Spontaneous Coronary Artery Dissection in a Woman with Depression without Coronary Atherosclerotic Risk Factors


Yen-Dong Ho, MD, Tomomi Koizumi, MD, PhD, David P. Lee, MD

Case Report. A 46-year-old female presented to a community hospital with acute coronary syndrome. One week prior to presentation, the patient had experienced chest tightness lasting 1 hour, occurring 1 day after lifting furniture. On the day of presentation, she developed recurrent chest tightness at rest. In the emergency room, her physical examination was normal. Her blood pressure was 109/60 mmHg. Serial electrocardiograms revealed transient minimal anterior ST-elevation and lateral T-wave inversions. Initial cardiac biomarkers were normal. The patient received aspirin, clopidogrel, metoprolol, nitrates and enoxaparin, and her chest pain resolved after 1.5 hours. However, her cardiac enzymes steadily rose over the next 2 days to a creatine kinase level of 567 U/L (normal < 200 U/L), CK-MB of 58 ng/ml (normal < 4 ng/ml), and troponin I of 28.1 ng/ml (normal < 0.3 ng/ml).
The patient had a history of depression and mitral valve prolapse, no risk factors for atherosclerosis and no family history of coronary disease or sudden cardiac death. There was no history of recreational drug use, recent trauma or recent pregnancy. Her only medication was duloxetine hydrochloride 60 mg daily. Upon transfer to our hospital, coronary angiography demonstrated left anterior descending artery (LAD) dissection from the takeoff of the first septal branch to the distal LAD (Figure 1). The remainder of the coronary arterial tree was angiographically normal. Intravenous heparin and tirofiban were administered. Via a 6 Fr JL4 Launcher guide catheter (Medtronic, Inc., Minneapolis, Minnesota), a 0.014 inch x 190 cm Balance guidewire (Guidant Corp., Indianapolis, Indiana) was manipulated into the second diagonal artery. Intravascular ultrasound (IVUS) examination using a 40 MHz Atlantis SR Pro catheter (Boston Scientific Corp., Natick, Massachusetts) revealed a LAD medial dissection with the true lumen compressed by a hematoma-filled false lumen (Figure 1). Minimal lumen area in the lesion segment was 1.79 mm2. No communication was visualized between the true and false lumens, and the normal vessel wall was observed from the proximal dissection edge to the left main trunk. IVUS also confirmed the location of guidewire in the true lumen of the LAD. The mid-LAD was directly stented with a 3.0 x 32 mm Taxus Express2 stent (Boston Scientific). Repeat angiography revealed no obvious proximal LAD dissection (Figure 2), but IVUS examination demonstrated dissection extending proximal to the stent, prompting deployment of a 3.5 x 12 mm Taxus Express2 stent proximal to and overlapping with the initial stent. Subsequent IVUS examination confirmed stent coverage of the proximal dissection edge. The minimal stent area was 5.82 mm2. By coronary angiography, LAD flow was observed to be TIMI 3, though there remained a dissection plane visible in the distal vessel (Figure 3). Postprocedure, the patient had no further chest pain and
her cardiac enzymes trended downward. She was discharged the following day on aspirin and clopidogrel.


Discussion. Spontaneous coronary artery dissection (SCAD) is a rare but potentially devastating cause of acute coronary syndrome.1–3 It is defined as hemorrhagic separation of the media of the coronary artery, with creation of a false lumen in the absence of chest trauma, aortic dissection extension, or iatrogenic trauma from cardiac catheterization or surgery.3,4 It can manifest as myocardial ischemia or infarction, pericardial tamponade, heart failure or sudden death, with clinical presentation dependent on the vessel involved, the extent and rate of dissection, and the amount of myocardium at risk.2,3 Unfortunately, its pathogenesis remains poorly elucidated.
SCAD has a predilection for women, especially in the peripartum state or with oral contraceptive use, as well as association with atherosclerosis, intense physical activity, cocaine use, collagen vascular disorders and autoimmune diseases.1,2,5–7 The predominance of women and the influence of pregnancy and oral contraceptives on SCAD incidence point towards a hormonal influence on vascular stability, possibly through impaired collagen synthesis.5–7 In addition, as intimal tears have been identified in only a minority of autopsy cases, primary rupture of the vasa vasorum with medial hemorrhage may account for some dissections.3 Inflammation is also implicated, with histology demonstrating periadventitial eosinophilic infiltrates.3,8 Finally, the association of SCAD with intense exercise suggests that hemodynamic stresses facilitate dissection.7,9
Here we present a case of spontaneous coronary dissection resulting in myocardial infarction in a woman without atherosclerotic risk factors, but with medically treated depression. No atherosclerosis was present by IVUS. Initial chest pain occurred 1 day after physical exertion. Given the temporal separation from the onset of chest pain, the role of physical exertion in the pathogenesis of this case is uncertain, though it is possible that hemodynamic stresses may have contributed to medial injury without initial coronary flow limitation. Nevertheless, her only clear risk factor for dissection was female sex.
Highlighting gender differences in vascular biology, the WISE study identified a subpopulation of women with increased risk of cardiac events despite angiographically normal coronary arteries.10 Interestingly, among women with suspected myocardial ischemia, depression predicts increased cardiac events, possibly via abnormal platelet aggregation, increased cortisol production and an imbalance of sympathetic/parasympathetic tone as demonstrated by decreased heart rate variability.11 We can speculate that in depression, increased sheer forces on the coronary wall secondary to increased sympathetic tone contribute to heightened risk of not only plaque rupture but also coronary dissection.
Though consensus is lacking concerning the treatment of SCAD, management decisions can be made on a case-by-case basis, integrating the clinical scenario with the angiographic assessment of dissection location and the extent and degree of compromise of vessel flow. Treatment options include medical therapy, percutaneous intervention and surgical revascularization.1,2,4,5,7,12–18 In hemodynamically stable patients without signs of ongoing ischemia and with limited dissection on angiography, medical management with aspirin, nitrates and beta-blockers has achieved reasonable results.1,2,4,5,12,13 Indeed, though SCAD carries high mortality, with nearly 70% of cases diagnosed at necroscopy, the prognosis is favorable for patients who survive the initial event.1
In contrast, ischemia refractory to medical management should prompt urgent revascularization. Thrombolysis may facilitate revascularization via intramural clot lysis, but is not recommended, given the risk of dissection extension via an increased medial hemorrhage.14 Surgical revascularization is indicated in left main or multivessel dissections, while percutaneous intervention has benefited patients with refractory ischemia secondary to single-vessel dissection.1,2,5,7,12,15–18 In our case, given the rising cardiac biomarkers despite 2 days of medical therapy with aspirin, clopidogrel, metoprolol, nitrates and enoxaparin, and given the extensive LAD luminal compromise, we elected to pursue percutaneous intervention.
Coronary stenting offers a rapid revascularization option and the ability to stem dissection propagation. Stent deployment at the proximal dissection edge can seal off potential intimal tears and/or tamponade further hemorrhage, thereby facilitating healing of the more distal vessel. However, guidelines for stent selection are lacking. Given their antiproliferative properties, drug-eluting stents have been theorized to interfere with dissection healing, but data are as yet limited.19 Therefore, the decision between drug-eluting and bare-metal stent use in SCAD must reflect a balance between the risk of restenosis and the risk of thrombosis, and should be individualized based on both patient characteristics (e.g., diabetes, bleeding risk, medical compliance) and angiographic assessment (e.g., location and length of dissection, diameter of vessel, presence of atherosclerosis).
In addition, determination of guidewire position prior to stenting and confirmation of optimal stent placement after stenting is crucial. Devastating consequences, including coronary occlusion or perforation, can result if the false lumen is stented. Also, retrograde propagation of an intramural hematoma with compromise of the proximal vessels after stent deployment has been reported in case studies.20 In our patient, IVUS examination corroborated the guidewire position in the true lumen, facilitating initial stent deployment. However, as the subsequent IVUS study demonstrated dissection extending proximal to the stent, a second stent was employed to cover the proximal dissection edge.

Conclusion. In summary, this case demonstrates spontaneous coronary artery dissection in a woman with medically treated depression. Though the pathogenesis of SCAD remains poorly elucidated, its predilection for women highlights gender differences in vascular biology. Its management requires the integration of the clinical scenario with angiographic assessment. In this woman with medically refractory SCAD, IVUS-guided percutaneous intervention led to a favorable angiographic and clinical outcome.




Angiographic image after deployment of the first stent in the mid LAD.
Angiographic and IVUS images of the LAD prior to intervention. Angiogram demonstrates narrowing with haziness in the mid-to-distal LAD. No intimal thickening is visible on IVUS cross-sectional images of the left main (A) and the proximal LAD (B). IVUS ima
Final angiographic and IVUS images after stenting of the LAD. LAD flow was TIMI 3, though there remains a dissection plane visible in the distal vessel by angiography. Minimal stent area by IVUS was 5.82 mm2 (D).


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