Spontaneous Coronary Artery Dissection: Management Options
in the Stent Era

ABSTRACT: Spontaneous coronary artery dissection (SCAD) is a rare cause of coronary obstruction, usually affecting women in the childbearing age. Pathogenetic mechanisms are elusive, and optimal treatment is not established. We describe a case of spontaneous coronary artery dissection that was successfully treated by coronary stenting. The published literature regarding the outcome of this modality of treatment in patients with SCAD is reviewed. A patient with spontaneous coronary artery dissection treated by stenting is described along with a review of the published literature regarding treatment of similar patients. J INVAS CARDIOL 2004;16:333–335 Key words: coronary artery, dissection, stent Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary obstruction.¹ Prompt recognition is crucial for appropriate patient management. We describe the occurrence of SCAD in a peri-menopausal woman that was successfully treated by emergency stenting. We also review the relevant literature with regard to management of this condition. Case Report. A 52-year-old lady presented to the emergency room with acute onset oppressive retrosternal chest pain of half hour duration. On examination, she was in severe pain. She had a blood pressure of 140/80 mmHg and a regular pulse of 95 bpm. Her electrocardiogram (ECG) showed ST elevations in leads II, III and aVF with ST depressions in the lateral leads. Echocardiography revealed akinesia of the inferior wall with preserved overall systolic function. She was mildly dyslipidemic with no other risk factors for coronary atherosclrerosis. She was given aspirin, 300 mg of clopidogrel and heparin. Thrombolytic therapy with 6000 units of tenecteplase (Metalyse®) intravenous bolus was administered. Pain and ECG changes improved, but recurred 45 minutes later. She was urgently transferred to the catheterization laboratory for rescue angioplasty. Coronary angiography revealed normal left coronary system. The right coronary artery (RCA) bore a long spiral dissection involving the proximal and mid segments with TIMI 2 flow, and total occlusion of a small posterior descending artery (Figure 1). Aortic root angiography was normal, without RCA ostial dissection. A 0.014 in. high torque floppy wire was successfully positioned in the true lumen of the RCA and two sirolimus-eluting (Cypher®) stents (3.0 x 23 mm and 2.75 x 23 mm) were deployed sequentially in the proximal and mid segments of the vessel (Figure 2). There was restoration of TIMI 3 flow with resolution of the ST segment elevations, and abolishment of chest pain. Cardiac enzymes exhibited an early peak. Subsequent clinical course was uneventful and she was discharged on the sixth hospital day. Thyroid function tests were normal. There were no manifestations of connective tissue disease, with negative assays for lupus anticoagulant, anticardiolipin antibodies (IgG and IgM), and antinuclear antibodies. Nine months later, patient was doing well with no recurrence of pain. Discussion Incidence. Since the first description by Pretty² in 1931, there have been few reported cases of SCAD, the majority being diagnosed on autopsy.³ Nearly 60% of the described cases were women, and commonly in the peripartum period.¹Pathogenesis. The pathogenesis of SCAD is not fully elucidated. Intramural hematoma results from disruption of the coronary artery, with hemorrhage separating the media and the external elastic lamina^4,5 leading to compression of the true vascular lumen. The initial event leading to dissection is not clear; an intimal tear being recognized in only few of the cases. This raises the possibility that the hematoma might originate from the vasa vasorum,³ and that the intimal tear when present, might be a site of egress rather than ingress of blood.^4,5 Other suggested mechanisms include alteration in the vascular wall properties⁴ leading to weakening of the media and connective tissue which occur in cystic medial necrosis,^5–7 pregnancy-related connective tissue changes,⁸ Marfan’s and Ehlers-Danlos⁹ syndromes, as well as a result of the action of proteases released from accumulated eosinophils.^5,10 An association with Polyarteritis Nodosa has also been reported.¹¹Presentation and angiographic diagnosis. The presentation of SCAD is variable and ranges from asymptomatic pathology¹² to myocardial infarction and sudden cardiac death. The diagnosis should be considered in young patients with few risk factors,³ and especially in women in the peripartum period.^1,3,13 The presence of a dissection on coronary angiography confirms the diagnosis. Filling of the dissection channel with delayed clearance of the contrast material can be noted.³ However, in the absence of an intimal tear, the false channel may not be visualized because of minimal communication with the intramural hematoma. In this situation, only luminal narrowing can be appreciated on angiography, and intravascular ultrasound can contribute significantly to the diagnosis and definition of the existing anatomy.¹⁴ Similar cases have been confirmed during bypass surgery.^15,16 Hence, the condition should be suspected in patients with a suggestive clinical presentation, despite absent angiographic evidence of dissection. Treatment. Several treatment options have been implemented in patients with SCAD, with variable outcomes. Some patients have been treated with antithrombotic and thrombolytic agents^17–19 with success. Theoretically however, thrombolysis may dissolve the intramural clot leading to enhanced flow in the false lumen and propagation of the dissection.²⁰ In few asymptomatic patients, healing of the dissection has been noted with medical therapy alone (beta-blockers, nitrates and calcium channel blockers).²¹ When ischemia is ongoing, revascularization is clearly indicated.³ Bypass surgery has been suggested.^22,23 However, effective revascularization can be hampered by difficulty in identifying the true lumen. Experience with balloon angioplasty is limited: results were suboptimal in two cases;^24,25 in others, balloon inflation resulted in further propagation of the dissection with emergent need for bypass surgery.^15,26 Coronary stenting has emerged as a rational modality aimed at limiting the propagation of the dissection. Successful stenting was initially described by Hong et al. in 1996.²⁷ An important limitation is represented by the risk of coronary perforation in case of entry and passage of the guidewire into the false lumen.¹⁵ Table 1 summarizes the published experience with stenting. A total of 32 patients treated by stenting could be identified in the literature: 23 were females, 7 of whom were peripartum. The average age was 45 years (range 27–69). Twenty-two (69%) patients presented with acute myocardial infarction. The involved vessel was the left anterior descending (LAD) in 15 (47%), RCA in 10 (31%) and circumflex (LCX) in 3 (9%). Four patients (13%) had multi-vessel involvement. More than one stent was needed in 19 (59%) of the cases. Clinical success was reported in 29 (91%) patients. Complications included extension of the dissection, necessitating additional stenting in one case,¹ inflation of a perfusion balloon in another,²⁸ and bypass surgery in 2 patients.^29,30 In-stent stenosis was reported in one patient at 5 months.³¹ Additionally, Hering et al.³² reported 24 patients who were successfully treated by intracoronary stenting. Of these, 3 patients subsequently developed in-stent stenosis. To this end, our patient presents the first reported deployment of Cypher stent for the treatment of SCAD. An added advantage is reduced incidence of in-stent restenosis, thus better long-term outcome. Conclusion In summary, our case represents the first case of SCAD treated by a drug-eluting stent. The triggers for the coronary dissection could not be elucidated. Intracoronary stenting appears to be a valid treatment option in patients with SCAD with a high success rate. Drug-coated stents offer an additional advantage by reducing the risk of stent-related neointimal growth.