ORIGINAL ARTICLE
Heart, Lung and Circulation (2014) 23, 422–427 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2013.10.086
Coronary Artery Embolism Causing Acute Myocardial Infarction in Patients with Mechanical Heart Valve Prosthesis: Which is the Optimal Treatment? Liang Tang, MD, Xin-qun Hu, MD, Sheng-hua Zhou, MD, PhD* Department of Cardiology, The Second Xiangya Hospital of Central South University, Changsha, China Received 21 September 2013; received in revised form 18 October 2013; accepted 22 October 2013; online published-ahead-of-print 30 October 2013
Objective
Coronary artery embolism resulting in acute myocardial infarction (AMI) is an infrequent but potentially life-threatening occurrence. To date, there is still no consensus in the literature regarding the optimal therapeutic algorithm for embolic myocardial infarction.
Patients
We present our experience with three patients who had mechanical valve prosthesis and suffered from AMI due to coronary artery embolism in the setting of sub-therapeutic or interrupted anti-coagulation therapy. Those patients were treated with intracoronary thrombolysis, thrombus aspiration followed by balloon angioplasty and thrombus aspiration alone, respectively.
Results
In our case 1, the coronary angiogram demonstrated extensive thrombus within the left circumflex coronary artery and extending into the left anterior descending (LAD). We performed intracoronary thrombolytic therapy, which results in completed thrombus resolution and favourable clinical outcome. In our case 3, coronary angiography revealed massive thrombus within the middle-LAD with a TIMI grade 3 distal flow. The patient underwent a successful thrombus aspiration procedure without stent implantation. In our case 2, the coronary angiography revealed total occlusion of the middle LAD, and thrombus aspiration was initially performed because of the large thrombus burden. However, this approach was unsuccessful and so the patient was then treated with balloon angioplasty, resulting in TIMI 2 flow.
Conclusion
Embolic myocardial infarction, although uncommon, can occur in predisposed groups such as those with prosthetic mechanical valves with sub-therapeutic anticoagulation. The treatment for this specific group of patients needs to be tailored individually.
Keywords
Coronary artery embolism Valve prosthesis Acute myocardial infarction Thrombolytic therapy Primary PCI
Introduction In patients with significant aortic and/or mitral valve disease, replacement with prosthetic mechanical valves or with tissue valves remains the current standard treatment. Mechanical prosthetic valves are highly thrombogenic, thereby necessitating life-long anticoagulation therapy with
warfarin to prevent thromboembolic events [1]. However, due to the narrow therapeutic window, need for frequent monitoring and dose adjustments, increased risk of bleeding complications, and poor patient tolerance, warfarin is underutilised in a substantial number of patients with prosthetic mechanical valves. Consequently, prosthetic valve thrombosis and systemic thromboembolic events can occur
*Corresponding author at: Department of Cardiology, The Second Xiangya Hospital of Central South University, No. 139, Middle Ren-min Road, Changsha, Hunan 410011, China. Tel.: +86 0731 85292012; fax: +86 0731 85294038., Emails: [email protected], [email protected] © 2013 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier Inc. All rights reserved.
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Coronary Embolism in Patients with Heart Valve Prosthesis
in this predisposed group of patients. The majority of embolic events present as ischaemic stroke [2]. Coronary artery embolism is a relatively rare but potentially life-threatening occurrence in this situation [2,3]. The management of patients with coronary embolism may present a treatment challenge for various reasons. In this article, we describe a case series of coronary artery embolism causing acute myocardial infarction (AMI) in patients with mechanical valve prosthesis. The management strategies of this unusual entity are discussed and the literature is reviewed.
Case 1 A 52 year-old woman was admitted to the emergency department complaining of sudden onset of severe retrosternal chest pain for three hours duration. Her past medical history was remarkable for aortic and mitral valve replacement with two mechanical tilting-disc valve 15 months earlier for symptomatic severe calcific aortic stenosis and mitral regurgitation. A coronary angiography performed prior to valve surgery, revealed completely normal coronary arteries. She had been maintained on warfarin therapy without complications; however, it had been suspended approximately seven days prior to the admission in preparation for an elective cystoscopy. No heparin cover was provided for this duration. At admission, physical examination revealed blood pressure of 95/60 mmHg and pulse rate of 93 bpm. Cardiac auscultation revealed normal prosthetic valve clicks and a grade II/VI ejection systolic murmur. The ECG showed sinus rhythm and marked ST-segment elevation in leads I, aVL, V4 to V6 and aVR. Serum cardiac biomarkers levels were elevated, with a creatine kinase level of 924 U/L, a creatine kinase-MB level of 118 ng/mL, and a troponin T level of 2.86 ng/mL. International normalised ratio (INR) was at a subtherapeutic level of 1.2. Transthoracic echocardiography showed normal prosthetic mitral valve functions and no
signs of thrombus on the valves or in the cardiac chambers. Urgent coronary angiography demonstrated extensive thrombus within the proximal left circumflex (LCX) and slightly extending into the left anterior descending (LAD) artery and the ramus medianus ostium (Fig. 1A and Video 1A). Moreover, all these three involved arteries with TIMI 3 flow distally, and were free of atherosclerotic lesions. The right coronary artery was normal. Since the high-burden thrombus was located at the left main bifurcation, percutaneous coronary intervention (PCI) therapy may carry a high risk of thrombus detachment and migration into the proximal LAD as well as distal embolisation. PCI was therefore not performed and a decision was made to proceed with intracoronary thrombolysis. Intracoronary injection of a bolus of 20 mg alteplase (tPA) was therefore administered slowly via a 6F guiding catheter in combination with a 24 h intravenous infusion of GP IIb/IIIa antagonist tirofiban and unfractionated heparin. Surprisingly, control coronary angiography performed 24 h later demonstrated complete dissolution of the massive thrombus, and no residual stenosis in the previous location (Fig. 1B and Video 1B). No bleeding complications occurred during the hospitalisation period. The patient made an uneventful recovery and was discharged five days later. She was maintained on lifelong warfarin therapy with target INR of 2.5–3.0 and was free from thromboembolic events at 18 months follow-up.
Case 2 A 49 year-old male patient was admitted to the emergency room because of retrosternal chest pain of 2 h duration. He had a history of rheumatic mitral and aortic regurgitation and had received two St. Jude mechanical prosthetic valves one year earlier. Preoperative coronary angiography revealed normal coronary arteries at that time. He had been receiving warfarin since then, but in the last two weeks it was
Figure 1 (A) Coronary angiogram showing extensive thrombus within the proximal left circumflex and slightly extending into the left anterior descending artery as well as the ramus medianus ostium (arrow); (B) Control angiography after intracoronary thrombolysis demonstrating complete resolution of the thrombi.
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Figure 2 (A) Coronary angiography showing complete occlusion of the middle portion of the left anterior descending artery (LAD) and a radiologic image suggestive of embolism (arrow). (B) Repeated angiography after balloon angioplasty revealing thrombus embolisation to the distal LAD with a TIMI grade 2 flow.
decided to discontinue it due to gross haematuria. The 12lead ECG showed atrial fibrillation and ST-segment elevation in leads V1-4, compatible with acute anterior wall AMI. After initial treatment with a loading dose of aspirin (300 mg), clopidogrel (600 mg) and a bolus of weight-adjusted heparin (5000 U), the patient was immediately taken to the catheterisation room for primary PCI. Coronary angiography revealed a complete occlusion of the middle portion of the LAD, with angiographic image features strongly suggestive of an embolic event (Fig. 2A). The LCX and RCA were normal with no evidence of atherosclerotic lesions. Given the clinical characteristics of the patient and the absence of evidence of an atherosclerotic basis for the lesion, thrombus aspiration (TA) was determined to be the optimal initial treatment for this case. TA was performed using a ZEEK aspiration catheter (Zeon Medical Inc., Tokyo, Japan); however, despite successive attempts, this failed to remove thrombus or improve coronary flow. Repeated balloon angioplasty was then performed, which resulted in thrombus dislodgement and embolisation to the distal LAD with a final TIMI grade 2 flow restored (Fig. 2B). At this point, the absence of underlying atherosclerotic lesions in the middle portion was confirmed. The patient was maintained on intravenous unfractioned heparin until therapeutic levels of warfarin were achieved and was discharged on oral anticoagulation but without the use of antiplatelet agents. He was symptom free without further clinical events at six month follow-up.
Case 3 A 48 year-old female, who had undergone aortic and mitral valve replacement with two St. Jude mechanical prosthetic valves one year earlier for rheumatic mitral and aortic regurgitation, was admitted with sudden onset of severe chest pain lasting about an hour. Preoperative angiography
revealed no significant coronary lesions. Although she had been maintained on anticoagulation with warfarin 2 mg daily, she had been missing her regular INR controls for about two months. The INR level was subtherapeutic at 1.63 on this admission. ECG showed sinus rhythm and STsegment elevation in leads V1-5, suggesting an anterior wall AMI. TTE did not demonstrate any obvious intracardiac thrombus or prosthesis malfunction. Treatment with 300 mg aspirin, clopidogrel and 5000 U of unfractionated heparin was initiated. Subsequently, the patient underwent emergent coronary angiography, which revealed large intraluminal filling defects consistent with intracoronary thrombus resulting in partial vessel occlusion in the middle segment of the LAD, with a TIMI grade 3 distal flow (Fig. 3A); otherwise, the coronary arteries were normal. Thrombus aspiration was attempted with a ZEEK aspiration catheter and simultaneously a glycoprotein IIb/IIIa inhibitor (tirofiban) infusion was administrated intravenously. After two passages of the aspiration catheter, the clot was successfully removed with complete restoration of TIMI grade 3 flow and only mild residual lesions in the mid-LAD (Fig. 3B), balloon angioplasty or stent implantation was therefore not performed. The patient was maintained on tirofiban and unfractioned heparin intravenous therapy for 24 h and commenced on long-term oral warfarin anticoagulation. She had made an uneventful recovery and discharged five days later with a therapeutic INR of 2.8.
Discussion Coronary artery embolism is a relatively rare cause of AMI, representing a distinct entity both in terms of aetiology and clinical treatment. Previous studies have shown that only 10– 13% of autopsy-studied myocardial infarctions are secondary to coronary artery embolism [3]. However, it should always be considered especially in high risk groups such as those
Coronary Embolism in Patients with Heart Valve Prosthesis
425
Figure 3 (A) Coronary angiography illustrating massive thrombus within the middle LAD, with a TIMI grade 3 distal flow (arrow). (B) Control angiography following thrombus aspiration showing the clot was totally removed.
with heart valve prosthesis particularly in the setting of suboptimal anti-coagulation, chronic atrial fibrillation, infective endocarditis, dilated cardiomyopathy, etc. [4]. It has been observed that the majority of emboli involve the left coronary system, which could be due to the preferential flow into the artery related to coronary flow volume characteristics and aortic valve morphology. Moreover, due to the LAD is straighter than the LCX; hence, coronary embolisms have been most frequently reported in the LAD territory [3,4], as highlighted in our case series. In the present case series, we speculate that the aetiology of STEMI were due to embolisation from the prosthetic mechanical valves. Evidence strongly supporting our diagnosis was (1) the absence of preceding symptoms of myocardial ischaemia together with normal appearance of the coronary arteries on the pre-operative angiogram, (2) the suggestive image of the culprit lesions and (3) the clinical setting of mechanical valve prosthesis with subtherapeutic or interrupted anti-coagulation. Admittedly, similar to the majority of previously described cases, the source of emboli in our case series were not clear, making the diagnosis of embolic AMI rather presumptive. Transoesophageal echocardiography is more sensitive for diagnosing potential cardiac thrombus; however, it was not performed in these critically ill patients because the lack of visualisation of a thrombus does not mean that it has not existed previously. Moreover, the finding of the exam would have not changed the management [5]. To date, the optimal therapeutic strategy for coronary embolism remains uncertain, and treatment decisions are usually difficult and individualised. Percutaneous interventions like catheter guided emboli aspiration, percutaneous transluminal coronary angioplasty (PTCA) with or without stenting, and medical approach with thrombolytic agents are current available modalities for this entity [6–8]. Ideally, thrombolytic therapy or use of an aspiration catheter achieves TIMI grade 3 flow without implantation of a coronary stent.
The role of thrombolysis in the treatment of coronary embolism has not been well established, but previous limited experience indicates that it can be a valid treatment option for selected patients in whom PCI procedures are difficult to perform because of inappropriate coronary anatomy or location of the thrombus. Dogan et al. [9] described a case of a 37 year-old female patient with nonST elevation myocardial infarction due to coronary embolism secondary to prosthetic mitral valve that was successfully managed using intravenous thrombolytic therapy with tissue plasminogen activator (tPA). Atmaca et al. [8] also reported that the use of combined regimen of half-dose tPA and tirofiban given intravenously was effective in achieving complete resolution of the embolic thrombi in a patient with mitral and aortic valve replacement when thrombectomy had failed. In the present case 1, we performed intracoronary thrombolytic therapy, which yielded a favourable result. We considered intracoronary thrombolytic therapy would be a reasonable option for this particular case because the involved arteries with TIMI 3 flow and the location of the coronary thrombus was a challenging place to treat with PCI. Any catheter-based intervention may lead to dislodgment of the thrombus, causing distal embolisation with further damage. Catheter aspiration embolectomy has been shown to be a feasible and effective strategy in this setting. Kotooka et al. [10] described three patients with AMI caused by coronary embolism secondary to paroxysmal or chronic atrial fibrillation, in two cases the emboli were completely removed using a thrombus aspiration device. Dagre et al. [11] reported a case of embolic anterior myocardial infarction in a middle-aged female with mechanical mitral valve prosthesis and subtherapeutic INR levels successfully treated with thrombus aspiration alone. Recently, Jaffe et al. [12] also present a case of a 46 year-old woman with anterior wall AMI due to left main coronary artery thrombus embolisation from a prosthetic mitral valve. The patient underwent a successful thrombus aspiration
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procedure without stent implantation and had a favourable outcome. In the present case 3, the angiogram showed a large thrombus burden in the mid-LAD with TIMI 3 flow, balloon angioplasty or coronary stenting would not be a rational choice in this setting, therefore, we decided to perform thrombus aspiration alone. After two passages of the aspiration catheter, the clot was completely removed with an excellent result. These reports suggest that thrombus aspiration alone is a feasible and effective strategy for the treatment of acute coronary embolism. However, due to the relatively small inner lumen diameter of the ordinary aspiration catheters, it makes aspiration thrombectomy usually of limited use for extraction of a large thrombus [13]. So PTCA or stent implantation is required in most cases in which the coronary is totally occluded. In our case 2, the coronary angiography revealed total occlusion of the middle LAD with no distal flow, thrombus aspiration was initially performed because of the large thrombus burden. However, despite several attempts, we could not exteriorise it and so balloon angioplasty was inevitable. The latter, unfortunately, produced successive distal embolisations, and yielded an unfavourable result. Saraiva et al. [14] presented a similar case of a 71 year-old female with aortic valve prosthesis who suffered an AMI secondary to an embolic occlusion of the LAD. They performed aspiration thrombectomy several times but it failed to aspirate the large thrombus and so the patient was then treated with balloon angioplasty, resulting in TIMI 2 flow. Interestingly, Aroney et al. [15] described an extremely rare case of a 30 month-old child with a mechanical mitral prosthesis who presented with refractory angina pectoris secondary to an embolic occlusion of the LAD. Successful balloon PTCA of the LAD was performed, resulting in resolution of angina symptoms and significant improvement of the left ventricular function. With the performance of PTCA, results are variable without stent placement. Since the embolus is usually firmer than the classic thrombus organised by plaque rupture, it may be transiently displaced laterally without undergoing any remodelling and obstruction will be unchanged [5]. Balloon dilation followed by stenting has been successfully employed by several authors in this context. Ranasinghe et al. [16] reported a case of a 59 year-old man presenting with cardiogenic shock caused by an acute left main occlusion secondary to emboli from aortic valve prosthesis. The patient was successfully treated with clot aspiration followed by PTCA and stenting. In another unusual case reported by Patel et al. [17], embolic occlusion of the left main coronary artery in a patient with mechanical aortic valve prosthesis was also treated with balloon dilatation and stenting successfully. It is worth noting that stent deployment in the setting of coronary embolism, however, is frequently complicated by distal embolisation resulting in no reflow and suboptimal myocardial reperfusion [5,18]. Besides the invasive strategy and thrombolysis, there have also been individual reports of using the new oral
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anticoagulants for the treatment of acute embolic myocardial infarction. Steinwender et al. [19] reported a case of non-STsegment myocardial infarction caused by coronary embolism from the left atrial appendage in which the embolus was completely resolved by intravenous application of bivalirudin. In summary, our case series demonstrates that although uncommon, embolic myocardial infarction can occur in predisposed groups such as those with prosthetic mechanical valves with subtherapeutic anticoagulation. Given the standard therapeutic algorithm remains uncertain, treatment for this specific group of patients needs to be tailored individually; that is to say, the decision should be made according to the acuity of the clinical presentation, the coronary angiographic features, etc.
Conflict of Interest None declared.
Appendix A. Supplementary data Supplementary data related to this article can be found, in the online version, at http://dx.doi.org/10.1016/j.hlc.2013. 10.086.
References [1] Roudaut R, Serri K, Lafitte S. Thrombosis of prosthetic heart valves: diagnosis and therapeutic considerations. Heart 2007;93:137–42. [2] Cannegieter SC, Rosendaal FR, Brier E. Thromboembolic and bleeding complications in patients with mechanical heart valve prosthesis. Circulation 1994;89:635–41. [3] Prizel KR, Hutchins GM, Bulkley BH. Coronary artery embolism and myocardial infarction, a clinicopathologic study of 55 patients. Ann Intern Med 1978;88:155–61. [4] Kraus PA, Lipman J. Coronary embolus causing myocardial infarction. Intens Care Med 1990;16:215–6. [5] Aslam MS, Sanghi V, Hersh S, Lakier JB. Coronary artery saddle embolus and myocardial infarction in a patient with prosthetic mitral valve. Catheter Cardiovasc Interv 2002;57:367–70. [6] Hung WC, Wu CJ, Chen WJ, Yang CH, Chang JP. Transradial intracoronary catheter-aspiration embolectomy for acute coronary embolism after mitral valve replacement. Tex Heart Inst J 2003;30:316–8. [7] Sial JA, Ferman MT, Saghir T, Rasool SI. Coronary embolism causing acute myocardial infarction in a patient with mitral valve prosthesis: successful management with angioplasty. J Pak Med Assoc 2009;59: 409–11. [8] Atmaca Y, Ozdol C, Erol C. Coronary embolism in a patient with mitral valve prosthesis: successful management with tirofiban and half-dose tissue-type plasminogen activator. Chin Med J 2007;120:2321–2. [9] Dogan M, Acikel S, Aksoy M, Cagirci G, Kilic H, Yesilay A, et al. Coronary saddle embolism causing myocardial infarction in a patient with mechanical mitral valve prosthesis: treatment with thrombolytic therapy. Int J Cardiol 2009;135:47–8. [10] Kotooka N, Otsuka Y, Yasuda S, Morii I, Kawamura A, Miyazaki S. Three cases of myocardial infarction due to coronary embolism. Jpn Heart J 2004;45:861–6. [11] Dagre A, Kouris N, Olympios C. Coronary artery disease: not always the case for ST-elevation myocardial infarction. J Invasive Cardiol 2012;24:e142–4. [12] Jaffe R, Shiran A, Rubinshtein R. Left main coronary artery occlusion due to thrombus embolization from a prosthetic mitral valve. JACC Cardiovasc Interv 2013;6:e43–4.
Coronary Embolism in Patients with Heart Valve Prosthesis
[13] Hosokawa Y, Tanaka K, Mizuno K. Successful treatment for refractory coronary thrombus with scoring balloon angioplasty. Catheter Cardiovasc Interv 2012;79:282–7. [14] Saraiva F, Matos V, Gonc¸alves L, Provideˆncia LA. Acute coronary embolism in a patient with a mechanical aortic prosthesis: case report. Rev Port Cardiol 2011;30(05):543–9. [15] Aroney CN, Justo RN, Radford DJ. Percutaneous transluminal coronary angioplasty in a 30-month-old child with embolic long segment occlusion of the left anterior descending artery. Catheter Cardiovasc Diagn 1998;44:206–9. [16] Ranasinghe I, Yiannikas J, Brieger D. Acute left main occlusion secondary to embolism from an aortic valve prosthesis: successful
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treatment with embolectomy and percutaneous coronary intervention. Int J Cardiol 2011;149:e110–2. [17] Patel M, Bhangoo M, Prasad A. Successful percutaneous treatment of suspected embolic left main thrombosis in a patient with a mechanical aortic valve. J Invasive Cardiol 2011;23:e263–6. [18] Camaro C, Aengevaeren WR. Acute myocardial infarction due to coronary artery embolism in a patient with atrial fibrillation. Neth Heart J 2009;17:297–9. [19] Steinwender C, Hofmann R, Hartenthaler B, Leisch F. Resolution of a coronary embolus by intravenous application of bivalirudin. Int J Cardiol 2009;132:e115–6.
Heart, Lung and Circulation (2014) 23, 422–427 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2013.10.086
Coronary Artery Embolism Causing Acute Myocardial Infarction in Patients with Mechanical Heart Valve Prosthesis: Which is the Optimal Treatment? Liang Tang, MD, Xin-qun Hu, MD, Sheng-hua Zhou, MD, PhD* Department of Cardiology, The Second Xiangya Hospital of Central South University, Changsha, China Received 21 September 2013; received in revised form 18 October 2013; accepted 22 October 2013; online published-ahead-of-print 30 October 2013
Objective
Coronary artery embolism resulting in acute myocardial infarction (AMI) is an infrequent but potentially life-threatening occurrence. To date, there is still no consensus in the literature regarding the optimal therapeutic algorithm for embolic myocardial infarction.
Patients
We present our experience with three patients who had mechanical valve prosthesis and suffered from AMI due to coronary artery embolism in the setting of sub-therapeutic or interrupted anti-coagulation therapy. Those patients were treated with intracoronary thrombolysis, thrombus aspiration followed by balloon angioplasty and thrombus aspiration alone, respectively.
Results
In our case 1, the coronary angiogram demonstrated extensive thrombus within the left circumflex coronary artery and extending into the left anterior descending (LAD). We performed intracoronary thrombolytic therapy, which results in completed thrombus resolution and favourable clinical outcome. In our case 3, coronary angiography revealed massive thrombus within the middle-LAD with a TIMI grade 3 distal flow. The patient underwent a successful thrombus aspiration procedure without stent implantation. In our case 2, the coronary angiography revealed total occlusion of the middle LAD, and thrombus aspiration was initially performed because of the large thrombus burden. However, this approach was unsuccessful and so the patient was then treated with balloon angioplasty, resulting in TIMI 2 flow.
Conclusion
Embolic myocardial infarction, although uncommon, can occur in predisposed groups such as those with prosthetic mechanical valves with sub-therapeutic anticoagulation. The treatment for this specific group of patients needs to be tailored individually.
Keywords
Coronary artery embolism Valve prosthesis Acute myocardial infarction Thrombolytic therapy Primary PCI
Introduction In patients with significant aortic and/or mitral valve disease, replacement with prosthetic mechanical valves or with tissue valves remains the current standard treatment. Mechanical prosthetic valves are highly thrombogenic, thereby necessitating life-long anticoagulation therapy with
warfarin to prevent thromboembolic events [1]. However, due to the narrow therapeutic window, need for frequent monitoring and dose adjustments, increased risk of bleeding complications, and poor patient tolerance, warfarin is underutilised in a substantial number of patients with prosthetic mechanical valves. Consequently, prosthetic valve thrombosis and systemic thromboembolic events can occur
*Corresponding author at: Department of Cardiology, The Second Xiangya Hospital of Central South University, No. 139, Middle Ren-min Road, Changsha, Hunan 410011, China. Tel.: +86 0731 85292012; fax: +86 0731 85294038., Emails: [email protected], [email protected] © 2013 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier Inc. All rights reserved.
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Coronary Embolism in Patients with Heart Valve Prosthesis
in this predisposed group of patients. The majority of embolic events present as ischaemic stroke [2]. Coronary artery embolism is a relatively rare but potentially life-threatening occurrence in this situation [2,3]. The management of patients with coronary embolism may present a treatment challenge for various reasons. In this article, we describe a case series of coronary artery embolism causing acute myocardial infarction (AMI) in patients with mechanical valve prosthesis. The management strategies of this unusual entity are discussed and the literature is reviewed.
Case 1 A 52 year-old woman was admitted to the emergency department complaining of sudden onset of severe retrosternal chest pain for three hours duration. Her past medical history was remarkable for aortic and mitral valve replacement with two mechanical tilting-disc valve 15 months earlier for symptomatic severe calcific aortic stenosis and mitral regurgitation. A coronary angiography performed prior to valve surgery, revealed completely normal coronary arteries. She had been maintained on warfarin therapy without complications; however, it had been suspended approximately seven days prior to the admission in preparation for an elective cystoscopy. No heparin cover was provided for this duration. At admission, physical examination revealed blood pressure of 95/60 mmHg and pulse rate of 93 bpm. Cardiac auscultation revealed normal prosthetic valve clicks and a grade II/VI ejection systolic murmur. The ECG showed sinus rhythm and marked ST-segment elevation in leads I, aVL, V4 to V6 and aVR. Serum cardiac biomarkers levels were elevated, with a creatine kinase level of 924 U/L, a creatine kinase-MB level of 118 ng/mL, and a troponin T level of 2.86 ng/mL. International normalised ratio (INR) was at a subtherapeutic level of 1.2. Transthoracic echocardiography showed normal prosthetic mitral valve functions and no
signs of thrombus on the valves or in the cardiac chambers. Urgent coronary angiography demonstrated extensive thrombus within the proximal left circumflex (LCX) and slightly extending into the left anterior descending (LAD) artery and the ramus medianus ostium (Fig. 1A and Video 1A). Moreover, all these three involved arteries with TIMI 3 flow distally, and were free of atherosclerotic lesions. The right coronary artery was normal. Since the high-burden thrombus was located at the left main bifurcation, percutaneous coronary intervention (PCI) therapy may carry a high risk of thrombus detachment and migration into the proximal LAD as well as distal embolisation. PCI was therefore not performed and a decision was made to proceed with intracoronary thrombolysis. Intracoronary injection of a bolus of 20 mg alteplase (tPA) was therefore administered slowly via a 6F guiding catheter in combination with a 24 h intravenous infusion of GP IIb/IIIa antagonist tirofiban and unfractionated heparin. Surprisingly, control coronary angiography performed 24 h later demonstrated complete dissolution of the massive thrombus, and no residual stenosis in the previous location (Fig. 1B and Video 1B). No bleeding complications occurred during the hospitalisation period. The patient made an uneventful recovery and was discharged five days later. She was maintained on lifelong warfarin therapy with target INR of 2.5–3.0 and was free from thromboembolic events at 18 months follow-up.
Case 2 A 49 year-old male patient was admitted to the emergency room because of retrosternal chest pain of 2 h duration. He had a history of rheumatic mitral and aortic regurgitation and had received two St. Jude mechanical prosthetic valves one year earlier. Preoperative coronary angiography revealed normal coronary arteries at that time. He had been receiving warfarin since then, but in the last two weeks it was
Figure 1 (A) Coronary angiogram showing extensive thrombus within the proximal left circumflex and slightly extending into the left anterior descending artery as well as the ramus medianus ostium (arrow); (B) Control angiography after intracoronary thrombolysis demonstrating complete resolution of the thrombi.
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Figure 2 (A) Coronary angiography showing complete occlusion of the middle portion of the left anterior descending artery (LAD) and a radiologic image suggestive of embolism (arrow). (B) Repeated angiography after balloon angioplasty revealing thrombus embolisation to the distal LAD with a TIMI grade 2 flow.
decided to discontinue it due to gross haematuria. The 12lead ECG showed atrial fibrillation and ST-segment elevation in leads V1-4, compatible with acute anterior wall AMI. After initial treatment with a loading dose of aspirin (300 mg), clopidogrel (600 mg) and a bolus of weight-adjusted heparin (5000 U), the patient was immediately taken to the catheterisation room for primary PCI. Coronary angiography revealed a complete occlusion of the middle portion of the LAD, with angiographic image features strongly suggestive of an embolic event (Fig. 2A). The LCX and RCA were normal with no evidence of atherosclerotic lesions. Given the clinical characteristics of the patient and the absence of evidence of an atherosclerotic basis for the lesion, thrombus aspiration (TA) was determined to be the optimal initial treatment for this case. TA was performed using a ZEEK aspiration catheter (Zeon Medical Inc., Tokyo, Japan); however, despite successive attempts, this failed to remove thrombus or improve coronary flow. Repeated balloon angioplasty was then performed, which resulted in thrombus dislodgement and embolisation to the distal LAD with a final TIMI grade 2 flow restored (Fig. 2B). At this point, the absence of underlying atherosclerotic lesions in the middle portion was confirmed. The patient was maintained on intravenous unfractioned heparin until therapeutic levels of warfarin were achieved and was discharged on oral anticoagulation but without the use of antiplatelet agents. He was symptom free without further clinical events at six month follow-up.
Case 3 A 48 year-old female, who had undergone aortic and mitral valve replacement with two St. Jude mechanical prosthetic valves one year earlier for rheumatic mitral and aortic regurgitation, was admitted with sudden onset of severe chest pain lasting about an hour. Preoperative angiography
revealed no significant coronary lesions. Although she had been maintained on anticoagulation with warfarin 2 mg daily, she had been missing her regular INR controls for about two months. The INR level was subtherapeutic at 1.63 on this admission. ECG showed sinus rhythm and STsegment elevation in leads V1-5, suggesting an anterior wall AMI. TTE did not demonstrate any obvious intracardiac thrombus or prosthesis malfunction. Treatment with 300 mg aspirin, clopidogrel and 5000 U of unfractionated heparin was initiated. Subsequently, the patient underwent emergent coronary angiography, which revealed large intraluminal filling defects consistent with intracoronary thrombus resulting in partial vessel occlusion in the middle segment of the LAD, with a TIMI grade 3 distal flow (Fig. 3A); otherwise, the coronary arteries were normal. Thrombus aspiration was attempted with a ZEEK aspiration catheter and simultaneously a glycoprotein IIb/IIIa inhibitor (tirofiban) infusion was administrated intravenously. After two passages of the aspiration catheter, the clot was successfully removed with complete restoration of TIMI grade 3 flow and only mild residual lesions in the mid-LAD (Fig. 3B), balloon angioplasty or stent implantation was therefore not performed. The patient was maintained on tirofiban and unfractioned heparin intravenous therapy for 24 h and commenced on long-term oral warfarin anticoagulation. She had made an uneventful recovery and discharged five days later with a therapeutic INR of 2.8.
Discussion Coronary artery embolism is a relatively rare cause of AMI, representing a distinct entity both in terms of aetiology and clinical treatment. Previous studies have shown that only 10– 13% of autopsy-studied myocardial infarctions are secondary to coronary artery embolism [3]. However, it should always be considered especially in high risk groups such as those
Coronary Embolism in Patients with Heart Valve Prosthesis
425
Figure 3 (A) Coronary angiography illustrating massive thrombus within the middle LAD, with a TIMI grade 3 distal flow (arrow). (B) Control angiography following thrombus aspiration showing the clot was totally removed.
with heart valve prosthesis particularly in the setting of suboptimal anti-coagulation, chronic atrial fibrillation, infective endocarditis, dilated cardiomyopathy, etc. [4]. It has been observed that the majority of emboli involve the left coronary system, which could be due to the preferential flow into the artery related to coronary flow volume characteristics and aortic valve morphology. Moreover, due to the LAD is straighter than the LCX; hence, coronary embolisms have been most frequently reported in the LAD territory [3,4], as highlighted in our case series. In the present case series, we speculate that the aetiology of STEMI were due to embolisation from the prosthetic mechanical valves. Evidence strongly supporting our diagnosis was (1) the absence of preceding symptoms of myocardial ischaemia together with normal appearance of the coronary arteries on the pre-operative angiogram, (2) the suggestive image of the culprit lesions and (3) the clinical setting of mechanical valve prosthesis with subtherapeutic or interrupted anti-coagulation. Admittedly, similar to the majority of previously described cases, the source of emboli in our case series were not clear, making the diagnosis of embolic AMI rather presumptive. Transoesophageal echocardiography is more sensitive for diagnosing potential cardiac thrombus; however, it was not performed in these critically ill patients because the lack of visualisation of a thrombus does not mean that it has not existed previously. Moreover, the finding of the exam would have not changed the management [5]. To date, the optimal therapeutic strategy for coronary embolism remains uncertain, and treatment decisions are usually difficult and individualised. Percutaneous interventions like catheter guided emboli aspiration, percutaneous transluminal coronary angioplasty (PTCA) with or without stenting, and medical approach with thrombolytic agents are current available modalities for this entity [6–8]. Ideally, thrombolytic therapy or use of an aspiration catheter achieves TIMI grade 3 flow without implantation of a coronary stent.
The role of thrombolysis in the treatment of coronary embolism has not been well established, but previous limited experience indicates that it can be a valid treatment option for selected patients in whom PCI procedures are difficult to perform because of inappropriate coronary anatomy or location of the thrombus. Dogan et al. [9] described a case of a 37 year-old female patient with nonST elevation myocardial infarction due to coronary embolism secondary to prosthetic mitral valve that was successfully managed using intravenous thrombolytic therapy with tissue plasminogen activator (tPA). Atmaca et al. [8] also reported that the use of combined regimen of half-dose tPA and tirofiban given intravenously was effective in achieving complete resolution of the embolic thrombi in a patient with mitral and aortic valve replacement when thrombectomy had failed. In the present case 1, we performed intracoronary thrombolytic therapy, which yielded a favourable result. We considered intracoronary thrombolytic therapy would be a reasonable option for this particular case because the involved arteries with TIMI 3 flow and the location of the coronary thrombus was a challenging place to treat with PCI. Any catheter-based intervention may lead to dislodgment of the thrombus, causing distal embolisation with further damage. Catheter aspiration embolectomy has been shown to be a feasible and effective strategy in this setting. Kotooka et al. [10] described three patients with AMI caused by coronary embolism secondary to paroxysmal or chronic atrial fibrillation, in two cases the emboli were completely removed using a thrombus aspiration device. Dagre et al. [11] reported a case of embolic anterior myocardial infarction in a middle-aged female with mechanical mitral valve prosthesis and subtherapeutic INR levels successfully treated with thrombus aspiration alone. Recently, Jaffe et al. [12] also present a case of a 46 year-old woman with anterior wall AMI due to left main coronary artery thrombus embolisation from a prosthetic mitral valve. The patient underwent a successful thrombus aspiration
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procedure without stent implantation and had a favourable outcome. In the present case 3, the angiogram showed a large thrombus burden in the mid-LAD with TIMI 3 flow, balloon angioplasty or coronary stenting would not be a rational choice in this setting, therefore, we decided to perform thrombus aspiration alone. After two passages of the aspiration catheter, the clot was completely removed with an excellent result. These reports suggest that thrombus aspiration alone is a feasible and effective strategy for the treatment of acute coronary embolism. However, due to the relatively small inner lumen diameter of the ordinary aspiration catheters, it makes aspiration thrombectomy usually of limited use for extraction of a large thrombus [13]. So PTCA or stent implantation is required in most cases in which the coronary is totally occluded. In our case 2, the coronary angiography revealed total occlusion of the middle LAD with no distal flow, thrombus aspiration was initially performed because of the large thrombus burden. However, despite several attempts, we could not exteriorise it and so balloon angioplasty was inevitable. The latter, unfortunately, produced successive distal embolisations, and yielded an unfavourable result. Saraiva et al. [14] presented a similar case of a 71 year-old female with aortic valve prosthesis who suffered an AMI secondary to an embolic occlusion of the LAD. They performed aspiration thrombectomy several times but it failed to aspirate the large thrombus and so the patient was then treated with balloon angioplasty, resulting in TIMI 2 flow. Interestingly, Aroney et al. [15] described an extremely rare case of a 30 month-old child with a mechanical mitral prosthesis who presented with refractory angina pectoris secondary to an embolic occlusion of the LAD. Successful balloon PTCA of the LAD was performed, resulting in resolution of angina symptoms and significant improvement of the left ventricular function. With the performance of PTCA, results are variable without stent placement. Since the embolus is usually firmer than the classic thrombus organised by plaque rupture, it may be transiently displaced laterally without undergoing any remodelling and obstruction will be unchanged [5]. Balloon dilation followed by stenting has been successfully employed by several authors in this context. Ranasinghe et al. [16] reported a case of a 59 year-old man presenting with cardiogenic shock caused by an acute left main occlusion secondary to emboli from aortic valve prosthesis. The patient was successfully treated with clot aspiration followed by PTCA and stenting. In another unusual case reported by Patel et al. [17], embolic occlusion of the left main coronary artery in a patient with mechanical aortic valve prosthesis was also treated with balloon dilatation and stenting successfully. It is worth noting that stent deployment in the setting of coronary embolism, however, is frequently complicated by distal embolisation resulting in no reflow and suboptimal myocardial reperfusion [5,18]. Besides the invasive strategy and thrombolysis, there have also been individual reports of using the new oral
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anticoagulants for the treatment of acute embolic myocardial infarction. Steinwender et al. [19] reported a case of non-STsegment myocardial infarction caused by coronary embolism from the left atrial appendage in which the embolus was completely resolved by intravenous application of bivalirudin. In summary, our case series demonstrates that although uncommon, embolic myocardial infarction can occur in predisposed groups such as those with prosthetic mechanical valves with subtherapeutic anticoagulation. Given the standard therapeutic algorithm remains uncertain, treatment for this specific group of patients needs to be tailored individually; that is to say, the decision should be made according to the acuity of the clinical presentation, the coronary angiographic features, etc.
Conflict of Interest None declared.
Appendix A. Supplementary data Supplementary data related to this article can be found, in the online version, at http://dx.doi.org/10.1016/j.hlc.2013. 10.086.
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