J INVASIVE CARDIOL 2008;20:E124-E125
An infrequent, but potentially lethal, complication after aortic valve replacement (AVR) is the occurrence of iatrogenic coronary ostial stenosis. This complication has been observed after both mechanical and bioprosthetic valve use and its reported incidence varied between 0.3% and 5%.1,2 The most likely pathophysiological mechanism proposed is posttraumatic fibrous intimal proliferation caused by coronary ostia cannulation for direct cardioplegia during the operation.2 We report a unique case of early occurrence of left main stem (LMS) obstruction 2 weeks after AVR with large thrombotic burden in a patient not receiving any antithrombotic or antiplatelet therapy.
Case Presentation. A 74-year-old female underwent aortic valve replacement with a 19 mm Magna bioprosthesis (Edwards Lifesciences, Irvine, California) for aortic stenosis. Preoperative coronary angiography was normal. No antiplatelet or anticoagulant therapy was prescribed due to perioperative thrombocytopenia. The platelet count (PLT) at discharge was 130,000. She was brought to our emergency room 2 weeks post discharge with symptoms of chest pain and shortness of breath that had developed over several hours. Physical examination revealed that the patient was in cardiogenic shock. The electrocardiogram showed sinus tachycardia, prolonged QRS, ST-elevation in the lateral leads and widespread ST-depression in the inferior leads. Cardiac enzymes were elevated and the PLT was 644,000. Echocardiography showed global hypokinesis of the left ventricle with a left ventricular ejection fraction (LVEF) of 0.15, and normal position and function of the prosthetic valve. Circulation was supported by inotropes and intra-aortic balloon counterpulsation.
Urgent coronary angiography showed severe ostial LMS obstruction with a large amount of mobile thrombus in the LMS and the adjacent sinus of Valsalva (Figure 1). This was crossed with a Balance Middleweight (Abbott Vascular, Abbott Park, Illinois) guidewire, predilated with a 3.0 x 20 mm Voyager balloon (Guidant Corp., Indianapolis, Indiana) and a 3.5 x 18 mm Endeavor stent (Medtronic, Inc., Minneapolis, Minnesota) was deployed at 16 atm (Figure 2). Following predilatation and stent deployment, a large piece of mobile thrombus remained in the body of the LMS (Figure 3), and this was successfully aspirated using a Pronto™ expiration catheter (Vascular Solutions, Inc., Minneapolis, Minnesota) (Figure 4). The patient’s symptoms improved immediately and the LVEF at discharge was 0.35. The antiplatelet and anticoagulant regimen used during the procedure was oral aspirin and clopidogrel loading and intravenous heparin and abciximab. She was discharged on aspirin and clopidogrel. The patient refused follow-up angiography and was hospitalized twice over the next 8 months with mild heart failure decompensation treated medically.
Discussion. Several pathophysiological mechanisms for the complication presented here have been proposed.2 The most likely is posttraumatic fibrous intimal proliferation caused by insertion of the self-inflating balloon cannula for direct cardioplegia during AVR. Other mechanisms suggested are direct obstruction by the prosthetic valve and its components or edematous reaction. Oversizing of the aortic valve and abnormally low ostia may be contributing factors. All reported cases of this complication presented over several months (usually 2 to 6, but up to 1 year) following AVR.1–5
The earlier-than-expected presentation and the presence of a large amount of thrombus in the LMS and the adjacent sinus of Valsalva necessitating thrombectomy distinguish our case from previous reports. These may have been related to the absence of any antithrombotic or antiplatelet protection, and can be viewed as an argument for its importance in the early postoperative period and as reinforcing the existing guidelines that recommend the use of an anticoagulation regimen for the first 3 months following bioprosthetic AVR.6 Recent guidelines recommend bioprosthetic valves for AVR in elderly patients, and their use has soared over the past decade, especially in high-volume centers.7 Therefore, knowledge of this potentially lethal complication and its management become crucial, and the point of course is to provide the highest standard of care to the increasing numbers of patients receiving an aortic bioprosthetic valve.
Conclusion. The case of LMS obstruction following bioprosthetic AVR describe here demonstrates that this potentially lethal complication can occur earlier than we had previously thought. Moreover, this early obstruction can have a prominent thrombotic nature in the absence of any antithrombotic or antiplatelet protection. High suspicion of this complication and immediate interventional management can be life-saving.
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