ABSTRACT: Left main coronary artery thrombosis is a rare but potentially fatal phenomenon. We present the unusual case of total occlusion of the left main coronary artery suspected to be secondary to embolized thrombus from a patient’s mechanical, prosthetic aortic valve resulting in an anterior wall ST elevation myocardial infarction and cardiogenic shock. The acute interventional management and review of literature of left main thrombosis is described.
J INVASIVE CARDIOL 2011;23(11):E263-E266
Key words: total occlusion, PCI, STEMI
The incidence of acute ST-elevation myocardial infarction (STEMI) secondary to occlusion of the left main coronary artery (LMCA) is rare with rates ranging from 0.8 to 1.7% of all STEMI cases.1 The optimal management of patients presenting with left main thrombosis is unclear based on the current literature. Most patients present in cardiogenic shock, which, in itself portends a grave prognosis, and is usually fatal without emergent revascularization. Unfortunately, revascularization either by emergency coronary artery bypass surgery or primary percutaneous coronary intervention (PCI) in the setting of acute myocardial infarction and cardiogenic shock are associated with mortality rates as high as 50%.2 Although plaque rupture and subsequent thrombosis represent the mechanism for infarction in the majority of STEMI patients, embolism to the LMCA has been previously described. We present a case of left main thrombosis and cardiogenic shock in a patient with a prosthetic mechanical aortic valve, subtherapeutic INR, and otherwise angiographically normal coronary arteries — suggesting an embolic etiology. The acute interventional management and review of literature of left main thrombosis is described.
Case Report. A 59-year-old female with a of history Type 2 diabetes mellitus and mechanical bi-leaflet aortic valve prosthesis presented with the acute onset of substernal chest pain and anterolateral ST elevations. The patient’s aortic valve replacement had been performed 4 years earlier for a stenotic bicuspid valve with no prior history of concomitant coronary artery disease. The patient was noted to have bibasilar rales and hypotension (systolic blood pressure of 70 mmHg) requiring intravenous dopamine. Given evidence of an evolving STEMI and shock, she was urgently taken to the cardiac catheterization laboratory.
Diagnostic angiography of the left coronary system demonstrated complete occlusion of the LMCA (Figure 1). Fluoroscopy was also notable for a normal opening and closing bi-leaflet mechanical aortic valve. Given the scenario of cardiogenic shock, the decision was made to proceed with primary percutaneous coronary intervention. An intra-aortic balloon pump was placed for hemodynamic support. Intraveneous heparin and eptifibatide were administered with a peak activated clotting time of 293 seconds. A 300 cm BMW wire (Abbott Vascular) was advanced across the LMCA and positioned in the left anterior descending artery. After confirmation of intra-luminal location, a 2.0 x 15-mm Maverick balloon (Boston Scientific) was used to perform initial angioplasty of the LMCA with restoration of TIMI 2 flow, but with significant residual thrombus burden. Next, a 6 Fr ExPort catheter (Medtronic) was used to perform aspiration thrombectomy without retrieval of visible thrombus. A 7 Fr ExPort catheter was subsequently used to perform additional thrombectomy passes with improvement in flow (Figure 2) and removal of visible clot (Figure 3). However, given a persistently large clot burden in the LMCA, the decision was made to stent the vessel and compress the thrombus against the vessel wall. The left circumflex was a small non-dominant vessel, and a 2.75 x 23-mm Vision bare-metal stent (Abbott Vascular) was deployed in the LMCA into the LAD. The stent was ultimately post-dilated with a 3.5 x 15-mm NC Quantum balloon (Boston Scientific) to high pressure. Final angiography revealed TIMI 3 flow and no significant disease in the LAD (Figure 4). The right coronary artery was similarly free of significant angiographic disease (Figure 5).
Laboratory results ultimately revealed a subtherapeutic INR at 1.4. The patient admitted to non-compliance with warfarin therapy. Subsequent transesophageal echocardiography revealed no evidence of aortic valve dysfunction or evidence of valvular thrombus. The patient was treated with low dose aspirin, clopidogrel and warfarin and discharged in excellent condition with a preserved ejection fraction.
Discussion. LMCA thrombosis has been described in prior studies and case reports and can have variable presentations.3–7 Although patients may present with unstable angina or non-ST elevation myocardial infarctions, the great majority present in either cardiogenic shock or as victims of sudden cardiac death.8,9 Prior studies have demonstrated that anywhere from 63 to 92% of patients presenting with LMCA occlusion present in cardiogenic shock.1,7,9,10 Two high volume interventional centers in Melbourne, Australia found that out of 1,115 consecutive primary percutaneous interventions for acute myocardial infarctions over a 4-year period, 28 (2.5%) were due to left main thrombosis. They noted 18 (64%) of these patients presented in cardiogenic shock, while 10 (36%) patients were survivors of cardiac arrest.1 Furthermore, subgroup analysis of the SHOCK trial in which the left main was the culprit vessel suggested a 1-year mortality of 75% irrespective of the randomized management strategy.11
Various etiologies of left main coronary artery occlusion have been previously described including acute plaque rupture,12,13 embolized thrombus from intracardiac sources,4,6,14,15 embolization of intracardiac masses,16 dissection,17 catheter-induced,5 cocaine-induced plaque rupture or spasm,18 mycotic aneurysms of the LMCA,19 extrinsic compression from the pulmonary artery,20 as a complication of radiofrequency ablation procedures involving the AV-node,21 fibrous intimal proliferation after cardioplegia during bypass or valve replacement surgery,22 and blunt chest trauma.23
The acute management of this morbid condition can be quite challenging, but life preserving. Although there is a paucity of information, the ACC/AHA guidelines as well as data from the SHOCK trial support emergent revascularization either percutaneously or surgically.2,24 In the stable subset of patients presenting without ST elevation or hemodynamic instability, individual case reports of treatment with intravenous heparin in addition to either thombolytics3,25 or glycoprotein IIb/IIIa inhibitors26,27 have shown favorable results. In the few studies involving patients with acute myocardial infarction due to left main thrombosis, emergent surgical management yielded in-hospital mortality rates ranging from 46–53% with patients in cardiogenic shock representing the high end of the range.28–30 Reports involving percutaneous management of acute left main thrombosis or occlusion have found comparatively lower rates of in-hospital mortality (35-46%) when compared to the aforementioned surgical outcomes.1,7,31
In the present case, we speculate that the etiology of the left main thrombus was due to embolism from the prosthetic aortic valve. This assertion is based on the absence of significant atherosclerosis in the remainder of the coronary arteries in the setting of a mechanical aortic valve with a subtherapeutic INR. However, given the patient’s history of diabetes and the lack of intravascular ultrasound evaluation of the coronary vessels, we cannot rule out the possibility of in situ plaque rupture.
From a technical standpoint, aspiration thrombectomy proved to be of limited utility for complete thrombus removal in our case due to what was felt to be organized clot. Initial aspiration with a 6 Fr aspiration catheter was unsuccessful, but use of a larger lumen 7 Fr catheter yielded several fragments of thrombus. Although prior case reports of aspiration thrombectomy in the LMCA are available, neither of the previously published cases involved acute STEMI due to LMCA thrombosis.32,33 The use of rheolytic thrombectomy with the Angiojet catheter may be helpful in this context.34 In addition, the intra-arterial injection of a glycoprotein 2b/3a inhibitor could be considered — particularly to reduce infarct size.35 Finally, data are lacking on the utility of intra-aortic balloon counterpulsation in emergent, unprotected left main intervention during STEMI. Restoration of flow with immediate balloon angioplasty or aspiration thrombectomy may, in itself, improve the patient’s hemodynamics and obviate the need for balloon pump support. However, these interventions may also lead to no-reflow which, in the setting of left main thrombosis, may have fatal consequences. In this particular circumstance, cardiogenic shock necessitated immediate balloon pump insertion, which provided excellent hemodynamic support during this complex case.
To our knowledge, the percutaneous management of left main occlusion due to suspected embolized thrombus has not been described in the literature. Our case demonstrates the feasibility of percutaneous intervention with aspiration and stenting for this otherwise morbid condition.
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- Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med 1999;341:625-634.
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- Marso SP, Steg G, Plokker T, et al. Catheter-based reperfusion of unprotected left main stenosis during an acute myocardial infarction (the ULTIMA experience). Unprotected Left Main Trunk Intervention Multi-center Assessment. Am J Cardiol 1999;83:1513-517.
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- Lee SW, Hong MK, Lee CW, et al. Early and late clinical outcomes after primary stenting of the unprotected left main coronary artery stenosis in the setting of acute myocardial infarction. Int J Cardiol 2004;97:73-76.
- Sanborn TA, Sleeper LA, Webb JG, et al. Correlates of one-year survival inpatients with cardiogenic shock complicating acute myocardial infarction: Angiographic findings from the SHOCK trial. J Am Coll Cardiol 2003;42:1373-1379.
- Rdzanek A, Pietrasik A, Kochman J, Wilczynska J, Opolski G. Acute coronary syndrome caused by left main coronary artery plaque rupture and thrombosis — resolution after pharmacological treatment. Int J Cardiol 2007;117:e92-e94.
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From the Division of Cardiology, University of California San Diego, San Diego, California.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. No conflicts of interest were reported regarding the content herein.
Manuscript submitted March 24, 2011, provisional acceptance given April 14, 2011, final version accepted May 2, 2011.
Address for correspondence: Dr. Anand Prasad, University of California San Diego, California Division of Cardiology, 200 West Arbor Drive, San Diego, CA 92103. Email: firstname.lastname@example.org