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Ann Thorac Surg 1995;59:1030-1035
© 1995 The Society of Thoracic Surgeons


Current Review

Coronary Artery Aneurysms After Angioplasty and Atherectomy

James G. Dralle, MD, Carol Turner, RN, MS, Jack Hsu, MD, Robert L. Replogle, MD

Cardiac Surgery Department, Columbus Hospital, Chicago, Illinois


    Abstract
 Top
 Footnotes
 Abstract
 Introduction
 Case Report
 Comment
 References
 
Coronary artery aneurysm formation after percutaneous transluminal coronary angioplasty and directional coronary atherectomy is unusual. We report the case of a left anterior descending coronary artery aneurysm that formed in such a patient. The left anterior descending coronary artery was bypassed and the aneurysm was plicated with the aid of coronary angioscopy. The English-language medical literature on the topic of coronary artery aneurysms is reviewed.


    Introduction
 Top
 Footnotes
 Abstract
 Introduction
 Case Report
 Comment
 References
 
Over the past several years, surgeons have become quite familiar with the complications of percutaneous transluminal coronary angioplasty (PTCA) and directional coronary atherectomy (DCA). Acute coronary occlusion requiring emergent surgical revascularization occurs in 3% to 7% of all patients [1]. Coronary restenosis requiring surgical revascularization is certainly common. The formation of a coronary artery aneurysm (CAA) after PTCA or DCA, however, is a complication that is not as familiar to most surgeons. We describe a case of CAA formation after DCA and PTCA. The incidence, natural history, and treatment of these PTCA-related and DCA-related CAAs are reviewed.


    Case Report
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 Footnotes
 Abstract
 Introduction
 Case Report
 Comment
 References
 
The patient was a 53-year-old hypertensive woman who initially presented in August 1993 with complaints of substernal chest pain. Coronary angiography showed a 95% stenosis in the proximal left anterior descending artery (LAD). Percutaneous transluminal coronary angioplasty was performed, after which the residual stenosis was only 10%. The patient was subsequently asymptomatic. In October 1993, chest pain recurred and coronary angiography showed an 80% stenosis at the site of the previous LAD angioplasty (Fig 1Go). Directional coronary atherectomy was performed on October 9, 1993, using a 7F atherectomy catheter. There was no residual stenosis (Fig 2Go) and no evidence of coronary perforation. A 0.042-g tissue specimen was submitted for histologic examination, which revealed evidence of intima and media but no evidence of adventitia. The patient experienced no further chest pain until January 1994. Coronary angiography at that time showed a 60% stenosis and a discrete coronary aneurysm at the site of the atherectomy (Figs 3, 4GoGo). The aneurysm was 7 mm wide and 8 mm long, and was located just beyond the first septal perforator and a large diagonal branch. Surgical revascularization was therefore recommended.



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Fig 1. . Angiogram showing restenosis of the left anterior descending artery 2 months after angioplasty.

 


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Fig 2. . Angiogram showing the left anterior descending artery immediately after atherectomy.

 


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Fig 3. . Angiogram showing an eccentric 60% stenosis in the left anterior descending artery just proximal to the aneurysm.

 


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Fig 4. . Angiogram showing the left anterior descending artery aneurysm 3 months after atherectomy. The septal and diagonal branches are immediately adjacent.

 
At operation on February 15, 1994, the aneurysm was found to be bluish and was soft to palpation. The LAD was opened 2 cm distal to the aneurysm and a 1.4-mm Olympus angioscope (Olympus Optical Co, Ltd, Japan) was passed proximally up the LAD. The aneurysm had a completely smooth, white interior and showed no trace of thrombus or atherosclerotic material. At this point, the aneurysm was opened longitudinally (Fig 5Go). The wall of the aneurysm was 1 to 1.5 mm thick and the tissue was firm but not sclerotic. The aneurysm was then plicated with a 7-0 running mattress suture followed by a 7-0 running over-and-over suture, using the angioscope as a stent. Angioscopy showed the walls of the plicated aneurysm to be smooth and its caliber to approximate that of the adjacent distal LAD. The left internal mammary artery was then anastomosed to the LAD. The patient was weaned from cardiopulmonary bypass without difficulty and was discharged home 5 days later.



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Fig 5. . Intraoperative view of the opened, thick-walled left anterior descending artery aneurysm. Note the smooth, white interior devoid of thrombus.

 
After discharge, the patient complained of atypical chest pain thought to be incisional in nature. Results of a postoperative stress test showed no ischemia. Five months postoperatively, the patient underwent repeat coronary angiography (Fig 6Go). The mammary artery graft was found to be widely patent, as were the large septal and diagonal branches. The segment of the LAD from the area that had shown 60% stenosis preoperatively to the mammary artery anastomosis had occluded. There is a threadlike, recanalized lumen that persists into the area where the CAA had been. The patient remains well 7 months postoperatively.




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Fig 6. . (A) Angiograms showing a widely patent left internal mammary artery graft and (B) widely patent first septal and diagonal branches. A threadlike lumen persists into the area of the aneurysm.

 

    Comment
 Top
 Footnotes
 Abstract
 Introduction
 Case Report
 Comment
 References
 
A CAA is defined by the Coronary Artery Surgery Study as a coronary dilatation that exceeds by 1.5 times the diameter of normal adjacent segments or the diameter of the patient's largest coronary vessel [2]. Various authors have used different definitions, and, for this reason, the exact incidence of CAAs after angioplasty and atherectomy is unknown. In a series of 728 patients with complete angiographic follow-up, there was a 3.9% incidence of CAA after PTCA [3]. After DCA, the incidence of CAA ranges from 0.5% to as high as 10% [46]. The Food and Drug Administration approved DCA for use in September 1990. Since then, approximately 80,000 procedures have been performed in the United States (personal communication, Devices for Vascular Intervention, Redwood City, CA). In 1991 alone, 331,000 PTCAs were done in this country [7]. Despite these large numbers, there are relatively few reports of PTCA-related or DCA-related CAAs. A Medline search located only 74 cases that have been reported in the English-language medical literature (Table 1Go).


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Table 1. . Cases of Coronary Artery Aneurysms Related to Percutaneous Transluminal Coronary Angioplasty or Directional Coronary Atherectomy
 
In 1983, Holmes and associates [8] reported the first case of a PTCA-related CAA. The aneurysm resulted from inadvertent balloon inflation in the diagonal artery, and it was found to have remained unchanged at the 6-month follow-up. Since this case, an additional 58 cases of PTCA-related CAA have been reported. In 1991, Bal and colleagues [3] presented the largest series of such patients, consisting of 28 cases with an average follow-up of 64 months. In terms of DCA-related CAAs, there are fewer cases and the follow-up has been shorter. Safian [22] described the first case of DCA-related CAA in 1990. Since then, only an additional 14 cases have been reported. The 1992 report from the Mayo Clinic represents the largest series of DCA-related CAA with the longest follow-up; it consists of only 7 cases with an average follow-up of only 19 months [6]. With the ever-increasing use of these interventional techniques, one would expect this rather limited experience to grow rapidly.

The mechanisms by which CAAs develop after PTCA or DCA are unclear. Different mechanisms may be responsible for causing different types of aneurysms. There appear to be two general groups of PTCA-related and DCA-related CAAs: early and late. The early aneurysms are those diagnosed at or very soon after the original procedure, and likely represent contained perforations, which would make them false aneurysms. van Suylen and associates [23] reported a case of a DCA-related aneurysm in the right coronary artery that ruptured 3 days after the procedure and resulted in tamponade and death. This was found to be a false aneurysm at autopsy. Garrand and co-workers [19] reported on a patient who underwent DCA of the right coronary artery that was complicated by contained perforation. Although the perforation appeared to have sealed the following day, an aneurysm in the right coronary artery was demonstrated angiographically 3 months later. Garrand and co-workers used intravascular ultrasound to characterize this as a false aneurysm. These findings were later confirmed surgically.

The majority of PTCA-related and DCA-related CAAs, however, would be classified as late aneurysms, and they are not associated with coronary perforation at the original procedure. In addition, the interval between the inciting procedure and the diagnosis of the CAA tends to be longer. Whether these also represent false aneurysms or are in fact true aneurysms is almost entirely unknown. There is only a single report in the literature addressing the nature of these late CAAs. Based on the findings yielded by intravascular ultrasound studies, Krolick and associates [25] concluded that a 7.8-mm LAD aneurysm diagnosed 1 month after DCA was a true aneurysm.

Because the nature of these late CAAs is unknown, the particular mechanisms responsible for their formation are largely conjectural. In the case of PTCA-related CAAs, most authors believe that medial damage resulting from either dissection or overexpansion, or both processes, leads to a weakening and subsequent dilatation of that particular segment of the coronary artery. In one series, PTCAs complicated by dissection were reported to be associated with a 9% incidence of CAA, whereas PTCAs without dissection were associated with only a 2.9% incidence of CAA [3]. Other predisposing factors that have been proposed as causes of PTCA-related CAAs have included PTCA of an infarct-related vessel [9] and the use of an oversized balloon [12]. The development of DCA-related CAAs also appears to involve subintimal damage. Recovery of media with DCA occurs in 51% to 67% of procedures whereas recovery of adventitia occurs in up to 30% [22, 27]. In one series, 29% of the patients with DCA-related CAAs had evidence of subintimal resection [6]. In patients without CAA after DCA, there was only a 22% incidence. Fourteen percent of the patients with CAAs underwent adventitial resection as opposed to only 7% of the patients without an aneurysm. The authors of that study concluded that deeper resection was associated with an increased incidence of DCA-related CAA. Therefore, with regard to both PTCA-related and DCA-related late CAAs, subintimal damage appears to be at the very least a contributing factor.

In view of the limited experience with these CAAs, both the natural history of these aneurysms and their ideal management remain to be elucidated. Although there are reports of the successful conservative treatment of early CAAs [8, 21], there is also documented evidence of their propensity to enlarge [19] and rupture [23]. Most of these ``early'' aneurysms have warranted operative intervention consisting of coronary ligation and distal bypass. ``Late'' CAAs after PTCA have been described since 1983. Their natural history appears to be clinically benign. All but one of the 28 late PTCA-related CAAs described by Bal and colleagues [3] were managed medically. The patients remained symptom-free and event-free for a mean follow-up of 64.2 months. Seven of Walford and associates' [14] 8 patients with PTCA-related CAA were successfully managed by medical means for a follow-up period of 20 months. Medical management also appears to be successful in patients with late DCA-related CAAs. Six of Bell and colleagues' [6] 7 patients were managed medically and did well for an average follow-up of 19 months. Safian and associates' [3] original patient with a DCA-related CAA was successfully managed medically and remained well during 11 months of follow-up. In fact, there appears to be a consensus that late PTCA-related and DCA-related CAAs have the ``same good prognosis as aneurysmal coronary artery disease occurring spontaneously in patients with coronary atherosclerosis'' [3]. Therefore, most authors would agree that the mere presence of a late PTCA-related or DCA-related CAA does not constitute an indication for operative intervention at this time.

Of the 74 cases of PTCA-related and DCA-related CAAs reported in the literature, only 16 of the patients involved have undergone operation (Table 2Go). Five of these patients had early CAAs and were operated on for fear of rupture. The remaining 11 patients had late CAAs. The presence of a CAA did not factor into the decision to operate on any of these 11 patients. All 11 had other indications for operation, and this included either restenosis of the affected vessel, progression of multivessel coronary artery disease, or the need for a concomitant cardiac procedure. For this group of patients, there appears to be little consensus as to the optimal approach to the CAA to be used at the time of operation. One patient who required aortic valve replacement underwent aneurysm ligation and distal bypass, with good results [3]. Some authors oppose ligation, however, and advocate only isolated coronary artery bypass grafting. Cohen and co-workers [24] recently reported on a patient with a DCA-related aneurysm of the LAD referred for operation because of LAD restenosis. They ligated the CAA proximally, distally, and posteriorly, but the patient could not be weaned from cardiopulmonary bypass until these ligatures were removed. The authors concluded that attempted ligation of LAD aneurysms may inadvertently sacrifice important septal perforators, and therefore should be avoided. Instead they recommended isolated coronary artery bypass grafting. Prewitt and associates [26] reported 1 case of DCA-related LAD aneurysm with associated restenosis treated by isolated left internal mammary artery grafting. Ueno and colleagues [11] reported 2 cases of PTCA-related LAD aneurysms with associated restenosis treated by isolated saphenous vein grafting. Both patients involved had postoperative angiograms that showed patent grafts with thrombosis of the aneurysms. In the remaining case reports, there was no information offered regarding the specific treatment of the CAA. Therefore, based on the findings from our review, there appear to be proponents of aneurysm ligation with distal bypass as well as proponents of isolated distal bypass. Ligation definitely eliminates all of the potential complications of CAA, including expansion, rupture, thrombosis, or embolization. Given the relatively short follow-up in these patients with CAAs, especially DCA-related CAAs, this is an attractive feature of this approach. However, as Cohen and associates' [24] point out, aneurysm ligation may be hazardous secondary to the inadvertent ligation of important coronary branches. In addition, ligation of a CAA associated with only a mild or moderate stenosis places a larger more immediate demand on the flow reserve of the bypass conduit to the distal coronary artery. Unlike vein grafts, not all mammary grafts may be able to meet this immediate demand. This may be analogous to ligating a stenotic vein graft to a totally obstructed LAD and replacing it with only a mammary artery graft. As Navia and colleagues [28] concluded, this may be ``associated with [an] increased incidence of death and hypoperfusion syndrome.''


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Table 2. . Surgically Treated Coronary Artery Aneurysms Related to Percutaneous Transluminal Coronary Angioplasty or Directional Coronary Atherectomy
 
In our case, we report a different approach to a DCA-related LAD aneurysm. Plication of the CAA was performed easily. By plicating the aneurysm, we believe we diminished the risk of the later complications of a CAA developing, as discussed previously. Plication, as opposed to ligation, may also cause some antegrade coronary flow to be maintained in the perioperative period, thus decreasing the immediate flow demands on the mammary artery graft. If the CAA had contained thrombus and atherosclerotic debris, plication would have been quite hazardous in the event of possible distal embolization. Through the use of intraoperative angioscopy, we were able to demonstrate that the interior of the CAA was smooth and contained no debris or thrombus. With this knowledge, we knew that plication could be performed easily and safely. Which of these surgical alternatives is the best is certainly unknown at this point. Only through greater experience and follow-up will this become clear. It may even be that the optimal surgical treatment will prove to differ for different patients.

In conclusion, early PTCA-related and DCA-related aneurysms, which most likely represent contained perforations, may require early operative intervention consisting of ligation and distal bypass. Late CAAs, however, appear to be more benign. The mere presence of these aneurysms does not at this point warrant operative intervention. The potential role of intravascular ultrasound in the differentiation between true and false aneurysms and whether this distinction has a bearing on prognosis and management remains to be studied. In those patients presenting for cardiac operation with an incidental PTCA-related or DCA-related CAA, the optimal way to handle the aneurysm is unknown. Ligation with distal bypass, plication with distal bypass, and distal bypass alone have all been performed with success.


    Footnotes
 Top
 Footnotes
 Abstract
 Introduction
 Case Report
 Comment
 References
 
Address reprint requests to Dr Dralle, Cardiac Surgery Division, Columbus Hospital, 2520 N Lakeview, Chicago, IL 60614.


    References
 Top
 Footnotes
 Abstract
 Introduction
 Case Report
 Comment
 References
 

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