Acute Left Main Coronary Arterial Thrombosis — A Case Series

Author Affiliations: From the *University of Colorado at Denver Health Sciences, Division of Cardiology, and the §Denver VA Medical Center, Division of Cardiology, Denver, Colorado. The authors report no conflicts of interest regarding the content herein. Manuscript submitted December 27, 2007, provisional acceptance given March 13, 2008, and accepted March 25, 2008. Address for correspondence: John C. Messenger, MD, University of Colorado Health Sciences, University of Colorado Hospital, 12401 E. 17th Avenue, P.O. Box 6511, B-132, Aurora, CO 80045. E-mail: John.Messenger@uchsc.edu

_______________________________________________ ABSTRACT: Acute left main coronary artery thrombosis is an uncommon, but important clinical entity. We report 6 consecutive cases of acute left main thrombosis that highlight the spectrum in clinical presentation of this entity, and the potential of an initial medical approach in managing a subset of these patients.

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J INVASIVE CARDIOL 2008;20:E243–E246 Thrombus formation in the left main coronary artery (LMCA) is considered a rare clinical event, although its true incidence is unknown. Plaque rupture with subsequent thrombus formation (i.e., atherothrombosis) is likely the most common etiology of a left main thrombus. We report a consecutive series of 6 patients who were found to have LMCA thrombosis by angiography that serve to highlight the spectrum in clinical presentation of this entity, and the potential of an initial medical approach in the management of a subset of these patients. Case Presentations Case 1. A 44-year-old male presented with an acute anterior myocardial infarction (MI) and underwent emergent angiography that demonstrated a large mobile intraluminal filling defect in the mid-portion of the left main coronary artery (LMCA) suggestive of thrombus (Figure 1A). Additionally, the left anterior descending artery (LAD) had evidence of distal embolization with an abrupt termination of its apical portion (Figure 1B). Intravascular ultrasound (IVUS) of the LMCA and the LAD demonstrated no evidence of LAD atherosclerosis and mild intimal thickening in the distal left main with a small eccentric plaque. A large filling defect at the site of the small LMCA plaque was noted (Figure 1C). The patient was hemodynamically stable and without chest pain while receiving intravenous (IV) heparin and abciximab. The decision was made to reassess the patient angiographically after 48 hours of IV heparin (target partial thromboplastin time of 60–80 seconds) and abciximab. In addition, the patient was treated with aspirin (325 mg daily), metoprolol (25 mg twice daily), lisinopril (2.5 mg daily), and atorvastatin (80 mg daily). A hypercoagulable evaluation was negative. Repeat angiography at 48 hours demonstrated near-complete resolution of the left main thrombus (Figure 1D) and recanalization of the distal LAD (Figure 1E). Repeat IVUS examination demonstrated a Case 2. A 51-year-old male admitted with new-onset chest pain underwent coronary angiography following a positive exercise treadmill test which demonstrated inferior ischemic changes. Left coronary angiography was significant for a 30% stenosis of the LMCA with a lucency noted in its proximal and mid-portion, suggestive of a thrombus (Figure 2A). IVUS revealed an eccentric plaque at the ostium of the LMCA extending to its mid-portion. There was an ulcer with a small overlying non-mobile echodensity (Figure 2B). Given the patient’s stable clinical condition, the decision was made to treat the patient medically with IV eptifibatide and heparin over 48 hours followed by repeat angiography. A hypercoagulable evaluation revealed the patient to be heterozygous for Factor V Leiden deficiency. Repeat coronary angiography at 48 hours noted near-complete resolution of the LMCA density seen on the first catheterization, suggesting resolution of the LMCA thrombus (Figure 2C). The patient was treated medically with dual antiplatelet therapy (aspirin and clopidogrel). At 3-year follow up, the patient has had no recurrent cardiac events. Case 3. A 66-year-old male with acute onset of chest pain, diffuse ST depression and elevated troponin underwent emergent coronary angiography that revealed an 80% stenosis of the left main with a filling defect consistent with thrombus (Figures 3A and B). The remainder of the coronary tree revealed mild luminal irregularities. The patient continued to experience chest pain, prompting the placement of an intra-aortic balloon pump (IABP) and referral for emergent coronary artery bypass grafting (CABG). Clinical follow up at 2 years revealed the patient was doing well with no recurrent events. Case 4. A 60-year-old male presenting with an acute anterolateral MI complicated by cardiogenic shock underwent emergent angiography. A large filling defect occupied the LMCA and extended into the LAD and circumflex arteries (Figure 4A). Toward the end of the cine acquisition, the thrombus prolapsed out of the LMCA into the aorta (Figures 4B and C). Repeat coronary angiography revealed TIMI 3 flow in the LAD and left circumflex arteries, but a subtotaled second diagonal, likely secondary to distal embolization. The patient was transferred to the medical intensive care unit in critical condition with heparin and abciximab infusions. The patient remained in critical condition with medically refractory cardiogenic shock and at the family’s request, support was withdrawn. Case 5. A 59-year-old male presented with a non-ST-elevation myocardial infarction and was referred for urgent cardiac catheterization. Left coronary angiography was remarkable for a “hazy” subtotal stenosis of the left main extending into the ostium of the left anterior descending artery with TIMI 2 flow in the LAD (Figures 5A and B). Given the extensive thrombus burden and suboptimal coronary flow, the patient was referred for emergent CABG. The patient underwent an uneventful 2-vessel CABG, and at 3 years post surgery was symptom-free. Case 6. A 65-year-old female with multiple cardiac risk factors including diabetes presented to the emergency room with severe chest pain and was found to have diffuse ST-segment depression. The patient was brought in for emergent angiography which revealed a prominent mobile filling defect in the LMCA consistent with thrombus (Figure 6A). There also appeared to be a thrombus at the origin of the first obtuse marginal with TIMI 1 flow in that vessel (Figure 6B). The patient was started on IV eptifibatide and heparin and an IABP was placed, which resulted in the patient becoming chest pain-free. Given the extensive thrombus burden and the patient’s diabetic status, cardiothoracic surgery was consulted and the patient underwent urgent 3-vessel CABG. At 1.5-year follow up, she was doing well with no further cardiac events. Discussion. This case series of 6 patients represents a contemporary experience of acute LMCA thrombosis. Atherosclerotic plaque rupture with superimposed thrombus formation was the likely underlying etiology in all of these cases. While the most common clinical presentation of LMCA thrombosis in this series was ST-elevation and non-ST-elevation MI, 1 patient presented with unstable angina. In an unselected population, acute LMCA thrombosis is also likely associated with sudden cardiac death. Data on the precise incidence of acute LMCA thrombosis are limited. Over the time course of this series (~17 months), 694 cardiac catheterizations were performed at our institution in patients with a diagnosis of acute coronary syndrome, resulting in an estimated incidence of LMCA thrombosis in this population of ~0.8%. Given the probable risk of sudden cardiac death with acute LMCA thrombosis, this likely represents an underestimate of the true incidence. The low frequency and exclusion of patients with LMCA thrombus from clinical trials presents a challenge when deciding the optimal management strategy in these patients. Based on our experience and other reports,1–9 the primary considerations in clinical management of these patients include: 1. Evidence of ongoing ischemia based on clinical symptoms or electrocardiographic findings; 2. The distribution and extent of coronary plaque burden in the LMCA and LMCA bifurcation; 3. The severity of coronary artery disease excluding the LMCA; 4. The extent of thrombus burden in the LMCA and LMCA bifurcation; 5. TIMI flow in the LAD and left circumflex (LCx) artery. Our series supports a role for medical treatment of acute LMCA thrombosis in the subset of patients with no evidence of ongoing ischemia, an absence of significant flow-limiting atherosclerotic disease in the left main artery, an absence of significant atherosclerotic disease in the remaining portions of the coronary tree, and TIMI 3 flow in the LAD and LCx arteries. In both of the patients in this series who met these criteria, medical management with 24–48 hours of IV heparin and glycoprotein IIb/IIIa inhibition and oral aspirin resulted in resolution of the thrombus burden, and effectively obviated the need for revascularization. Although the use of IVUS in the setting of acute LMCA thrombosis may be controversial, it facilitated the decision-making process in these cases by providing an accurate assessment of plaque burden in the LMCA and LMCA bifurcation, excluding the presence of LMCA dissection and documenting the resolution of thrombus following medical therapy. The choice of antiplatelet agent during the initial approach to medical therapy in these patients deserves some discussion. In contrast to small-molecule glycoprotein IIb/IIIa inhibitors, the ability to reverse the antiplatelet effects of abciximab using platelet transfusions should emergent CABG be required likely makes this the glycoprotein IIb/IIIa inhibitor of choice in this setting. The decision to add clopidogrel to this regimen may also be complicated by the increased bleeding risk should emergent CABG become necessary. An alternative strategy may be to defer the addition of clopidogrel until repeat angiography has confirmed the resolution of the LMCA thrombus, as was done in our second case. If medical therapy is employed as the primary treatment strategy, empiric data supports repeat coronary angiography at 48 hours (6–8) to confirm thrombus resolution. A variety of percutaneous treatments have been reported for the treatment of acute LMCA thrombosis. Generally, these treatments were attempted in patients who were critically ill with ongoing ischemia and hemodynamic instability. Most percutaneous treatments incorporate either mechanical (e.g., aspiration) or pharmacological thrombectomy (direct injection of tPA or streptokinase),1,4,10 alone, or as an adjunct to stenting. Emergent CABG is generally considered the standard of care for the treatment of patients with acute LMCA thrombosis. In this series, 3 of the 6 patients proceeded to CABG with excellent outcomes, although the perioperative mortality of emergent CABG and acute LMCA thrombotic occlusion has been reported to be as high as 40–50%.5,11,12 The decision to proceed with emergent PCI or CABG will largely depend on whether the patient is stable enough to wait for mobilization of the surgical team and can withstand induction with general anesthesia. With the increasing availability of percutaneous techniques for the treatment of bifurcation disease and interventional tools for the treatment of thrombus, the critically ill patient with acute LMCA thrombus should generally be treated with PCI. The use of circulatory support with IABPs13 or newer percutaneous left ventricular assist devices (e.g., Tandem Heart™, Cardiac Assist, Pittsburgh, Pennsylvania; Impella Recover Devices™, ABIOMED, Inc., Danvers, Massachusetts), where available, is generally recommended during such procedures. Acknowledgements. The authors would like to express their appreciation to Adam Hansgen for his assistance with graphics, and to Drs. John D. Carroll and Joel A. Garcia for critical review of the paper.

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