Aortocoronary Dissection with Acute Left Main Artery Occlusion: Successful Treatment with Emergent Stenting

Case Report. A 65-year-old female with a past history of hypertension, hyperlipidemia, distant tobacco use and coronary artery disease (CAD) presented to an outside hospital with chest pain. Upon arrival to the emergency department, she developed ventricular fibrillation and was promptly defibrillated. Initial electrocardiography (ECG) showed 1 mm ST-segment elevations in leads I and aVL, with inferior ST-segment depressions. The patient was transferred to our hospital for urgent cardiac catheterization. Angiography revealed three-vessel coronary artery disease with thrombus at the origin of the first obtuse marginal (OM-1) branch, and a severe LCx-OM bifurcation stenosis (Figure 1). The LCx-OM system was believed to be the culprit vessel. The patient was chest pain-free, and the option of coronary artery bypass grafting surgery (CABG) was discussed. The patient and her family opted to proceed with percutaneous intervention on the culprit vessel. Heparin and eptifibatide were administered for anticoagulation. A 7 French (Fr) XBLAD 3.5 guiding catheter (Cordis Corp., Miami, Florida) was used. A ChoICE^® PT Extra Support guidewire (Boston Scientific, Natick, Massachusetts) was used to cross OM-1, and a PT Graphix™ intermediate wire (Boston Scientific) was used to cross the LCx stenosis (recanalized total occlusion). The mid-LCx stenosis was predilated using a 2.0 x 15 mm OpenSail™ balloon (Guidant Corp., Indianapolis, Indiana) inflated to 12 atm. Thrombectomy was then performed using an Export^® aspiration catheter (Medtronic, Inc., Minneapolis, Minnesota). Several large thrombi were successfully aspirated. Delivery of the Export catheter required aggressive guiding catheter manipulation. Subsequent angiography revealed occlusion of the left main, with a dissection extending into the aortic root approximately 8 cm above the coronary sinus (Figure 1). Subsequent angiography revealed no flow into the LAD or the LCx arteries. The patient rapidly developed severe chest pain and hypotension, and circulatory collapse appeared imminent. A new ChoICE PT Extra Support guidewire was rapidly advanced across the dissected left main into the LAD with rapid balloon dilation (2.5 x 20 mm balloon) and stenting (2.5 x 23 mm Hepacoat™ stent, Cordis). With the stent positioned in the distal left main artery, extending into the proximal LAD, flow into the LAD was restored and the patient’s hemodynamic parameters stabilized. To contain the expanding aortic dissection, a 4.0 x 13 mm Hepacoat stent was positioned at the left main ostium, overlapping the first distal left main/LAD stent, and was deployed at 14 atm, with an excellent result (Figure 1). Subsequent angiography revealed restored flow across the left main, LAD and LCx arteries. Concurrent with salvage of the left main artery, dopamine and atropine were administered and eptifibatide was discontinued (in anticipation of surgery). A new ChoICE PT XS wire was advanced across the left main into the LCx. Balloon dilatation was performed using 1.5 x 9 mm and a 2.0 x 20 mm balloons. Final angiography revealed a stable angioplasty result in the mid-LCx, with 30% diffuse residual disease. The OM-1 had 20% residual stenosis, with no angiographic evidence of residual thrombus. The 2 overlapping stents extending from the left main ostium to the proximal LAD were widely patent. There remained a visible dissection plane in the left main, which appeared to be stable, with no further extravasation of contrast into the ascending aorta. There was normal flow in the left main, LAD, LCx, and OM-1 (Figure 1). The patient remained hemodynamically stable. Cardiothoracic surgery was consulted for the possibility of urgent CABG and aortic repair. The patient was intubated and transesophageal echocardiography was performed to further assess the extent of the aortic dissection (Figure 2). The dopamine infusion was stopped and intravenous nitroglycerin was started for hypertension. Transesophageal echocardiography showed a small residual ascending aorta dissection and no aortic valve pathology (Figure 2). There was no aortic regurgitation and no pericardial effusion. Repeat hemodynamic evaluation revealed relatively low right-sided filling pressures and a normal cardiac index. The patient was then transported from the catheterization laboratory to the Coronary Care Unit in stable condition. She was discharged home on the third post-procedural day on aspirin 325 mg daily for life, and clopidogrel 75 mg daily for a minimum of 1 year. Repeat coronary angiography at 3 months after the initial procedure showed widely patent left main coronary artery stents. The LCx had a 30% stenosis at the origin of OM (site of prior angioplasty). Repeat coronary angiography at 1 year showed a stable and patent left coronary system, with a new lesion in the RCA, which was stented (Figure 3). Discussion. According to the IRAD registry, aortic dissections are usually caused by retrograde propagation of coronary dissection.² Patients tend to be older (mean age of 71) and have a history of hypertension, coronary artery disease and prior CABG. The diagnosis is often challenging because unlike spontaneous dissection, chest and back pain are often absent and less abrupt. Physical exam findings such as a murmur of aortic regurgitation and diminished peripheral pulses are less prevalent. Thus, any patient undergoing a percutaneous coronary artery intervention who develops otherwise unexplained hypotension and hemodynamic compromise should be evaluated for aortic dissection. In addition, neointimal flaps are often not as well visualized in iatrogenic cases on imaging (transesophageal echocardiography, computed tomography or magnetic resonance). This may be partly due to the fact that some of these cases result in intramural hematomas, rather than classic dissections. Iatrogenic dissections, however, carry a mortality rate as high as that of spontaneous dissections (up to 35%), and have a higher incidence of concomitant myocardial infarction.^2,5 The majority of reported cases involve right coronary artery dissection extending into the aorta,^5–7 which is likely secondary to catheter manipulation and injection with deep catheter engagement (underscoring the continuous need to monitor catheter tip pressures). Aortocoronary dissections have been amenable to treatment with ostial stenting of the right coronary artery and left main ostium. According to a published case series,³ dissections extending less than 4 cm above the coronary sinuses are amenable to percutaneous treatment and medical management, whereas dissections involving more than 4 cm of the ascending aorta require surgical management. This case has several unique features. The dissection was localized to the left main coronary artery and resulted in an abrupt closure of the vessel with hemodynamic collapse, as well as extensive involvement of the ascending aorta. Despite the fact that the aortic dissection flap extended as far as 8 cm above the coronary sinus, it could nevertheless be stabilized and managed by emergent ostial left main coronary artery stenting alone, without the need for surgical management. To our knowledge, this is the first such reported case in the literature. In this patient, we elected not to use a drug-eluting stent to allow adequate healing of the intima and adventitia, however, this has to be weighed against a higher restenosis rate (which is easily treatable). We used a heparin-coated stent while it was still available in the U.S. for fear of not being able to use dual antiplatelet therapy and the possible need for surgical intervention. Our patient had a high burden of atherosclerosis as evidenced by her three-vessel disease, as well as the presence of protruding atheromas in her aorta. In the context of an acute coronary syndrome such as presented here, the pro-inflammatory markers and pro-apoptotic protein expression (cathepsin B)⁸ can be increased in the aorta, further predisposing patients to aortic dissection during various wire manipulations. Recent reports suggest the possibility of endovascular repair of aortic arch dissections which may offer a less morbid alternative to open-heart surgery for aortic dissections complicating coronary dissection.⁹ Such procedures can be performed in two stages, with coronary ostium stenting followed by ascending aorta and aortic arch stenting if the coronary ostial stenting fails to completely seal the dissection. This would expand our armamentarium for the treatment of complications in percutaneous coronary interventions. Acknowledgement. We would like to acknowledge Daniel R. Frisch, MD, Ralph De La Torre, MD, Warren Manning, MD, and James Alderman, MD, for their substantial contribution to the management of this case.

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