Conservative Management of Ascending Aortic Dissection Caused by Percutaneous Coronary Intervention

ABSTRACT: Despite notable refinements in percutaneous coronary intervention (PCI) techniques, these procedures are still associated with some morbidity and mortality. A case of elective coronary angioplasty is described that was complicated by coronary dissection and ST-elevation myocardial infarction. Subsequent efforts to recanalize the coronary artery resulted in a catheter-induced tear at the origin of the vessel, with proximal extension of the dissection to involve the ascending aorta. Literature relating to this complication (reviewed here) suggests that surgical management may be indicated under the circumstances we describe. However, a conservative approach was adopted in this instance with excellent long-term results.

Key words: aortic dissection, coronary intervention

A case of extensive ascending aortic dissection caused by a percutaneous coronary intervention (PCI) procedure is described. The patient was managed conservatively with a satisfactory outcome. The literature relating to this rare complication of PCI is reviewed. Case Report. A 64-year-old woman was referred to our department for coronary angiography. She had been experiencing effort-related chest discomfort for several months, and a thallium scan was suggestive of myocardial ischemia. Bilateral internal carotid artery stenoses of > 70% had been previously documented, with planned carotid endarterectomy following the recent development of left hemispheric transient ischemic attacks. She also had symptomatic lower limb vascular disease, which was non-critical. Coronary angiography revealed minor left anterior descending and left circumflex disease. The right coronary artery (RCA) was tortuous, with a 90% mid-vessel lesion just beyond a marginal branch. The vessel was quite calcified angiographically. Left ventriculography was normal with an ejection fraction of 70%. In light of the patient’s exercise-limiting angina and scheduled carotid endarterectomy, a decision was taken to proceed with PCI. Despite a significant degree of calcification, it was felt that the vessel was too tortuous to consider high-speed rotational atherectomy of the lesion. Therefore, elective angioplasty was arranged. Arterial access was obtained from the left femoral artery, following a failed attempt to cannulate the right femoral artery. A right femoral vein catheter was also inserted and 10,000 units of intravenous heparin were administered. We had great difficulty finding a guide that would seat adequately in the origin of the RCA, and finally settled on an 8 French (Fr) AL1 Cyber guide (Boston Scientific/Scimed, Inc., Maple Grove, Minnesota), which provided reasonable but not perfect back-up. A 0.014´´ Choice PT wire (Boston Scientific/Scimed, Inc.) was loaded within a 3.0 x 20 mm Bandit balloon (Boston Scientific/Scimed, Inc.) and advanced into the distal part of the RCA. Quite active guide manipulation was required in order to pass the balloon across the lesion. This was twice inflated to 6 atmospheres and then withdrawn. Subsequent angiography revealed a significant coronary dissection at the site of the lesion. We then attempted to deliver three different types of stent, without success. An attempt to pass a perfusion balloon was also unsuccessful. In the course of our efforts to advance the stents, wire position was lost. When position was reestablished the lesion was dilated several more times using a combination of balloons, but we were unable to restore and maintain good anterograde flow. The patient developed significant chest pain and ST segment elevation. At this time, it also became apparent that there was a catheter-induced dissection of the origin of the RCA that extended proximally 7 cm into the ascending aorta (Figure 1). The patient’s blood pressure rose to 160/90 mmHg, but she exhibited no signs of cerebrovascular (or other end-organ) compromise. The case was discussed with a cardiothoracic surgeon. It was concluded that the risks associated with emergent coronary artery bypass grafting and aortic arch replacement in the context of the patient’s carotid disease and evolving myocardial infarction were prohibitively high and it was decided she should be treated conservatively. Therefore, the patient was transferred to the Coronary Care Unit where intravenous sodium nitroprusside was commenced in order to optimally manage her blood pressure. Serial creatine kinase levels peaked at 671 U/L (normal range, 25–195 U/L) and serial electrocardiograms showed evolution of inferior Q-waves. The following morning, a transesophageal echocardiogram was carried out. This showed an ascending aortic dissection involving the origin of the RCA and stopping at the posterior margin of the left main coronary artery, extending 70 mm superiorly. Most of the false lumen appeared thrombosed apart from the superior third. There was no communication detected between the true and false lumen. There was mild central aortic regurgitation, which was known to be longstanding. A very small region of infero-posterobasal akinesia was demonstrated. Four days later the study was repeated, revealing a marked decrease in the size of the dissection. A third transesophageal echocardiogram was carried out six weeks later; it showed no evidence of residual aortic dissection and minimal wall motion abnormalities in the right coronary distribution. At six months, the patient underwent successful carotid endarterectomy without further cardiac complications. In the intervening four years, she has remained well. To the best of our knowledge, this case represents the first report of catheter-induced extensive ascending aortic dissection associated with acute ST-elevation MI to be successfully managed employing a conservative strategy. Discussion. Dissection of the ascending aorta is one of the most lethal of all acute cardiovascular conditions. Arising de novo, it is associated with an in-hospital mortality of up to 20%,¹ and when recognized in time mandates immediate surgical intervention. As a complication of cardiac catheterization it is extremely rare, with an incidence of 0.02–0.03%.^2–4 PCI appears to carry greater risk than diagnostic catheterization, with a risk of 0.07%.⁴ In the largest series to date (43,143 procedures), the incidence was significantly higher in patients undergoing catheterization for acute myocardial infarction, with a risk of 0.19% in this setting.² There have been 21 cases of cardiac-catheter induced aortic dissection reported in detail in the literature to date.^2–13 The mean age of the patients reported is 60 years (range, 42–77 years) and the majority of patients have been male (15/21; 71%). Overall mortality associated with the development of this complication is 9.5% of reported cases. The etiology of this condition is most likely multifactorial. The nature of the coronary lesion to be treated probably has the greatest bearing on the probability of aortic dissection occurring as a result of catheterization. Heavily calcified vessels, which often require more aggressive guiding catheter manipulation in order to deliver coronary balloons and stents (as was the case in our patient), are inherently more likely to result in dissection. Similarly, attempts to electively recanalize total occlusions (with the need for greater device manipulation and potential for luminal damage) may also pose a greater threat than PCI on non-occluded vessels. In addition, over-vigorous hand injection of radiocontrast dye has been alluded to as a potential contributing factor in several case reports,^2,5,6 where it was felt that contrast forcefully injected into a catheter that had probably already pierced the luminal surface may have been the primary dissecting agent. The small number of pathological specimens examined to date do not indicate that marked degeneration of the medial layer of the aorta is a prerequisite for the development of catheter-induced aortocoronary dissection. Pathology has been described in four cases of catheter-induced ascending aortic dissection.^3,7,8 Each has shown evidence of cystic medial necrosis, although where graded was not of any greater severity than which might be expected in otherwise healthy age-matched controls.^14,15 In one instance, a chronic penetrating atherosclerotic ulcer that extended the full thickness through the median layer of the ascending aorta was also noted, but was felt to be a coincidental lesion distinct and unrelated to the dissection of the vessel wall.³ Further pathological studies are required to clarify this issue. The majority of reported cases (17; 81%) have involved the RCA as the culprit vessel, with three cases involving the left system and one case arising from an aberrant conal vessel. The increased occurrence with the RCA appears genuine, as evidenced by the data from 1 series of patients at a single institution where all nine cases described had experienced RCA-related aortic dissection.³ Whether technical or anatomical/physiological differences between the left and right coronary arteries are responsible for this association is unclear. It is possible that the larger ostium of the left main coronary artery (and possibly the manner in which it is engaged) may decrease the incidence of catheter-induced trauma to this vessel. With such a small number of cases described in the literature to date, there are insufficient data upon which to base firm recommendations for prevention and management of this complication. The options reported include urgent surgical intervention, placement of an intracoronary stent at the origin of the culprit vessel or conservative therapy, as was the case with our patient. Of the cases reported in detail, thirteen patients were managed medically and the remaining eight required emergent cardiothoracic surgery. An “extensive” aortic dissection has arbitrarily been defined in the largest reported series to date as one that extends > 40 mm up the aorta from the coronary cusp.³ Applying this definition (using angiographic/echocardiographic images for this purpose in case reports where the extent is not precisely quantified), seven of eight extensive aortic dissections reported in the literature to date have been surgically managed, with two deaths. One patient with an extensive dissection was deemed unsuitable for surgery (due to the extent of dissection and history of prior cardiac surgery) and was successfully managed with a conservative strategy.⁹ However, on this occasion it was possible to deploy stents in the culprit coronary artery, which restored vessel patency and normal anterograde flow at the time the complication was recognized, thus preventing myocardial infarction and sealing the entry-door for the aortic dissection. Of the thirteen patients with dissection limited to 3 Stenting at the site of the presumed entry-door for aortic dissection in the culprit coronary vessel has been attempted in thirteen patients. The stent was successfully deployed angiographically in all of these cases. All patients survived to hospital discharge, and only two patients required subsequent surgery (in one case due to the development of hemopericardium, in the other due to the very extensive nature of the dissection, which had progressed to the aortic bifurcation). Six patients did not undergo coronary stenting as part of the management of this complication. Four of these patients were surgically treated, all of whom had suffered an extensive dissection. The remaining two patients had suffered a limited dissection. In one instance, stenting was not available as a treatment (case report from 1973); in the other, it was not felt to be indicated since the culprit coronary vessel (LAD) was chronically occluded. All six of these patients survived to hospital discharge. We did not place a stent in our patient. With regard to the remaining two cases in the literature, it is unclear whether or not stenting was attempted prior to the emergent surgery that was required in both instances. Both of these patients died An analysis of the case we present and those published previously suggests that the differences between spontaneous and cardiac-catheter related dissection of the ascending aorta may be significant, both in terms of pathophysiology and prognosis, and consequently in terms of optimal management. The critical difference is possibly the condition of the aorta prior to the development of the intimal tear. In spontaneous aortic dissection, significant degeneration of the media is almost universal,¹⁶ facilitating the propagation of any dissection that may occur. It would appear from the limited data to date that this may not be the case in iatrogenic aortic dissection. Another notable difference is the entry site for the aortic dissection, and the setting in which this occurs. The fact that a coronary-based dissection may be effectively sealed by stenting within minutes of this complication developing should limit the potential for further propagation. It is possible that occlusion (acute or chronic) of the coronary vessel with resultant diminished flow across the lesion may also effectively “seal” the entry door. The excellent results in patients with limited dissections and successful stenting indicate that the recommended surgical treatment for spontaneous ascending aortic dissection may indeed be inappropriate in these circumstances. Careful surveillance with optimal blood pressure control and appropriate imaging could be used to ensure stability and healing of the dissection. Serial transesophageal echocardiography studies certainly showed this in our patient. In the case of more extensive dissection, the evidence to date indicates that a surgical approach is preferred (7/8 patients, mortality 29% at 30 days). However, the case we report demonstrates that under unfavorable circumstances extensive ascending aortic dissection may be successfully managed employing a conservative strategy.