Aortocoronary Dissection Complicating a Percutaneous Coronary Intervention<br />

Small intimal dissections occur frequently after percutaneous coronary intervention (PCI), but are usually associated with a benign course. Following balloon angioplasty, coronary dissection is detected by angiography in 20–40% of cases1–3 and by intravascular ultrasound (IVUS) and angioscopy in 60–80% of cases.4,5 Considering the mechanism of lumen enlargement after percutaneous transluminal coronary angioplasty (PTCA) is predominately stretching of the vessel wall and plaque fracture, non-flow limiting dissections should not necessarily be considered a complication since they are easily treated with intracoronary stenting. Acute spontaneous aortic dissection involving the ascending aorta is a life-threatening condition that warrants urgent surgical therapy. Acute dissection of the ascending aorta complicating diagnostic coronary angiography or PCI is an uncommon but recognized occurrence. Its frequency has been reported to be 0.03–0.06%.6,7 The appropriate therapy and outcome of this rare entity is not well established. We present a case of aortocoronary dissection complicating PCI of the right coronary artery (RCA) and compare our therapy and outcome to previously reported cases. Case Report. A 62-year-old man presented to our hospital with a 1-hour history of substernal chest pressure associated with nausea. His medical history was significant for coronary artery disease (status post-coronary artery bypass grafting), type 2 diabetes mellitus and hypertension. Presenting electrocardiogram (ECG) demonstrated an acute inferoposterior myocardial infarction (MI). He was given thrombolytics with clinical evidence of reperfusion and was transferred to the cardiac intensive care unit. MI was confirmed with a peak troponin I of 35.5 ng/dl. The next day, coronary angiography demonstrated a patent left internal mammary artery graft to the left anterior descending (LAD) coronary artery, patent saphenous vein graft (SVG) to a diagonal branch with an occluded sequential segment to the LAD and a patent SVG to the RCA. The dominant RCA had a 90% mid stenosis and a 95% ungrafted, right posterior left ventricular (RPLV) branch occlusion with Thrombolysis In Myocardial Infarction (TIMI) grade 1 flow. Left ventriculography demonstrated severe hypokinesis of the mid-diaphragmatic segment with preserved overall left ventricular function. Initial plans were for conservative medical management. The next morning, the patient awoke complaining of substernal chest discomfort; ECG demonstrated 4 mm of recurrent inferior ST-segment elevation. Emergent cardiac catheterization demonstrated total occlusion of the mid-RCA with TIMI 1 flow. The RCA was intubated with an 8 French (Fr) Cordis JR 4 guide catheter (Cordis Corporation, Miami Lakes, Florida). A 0.014´´ Balance wire (Advanced Cardiovascular Systems Inc., Temecula, California) was then advanced through the occlusion. A 2.5 x 20 mm Maverick dilation catheter (Boston Scientific/Scimed, Inc., Maple Grove, Minnesota) was positioned in the RPLV and the Balance wire was removed. Intraluminal positioning of the dilation catheter was confirmed by injection of contrast through the central port. A 0.014´´ Luge wire (Boston Scientific/Scimed, Inc.) was advanced into the distal vessel. Following inflations in the distal and mid vessel, the patient was noted to have no-reflow. This was treated with intracoronary adenosine and nicardipine, as well as subsequent balloon inflation in the distal vessel with restoration of antegrade flow. At this point, a long linear dissection extending from the initial lesion in the mid-to-distal RCA to the ostium with contrast extension into the wall of the ascending aorta was noted (Figure 1). Five overlapping BX Velocity Hepacoat stents (Cordis Corporation) were then placed distal to proximal in an effort to cover the dissection and seal the entry port. An emergent transesophageal echocardiogram (TEE) was performed in the cath lab; it demonstrated an aortic intramural hematoma extending 5–7 cm superiorly along the anterior wall from the origin of the RCA. There was no color flow into the false lumen and there was no aortic insufficiency. The heparin was not reversed. Plavix (Bristol-Myers Squibb/Sanofi Pharmaceuticals, New York, New York) 300 mg was given post-procedure and 75 mg daily for 30 days in addition to aspirin 325 mg daily. A computed tomography (CT) scan of the chest later that day demonstrated a focal, type A, thrombosed intramural hematoma extending from 1.5 cm above the RCA to the proximal portion of the aortic arch (Figure 2). A repeat CT scan the following day demonstrated that the intramural hematoma decreased in size (Figure 3). A follow-up CT scan 3 months later demonstrated a normal aorta diameter with no areas of dilation or dissection (Figure 4). Discussion. Aortocoronary dissection is an extremely infrequent complication of coronary angiography or intervention. There are 28 previously reported cases in the literature (Table 1). Of these cases, 89% (n = 25) involved the RCA, 39% (n =11) were secondary to balloon inflation, 14% (n = 4) were due to wire manipulation, 29% (n = 8) were due to guide catheter manipulation, and 2 cases occurred during diagnostic coronary angiography. The mechanism is different than spontaneous aortic dissection and likely involves disruption of the coronary intima followed by subintimal injection of contrast and retrograde dispersion of contrast or blood. The increased incidence of aortocoronary dissections involving the RCA may be due to inherent differences in the histologic structure of the ostia of the RCA and left main coronary artery (LMCA).8 The optimal treatment for this complication is not established. In the previously reported cases, 64% (n = 18) consisted of localized aortic dissections involving the aortic root or ascending aorta and 36% (n = 10) involved more extensive dissections extending to or beyond the aortic arch, or associated with epicardial contrast. Of the cases involving localized aortic dissections, 50% (n = 9) were treated with intracoronary stenting, 44% (n = 8) were treated conservatively and 1 was treated with coronary artery bypass surgery for a LMCA dissection. Ninety-four percent (n = 17) of the patients with localized dissections survived to discharge. One patient died from refractory ventricular fibrillation after suffering an inferior MI. In the 8 patients who received follow-up imaging, the size of the dissection had decreased in all cases. Of the patients with extensive dissection, 80% (n = 8) were treated surgically while 1 was treated with intracoronary stenting and 1 was treated conservatively. Seventy-five percent of the surgically treated patients survived to discharge. The stented patient was noted to have a chronic dissection by CT scan at 6 months and to be asymptomatic at 36 months. The conservatively managed patient expired. It is interesting to note that 2 of the 8 patients with extensive dissections were determined to have cystic medial necrosis by histologic exam. After intracoronary stenting, our patient was determined by TEE to have a localized aortic dissection with no discernable color flow into the false lumen. Thus, a conservative approach of serial non-invasive evaluations of the extent of dissection was pursued. In the current era of coronary intervention, most operators choose to stabilize the lumen of a dissected coronary artery with stenting. Likewise, in the setting of aortocoronary dissection, covering the intracoronary dissection with a stent may seal the entry port of the dissection. This may now be even more effective with the availability of covered stents. IVUS is a powerful tool that can identify coronary dissections not visible by angiography. Although it has not previously been described in this setting, IVUS imaging may help evaluate for complete coverage of the intracoronary dissection, which presumably will prevent further propagation. After the intracoronary dissection is stabilized, attention should be turned to evaluation of the extent of aortic dissection. This can be accomplished immediately in the cath lab with TEE. If initial evaluation demonstrates only localized dissection without flow into the false lumen, then serial evaluation with either TEE, CT or magnetic resonance imaging (MRI) seems most appropriate. However, if initial evaluation demonstrates extensive dissection, particularly if it propagates to an adjacent coronary ostium or into the great vessels or if it is associated with aortic insufficiency, then surgical repair should be considered. In the reports reviewed, only Bae et al. make mention of their use of anticoagulants. They administered ticlid (Bristol-Myers Squibb/Sanofi Pharmaceuticals) and aspirin beginning 1 day post-PCI. In our case, because the dissection was not extensive and flow into the dissection was prevented by stenting, we chose not to reverse the anticoagulation and treated the patient with a standard regimen of Plavix and aspirin.

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