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J Thorac Cardiovasc Surg 2001;121:552-560
© 2001 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology |
From the Istituto di Chirurgia Cardiovascolarea Università agli Studi di Siena, Unita' Operativa di Chirurgia dell' Aorta Toracica, Istituto di Istituto di Chirurgia del Cuore e Grossi Vasi,b Università "La Sapienza," Rome, Italy.
Received for publication July 12, 2000. Revisions requested Sept 7, 2000; revisions received Oct 6, 2000. Accepted for publication Oct 26, 2000. Address for reprints: Eugenio Neri, MD, Istituto di Chirurgia Cardiovascolare Universita' agli Studi di Siena, Policlinico le Scotte, Viale M. Bracci, 53100 Siena, Italy (E-mail: euxneri{at}tin.it nerie@unisi.it).
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Abstract |
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 Top Abstract IntroductionPatients and methodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionPatients and methodsResultsDiscussionReferences |
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1 and it is a relatively common clinical finding. 2 In acute type A aortic dissection, acute myocardial ischemia and infarction due to this mechanism are severe complications, potentially leading to irreversible myocardial damage. Aortic dissection is not often considered a cause of myocardial malperfusion; thus, fatal accidents resulting from the thrombolytic treatment given to these patients are not uncommon. 3,4 Surgical treatment of patients with acute dissection of the coronary arteries is challenging. Management of this condition should take into account the re-establishment of an adequate coronary blood flow and involves important issues such as postischemic myocardial salvage/restoration and postoperative treatment for low cardiac output.
The approach to coronary revascularization in these patients relies on various techniques that span from coronary artery bypass grafting to the strategies of repair of torn coronary vessels.
This article reports the results of a selected group of 24 patients with type A acute aortic dissection and coronary artery dissection. We review our experience and illustrate our approach to this condition, which evolved over a 15-year period.
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Patients and methods |
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TopAbstractIntroductionPatients and methodsResultsDiscussionReferences |
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Clinical characteristics of patients with dissection of the coronary ostia are illustrated in Table I. There were 14 men and 10 women. The mean age of patients was 65.5 years (median 61.7; range 41-78 years). The right coronary artery was involved in 11 patients, the left in 4 patients, and both coronary arteries in 9 patients.
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Preoperative electrocardiography revealed ST or T-wave abnormalities in all 24 patients; of these, 16 (66%) had Q waves, inferior in 6 (25%) and anterior, lateral, septal, or posterior in 10 (41%). Preoperative echocardiograms revealed severe abnormalities of segmental wall motion of both ventricles in 7 patients and of the left ventricle in 17. Mean preoperative left ventricular ejection fraction, calculated at echocardiography, was 31% (median 32%; range 18%-44%). Acute mitral regurgitation from papillary muscle dysfunction was present in 6 patients. Nine patients had frank pulmonary edema. Average peak preoperative creatine kinase MB (CK-MB) level was 58.7 IU/L (median 44 IU/L, range 19-250 IU/L).
Preoperative coronary angiography was performed in 8 of the 24 patients with coronary dissection, none of whom had chronic CAD. In patients who did not undergo angiography, the coronary arteries were evaluated for chronic CAD at operation by epicardial palpation and in some cases by probing the coronary orifices from within the opened ascending aorta. No sign of chronic CAD was found in these patients. Preoperative investigations are listed in Table II.
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Average peak postoperative CK-MB level was 77.3 IU/L (median 48 IU/L, range 29-320 IU/L). Postoperative mean peak CK-MB level for patients who did not have a perioperative Q-wave myocardial infarction was 42 IU/L (median 38.5 IU/L, range 29-73 IU/L) versus 95.0 IU/L (median 50 IU/L, range 32-320 IU/L) in patients who did have a perioperative Q-wave myocardial infarction.
In all patients, histologic examination of aortic tissue specimens revealed the typical features of cystic medial necrosis with mucoid degeneration (grade 3 or 4 medial degeneration). Histologic examination of the coronary arteries of patients who died after the operation and of the specimen of the coronary arteries resected during the operation did not demonstrate any degenerative changes.
Types of coronary ostial lesions
We differentiate among three main types of lesions (Fig 1): (1) type A, ostial dissection; (2) type B, dissection with a coronary false channel; and (3) type C, circumferential detachment with an inner cylinder intussusception.
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In the third type, the dissection encircles the affected coronary ostium and may extend along the course of the left or right main coronary artery. In such cases, the affected ostium is totally dehisced from the true aortic lumen with intussusception of the inner wall cylinder into the outer coat of the respective coronary artery. Malperfusion in these cases is produced by direct obstruction of coronary blood flow.
In our series we have found 12 type A lesions (9 of the right and 3 of the left coronary artery), of which 4 were responsible for malperfusion. Type B lesions were found in 12 patients (8 of the right and 4 of the left coronary artery) and type C lesions in 9 (3 of the right and 6 of the left coronary artery). Lesions of both coronary ostia were found in 8 patients; in none of these did type B and type C lesions coexist.
Operative technique
All operations in this series (Table III
) were performed through a median sternotomy. In all cases hypothermic circulatory arrest was a planned procedure to allow distal anastomosis by means of an open technique. In the present protocol, in use since 1988, the right atrium and the femoral artery with the best pulsation, or one of the axillary arteries, are cannulated. The coronary sinus is cannulated for retrograde cardioplegia. CPB is established, with cardiac indices of 2.0 to 2.5 L · min–1 · m–2, systemic cooling is initiated immediately, and the left ventricle is vented via the right superior pulmonary vein. As CPB is started, the ascending aorta is crossclamped in its midportion, a few centimeters above the sinotubular junction, and opened. The heart is covered with cold saline solution. Cold blood cardioplegic solution is administered either retrogradely via the coronary sinus at 250 mL/min or retrogradely plus antegradely (350 mL/min) through the nondissected coronary ostium, for a total of 4 minutes, with coronary sinus pressures nearing 40 mm Hg. The dose is repeated every 15 to 20 minutes during systemic cooling and rewarming. During the cooling period, the aorta is freed from the pulmonary artery and transected above the aortic commissures. The presence and the extent of the dissection, in relation to the coronary ostia, are then assessed. In the event that one or two coronary ostia are torn by proximal dissection, repair is accomplished after completion of the distal anastomosis.
By means of an open technique, the intimal tear is resected and the dissected layers of aorta are reapproximated with gelatin-resorcin-formalin glue at the site of the distal anastomosis. Systemic cooling is considered adequate for hypothermic circulatory arrest when the nasopharyngeal temperature has reached 20°C and the bladder temperature is below 28°C. The dissected aortic valve commissures are resuspended if the valve can be preserved, or else the valve is replaced with a composite graft conduit. Normothermic controlled reperfusion is administered either antegradely or retrogradely for 20 minutes after the completion of proximal repair, before crossclamp release. The heart is vented and assisted throughout the controlled reperfusion and at least for an additional 30 minutes after completion of controlled reperfusion.
Before any attempt at weaning from CPB, a precise assessment of the regional contractility and of the extent of the myocardial damage is obtained with the aid of transesophageal echocardiography. The presence of ventricular arrhythmias may represent an expression of reperfusion injury and should lead to the continuance of CPB with the heart vented.
Techniques of coronary repair
The technique of repair depends on the type and the extent of the lesion and on which coronary artery is involved. If the dissection has reached the ostium without disrupting the coronary vessel (type A), the coronary ostium is repaired with a continuous 6-0 over-and-over suture conjoining the dissected arterial layers, leaving the ostium in continuity with the aortic wall. In ostia completely surrounded by the dissection, or in the presence of extremely fragile tissues, we prefer to excise the ostium in button form with a 4-mm margin of the surrounding aortic wall (Fig 2). The dissected aortic layers of the ostial button are then conjoined with gelatin-resorcin-formalin glue and an over-and-over 6-0 suture: attention is paid to not put glue inside the layers of the coronary artery to avoid secondary stenosis. The ostial button then is anastomosed to the tube graft without torsion or tension.
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The extent of the lesion is assessed by freeing the coronary artery, to a variable extent, along its course. In the case of left main coronary artery dissection, it may be necessary to divide the main pulmonary artery to visualize the bifurcation between the circumflex and left anterior descending arteries. The typical bluish aspect of dissection on the vessel surface indicates precisely the extent of the lesion.
In the absence of intussusception (type B), the coronary artery is incised longitudinally and patch repair is performed with a continuous 7-0 polypropylene suture conjoining the dissected arterial layers and the patch (Fig 3). The patch can be created with either a saphenous vein or autologous pericardium. In the presence of coronary intussusception (type C), the coronary artery is transected in a nondiseased zone and saphenous vein reconstruction of the vessel is performed with an end-to-end anastomosis (Fig 4). In general, for the left coronary artery, reconstruction is possible only if dissection does not go beyond the left main bifurcation. There are no precise limits for repair of the right coronary artery. However, too long a patch should be avoided because the excess length may result in kinking of the vessel. In the presence of extensive distal dissection, coronary bypass grafting is the only alternative to ostial reconstruction. Saphenous vein grafts are used, because thoracic artery bypass in emergency surgery for acute aortic dissection is not advisable. Polytetrafluoroethylene artificial grafts have never been used in our patients. None of the repaired coronary arteries was treated with a supplemental bypass. Table III summarizes our experience with these techniques.
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Results |
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TopAbstractIntroductionPatients and methodsResultsDiscussionReferences |
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The second patient had a type C lesion of the right coronary artery and right ventricular infarction. He was treated with ascending aorta replacement and saphenous vein bypass grafting of the right coronary artery because of extensive dissection of the vessel. Both of these patients were treated without controlled reperfusion, and cardioplegic solution was administered only at the end of circulatory arrest.
The third patient was admitted after 2 episodes of cardiac arrest. He had signs of anterior myocardial infarction and inferior ischemia due to a type A lesion of a dominant right coronary artery, with malperfusion, and a type C lesion of the left main trunk. He was treated with a composite graft aortic root replacement, direct repair of the right ostium, and left main reconstruction with a short saphenous graft. The patient could not be weaned, after 6 hours of assistance, because of intractable ventricular fibrillation. Two (8.3%) deaths occurred on postoperative days 4 and 10, respectively, as a result of multiorgan system failure caused by a low cardiac output syndrome.
One patient was treated without controlled reperfusion after preoperative left ventricular ischemia. Her type B lesion of the left coronary artery was treated with bypass grafting. She required maximal inotropic support to be weaned from the pump and displayed early postoperative renal and hepatic failure. The other patient was treated with ascending aorta replacement, repair of a type A lesion of the left coronary ostium, causing malperfusion, and short graft reconstruction of the right coronary type C lesion. Postoperative right ventricular failure was associated with a low cardiac output syndrome and multiorgan failure. Necropsy indicated perfect patency of both of the repaired arteries.
As indicated by univariate analysis (Table IV), significant perioperative patient variables correlated to operative mortality were as follows: preoperative ejection fraction less than 0.25 (P < .001), preoperative CK-MB levels (P < .001), presence of ventricular arrhythmias at the end of the procedure (P < .001), persistence of mitral regurgitation at the end of the procedure (P < .001), ejection fraction less than 0.25 at the end of the procedure (P < .001), and postprocedure CK-MB levels (P < .001). The presence of Q waves and the type of coronary lesion were weakly correlated to operative mortality.
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The 19 patients who survived the operation had a mean intensive care unit stay of 6.1 ± 2.6 days, with a mean hospital stay of 15.1 ± 5.1 days.
Follow-up
The 19 patients who survived the operation were observed from 1 to 161 months (mean 48.5 months) after the operation. There were 4 late deaths at 11, 24, 29, and 40 months, postoperatively. Of these, the cause of death in only 1 patient was related to cardiac problems (ventricular fibrillation during hemodialysis); the other 3 patients died of lung cancer, breast cancer, and a car accident, respectively. Three patients were uneventfully reoperated on for secondary aortic valve regurgitation. Fifteen patients are alive in New York Heart Association functional class I (4 patients), class II (6 patients), and class III (5 patients).
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Discussion |
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TopAbstractIntroductionPatients and methodsResultsDiscussionReferences |
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Our approach is based on the concept that repair of torn coronary arteries is preferable to coronary bypass grafting. The rationale for this attitude resides in both technical and hemodynamic considerations. The advantages are as follows: (1) Reconstruction of the coronary ostia is anatomic, and it avoids extensive revascularization on vessels whose diameter, importance, and status are often undetermined; (2) it avoids ligature of the coronary ostium and the consequent complete graft-dependent perfusion of large territories of the myocardium; and (3) it provides antegrade flow in the coronary tree, thus avoiding the risk of competitive flows 5 and of coronary redissection. The latter point is of particular importance to us. In 2 cases of right coronary artery reconstruction for type B lesions, we have found distal re-entries some millimeters distal to the ostium. If we had performed bypass grafting, we could not exclude that a local re-entry would have determined a redissection along the artery, beyond the site of anastomosis, favored by the pressure on the proximal stump.
Development of the technique was stimulated by the dismal results with coronary artery bypass grafting observed at the beginning of our experience (Table V). At that time we regarded the ligature of the coronary ostia and the diversion of blood through the bypass grafts as causes of failure. Subsequent developments in myocardial protection and the clinical application of the concepts of myocardial resuscitation 6,7 greatly improved the results in these operations without diverting our efforts to ensure anatomic reconstruction of the coronary tree. The results obtained with this approach demonstrate that coronary repair is feasible in most cases (Tables III and V) and that the integrated approach of coronary reconstruction and aggressive myocardial management provides encouraging results (Table V).
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Composite graft replacement of the aortic root for reimplantation of the restored coronary orifices has been extensively applied in this series, mostly because of the high incidence of bicuspid aortic valves (10 patients). We now prefer to perform aortic valve–sparing techniques when possible. The results with the Yacoub technique in 4 patients are encouraging even though 1 patient required reoperation.
Distal repair with hemiarch replacement is our standard approach in patients with aortic dissection; the technique was used in the last 20 patients of this series without particular complications.
In recent years, progress in noninvasive diagnostic techniques, in particular transesophageal echocardiography, allows aortic dissection to be diagnosed accurately and the extension of the dissection, the presence and the degree of valvular regurgitation, and the entity of myocardial impairment to be evaluated precisely.
If angiography is no longer needed to establish or confirm the diagnosis of acute dissection, it still represents the gold standard to evaluate the coronary anatomy and to discriminate acute CAD caused by ostial involvement from chronic CAD. Nevertheless, the role of coronary angiography before emergency repair of acute aortic dissection is controversial. A recent article by Penn and colleagues 8 indicates that determination of coronary anatomy has no impact on survival. Rizzo and coworkers 9 found angiography to be associated with increased mortality owing to aortic rupture during the delay to surgical intervention.
We have found an intrinsic difficulty in performing coronary angiography in patients with coronary malperfusion because of their hemodynamic instability. Moreover, the visualization of the coronary tree may be suboptimal because of flow obstruction, as we observed in 3 of the 8 patients who have undergone preoperative coronary angiography. Nevertheless, we are convinced of the necessity to obtain information about coronary anatomy in patients with aortic dissection and, in particular, in those with coronary malperfusion. Intraoperative coronary angiography is now possible and its routine application in patients with aortic dissection will allow these difficulties to be overcome.
Interestingly, in our series none of the patients had evidence of occlusive CAD: this finding is in variance with the results of studies about CAD in patients with type A aortic dissection, which reported a prevalence between 22% and 35%. 10,11 To explain this circumstance, we hypothesized that chronic CAD, in particular at the origin of the coronary artery, could somehow protect from extensive dissection.
In the absence of coronary angiography, electrocardiography maintains its importance in topographic evaluation of malperfused myocardium. We observed that preoperatively the location of Q waves accurately correlated with wall motion abnormalities and with the actual coronary involvement, thus giving precious information about the degree of functional coronary impairment. Postoperatively, the correlation between topography of Q waves and wall motion abnormalities was less specific, suggesting that electrocardiographic signs may persist also in areas of rescued myocardium.
Type B and C lesions were accompanied by the most serious clinical conditions, and Q waves accurately reflected the severity of coronary malperfusion: all 16 patients with preoperative Q waves had at least one type B or C lesion. The survival of 5 of the 9 patients with type C lesions and of 11 of the 12 patients with type B lesions, as well as the weak correlation between mortality and the presence of preoperative Q waves (P = .10), illustrates that the operation effectively reversed severe degrees of malperfusion (Table IV).
In summary, aggressive myocardial resuscitation and early operation are the key factors in the management of these patients. The technical feasibility of coronary repair and its relative safety represent an alternative to bypass grafting, guarantee anatomic reconstruction, and overcome the difficulties of revascularization when a coronary angiogram cannot be obtained.
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TopAbstractIntroductionPatients and methodsResultsDiscussionReferences |
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