The only thing that I can say, when they came to us and presented as dissection, every single case was in excess of 50 mm. That will mean we would have to perform regular CT on every CABG case. We can't do this.
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References |
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TopAbstract1. Introduction2. Patients and methods3. Results4. DiscussionAppendix A. Conference...References |
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  Z. Masuda, T. Murakami, E. Shishido, and M. Kuinose A Rare Cause of Dissection of Ascending Aorta after Aortic Valve Replacement Asian Cardiovasc Thorac Ann, February 1, 2008; 16(1): e4 - e6. [Abstract] [Full Text] [PDF]
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 J. S. Collins, A. Evangelista, C. A. Nienaber, E. Bossone, J. Fang, J. V. Cooper, D. E. Smith, P. T. O'Gara, T. Myrmel, D. Gilon, et al. Differences in Clinical Presentation, Management, and Outcomes of Acute Type A Aortic Dissection in Patients With and Without Previous Cardiac Surgery Circulation, September 14, 2004; 110(11_suppl_1): II-237 - II-242. [Abstract] [Full Text] [PDF]
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