Case Report and Brief Review

Spontaneous Dissection of the Left Main Coronary Artery Treated
with Percutaneous Coronary Stenting

Mimi Q. Le, MD and Frederick S. Ling, MD
Mimi Q. Le, MD and Frederick S. Ling, MD

Spontaneous coronary artery dissection (SCAD) is an unusual cause of acute myocardial ischemia, with approximately 300 cases reported in the literature.1,2 It is often fatal and is mostly recognized at postmortem examination in young victims of sudden death.2 More than 70% of the reported cases occurred in women, particularly during pregnancy and peripartum, with highest risk in the immediate postpartum period.2 Treatment options include medical therapy, revascularization with coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI).3 Reported cases of left main spontaneous dissection are mainly treated with CABG.2,4–7 To the best of our knowledge, there has only been 1 reported case of spontaneous left main dissection treated with percutaneous coronary stenting.8 We describe a case of spontaneous left main dissection in a young woman that was successfully treated with bare-metal stenting (BMS) guided by intravascular ultrasound (IVUS).

Case Report. The patient is a 37-year-old female with a medical history notable only for migraines. She presented to our institution with chest pain, shortness of breath and diaphoresis of 1 hour’s duration. Her only cardiac risk factor is current tobacco abuse. She has no history of connective tissue disease, illicit drug use and her last menstrual period was 2–3 weeks prior to presentation. En route to the hospital, she underwent defibrillation 5 times due to ventricular tachycardia/ventricular fibrillation. Upon presentation to our institution, her initial blood pressure was 78/52 and her electrocardiogram showed normal sinus rhythm with anterior ST-segment elevation. She subsequently underwent emergent cardiac catheterization which showed severely reduced left ventricular (LV) systolic function, an ejection fraction of 22% and akinesis of the anterolateral wall and LV apex. The right coronary artery (RCA) appeared angiographically normal. There was severe disease of the proximal left anterior descending artery (LAD) with impaired TIMI 1 antegrade flow (Figures 1 and 2).

We subsequently proceeded with percutaneous intervention in order to restore normal flow. Heparin and eptifibatide were used for anticoagulation. The left main coronary artery was engaged with a 6 Fr EBU 3.5 Launcher guide catheter (Medtronic, Inc., Minneapolis, Minnesota), and the LAD was wired with a Balance Middleweight wire (Guidant Corp., Indianapolis, Indiana). Angioplasty was performed on the proximal-to-mid LAD lesion using a 2.75 x 20 mm2 Sprinter balloon (Medtronic), with minimal improvement in the stenosis. Due to the appearance of the LAD lesion (smooth linear edge) without angiographic evidence of atherosclerotic disease in the remainder of the vessels, we proceeded with IVUS evaluation of the lesion. This was performed with a 2.9 Fr Eagle Eye Gold IVUS catheter (Volcano Corp., Rancho Cordova, California), which showed a spontaneous coronary dissection in the LAD with intramural hematoma compromising the proximal-to-mid LAD lumen (Figure 3). The extent of the dissection was noted from the proximalLAD and halted at the first diagonal branch without a clearlyevident entry point. As the patient was still in extremis, the proximal- to-mid LAD was stented using a 3.5 x 28 mm2 Vision stent (Guidant) to 12 atm, and the proximal stent was postdilated with a 4.0 x 15 mm2 Maverick balloon (Boston Scientific Corp., Natick, Massachusetts) to 10 atm. BMS was chosen, given the lack of data for use of drug-eluting stents in spontaneous coronary artery dissection. Subsequent angiography revealed extension of the hematoma into the first diagonal branch with compromise (Figure 4), thus angioplasty of this vessel was performed with a 2.0 x 20 mm2 Maverick balloon (Boston Scientific) to 8 atm with a good result (Figure 5). IVUS was performed again, which showed good apposition of the LAD stent and no residual unstented dissection of the LAD. As there was evidence of mild left circumflex artery (LCx) narrowing, we proceeded to examine the LCx and first obtuse marginal branch (OM1) by IVUS. The LCx was wired into the high OM1 branch and IVUS was performed, which showed a dissection in the OM1 branch extending all the way back to the ostium of the left main (Figure 6). The dissection in the left main was not well visualized during the initial pullback IVUS of the LAD. Review of that IVUS did reveal what had been interpreted initially as mild intimal thickening of the distal left main, but in retrospect, was an intramural hematoma. The origin of the left main clearly showed that the flap was not imaged during the initial IVUS due to deeper guide catheter intubation. It is also possible that the dissection in the left main became more prominent in the subsequent IVUS now that flow into the false lumen in the LAD was terminated by stenting of the LAD.

Aortography was performed at this time, showing no evidence of aortic root dissection. A transesophageal echocardiogram was also performed at this time, which also revealed no evidence of aortic root dissection. After extensive discussion with the cardiothoracic surgery department, the decision was made to proceed with percutaneous ostial left main intervention to seal off the dissection entry point, especially as serial angiography started to show progressive compromise of the LCx, particularly the OM1 branch, with a 30% stenosis likely from an expanding intramural hematoma compressing the lumen. Access was obtained in the left common femoral artery in anticipation of possible need for intra-aortic balloon pump support during the left main intervention. The left main coronary artery was engaged using a 7 Fr EBU JL 3.5 guiding catheter (Medtronic) and the left main was wired to the distal OM1 branch. Position of the guidewire in the true lumen was confirmed with IVUS. The ostium of the left main was primarily stented with a 4.0 x 8 mm2 Vision stent (Guidant) to 18 atm, and the proximal edge of the stent was postdilated with a 5.0 x 13 mm2 Powersail balloon (Guidant) to 12 atm to flare the proximal stent edge. IVUS was then performed, confirming good apposition of the stent with the proximal edge of the stent extending into the aorta (Figure 7). The stent did not cover the LCx origin. Final angiography revealed TIMI 3 flow with only mild residual narrowing of the circumflex origin and OM1 branch (Figure 8). The remainder of the patient’s hospital course was uneventful, and she was discharged on hospital day 6. Her troponin T peaked at 5.5 ng/mL and her peak creatine kinase was 6,414 units/L.

The patient returned 5 weeks later for follow-up coronary angiography. Her LV systolic function had returned to normal with mild residual anterolateral and apical wall motion abnormalities. The left main stent was widely patent. The proximal LAD stent was also patent, but there were 2 focal areas of stent nonapposition (Figure 9), likely due to luminal enlargement with resolution of the intramural hematoma from the original dissection. The first diagonal branch as well as the LCx/OM1 branch were patent, with no evidence of residual hematoma (Figures 10 and 11). The patient isto return for repeat follow-up coronary angiography in 3–4 months.

Discussion. Approximately 300 cases of spontaneous coronary artery dissection have been reported in the literature.1 SCAD results in the formation of an intramural hematoma in the media of the arterial wall that creates a false lumen. Expansion of this lumen through blood or clot accumulation leads to compression of the real lumen with myocardial ischemia.2 Patients may present with chronic stable angina, acute coronary syndromes, myocardial infarction, cardiogenic shock, sudden cardiac death or cardiac tamponade.3


Patients with SCAD have traditionally been assigned to three groups: those presenting with (a) significant preexisting atherosclerosis; (b) during the peripartum period, with most cases occurring within 2 weeks of delivery, or in association with oral contraceptive use; and (c) idiopathic presentation.3 Conditions associated with SCAD include connective tissue disorders (more common in women), Marfan’s syndrome, vasculitis, after intense physical activity, cocaine use or blunt chest trauma.3 SCAD has also been reported with elevated homocysteine levels.9 Left coronary artery dissections are more common in women and right coronary artery dissections occur more frequently in men.2 Overall, the LAD is affected in 75% of cases, the RCA in 20% of cases, the LCx in 4% of cases and the left main coronary artery in < 1% of cases.3

There are no established guidelines available to guide treatment of patients with SCAD. Treatment options include medical therapy and revascularization with either CABG or PCI. Thrombolytic therapy is relatively contraindicated in SCAD due to the potential risk of worsening the dissection and contributing to expansion of the hematoma.3 Extension of dissection is possible,10,11 although successful use of thrombolysis has been described.12 Medical therapy including aspirin, other antiplatelets, nitrates and beta-blockers has been successful in several cases with documentation of healing of the dissection on subsequent angiography.9,13,14

Revascularization for SCAD is warranted in those patients who present with ongoing ischemia refractory to medical treatment. Cases of spontaneous left main dissections reported in the literature have mainly been treated with CABG,2,4–7 as well as those with RCA involvement15 and triple-vessel SCAD.16 Successful revascularization with percutaneous stenting has also been described.17–19 In cases of severe heart failure, bridging to orthotopic heart transplantation with a left ventricular assist device (LVAD) may be the only option.20

Conclusion. Spontaneous left main coronary artery dissection is a rare event and has mostly been managed by CABG. The case described is an unusual presentation of SCAD in that the patient did not have the associated conditions traditionally described with SCAD. In our case, given the rapidly progressive nature of the dissection presenting as acute myocardial infarction, the unstable hemodynamics at the time of procedure and the severity of LV dysfunction, it was felt that percutaneous stenting of the left main coronary artery to seal the entry point of the dissection would be the most expeditious therapy. The patient subsequently had an uneventful hospital course, and follow-up angiography revealed patent stents. To our knowledge, this is the second reported case of left main stenting in a patient with SCAD. This is a potential option for the treatment of SCAD with left main involvement presenting with an acute coronary syndrome, particularly with the use of IVUS guidance and judicious followup angiography to monitor for in-stent restenosis.



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