Intravascular Ultrasound Imaging in the Diagnosis and Treatment of Spontaneous Coronary Dissection with Drug-Eluting Stents

ABSTRACT: Spontaneous coronary artery dissection is a rare cause of coronary ischemia. Its prognosis is uncertain and the optimal treatment is not fully defined. We report a case of spontaneous dissection of the left anterior descending artery in a healthy post-menopausal woman, in whom the initial strategy of medical therapy was unsuccessful. After repeated angiography, we implanted 2 drug-eluting stents using intravascular ultrasound guidance with excellent immediate result and long-term symptomatic relief. This is the first report of implantation of drug-eluting stents in spontaneous coronary dissection.

Key words: drug-eluting stent, IVUS, spontaneous coronary dissection

Spontaneous coronary artery dissection (SCAD) is rare,^1–4 but may sometimes result in sudden coronary occlusion, acute myocardial infarction (AMI) and sudden cardiac death.5 Although first described more than 70 years ago,⁶ the pathogenesis and treatment are not yet completely defined. We report on a case of SCAD involving the left anterior descending (LAD) artery in a post-menopausal woman, presenting with unstable angina, in whom the initial medical management failed to achieve resolution of symptoms. After repeated angiography, and on the basis of intravascular ultrasound (IVUS) imaging, drug-eluting stents (DES) were implanted. IVUS imaging was useful diagnostically and in detecting persistence of medial hematoma, despite a good angiographic appearance. Using IVUS guidance, the stent result was optimized, resulting in good apposition of stent struts to the media of the artery and to hematoma sealing. Case Report. A 54-year-old woman presented with an acute coronary syndrome. She had undergone surgical hysterectomy and oophorectomy twenty years previously. She had taken oral estrogen for fifteen years, but had stopped more than five years earlier. With the exception of slightly elevated blood cholesterol, she had no risk factors for coronary atherosclerosis. There was no family history of sudden death and no history of connective tissue disease, drug abuse or recent trauma. The patient had been experiencing recurrent episodes of chest tightness for a week, both at rest and with exercise. Unstable angina was diagnosed, based on some anterior electrocardiographic (ECG) changes and raised troponin I (0.5 ng/ml; local reference limit, 0.15 ng/ml). Low-molecular-weight heparin, aspirin, atorvastatin, ramipril and atenolol were prescribed, but she continued to experience chest pain and was referred for cardiac catheterization. Coronary angiography demonstrated normal right coronary and circumflex arteries, with no evidence of atheroma. However, the mid-LAD showed clear angiographic evidence of dissection (Figure 1), with a radiolucent intimal flap and contrast staining after injection (not shown). After an aneurysmal segment (due to contrast entering the false lumen), the distal LAD was small, with TIMI 2 flow. This was judged to be due to extensive dissection compressing the true lumen and/or to associated vasospasm. It did not improve after intracoronary nitrates. Left ventricular angiography showed good left ventricular function and minimal anterior hypokinesia. In view of the long diseased segment, with a very small distal vessel, a conservative approach was chosen and the patient was discharged home on medical therapy with aspirin and atenolol. Unfortunately, after temporary relief of symptoms, she continued to experience exercise chest discomfort, associated with fatigue and breathlessness. Outpatient ECG exercise test two months later was limited by chest pain and showed very low effort tolerance (3 minutes of a standard Bruce protocol), with anterior ST-segment depression. Further angiography (three months after the initial catheterization; Figure 2) showed an unsealed dissection in the mid-LAD with persistence of the enlarged segment and of the intimal flap. There was some improvement in diameter and flow of the distal vessel (now TIMI 3). The lesion was crossed with a 0.014" ACS BMW wire (Guidant Corporation, Temecula, California) and IVUS examination (Galaxy IVUS System, Boston Scientific/Scimed, Inc., Maple Grove, Minnesota) was performed to investigate the real extension of the dissection and to confirm the correct placement of the guidewire. IVUS showed the presence of a near-circumferential hematoma, extending deep into the media layer (Figure 3). No atheroma was visualized. Echo images also showed that dissection did not extend proximally after the enlarged segment, and only a few millimeters distally. Two 3.0 x 18 mm Cypher stents (Cordis Corporation, Miami, Florida) were placed over the dissection with overlap and inflated at 12 atms. Angiographic appearance was judged to be good (Figure 4), and another IVUS examination was performed to confirm full apposition, symmetry and expansion of the stents, sealing of the hematoma and absence of propagation of the dissection. Surprisingly, the images showed persistence of an echolucent space between the first stent struts and the internal elastic lamina, due to a non-completely sealed intramural hematoma (Figure 5). Post-dilatation with a non-compliant balloon (3.0 x 15 mm) was undertaken with multiple inflations at a maximum of 16 atmospheres. Repeat IVUS confirmed complete sealing of the dissection with full stent apposition (Figure 6). The patient did well after the intervention and was discharged on aspirin and clopidogrel. She is currently asymptomatic and a repeated exercise test performed six months after the intervention was terminated at eight minutes of the Bruce protocol without ECG changes. Discussion. SCAD refers to the unprovoked occurrence of a medial dissection and/or an intramural hematoma, with or without symptoms and signs (i.e., iatrogenic or traumatic causes are not included).^2,5 This rare condition remains an unresolved matter of debate for the medical community, as there is no agreement on its pathogenesis or on the optimal treatment. Many of the described cases were pregnant or peripartum women.⁷ The mean age of SCAD patients is around 40 years.⁸ SCAD may present clinically with a range of coronary syndromes, from fixed anginal symptoms to sudden coronary death. Although it mimics atherosclerotic disease, prompt recognization and treatment are imperative, as therapies used for obstructive atheroma may be harmful to patients with SCAD. Potential origin. The cause of spontaneous dissection is unclear, but links with pregnancy, oral contraceptives, vasculitis with a predominant eosinophilic infiltrate, intense physical activity, collagen vascular disease (including Ehlers-Danlos type IV disease), aortic dissection,^1,9 and, more recently, with forceful retching¹⁰ and cocaine use,¹¹ have been described. Diagnosis is usually made at post-mortem examination.⁵ Interestingly, the landmark of the angiographic diagnosis of SCAD, the “intimal flap,” is seldom found at autopsy, while an eosinophilic infiltration into the adventitia (in 43%) and cystic medial necrosis (in 37%) are quite common.^6,12–14 The most convincing explanation for this appears to be that the higher-risk patients may die suddenly, while the patients diagnosed at angiography may be at lower risk. The intimal rupture may constitute a protective effect by which an obstructive hematoma may decompress and prevent complete occlusion of the artery. This supports the theory that the dissection is a primarily intramural disease, and may help to explain why most patients demonstrate persistent or new dissections (67% at six months in a series).¹⁵ A recent paper that analyzed an IVUS database of 15,000 preintervention patients identified five cases of unsuspected dissection without the classic angiographic appearance; these patients showed only moderate coronary luminal narrowing and no evidence on intimal tears.¹⁶ Thus, it is likely that the described cases derive from the mixing of two types of spontaneous coronary dissection, with and without an intimal tear, with the latter more consistent with pathology reports. Whether these conditions are the extremities of a single spectrum, or actually two different diseases, is largely unknown at the moment and remains to be ascertained, as the respective role of mechanical and primary arterial factors. Optimal management and the role of percutaneous coronary intervention. SCAD patients have been treated with coronary artery bypass graft surgery, medical therapy (with and without thrombolysis and aggressive antiplatelet treatment) and coronary stenting.^1,8,17,18,23 Aggressive surgical revascularization has provided survival benefit in some series,^17,18 and some authors recommend it for all patients,¹⁹ but it is limited by the anatomic problem of grafting a dissected artery, which can result in dissection extension or incomplete revascularization. Currently, it is best suited for patients with left main involvement or multivessel disease (i.e., similar indications as for atherosclerotic disease).⁸ Thrombolysis is similarly associated with mixed outcomes. Although a number of successful outcomes using thrombolytic therapy for the acute presentation of an acute SCAD have been described,^20,21 there also have been reports of thrombolytic-induced extension of the dissection.^22,28 Other medical approaches have included long-term therapy with aspirin and beta-blockers, with good long-term results in one series.²⁴ Recently, the first use of abciximab was described, with good outcome and rapid sealing.⁹ Our patient, however, remained symptomatic despite long-term medical treatment. Coronary stenting is probably the therapy of choice for SCAD, as it has proven to be extremely efficacious in the context of balloon-induced dissection. The first report of stenting as SCAD therapy appeared in 199425 and other reports have confirmed the safety and efficacy of this approach.8,26,27,30 However, it remains limited by the possible longitudinal extension of the dissection, with vessel occlusion or need for extensive stenting, and by the risk of in-stent restenosis in a generally young and otherwise healthy patient. The future: IVUS-guided DES implantation? We believe that the combined use of IVUS and DES is the optimal management for this condition. IVUS in SCAD patients has already been described;^29,30 it is useful to differentiate atherosclerotic disease from SCAD in cases with ambiguous coronary angiography, to determine the morphology and the real extension of dissection (risk of occult dissection), to confirm correct guidewire placement before stenting (risk of false-lumen stenting), to confirm stent apposition, symmetry and expansion, and to rule out dissection extension. In our case, IVUS confirmed the absence of an extended distal dissection before stenting, allowed us to select the correct stent lengths, and also showed the presence of an unsealed dissection in the enlarged segment, which was angiographically silent and was corrected with high-pressure postdilatation. Conclusion. Stent-based therapy of SCAD is both safe and efficacious. Our case highlights a successful interventional therapy in the context of failed medical therapy for a relatively young patient with SCAD. In consideration of the patient’s age and of the diseased segment length, the use of two DESs was preferred. IVUS guidance allowed us to obtain an optimal result with complete stent apposition, and we propose IVUS-guided DES implantation as a first-line treatment for patients with SCAD.