Distal Coronary Artery Dissection Following Percutaneous Transluminal Coronary Angioplasty Douglas A. Murphy, M.D., Joseph M. Craver, M.D., and Spencer B. King 111, M.D.
ABSTRACT The most common cause of acute myocardial ischemia following percutaneous transluminal coronary angioplasty is coronary dissection, which characteristically remains localized to the site of balloon dilation. In this article, however, we report on 4 patients in whom percutaneous transluminal coronary angioplasty was complicated by coronary artery dissection extending distally beyond the site of anticipated vein graft anastomosis. Intraoperative diagnosis of distal coronary dissection is suggested by a characteristic appearance of the artery and confirmed by the finding of true and false lumens at the time of coronary arteriotomy. Successful revascularization is achieved by anastomosis of a vein graft to the true lumen with reapproximation of the dissected arterial layers. Proximal coronary artery ligation in this setting is unnecessary. Coronary artery dissection is the most common cause of acute myocardial ischemia in patients undergoing percutaneous transluminal coronary angioplasty [1, 21. Morphologically, such dissections are thought to arise from an intimal fracture at the site of balloon dilation of the atherosclerotic plaque [3]. Dissections originating at the angioplasty site have characteristically been limited to the immediate vicinity of the atherosclerotic lesion undergoing instrumentation [2]. This limitation of dissection may relate to fibrosis of the arterial wall surrounding the atherosclerotic process (31. However, distal propagation of coronary dissection after angioplasty does occur [4]. We have encountered 4 patients with acute myocardial ischemia after transluminal angioplasty who at operation were found to have coronary artery dissection extending distally beyond the point of anticipated vein graft anastomosis. The mechanism of arterial injury and the pathophysiology of these distal coronary dissections may differ from those of the localized dissection occurring at the angioplasty site. Successful emergency revascularization of patients with distal coronary dissection requires intraoperative recognition and modified technical management.
From the Joseph 8. Whitehead Department of Surgery and the Department of Medicine, Emory University School of Medicine, Atlanta, GA. Accepted for publication Dec 12, 1983. Address reprint requests to Dr.Murphy, Emory University Clinic, 1365 Clifton Rd, NE, Atlanta, GA 30322.
473
Case Reports Patient 1 A 53-year-old man was admitted to the hospital for transluminal angioplasty of a proximal left anterior descending (LAD) coronary artery stenosis 1 month after an anterior subendocardial infarction. Balloon angioplasty of the lesion shown in Figure 1 was performed using techniques described previously [5]. Following an uneventful angioplasty, there was no pressure gradient across the lesion. Thirty minutes after completion of the procedure, chest pain developed and there was elevation of the anterior lead ST segment on the electrocardiogram. Immediate coronary angiography revealed total occlusion of the LAD coronary artery at a point distal to the balloon angioplasty site (Fig 2). Intraaortic balloon pumping was initiated, and emergency revascularization was performed. At operation, the anterior left ventricular wall was dusky in color and hypokinetic. The LAD artery was dark blue in color nearly to the apex of the heart. Following the administration of cardioplegic solution into the aortic root, the LAD artery was opened in its middle portion and a false lumen filled with a bloody fluid was revealed. The true lumen then was opened by a second arteriotomy. A vein graft was sutured to the true lumen incorporating all layers of the dissected vessel. Carefully placed stay sutures of 7-0 monofilament were used to reapproximate the dissected vessel wall layers during the anastomosis. A second vein graft was anastomosed to the diagonal coronary artery. Following performance of proximal anastomoses, flow was established through the vein grafts and prompt improvement in left ventricular anterior wall color and motion was noted. Proximal ligation of the dissected coronary artery was not performed. The ECG indicated only minor loss of anterior wall R wave voltage postoperatively. Cardiac catheterization performed eight days postoperatively showed a left ventricular ejection fraction of 0.68, patent vein grafts, and obliteration of the false lumen in the LAD artery proximal and distal to the site of vein graft anastomosis (Fig 3). The proximal coronary artery remained patent. The padent was asymptomatic 15 months after the procedure. Patient 2 A 61-year-old man was admitted with a 7-month history of angina. Coronary angiography revealed a stenotic lesion of the proximal LAD coronary artery with normal
474 T h e Annals of Thoracic Surgery Vol 37
No 6 June 1984
Fig I . (Patient 1 .) Angiogram done prior to balloon angioplasty showing stenotic lesion of left anterior descending (LAD) coronary artery (arrow).
Fig 2. (Patient 1 . ) Angiogram done after balloon angioplasty. Total occlusion of the LAD artery (arrow) occurred distal to the site of balloon inpation. At operation, a distal dissection of the LAD artery was found.
left ventricular function (Fig 4). Transluminal angioplasty of the lesion was performed with a reduction in the gradient across the atherosclerotic lesion to 0 mm Hg. Immediately following this seemingly successful angioplasty, the patient complained of chest pain, ST segment elevation was noted in the anterior ECG leads, and the systolic blood pressure fell to 70 mm Hg. Coro-
Fig 3 . (Patient 1 J Postoperative angiogram shuwing a patent vein graft to the LAD artery. Proximal flow in the native artery is apparent from filling of the large diagonal branch (arrow).
nary angiography demonstrated a dissection of the LAD artery beginning at a point distal to the angioplasty site. Intraaortic balloon pumping was initiated, and the patient was transported to the operating room. At operation, the anterior left ventricular wall was noted to be discolored and very firm, suggesting an ischemic contracture of the muscle in the distribution of the injured artery. The LAD artery was dark blue in color and remained so after cross-clamping and administration of crystalloid cardioplegic solution. Arteriotomy in the LAD artery revealed the suspected distal coronary dissection. The false lumen was filled with bloody fluid, while the true lumen contained only clear cardioplegic solution. A vein graft was sutured to the true lumen of the artery using the same technique used in Patient 1. A second vein graft was performed to a diagonal coronary artery arising from the LAD artery proximal to the dissection process but distal to the known atherosclerotic lesion. With establishment of flow in the vein graft, there was improvement in the color and function of the anterior left ventricular wall. Proximal ligation of the coronary artery was not performed. The patient’s postoperative course was unremarkable, and an ECG showed no evidence of myocardial injury. Cardiac catheterization performed eight days after operation demonstrated patent vein grafts, obliterationof the false lumen in the LAD artery proximal and distal to the vein graft anastomosis, and patent proximal coronary arteries (Fig 5). Left ventricular function was normal. He remained well 6 months after operation.
475 Murphy, Craver, and King: Coronary Artery Dissection following PTCA
A
B
Fig 4. (Patient 2.) Angiograms performed prior to balloon angioplasty. (A)Right anterior oblique view of a LAD artery stenosis. (B)Left anterior oblique view of the same lesion (arrow).
A
B
Fig 5. (Patient 2.) Postoperative coronary angiograrns. (A)The saphenous vein graft is patent, and there is obliteration of the false lumen proximally and distally within the native artery. (B)Note patent proximal LAD artery with runofl into the first septal perforator (arrow).
Patient 3 A 40-year-old man was admitted to the hospital with angina and a history of a recent inferior myocardial infarction. Cardiac catheterization demonstrated stenotic lesions of the proximal right and circumflex coronary arteries and inferior left ventricular hypokinesis. The patient underwent transluminal angioplasty of the circumflex lesion shown in Figure 6. Following balloon
476 The Annals of Thoracic Surgery Vol 37 No 6 June 1984
ginal branches seen in Figure 7 was discolored and remained so after administration of crystalloid cardioplegic solution into the cross-clamped aortic root. Arteriotomy into the discolored marginal branch revealed a false lumen containing bloody fluid and a true lumen containing only cardioplegic solution. Vein graft anastomosis was performed as described in the two previous case reports. Vein grafts were also performed to the nondissected marginal branch and the posterior descending artery. The patient’s postoperative course was uneventful with no evidence of myocardial injury by ECG.The patient refused postoperative coronary angiography. He was asymptomatic 5 months after operation.
Fig 6 . (Patient 3.) Angiogram performed prior to balloon angioplasfy showing stenosis of the circumflex artery (arrow).
Fig 7 . (Patient 3.) Angiogram performed after balloon angioplasfy. Dissection (black arrow) of the circumflex artery occurred distal to the site of balloon inflation (white arrow).
dilation, the pressure gradient across the dilated lesion fell from 72 to 0 mm Hg. Coronary angiography showed a successful dilation of the atherosclerotic lesion, but also noted was a dissection of a large, more distal circumflex marginal branch associated with ischemic chest pain and electrocardiographic ST segment elevation (Fig 7). At operation, the posterolateral wall was found to be contracting poorly. The more anterior of the two mar-
Patient 4 A 67-year-old man was referred for transluminal coronary angioplasty of a proximal LAD coronary artery stenosis (Fig 8). Several hours after successful balloon dilation, which reduced the pressure gradient across the lesion from 50 to 12 mm Hg, chest pain developed. Pronounced ST segment elevation was evident in the anterior chest leads of the ECG. Ventricular fibrillation occurred; the patient was successfully resuscitated but required the insertion of an intraaortic balloon pump for hemodynamic support. At operation, the anterior left ventricular wall was markedly hypokinetic. Following aortic cross-clamping and administration of cardioplegic solution, the LAD artery was opened in its middle portion and a false lumen containing blood was revealed. A second arteriotomy opened a true lumen. Repair of the dissected vessel with anastomosis of a vein graft to the true lumen was carried out as described in the previous case reports. Following completion of the graft, improvement in the anterior ventricular contractions was marked and the patient demonstrated no subsequent evidence of myocardial infarction. Review of the angiograms performed during the transluminal angioplasty indicated that during the procedure, the tip of the guidewire had penetrated the wall of the artery distal to the balloon angioplasty site (see Fig 8). The patient declined postoperative angiography but was asymptomatic eight weeks after operation.
Comment Percutaneous transluminal coronary angiography continues to grow in popularity as a method of treatment for coronary heart disease. Approximately 3 to 7% of patients will require emergency revascularization for acute ischemia following attempted angioplasty [2, 61. All surgeons involved in the cardiac surgical support of angioplasty teams must be familiar with the mechanisms of coronary arterial injury by percutaneous transluminal angioplasty. Distal coronary artery dissection is an unusual complication of transluminal angioplasty, occurring in 7% of patients having angioplasty and requiring emergency revascularization at our institution. Nonetheless, recognition of this entity and proper technical
477 Murphy, Craver, and King: Coronary Artery Dissection following PTCA
B
A
Fig 8. (Patient 4 . ) (A) Angiogram performed prior to balloon angioplasty showing stenosis of the proximal LAD artery. (B)Angiogram performed during balloon angioplasty. Note inadvertent perforation of the distal artery by the tip of the guidmire (arrow). '
-. . .
A
Fig 9. Technique of repair of distal coronary dissection: (A) Initial coronay arteriotomy opens the false lumen. (B)Second arteriotomy opens the true lumen. (0Arterial layers are reapproximated with temporay stay sutures. (D, E ) A running anastomosis is performed to the vein graft, and the stay sutures are removed.
B
478 The Annals of Thoracic Surgery Vol 37 No 6 June 1984
management are mandatory for successful revascularization. The pathophysiology of distal coronary artery dissection following transluminal angioplasty is uncertain, but at least three factors are likely to play a role. First, an intimal flap must be created by arterial trauma, either proximally from the balloon dilation itself or more distally from the tip of the balloon catheter or guidewire. Second, this intimal flap must be acted on by hydrodynamic forces of sufficient strength to propagate the dissection process distally. In this regard, reduction of the pressure gradient across the proximal atherosclerotic lesion by angioplasty may contribute to these hydrodynamic forces in the more distal portion of the artery. Last, the character of the arterial wall may be an important factor, with severely fibrotic arteries being resistant to dissection and less diseased arteries being more susceptible. Recognition of distal coronary dissection is critical to successful management. It may be possible in some instances to recognize angiographically the dissection process extending distal to the site of angioplasty; however, the diagnosis will usually be made in the operating room. The surgeon should suspect this lesion when gross examination of the instrumented artery shows a blue discoloration caused by blood in the false lumen. The diagnosis is then confirmed by coronary arteriotomy, which reveals separation of the arterial wall layers with false and true lumens as depicted in Figure 9. The initial incision into the artery in our 4 patients opened the false lumen only. The true lumen was recognized by the convex rather than concave nature of the posterior wall of the artery. The goals in the surgical therapy of this lesion are to restore flow to the true arterial lumen and to obliterate the false lumen. There are three technical principles that are important to the achievement of these goals. First, the location of the coronary arteriotomy should not be influenced by the suspicion of distal coronary dissection but rather, should be based on the presence of known atherosclerotic lesions. Avoiding a dissection process by making the coronary arteriotomy at a very distal point, where coronary artery diameter is naturally smaller, forces the surgeon to perform a technically more difficult anastomosis; it also may result in inadequate coronary flow and reduce the chances for long-term graft patency.
Second, in performing the anastomosis of the vein graft to the true lumen, the layers of the dissected vessel wall must be reapproximated (see Fig 9). To realign the edges of the arterial wall, we have found temporary stay sutures of 7-0 polypropylene useful during the construction of the anastomosis. Finally, although proximal coronary artery ligation with concomitant vein bypass grafting has been advocated as the treatment for coronary artery dissections [7], we believe such proximal interruption is unnecessary in these patients. Postoperative angiography performed in 2 of our patients demonstrated obliteration of the false lumen, presumably by retrograde and antegrade arterial flow through the vein graft, despite residual patency of the proximal native coronary artery. Since resolution of the dissection process does not seem to be prevented by patency of the proximal native artery, ligation of this vessel involves an unnecessary loss of native coronary artery and serves only to make the distal coronary circulation totally dependent on vein graft patency. Supported in part by a grant from the Wasie Foundation.
References 1. Murphy DA, Craver JM,Jones EL, et al: Surgical revascularization following unsuccessful percutaneous transluminal coronary angioplasty. J Thorac Cardiovasc Surg 84:342,1982 2. Murphy DA, Craver JM, Jones EL, et al: Surgical management of acute myocardial ischemia following PTCA: role of the intraaortic balloon pump. J Thorac Cardiovasc Surg 8 7 3 2 , 1984 3. Block PC, Myler RK, Stertzer S, Fallon IT:Morphology after transluminal angioplasty in human beings. N Engl J Med 305:382, 1981 4. Wood WG: Transluminal coronary angioplasty. N Engl J Med 3051055, 1982 5. Gruentzig AR, Senning A, Siegenthaler WE: Nonoperative dilatation of coronary-artery stenosis: percutaneous transluminal coronary angioplasty. N Engl J Med 301:61, 1979 6. Dorros G, Cowley MJ, Simpson J, et al: Percutaneous transluminal coronary angioplasty: report of complications from the National Heart, Lung, and Blood Institute PTCA Registry. Circulation 67723, 1983 7. Harrison LH, Gregg DL, Itscoitz SB, et al: Delayed coronary artery dissection after angiography. J Thorac Cardiovasc Surg 69:880, 1975