Acute myocardial infarction (MI) due to extension of

Coronary Malperfusion Due to Type A Aortic Dissection: Mechanism and Surgical Management Koji Kawahito, MD, Hideo Adachi, MD, Sei-ichiro Murata, MD, Atsushi Yamaguchi, MD, and Takashi Ino, MD Department of Cardiovascular Surgery, Omiya Medical Center, Jichi Medical School, Saitama, Japan CARDIOVASCULAR Background. Coronary malperfusion associated with aortic dissection is relatively rare, but when it occurs, it is fatal to the patient. To salvage such moribund patients, aggressive coronary revascularization concomitant with aortic repair is essential. We review the surgical results and mechanism of malperfusion in a group of 12 patients with coronary malperfusion caused by type A aortic dissection, and we discuss our surgical approach. Methods. Between March 1990 and March 2003, 12 patients (6.1%) from a total of 196 consecutive patients with acute type A aortic dissection undergoing surgery suffered coronary malperfusion associated with the dissection. There were 4 men and 8 women (mean age, 60.8 8.3 years). Nine patients had acute myocardial infarction due to dissection before surgery, and 3 patients suffered coronary malperfusion after aortic declamping. Results. Hospital mortality rate was 33.3% (4 patients). The mortality rate was higher than that in patients without coronary malperfusion (33.3% vs. 8.2%, p 0.019). Three patients could not be weaned from cardiopulmonary bypass, and 1 patient died of heart failure in the intensive care unit. Involved coronary arteries included the right coronary artery (8 patients), left coronary (2 patients), and both (2 patients). Mechanisms of coronary obstruction were compression (2 patients), coronary dissection (7 patients), and coronary disruption (3 patients). Coronary artery bypass grafting was performed concomitant with aortic repair. Conclusions. Acute type A aortic dissection with coronary involvement is associated with high mortality rate, aggressive coronary revascularization and early aortic repair with simple techniques are necessary to salvage these critically ill patients. (Ann Thorac Surg 2003;76:1471 6) 2003 by The Society of Thoracic Surgeons Acute myocardial infarction (MI) due to extension of an aortic dissection into the coronary arterial wall or compression of the coronary arteries by a hematoma is a potentially fatal condition [1, 2]. Although surgical outcomes of type A aortic dissection have been improving [3 5], aortic dissection with coronary malperfusion remains a surgical challenge because preoperative diagnosis is not easily made, even during surgery [6, 7], and the mortality rate is high. To salvage critically ill patients with this problem, prompt coronary revascularization and concomitant surgical repair of the aorta are essential. Only a few reports have discussed the mechanisms of coronary malperfusion and surgical management, however [7, 8]. We have been performing aggressive myocardial revascularization for coronary dissection resulting from type A aortic dissection. In the present study, we review our experience with aortic dissection involving the coronary artery, experience that has evolved over a 10-year period with 196 consecutive acute type A dissections, and report the results of a selected group of 12 patients with coronary malperfusion due to acute type A aortic dissection. Accepted for publication May 14, 2003. Address reprint requests to Dr Kawahito, Department of Cardiovascular Surgery, Omiya Medical Center, Jichi Medical School, Amanuma 1-847, Saitama 330-8503, Japan; e-mail: kawahito@omiya.jichi.ac.jp. Patients and Methods Patients Between March 1990 and March 2003, 12 patients (6.1%; 4 men and 8 women; mean age, 60.8 8.3 years) from a total of 196 consecutive patients (111 men and 85 women) with type A aortic dissection undergoing surgery at Omiya Medical Center, Jichi Medical School, suffered coronary malperfusion due to dissection. Urgent operations were performed within 48 hours of acute onset in all 196 patients. Among these 196 patients, 9 patients (4.6%) had, on admission, acute MI due to dissection that was defined on the basis of new ST-segment elevation more than 0.1 mv, abnormal left ventricular wall motion on echocardiogram, and significant elevation of serum creatine kinase (CK) before surgery. Three other patients (1.5%), who had no signs of myocardial ischemia before surgery, developed myocardial ischemia caused by dissection after aortic declamping. In these 3 patients, coronary malperfusion was diagnosed by intraoperative transesophageal echocardiogram, postoperative coronary angiogram, or at autopsy. To reduce diagnostic time to a minimum, we do not perform preoperative coronary angiography; however, 4 of the MI patients were transferred to our hospital after coronary angiography (these patients were misdiagnosed with primary MI, and thrombolytic therapy, which is absolutely contraindicated in aortic dissection, had been given in 2 patients). 2003 by The Society of Thoracic Surgeons 0003-4975/03/$30.00 Published by Elsevier Inc doi:10.1016/s0003-4975(03)00899-3

CARDIOVASCULAR 1472 KAWAHITO ET AL Ann Thorac Surg CORONARY MALPERFUSION DUE TO AORTIC DISSECTION 2003;76:1471 6 Chronic coronary artery disease (CAD) was evaluated by epicardial palpitation in all patients at surgery. Furthermore, preoperative coronary angiography was performed in 4 patients, postoperative coronary angiography in 2 patients, autopsy in 3 patients, and postoperative three-dimensional computed tomography for coronary arteries in 2 patients. The remaining 1 patient was evaluated by epicardial palpitation and probing of the coronary orifices from within the opened ascending aorta at surgery. No signs of chronic CAD were found in these 12 patients. Two patients with chronic CAD who suffered coronary malperfusion were excluded from this study. One patient required cardiopulmonary resuscitation and percutaneous cardiopulmonary support before surgery. New ST elevation and abnormal left ventricular wall motion were observed after aortic declamping. This human could not weaned from cardiopulmonary bypass due to deep cardiogenic shock. He had a history of MI, and epicardial palpitation during surgery indicated chronic CAD. Although coronary malperfusion was suspected, we excluded him from this study because we could not confirm myocardial ischemia attributable to dissection. The other patient had history of angina pectoris and was suspected of having chronic CAD before surgery. He had undergone preoperative coronary angiography and was diagnosed as having severe three-vessel disease. His clinical presentation had indicated acute myocardial ischemia, and intraoperative findings strongly suggested ischemia caused by chronic CAD. He underwent ascending aorta replacement concomitant with coronary artery bypass grafting (CABG) using bilateral internal thoracic arteries. These 2 patients were excluded from this study because myocardial ischemia might have been attributable to chronic CAD. Clinical characteristics of the 12 patients with coronary malperfusion are listed in Table 1. Most of the patients with MI (n 9) were hemodynamically unstable and moribund at admission. Eight of these MI patients suffered deep cardiogenic shock, and 5 patients required cardiopulmonary resuscitation. In the patients in whom coronary malperfusion occurred during surgery (n 3), preoperative hemodynamics were stable. Average peak CK-MB level was 302 346 IU/L (median 147 IU/L, range 4 to 1000 IU/L). Electrocardiogram (ECG) changes and wall motion abnormalities on preoperative or intraoperative echocardiography revealed inferior ischemia in 8 patients, anteroseptolateral ischemia in 2 patients, and global ischemia in 2 patients. None of these 12 patients had diabetes, chronic obstructive pulmonary disease, or history of cerebral infarction. Hypertension was observed in 8 patients and Marfan syndrome in 1 patient. Mechanisms of Coronary Dissections According to the Neri definition of coronary malperfusion in acute aortic dissection [8], we differentiate among three types of lesions based upon operative findings: type A, ostial dissection is defined as a disruption of the inner layer limited to the area of the coronary ostium; type B, Table 1. Clinical Characteristics of Patients Number Age 60.8 8.3 Male/female 4/8 Preoperative myocardial 9 infarction Shock 8 Resuscitation 5 Acute aortic regurgitation 0 ( 3) Ascending aorta 6cm 3 Cardiac tamponade 2 Rupture 0 Neurologic deficit 2 Preoperative peak creatine kinase (IU/L) 4594 4158 (median 4038, range 72 12538) Preoperative peak creatine kinase-mb (IU/L) 302 346 (median 147, range 4 1000) Preoperative coronary 4 angiogram Other organ ischemia 3 leg: 2, kidney: 1 Onset to surgery (hours) 13.9 17.4 (median 6, range 2 48) Location of myocardial ischemia Inferior 8 Anteroseptolateral 2 Global 2 dissection extending into the coronary artery; and type C, coronary disruption (intimal detachment). Type A is a coronary artery occlusion resulting from compression by the bulging dissected false lumen or by secondary extravasation of blood into the pericardial or perivascular tissues. Type B is a retrograde extension of the dissection into the coronary arterial wall. The mechanism of this coronary obstruction has been attributed to compression by the enlarged intracoronary false lumen. Type C is the most severe type of coronary dissection. The coronary artery is detached from the aortic root, and malperfusion is produced by direct coronary obstruction. Surgical Procedures All procedures were done on an emergent or urgent basis within 48 hours after onset (emergent surgery within 10 hours in 10 patients and urgent surgery within 11 to 48 hours in 2 patients). Operative techniques used on and intraoperative data from the 12 patients are summarized in Tables 2 and 3, respectively. The procedures consisted of a median sternotomy with standard cardiopulmonary bypass. A femoral or axillary artery was used for arterial cannulation, and the right atrium was cannulated with a single atriocaval cannula. A left ventricular drain was inserted through the right upper pulmonary vein. From 1998, 2 million units of aprotinin were administered before initiation of extracorporeal circulation. The patients with MI on admission (n 9) were treated

Ann Thorac Surg KAWAHITO ET AL 2003;76:1471 6 CORONARY MALPERFUSION DUE TO AORTIC DISSECTION Table 2. Operations Number Ascending aorta replacement 1 CABG to RCA 7 CABG to RCA Ax-F bypass 1 CABG to LAD 2 CABG to RCA & LAD 1 Ax-F axillary-femoral artery; CABG coronary artery bypass grafting; LAD left anterior descending branch; RCA right coronary artery. for ischemia early. Once cardiopulmonary bypass was established, systemic cooling was initiated. The heart was covered with cold saline solution. After the onset of ventricular fibrillation, the ascending aorta was clamped and opened. The presence and the extent of the primary tear in relation to the coronary artery ostia were assessed. In the event that the primary tear involves both coronary ostia or annuloaortic ectasia is observed, we usually replace the aortic root with a composite graft conduit. However, no patients in this study required root replacement. For myocardial protection, cold blood cardioplegic solution was administered either retrogradely through coronary sinus or retrogradely plus antegradely through the nondissected coronary ostium. Lesions causing regional ischemia were grafted with saphenous veins. After that, intermittent myocardial protection was administered down the newly placed vein grafts and nondissected coronary ostium. After treating ischemia, aortic replacement was performed. Myocardial protection was administered every 20 minutes during systemic cooling and rewarming. In the patients in whom coronary malperfusion occurred after declamping (n 3), coronary grafting with saphenous veins was performed during rewarming in 2 patients (the third patient was diagnosed as having coronary malperfusion at autopsy). The low output syndrome observed in these 3 patients after declamping was possibly the result of myocardial ischemia. Precise assessment of regional contractility and extent of myocardial damage obtained with transesophageal echocardiography suggested that coronary malperfusion was due to dissection. 1473 technique always included the interpositioning of a tubular woven collagen-impregnated or albumin-sealed graft with Teflon strip reinforcement of the aortic stump. Gelatin-resorcin-formalin adhesive was not used. If the intimal tear was present or extended to the aortic arch, we partially or totally replace the arch using selective cerebral perfusion; however, no patients in this study required arch replacement. When the site of the intimal tear could not be identified, we simply replaced the ascending aorta. Coronary Revascularization In all patients with coronary dissection, we performed CABG with saphenous veins and did not perform local coronary repair or reimplantation (Table 2). We prefer not to operate on extremely fragile proximal coronary arteries because of the potential danger and problems involved. When the primary tear was limited to that occurring above the coronary ostia, the proximal stump was trimmed with Teflon strips just above the coronary ostia, and CABG to the involved coronary artery was performed using a saphenous vein graft. If the coronary artery was disrupted or the primary tear involved the coronary ostium, proximal trimming was performed below the coronary ostia and the coronary artery was sacrificed. The proximal end of the saphenous vein graft was directly anastomosed to the aortic graft. Statistical Analysis Statistical analysis consisting of the Fischer s exact test, the Kaplan-Meier method, and log rank test (Mantel-Cox test) was performed with StatView 5.0 (SAS Institute Inc, Cary, NC). Results Type of Coronary Dissection Type A coronary malperfusion was found in 2 patients, type B in 7 patients, and type C in 3 patients. Involved coronary arteries included the right coronary in 8 patients, the left coronary in 2 patients, and both in 2 patients. CARDIOVASCULAR Aortic Repair Aortic repair was performed by means of an open technique. The proximal stump was trimmed and reinforced with a Teflon strip. The dissected aortic valve commissures were resuspended if the valve could be preserved. The arch was explored under hypothermic circulatory arrest at a rectal temperature of 20 C. If the intimal tear was found in the ascending aorta, the tear was resected, and we simply replaced the ascending aorta by an open technique under circulatory arrest. After finishing the distal anastomosis, the graft was clamped and cardiopulmonary bypass was restarted; the proximal anastomosis was then done. The patients were rewarmed by antegrade or retrograde perfusion. The aortic replacement Table 3. Intraoperative Data Mean Range (median) Operation time (hours) 8.29 2.51 5.17 12.17 (8.21) CPB time (hours) 3.53 1.25 1.93 5.65 (3.35) Circulatory arrest (min) 32.8 7.5 24 46 (32) Blood transfusion (U) 37 30 0 102 (34) Site of primary aortic tear Ascending 7 Arch 0 Descending 5 CPB cardiopulmonary bypass.

CARDIOVASCULAR 1474 KAWAHITO ET AL Ann Thorac Surg CORONARY MALPERFUSION DUE TO AORTIC DISSECTION 2003;76:1471 6 Table 4. Hospital Mortality, Cause of Mortality, and Morbidity Number Mortality 4 Cause of death Heart failure 4 Morbidity Re-exploration 1 Right heart failure 1 Cerebral infarction/bleeding 2 Respiratory failure 1 Renal failure 1 Leg ischemia 1 Fig 1. Kaplan-Meier curves illustrating long-term survival rate in patients with and without coronary malperfusion. Hospital Mortality Overall hospital mortality (33.3%, 4 of 12 patients) and morbidities are illustrated in Table 4. The mortality rate was higher in patients with coronary malperfusion than in patients without coronary malperfusion (8.2%, 15/184, p 0.019). Three patients could not be weaned from cardiopulmonary bypass and died in the operating room; 1 patient died of heart failure in the intensive care unit. The first of these 4 patients had a massive acute MI before surgery, and intraoperative findings revealed that both coronary arteries were disrupted (type C). She required cardiopulmonary resuscitation before surgery and was moved to the operating room on a percutaneous cardiopulmonary support system. The second patient suffered cardiac arrest and required cardiopulmonary resuscitation before surgery. Postmortem examination revealed type B coronary dissection in the right coronary artery. The third patient, who had no symptom of ischemia before surgery, went into cardiogenic shock after completion of the ascending aorta replacement and died on bypass. Postmortem examination revealed dissection of both the right and left coronary arteries (type B). The fourth patient presented with deep cardiogenic shock on admission and required controlled ventilation before surgery. He had a type C dissection of the right coronary artery with inferior MI and severe right lower leg ischemia. Although he was treated with ascending aorta replacement, CABG to the right coronary artery and aortobifemoral bypass, he did not recover from shock and died on the eighth postoperative day. Morbidity Of the 8 surgical survivors, 1 patient suffered cerebral infarction and 1 patient had cerebral bleeding (the first patient recovered well and was discharged from hospital without neurologic deficit; the second remained hemiplegic). One patient suffered prolonged heart failure and required long hospitalization. Postoperative hemorrhage necessitating reoperation developed in 1 patient, and 1 patient required an additional femorofemoral bypass because of progression of right leg ischemia. One patient had prolonged respiratory failure, and 1 patient suffered renal failure requiring temporary hemodialysis (Table 4). Follow-Up The 8 operative survivors were observed during a 1- to 76-month follow-up period (mean 22 26 months). During follow-up, 1 patient died of bleeding during urologic surgery at 55 months after aortic surgery. The 7 other patients have suffered no late events including reoperation, heart failure, or cerebrovascular accidents. The actuarial survival rate including hospital mortality was 66.7% 13.6% at 1 year and 33.3% 24.5% at 5 years (Figure 1). The actuarial survival rate was lower in patients with coronary malperfusion than in those without it (p 0.010, Mantel-Cox test). Comment Although coronary malperfusion associated with type A dissection is relatively rare, when it does occur the patient s condition deteriorates rapidly, resulting in death [1, 2]. The incidence of acute myocardial ischemia due to type A aortic dissection has been reported at 5.7% to 11.3% in clinical reports [7, 8] and 7% in autopsy reports [1]. Similar to these previous reports, the current study demonstrated the incidence of coronary malperfusion associated with acute type A aortic dissection to be 6.1% (4.6% in patients with definite MI before surgery). Cambria and coworkers [9] reported four mechanisms of aortic branch obstruction based upon autopsy findings. The basic mechanisms involve bulging of the dissected false lumen at the branch orifice, subsequent distal thrombosis, eventual intimal detachment at the branch orifice, and dissection extending into the branch orifice. In discussing the mechanism of malperfusion caused by coronary dissections, Neri and associates [8] differentiated among three main types of coronary dissection based on extension of the dissection. This classification system is simple and useful when making a decision during surgery. We frequently observed type B and C coronary dissections in patients in this study. In regard to type A coronary involvement, Neri reported that this type may create a local flap and cause coronary malperfusion by a trapdoor mechanism [10, 11]. The type A coronary involvement seen in 2 patients was caused by

Ann Thorac Surg KAWAHITO ET AL 2003;76:1471 6 CORONARY MALPERFUSION DUE TO AORTIC DISSECTION an enlarged false lumen or a perivascular hematoma. Other reports have indicated that the enlarged false lumen or hematoma extension (secondary to extravasation of blood into pericardial or perivascular tissues) may compress the coronary arteries [6, 12]. Coronary malperfusion caused by acute aortic dissection is not easily evaluated even during surgery [6, 7]. We often observe acute aortic dissection that extends to the coronary ostia (especially the right coronary artery); however, it does not always cause myocardial ischemia. Some factors, such as location and size of the primary entry, existence of reentry, and flow pattern in the false lumen, may impact the onset of coronary malperfusion. Furthermore, the condition of the false lumen may change dramatically both proximally and distally after repair of the aortic dissection. When residual flow is created accidentally in the proximal false lumen by a needle hole or intimal cutting by a suture, the false lumen cannot be decompressed. The coronary false lumen may enlarge and obstruct the true lumen during the diastolic phase. Such phenomena cannot be evaluated under static conditions, but they may result in coronary malperfusion when flow is reestablished after aortic declamping. In our experience, the 3 patients who had no signs of myocardial ischemia before surgery developed low output syndrome due to myocardial ischemia after aortic repair. Two of these 3 patients were salvaged by additional beating heart coronary bypass (right coronary artery in 1 patient and left coronary artery in 1 patient). One patient died on bypass because coronary malperfusion was not recognized. Autopsy revealed a global MI caused by extensive right and left coronary dissection. The occurrence of low output syndrome after declamping may be an indication of myocardial ischemia caused by coronary malperfusion. In such instances, left ventricular wall motion abnormalities detected by intraoperative transesophageal echocardiography can be informative, and additional CABG should be performed. Recently, surgical outcomes of type A acute dissection have been improving [3 5]. However, the degree of associated myocardial damage caused by coronary dissection is one of the leading predictors of hospital death. We have reported previously that preoperative ST-T elevation identified on the ECG is a significant independent risk factor for hospital mortality after surgery for acute aortic dissection [5]. Coronary ischemia and concomitant CABG have also been reported to be risk factors for mortality [13, 14]. There were four (33.3%) early postoperative deaths in the current study, and this mortality rate was significantly worse than that in patients without coronary involvement over the same period of study (mortality rate 8.2%, p 0.019). Results suggest, however, that although it carries a high risk, the involvement of the coronary arteries in aortic dissection can be successfully managed by early coronary revascularization concomitant with aortic repair. Although a few reports mention the mechanism of coronary involvement, the strategy for surgical repair and the outcome from surgical repair of coronary dissection in regard to surgical management of coronary dissection have not been fully investigated. Neri and colleagues [8] treated 24 dissected coronary patients from a total of 211 patients with acute type A dissections. They preferred repair of dissected coronary arteries over CABG and described various local repair techniques. They mentioned the advantages of local repair to be anatomic reconstruction of the coronary artery ostia, avoidance of complete graft-dependent perfusion of large areas of the myocardium, and preservation of antegrade flow in the coronary trees, thus avoiding the risk of competitive flow and coronary redissection. However, mobilization and repair of acutely dissected coronary arteries is potentially dangerous and problematic. In other reports most patients received CABG and ascending aorta replacement [6, 15]. Our approach is based on the concept that CABG is preferable to local repair because the procedure is simple and less invasive, and, furthermore, recent reports of short- and long-term outcomes of primary CABG are acceptable. However, local coronary repair may be more suitable than CABG for some type A patients. For one of the type A coronary dissections occurring after declamping in this study we simply performed CABG during rewarming. In the other patient, the type A coronary involvement was identified when the aorta was opened. Local coronary repair may be considered for this type of patient. In summary, the overall incidence of coronary malperfusion with acute aortic dissection was 6.1% (12/196 patients) in the present study, and hospital mortality was 33.3% (4/12 patients). Acute type A dissection with coronary involvement is associated with high mortality rate; early coronary revascularization and aortic repair with simple techniques is essential to salvage these critically ill patients. References 1475 1. Hirst AE, Johns VJ, Kime SW. Dissecting aneurysms of the aorta: a review of 505 cases. Medicine 1958;37:217 71. 2. Coselli JS. Treatment of acute aortic dissection involving the right coronary artery and aortic valve. J Cardiovasc Surg (Torino) 1990;31:305 9. 3. Westaby S, Saito S, Katsumata T. Acute type A dissection: conservative methods provide consistently low mortality. Ann Thorac Surg 2002;73:707 13. 4. Takahara Y, Sudo Y, Mogi K, Nakayama M, Sakurai M. Total aortic arch grafting for acute type A dissection: analysis of residual false lumen. Ann Thorac Surg 2002;73:450 4. 5. Kawahito K, Adachi H, Yamaguchi A, Ino T. Preoperative risk factors for hospital mortality in acute type A aortic dissection. Ann Thorac Surg 2001;71:1239 43. 6. Paidipaty BB, Husain M, Puri VK. Right coronary artery occlusion after acute proximal dissection (hematoma). Crit Care Med 1983;11:574 5. 7. Pego-Fernandes PM, Stolf NA, Hervoso CM, Silva JM, Arteaga E, Jatene AD. Management of aortic dissection that involves the right coronary artery. Cardiovasc Surg 1999;7: 545 8. 8. Neri E, Toscano T, Papalia U, et al. Proximal aortic dissection with coronary malperfusion: presentation, management, and outcome. J Thorac Cardiovasc Surg 2001;121:552 60. 9. Cambria RP, Brewster DC, Gertler J, et al. Vascular compli- CARDIOVASCULAR

CARDIOVASCULAR 1476 KAWAHITO ET AL Ann Thorac Surg CORONARY MALPERFUSION DUE TO AORTIC DISSECTION 2003;76:1471 6 cations associated with spontaneous aortic dissection. J Vasc Surg 1988;7:199 209. 10. Shapira OM, Davidoff R. Images in cardiovascular medicine. Functional left main coronary artery obstruction due to aortic dissection. Circulation 1998;98:278 80. 11. Ashida K, Arakawa K, Yamagishi T, et al. A case of aortic dissection with transient ST-segment elevation due to functional left main coronary artery obstruction. Jpn Circ J 2000;64:130 4. 12. Oram S, Holt MC. Coronary involvement in dissection aneurysm of the aorta. Br Heart J 1950;12:10 16. 13. Chirillo F, Marchiori MC, Andriolo L, et al. Outcome of 290 patients with aortic dissection. A 12-year multicentre experience. Eur Heart J 1990;11:311 9. 14. Crawford ES, Kirklin JW, Naftel DC, Svensson LG, Coselli JS, Safi HJ. Surgery for acute dissection of ascending aorta. Should the arch be included? J Thorac Cardiovasc Surg 1992;104:46 59. 15. Tominaga R, Tomita Y, Toshima Y, et al. Acute type A aortic dissection involving the left main trunk of the coronary artery a report of two successful cases. Jpn Circ J 1999;63: 722 4. INVITED COMMENTARY Acute myocardial ischemia or infarction due to retrograde dissection extending into the coronary artery is not uncommon in acute aortic dissection, as witnessed by the 5% 10% incidence of this complication. Although emergent coronary revascularization associated with aortic repair is mandatory to salvage these critically ill patients, few reports have been published so far. Furthermore, it is well recognized that coronary malperfusion requiring concomitant CABG is one of the risk factors for early mortality in acute type A aortic dissection. In 2001, Neri et al described the mechanism of coronary malperfusion in acute aortic dissection and divided it into three groups depending on the extension of coronary artery dissection. Neri claimed that direct coronary artery repair was preferable to CABG. Meanwhile, Dr Kawahito and colleagues advocate that CABG is a useful technique in revascularizing a dissected coronary artery regardless of the mechanism of coronary dissection, even though the number of patients is too small to draw a definitive conclusion. I believe there are two technical issues here when dealing with revascularization of jeopardized myocardium. One is how to protect the myocardium in patients presenting with acute myocardial ischemia or infarction during the operation. Our way follows: after cardiopulmonary bypass is instituted, blood cardioplegia is administered retrograde via the coronary sinus, and also antegrade through the nondissected coronary ostium. Subsequently, after the dissected coronary artery is revascularized, blood cardioplegia is administered through the vein bypass graft. Controlled reperfusion after ischemia seems only rational. The other issue is how to restore blood flow to the jeopardized myocardium. The surgical techniques used vary from local direct coronary repair to CABG, depending on the mechanism of the coronary dissection. Type A lesions with ostial dissection can be directly repaired. On the other hand, type B lesions with a coronary false channel or type C lesions with circumferential detachment and an inner cylinder intussception can both be treated by either direct coronary repair or CABG. If the dissection extends to the distal coronary artery, CABG is preferable to direct coronary repair. CABG can be used in all types of coronary artery dissection, as suggested by Dr Kawahito and colleagues, but its potential disadvantages include complete graftdependent perfusion of the myocardium, risk of closure of the vein graft attached to a woven Dacron graft, competitive flow, and coronary redissection. Even with earlier referral for surgery and enhanced myocardial protection and refined surgical technique, which have all contributed to the improvement of surgical outcomes of acute type A dissection, the salvage rate in patients with extensive myocardial infarction remains dismal and is not likely to improve much. Therefore, it is advisable to establish exclusion criteria for emergency operation in these patients. Teruhisa Kazui, MD, PhD 1st Department of Surgery Hamamatsu University School of Medicine 1-20-1 Handayama Hamamatsu 431-3192 Japan e-mail: tkazui@hama-med.ac.jp 2003 by The Society of Thoracic Surgeons 0003-4975/03/$30.00 Published by Elsevier Inc doi.10:1016/s0003-4975(03)01484-x