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Case Report

Treatment of Spontaneous Coronary Dissection with Drug-Eluting Stents — Late Clinical, Angiographic and IVUS Follow Up

William J. van Gaal, III, MBBS, FRACP, Italo Porto, MD, Adrian P. Banning, MD, MRCP
February 2006
Spontaneous coronary artery dissection (SCAD) is a rare condition which may result in sudden coronary occlusion, acute myocardial infarction (AMI) and sudden cardiac death.1–3 We previously reported a case of SCAD involving the left anterior descending (LAD) artery confirmed with coronary angiography and intravascular ultrasound (IVUS).4 After failure of medical management, the patient was successfully treated with implantation of drug-eluting stents (DES), achieving a good immediate angiographic and intravascular ultrasound (IVUS) result with resolution of symptoms. We now report the late clinical, angiographic and IVUS follow up after treatment of SCAD with implantation of DES. Case Report. A 54-year-old postmenopausal woman presented with 1 week of chest pain on exertion and at rest. She had no risk factors for coronary atherosclerosis. The electrocardiograph (ECG) demonstrated anterior T-wave changes and the troponin I was elevated (0.5 ng/ml; local reference limit, 0.15 ng/ml). Low-molecular weight heparin, aspirin, atorvastatin, ramipril and atenolol were prescribed. She had recurrent chest pain and underwent cardiac catheterization. Coronary angiography demonstrated dissection of the mid-LAD (Figure 1). In view of the long diseased segment and small distal vessel, the patient was treated medically. After temporary relief of symptoms, she began to experience exertional chest discomfort. An exercise ECG was positive and repeat angiography at 3 months showed persistent dissection. IVUS examination (Galaxy IVUS System, Boston Scientific Corp., Natick Massachusetts) showed near-circumferential hematoma extending deep into the media. No atheroma was visualized (Figure 2). Two 3.0 x 18 mm Cypher™ stents (Cordis Corp., Miami, Florida) were deployed over the dissection with overlap and inflated at 12 atm. Postdilatation with a noncompliant balloon (3.0 x 15 mm) was undertaken after IVUS demonstrated incomplete stent deployment (not shown). The immediate angiographic result appeared good. Repeat IVUS confirmed complete sealing of the dissection, with full stent apposition (Figure 3). The patient was discharged on long-term aspirin and 6 months of clopidogrel therapy. A repeat exercise test performed 6 months after the intervention was terminated at 8 minutes of the Bruce protocol without ECG changes. More than 18 months later, the patient complained of mild exertional breathlessness, and coronary angiography was again performed. There was good flow in the LAD, and IVUS examination confirmed widely patent stents without evidence of neointimal proliferation (Figure 4). At review more than 2 years following intervention, she remains on aspirin and is asymptomatic, with a normal cardiovascular examination and normal ECG. Transthoracic echocardiography demonstrated only minimal anterior hypokinesia. Discussion Reported treatment options for SCAD include medical therapy, thrombolysis, balloon angioplasty and coronary artery bypass surgery. There have been varied reports of success in the literature for each approach.5 Coronary stenting for SCAD was first reported in 1996,6 and has become the treatment of choice for preventing further propagation of dissection. There are now over 30 case reports of bare metal stenting for SCAD in the literature, however, in-stent stenosis has been problematic.7 In the absence of atheromatous coronary artery disease, reports of DES use for SCAD are rare, and there are no reports of long-term angiographic outcomes with either approach. In our case, therapy with low-molecular weight heparin, aspirin and atenolol failed to allow for healing and did not relieve the patient’s symptoms after nearly 3 months. Repeat angiography confirmed persistent dissection, and the patient was treated with the first reported use of DES for SCAD.4 We now report the late angiographic and IVUS follow up at 18 months, which confirmed a patent stent without neointimal proliferation and at 2-year clinical follow up, the patient was asymptomatic. Conclusion A trial of initial medical therapy for SCAD appears to be supported by the literature, however if symptoms or dissection persist, stenting appears to be the treatment of choice. Only isolated reports of DES for SCAD exist, and long-term results are not known. Our case demonstrates the utility of DES in providing a good long-term clinical, angiographic and IVUS outcome for SCAD in the absence of atherosclerotic coronary artery disease.
1. Kamineni R, Sadhu A, Alpert JS. Spontaneous coronary artery dissection: Report of two cases and a 50-year review of the literature. Cardiol Rev 2002;10:279–284. 2. DeMaio SJ Jr, Kinsella SH, Silverman ME. Clinical course and long-term prognosis of spontaneous coronary dissection. Am J Cardiol 1989;64:471–474. 3. Basso C, Morgagni GL, Thiene G. Spontaneous coronary artery dissection: A neglected cause of acute myocardial ischaemia and sudden death. Heart 1996;75:451–454. 4. Porto I, Banning AP. Intravascular ultrasound imaging in the diagnosis and treatment of spontaneous coronary artery dissection with drug-eluting stents. J Invasive Cardiol 2004;16:78–80. 5. Mourkabel G, Alam S. Case Report and Brief Review: Spontaneous Coronary Artery Dissection: Management option in the Stent Era. J Invasive Cardiol 2004;16:333-335. 6. Hong MK, Satler LF, Mintz GS, et al. Treatment of spontaneous coronary artery dissection with intracoronary stenting. Am Heart J 1996;132:200–202. 7. Hering D, Piper C, Hohmann C, et al. Prospective study of the incidence, pathogenesis and therapy of spontaneous, by coronary angiography diagnosed coronary artery dissection. Z Kardiol 1998;87:961–970.

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