Spontaneous coronary artery dissection (SCAD) is a rare angiographic finding with a female preponderance and is usually associated with the peripartum period, cocaine use, severe hypertension or physical stress.1 The markedly heightened coronary sheer stress associated with the above conditions is undoubtedly a major etiologic mechanism. Not infrequently, patients present with dramatic clinical and hemodynamic compromise. Aliyary et al reported a woman with acute myocardial infarction and cardiogenic shock at 36 weeks of pregnancy. With intra-aortic balloon pump-assisted hemodynamic support, she underwent emergent but successful Cesarean section and subsequent off-pump coronary bypass surgery for SCAD.2 Hormonal variations during menstruation, pregnancy and oral contraceptive use, as well as collagen-vascular diseases and elevated anticardiolipin antibodies, have likewise been implicated as etiological factors. While SCAD tends to occur in segments free of significant atherosclerosis, acute plaque rupture may appear angiographically identical. Pathological series have found associated cystic medial necrosis as well as eosinophilic infiltration. Disorders of collagen and elastin can lead to vessel wall weakening, predisposing a patient to SCAD.3 Although this condition has been described in all coronary distributions, the most common location is the left anterior descending artery (LAD).1 A representative angiogram is depicted in Figure 1. This morbidly obese 39-year-old woman, non-gravid, with no previous medical or drug-abuse history, underwent evaluation for exertional angina prior to cholecystectomy. Stress echocardiography revealed anterior ischemia, and she underwent cardiac catheterization. A flow-limiting, long-spiral SCAD was seen in the proximal LAD, with no disease observed elsewhere. Subsequent percutaneous intervention with a 3.0 x 28 mm Express stent (Boston Scientific Corp., Natick, Massachusetts) was successful and uneventful (Figure 2). A bare-metal stent was selected due to the patient’s upcoming surgery. She was discharged on atenolol, aspirin, clopidogrel and simvastatin. Although a full collagen-vascular disease evaluation was not performed, her erythrocyte sedimentation rate and rheumatoid factor were within normal limits. In contrast to our patient, most cases occur in the peri-partum period. This particular case was unusual in that, aside from the patient’s gender, no other traditional SCAD risk factors were present. While the optimal therapeutic modality for SCAD is yet undefined, successful outcomes have been reported for both conservative medical therapy as well as invasive revascularization. Boztosun et al described an unusual case of spontaneous healing of a SCAD within 24 hours. The patient had been scheduled for stent implantation 1 day after initial angiography, and subsequent guiding angiogram revealed complete luminal normalization.1 Additionally, sleep deprivation apparently led to SCAD in a woman after 72 hours of continuous work. Conservative medical therapy for the culprit small diagonal branch resulted in spontaneous healing after 6 months. A hypercatecholaminergic state from the stress of overwhelming fatigue may have led to increased coronary sheer stress.4 More often, however, conservative observation results in symptomatic recurrence. In these instances, in the presence of suitable anatomy, stent implantation is recommended. Identification of the true lumen is crucial during percutaneous SCAD intervention. Inadvertent guidewire advancement or stent deployment into the false lumen can result in disastrous dissection propagation and abrupt vessel closure. Intravascular ultrasound (IVUS) can be invaluable in these cases both for true-lumen selection, as well as evaluation of the presence and extent of a coexistent intramural hematoma. Cardiac computerized tomographic angiography can likewise clearly define dual lumens in cross-sectional imaging.5 Ohlmann and colleagues described a case of diffuse LAD narrowing in a patient who presented with elevated cardiac markers. Because no obvious dissection was seen, the patient was initially treated medically. However, one week later she re-presented with a similar event. IVUS was performed with repeat catheterization and revealed a “double barrel”, with an intramural hematoma filling a segment of the false lumen. Subsequent stent deployment was successful, and the patient has remained asymptomatic.5 In his editorial comment, Vassanelli pointed out that “spontaneous means unknown.” Given the usual lack of antecedent information, the finding of SCAD rarely allows the investigator the ability for extensive inquiry regarding the etiologic mechanism.3 It is certainly plausible that SCAD is simply a common manifestation of multiple pathophysiologic entities such as enhanced coronary sheer stress, defects of vascular collagen and/or “generic” plaque rupture. We await findings from the ongoing DISCOVERY (DISsections of the Coronary arteries: Veneto and Emilia RegistrY) study, which aims to identify and study genetic and circulating biomarkers of this rare but perplexing syndrome.
1. Boztosun B, Gunes Y, Olcay A. Spontaneous closure of a spontaneous coronary artery dissection in one day. Vasc Disease Management 2006;3:356–357. 2. Chen J, Aliyary S, Mariani MA, et al. Staged therapeutic approach in spontaneous coronary dissection. Ann Thorac Surg 2007;83:1879–1881. 3. Vassenelli C. Spontaneous coronary artery dissection: When spontaneous means unknown. J Cardiovasc Med 2006;7:71–73. 4. Chen J, Suh SY, Kim JW, et al. Complete angiographic resolution of spontaneous coronary artery dissection associated with sleep deprivation. Int J Cardiol 2007;119:E38–E39. 5. Ohlmann P, Weigold G, Kim SW, et al. Images in cardiovascular medicine. Spontaneous coronary dissection: Computed tomography appearance and insights from intravascular ultrasound examination. Circulation 2006;113:E403–405. The authors can be reached at: firstname.lastname@example.org Address for correspondence: Jack P. Chen, MD, FACC, FSCAI, FCCP, 5670, Peachtree Dunwoody Road, #880, Atlanta, GA 30342.