Case Report

Spontaneous Coronary Artery Dissection and the Role for Percutaneous Coronary Intervention: To Treat or Not To Treat?

*Colin D. Chue, MBChB (Hons), MRCP, §Helen C. Routledge, MD, MRCP, §Jonathan N. Townend, MD, FRCP, FESC
*Colin D. Chue, MBChB (Hons), MRCP, §Helen C. Routledge, MD, MRCP, §Jonathan N. Townend, MD, FRCP, FESC
From the *Department of Cardiovascular Medicine, University of Birmingham, Edgbaston, Birmingham, West Midlands, and the §Department of Cardiology, University Hospital Birmingham NHS Foundation Trust, Queen Elizabeth Hospital, Edgbaston, Birmingham, United Kingdom. The authors report no conflicts of interest regarding the content herein. Manuscript submitted October 8, 2008, provisional acceptance given December 3, 2008, and final version accepted December 4, 2008. Address for correspondence: Dr. Jonathan N. Townend, Consultant Cardiologist, Department of Cardiology, Queen Elizabeth Hospital, Edgbaston, Birmingham, West Midlands B15 2TH, United Kingdom.

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ABSTRACT: Spontaneous coronary artery dissection is a rare but occasionally lethal condition that is more common in the peri- and post-partum periods. Recommendations for its management are derived from the literature only in the form of single case reports and few small case series in which successful outcomes were obtained. No consensus of opinion or guideline for optimal treatment exists. We present a case of post-partum coronary artery dissection initially treated with drug-eluting stents, but complicated by the extension of intramural hematoma and further dissection. After consideration of surgical revascularization, medical management with dual-antiplatelet therapy resulted in complete healing of the dissection and spontaneous gradual resolution of intramural hematoma after three weeks. Unfortunately development of in-stent restenosis necessitated reintervention with further coronary stenting 2 months later.

J INVASIVE CARDIOL 2009;21:E44–E47

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Case Report. A 39-year-old Afro-Caribbean female presented with an 8-day history of chest pain 9 weeks following uncomplicated Caesarean delivery of her third child. She had no risk factors for cardiovascular disease and no features of connective tissue disease. An electrocardiogram (ECG) revealed T-wave inversion in the anterior leads and serum Troponin T was elevated at 0.21 (normal range 1 At clinical follow up 2 months later, she described Canadian Cardiovascular Society (CCS) Class II symptoms of exertional angina, confirmed on exercise testing by chest pain and ST depression in Stage II of the standard Bruce protocol. Subsequent angiography revealed a normal-caliber proximal LAD and normal intravascular ultrasound (IVUS) appearances of the LAD and LMS with no evidence of recurrent dissection (Figure 5A). Distal edge in-stent restenosis was, however, evident in the distal LAD stent (Figure 5B). She underwent successful reintervention to the distal LAD with implantation of a Taxus® paclitaxel-eluting stent (Boston Scientific Corp.) (Figure 5C). At follow up she remains symptom-free with unlimited exercise capacity. Discussion. Spontaneous coronary artery dissection (SCAD) is a rare finding in patients presenting with an acute coronary syndrome.2–4 It is potentially fatal and the diagnosis may be made only at autopsy.5 The proportion of acute coronary events caused by SCAD is higher in the peri- and post-partum periods; this has been attributed to hormonal changes and hemodynamic stresses related to pregnancy, labor and delivery.6,7 No guidelines currently exist for the management of SCAD owing to the condition’s scarcity. It has been previously recommended that patients without myocardial ischemia or hemodynamic instability might be treated medically.8 This is supported by reports of successful resolution of dissection following therapy with aspirin and warfarin.9 In the case presented here, persistent chest pain suggesting ongoing myocardial ischemia and the presence of complete vessel occlusion led the operators to proceed immediately with mechanical revascularization. We accept that a trial of medical therapy and assessment of myocardial ischemia by noninvasive testing would have been a reasonable alternative strategy. Some concern was present, however, about the use of combined aspirin and warfarin therapy with its risk of hemorrhagic complications in a Jehovah’s Witness with anemia. PCI is likely to be used more frequently in SCAD as a result of widespread uptake of primary or early intervention in ST- and non-ST-segment elevation MI. A number of cases of pregnancy-related coronary dissection successfully treated by PCI have been described.3,4,10,11 The rationale that stent deployment reduces the risk of recurrent dissection seems reasonable, although there are reports that, as in this case, stent deployment may be immediately followed by extension of the dissection distally or proximally, presumably as a result of displacement and propagation of intramural hematoma, which then exits to cause dissection and vessel occlusion at a remote site or perhaps by further damage to a fragile vessel wall.12 It is suggested that the absence of significant atheroma in many cases of coronary dissection could facilitate propagation of the dissection through the media.13 We do not believe that the choice of inflation pressures in this case contributed to propagation of hematoma. PCI carries another potential risk of stent deployment into the false lumen, causing either obliteration of coronary flow or arterial rupture.14 The incidence of such complications may be minimized through the use of IVUS, which has proveughn to be useful for not only differentiating the etiology of atypical angiographic appearances,13 but also determining the optimal position for stent deployment.15,16 Altho IVUS might have provided important information regarding the extent of proximal dissection in our patient, it was not performed in the acute setting because of symptoms and hemodynamic instability associated with the LAD occlusion. It remains unclear which treatment strategy should be adopted if further dissection or intramural hematoma is identified following PCI. With hindsight, it can be seen that although stenting of the intramural hematoma in the proximal LAD might have prevented further dissection, it would not have improved the eventual caliber of this vessel. Stenting at that time might also have resulted in immediate further dissection or proximal displacement of the intramural hematoma with compromise of the LMS. Almost all reported cases of SCAD successfully treated with coronary stenting have involved the use of bare-metal stents. As highlighted by our case, the length of stent required in an extensive dissection should raise concern regarding restenosis and the need for repeated interventions. This case also serves as a reminder that both intramural hematoma and extensive coronary dissection can heal spontaneously.17 This should be remembered when encountering SCAD, and the possibility of conservative therapy in stable asymptomatic patients, even those with extensive dissection, should always be considered. Conclusion. We describe a case of peri-partum SCAD in which PCI with stent implantation to restore distal flow precipitated propagation of an intramural hematoma and retrograde extension of the dissection. With conservative management and medical therapy, the resulting dissection resolved without the need for further intervention. We propose that while percutaneous intervention may be necessary to restore flow in an occluded vessel, a conservative approach with medical management and repeat angiography should be adopted for stable asymptomatic patients to avoid the potential complications associated with coronary intervention. Figure Legends: Figure 1. Coronary angiography following the initial presentation of chest pain 9 weeks after childbirth shows the left coronary system in the right anterior oblique view (A). The left anterior descending artery (LAD) is occluded in its mid-portion (arrow). Following successful implantation of 3 overlapping everolimus-eluting stents in the LAD, the proximal part of the vessel developed an abnormal appearance (arrow) consistent with spasm or intramural hematoma (B). This appearance improved following administration of intracoronary nitrates (C) and no further intervention was performed. Figure 2. Repeat coronary angiography performed a few hours later due to recurrent chest pain and new inferior ST-elevation on the 12-lead electrocardiogram demonstrated patent left anterior descending artery (LAD) stents, but persistent changes in the proximal LAD with haziness extending into the second obtuse marginal branch of the circumflex system, suggestive of retrograde propagation of an intramural hematoma and extending dissection (arrow). No further intervention was performed. Figure 3. Repeat coronary angiography 7 days later showed dissection of the proximal left anterior descending artery (arrows) extending into the left main stem (arrowheads) and circumflex artery, prompting referral for urgent coronary artery bypass grafting. Figure 4. Surgery was delayed owing to clinical stability and anemia. Repeat angiography 3 weeks later revealed complete healing of the dissection with only moderate residual narrowing in the proximal left anterior descending artery. Medical therapy was continued and the patient was discharged. Figure 5. Angiography was repeated 2 months later as the patient developed exertional chest pain. An intravascular ultrasound study of the proximal left anterior descending artery (LAD) showed a normal-caliber vessel with no evidence of dissection, intramural hematoma or atheroma (A). Distal edge in-stent restenosis (arrow) had, however, developed in the distal LAD stent (B). This was successfully treated with implantation of a paclitaxel-eluting stent (C). The patient remains asymptomatic at follow up.

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