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Resolution of a coronary embolus by intravenous application of bivalirudin
International Journal of Cardiology 132 (2009) e115 – e116 www.elsevier.com/locate/ijcard
Letter to the Editor
Resolution of a coronary embolus by intravenous application of bivalirudin Clemens Steinwender ⁎, Robert Hofmann, Bernhard Hartenthaler, Franz Leisch Cardiovascular Division, Academic Teaching and General Hospital Linz, Linz, Austria Received 1 August 2007; accepted 10 August 2007 Available online 26 November 2007
Abstract We report on a case of non-ST-segment myocardial infarction in the absence of coronary artery disease, caused by coronary embolism from the left atrial appendage. Due to the fact that the angiographically confirmed embolus did not resolve within 4 days of treatment with aspirin, clopidogrel and low molecular weight heparin (LMWH), we intravenously administered bivalirudin instead of LMWH for another 2 days and could demonstrate complete resolution of the embolus following this protocol. No bleeding complications or recurrence of myocardial ischemia occurred. Our observations may draw attention to bivalirudin therapy for coronary emboli, when LMWH is not effective. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Coronary embolism; Acute myocardial infarction; Bivalirudin
A 60-year-old man was referred from the emergency room to our intensive care unit for typical chest pain since 3 h. Shortly after admission the symptoms completely disappeared and did not reoccur. Apart from persistent atrial fibrillation, diagnosed by the general practitioner months ago, the medical history was inconspicuous. Though recommended, the patient was not on oral anticoagulation. Serial ECGs displayed normfrequent atrial fibrillation without signs of ongoing or recent myocardial ischemia. Though conservative treatment with aspirin, clopidogrel and subcutaneousely applied weightadjusted low molecular weight heparin (LMWH) was initiated immediately after admission, the initially normal creatinekinase rose to a level of 559 U/L, its MB-fraction to 79 U/L and troponine T to 2.31 μg/L. Transthoracic echocardiography showed a dilated cardiomyopathy with severe impairment of left ventricular systolic function but no distinct regional akinesis.
⁎ Corresponding author. Cardiovascular Division, Academic Teaching and General Hospital Linz, Linz, Austria, Krankenhausstraβe 9, A – 4020 Linz, Austria. Tel.: +43 732 7806 73211; fax: +43 732 7806 6205. E-mail address: [email protected] (C. Steinwender). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.08.032
Fig. 1. Angiography (LAO-projection) of the right coronary artery after treatment with aspirin, clopidogrel and subcutaneously applied low molecular weight heparin (LMWH) for 4 days. Free-floating Y-shaped thrombus at the bifurcation of the posterior descending artery and the posterolateral artery (arrow).
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C. Steinwender et al. / International Journal of Cardiology 132 (2009) e115–e116
Fig. 2. Control angiography (LAO-projection). Complete resolution of the embolus after intravenous administration of bivalirudin for 48 h.
Diagnostic cardiac catheterisation was performed after 4 days of treatment and revealed angiographically normal coronary arteries, but a single free-floating Y-shaped thrombus in the right coronary artery, located at the bifurcation of the posterior descending artery and the posterolateral artery (Fig. 1). As no evidence of a ruptured atherosclerotic plaque or signs of ongoing ischemia were present, no percutaneous coronary intervention was performed. The suspicion of coronary embolism from the left atrial appendage was substantiated by subsequent transesophageal echocardiography, which revealed solid and mobile thrombus formations herein. Due to the fact that the embolus had not resolved within 4 days of treatment with LMWH, this therapy was interrupted and bivalirudin was applied with an intravenous bolus of 0.75 mg/kg body weight, followed by an infusion of 1.75 mg/kg body weight/hour for 48 h. No bleeding complications or recurrence of myocardial ischemia occurred. After completion of this protocol, control angiography demonstrated complete resolution of the embolus with no evidence of distal migration or small branch occlusion (Fig. 2). Antiplatelet medication with aspirin and clopidogrel was stopped this day and permanent oral anticoagulation, overlapping with LMWH therapy, was initiated. The patient could be discharged from inpatient care after enrolment in our institution's ambulatory heart failure program. Atherosclerotic plaque rupture with consecutive superimposed thrombus formation is the major cause for acute coronary syndromes including ST-elevation myocardial infarction. However, up to 7% of patients undergoing coronary angiography for this indication do not have morphological changes typical for atherosclerotic coronary
disease. In these patients, coronary embolism, usually arising from the left atrium during or after atrial fibrillation, is the most probable pathophysiological mechanism [1]. Appropriate treatment of coronary embolism remains a therapeutic challenge. The strategy of intervention varies according to the acuity of the clinical presentation. If coronary embolism results in ST-elevation myocardial infarction, various interventional procedures, including Fogarty manoeuvres, sole balloon angioplasty, stenting or thrombus aspiration, have been suggested. However, in the case of non-ST-elevation myocardial infarction (NSTEMI), there is no conclusive evidence favouring an interventional or conservative strategy [2,3]. In our patients with NSTEMI and no signs of ongoing ischemia we tried to avoid any mechanical intervention at the site of the free-floating embolus. As standard treatment had failed to cause embolus resolution within 4 days, we successfully administered bivalirudin instead of LMWH. Bivalirudin has been shown to be as effective as LMWH plus a glycoprotein IIb/IIIa inhibitor in reducing ischemic events in patients with NSTEMI [4]. Despite the fact that the histologic composition of coronary emboli differs from thrombi agglomerating on ruptured plaques bivalirudin seems to have the potential to trigger and maintain complete resolution of both types of clots [3,5,6]. Our observations may therefore draw attention to bivalirudin as conservative therapeutic strategy for coronary emboli when administration of LMWH is not effective. Appendix A. Supplementary data Supplementary data associated with this article can be found, in the online version, at doi:10.1016/j.ijcard.2007.08.032. References [1] Rigatelli G. Normal angiogram in patients with acute coronary syndrome: searching for unusual substrates of myocardial ischemia. Int J Cardiol 2005;99:25–7. [2] Hernandez F, Pombo M, Dalmau R, et al. Acute coronary embolism: angiographic diagnosis and treatment with primary angioplasty. Catheter Cardiovasc Interv 2002;50:362–70. [3] 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. [4] Stone GW, McLaurin BT, Cox DA, et al. Bivalirudin for patients with acute coronary syndromes. N Engl J Med 2006;355:2203–16. [5] Von Korn H, Ohlow M, Donev S, et al. Export aspiration system in patients with acute coronary syndrome and visible thrombus provides no substantial benefit. Catheter Cardiovasc Interv 2007;70:36–43. [6] Saito T, Tamura K, Uchida D, Saito T, Nitta T, Sugisaki Y. Histopathological evaluation of left atrial appendage thrombogenesis removed during surgery for atrial fibrillation. Am Heart J 2007;153:704–11.
Letter to the Editor
Resolution of a coronary embolus by intravenous application of bivalirudin Clemens Steinwender ⁎, Robert Hofmann, Bernhard Hartenthaler, Franz Leisch Cardiovascular Division, Academic Teaching and General Hospital Linz, Linz, Austria Received 1 August 2007; accepted 10 August 2007 Available online 26 November 2007
Abstract We report on a case of non-ST-segment myocardial infarction in the absence of coronary artery disease, caused by coronary embolism from the left atrial appendage. Due to the fact that the angiographically confirmed embolus did not resolve within 4 days of treatment with aspirin, clopidogrel and low molecular weight heparin (LMWH), we intravenously administered bivalirudin instead of LMWH for another 2 days and could demonstrate complete resolution of the embolus following this protocol. No bleeding complications or recurrence of myocardial ischemia occurred. Our observations may draw attention to bivalirudin therapy for coronary emboli, when LMWH is not effective. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Coronary embolism; Acute myocardial infarction; Bivalirudin
A 60-year-old man was referred from the emergency room to our intensive care unit for typical chest pain since 3 h. Shortly after admission the symptoms completely disappeared and did not reoccur. Apart from persistent atrial fibrillation, diagnosed by the general practitioner months ago, the medical history was inconspicuous. Though recommended, the patient was not on oral anticoagulation. Serial ECGs displayed normfrequent atrial fibrillation without signs of ongoing or recent myocardial ischemia. Though conservative treatment with aspirin, clopidogrel and subcutaneousely applied weightadjusted low molecular weight heparin (LMWH) was initiated immediately after admission, the initially normal creatinekinase rose to a level of 559 U/L, its MB-fraction to 79 U/L and troponine T to 2.31 μg/L. Transthoracic echocardiography showed a dilated cardiomyopathy with severe impairment of left ventricular systolic function but no distinct regional akinesis.
⁎ Corresponding author. Cardiovascular Division, Academic Teaching and General Hospital Linz, Linz, Austria, Krankenhausstraβe 9, A – 4020 Linz, Austria. Tel.: +43 732 7806 73211; fax: +43 732 7806 6205. E-mail address: [email protected] (C. Steinwender). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.08.032
Fig. 1. Angiography (LAO-projection) of the right coronary artery after treatment with aspirin, clopidogrel and subcutaneously applied low molecular weight heparin (LMWH) for 4 days. Free-floating Y-shaped thrombus at the bifurcation of the posterior descending artery and the posterolateral artery (arrow).
e116
C. Steinwender et al. / International Journal of Cardiology 132 (2009) e115–e116
Fig. 2. Control angiography (LAO-projection). Complete resolution of the embolus after intravenous administration of bivalirudin for 48 h.
Diagnostic cardiac catheterisation was performed after 4 days of treatment and revealed angiographically normal coronary arteries, but a single free-floating Y-shaped thrombus in the right coronary artery, located at the bifurcation of the posterior descending artery and the posterolateral artery (Fig. 1). As no evidence of a ruptured atherosclerotic plaque or signs of ongoing ischemia were present, no percutaneous coronary intervention was performed. The suspicion of coronary embolism from the left atrial appendage was substantiated by subsequent transesophageal echocardiography, which revealed solid and mobile thrombus formations herein. Due to the fact that the embolus had not resolved within 4 days of treatment with LMWH, this therapy was interrupted and bivalirudin was applied with an intravenous bolus of 0.75 mg/kg body weight, followed by an infusion of 1.75 mg/kg body weight/hour for 48 h. No bleeding complications or recurrence of myocardial ischemia occurred. After completion of this protocol, control angiography demonstrated complete resolution of the embolus with no evidence of distal migration or small branch occlusion (Fig. 2). Antiplatelet medication with aspirin and clopidogrel was stopped this day and permanent oral anticoagulation, overlapping with LMWH therapy, was initiated. The patient could be discharged from inpatient care after enrolment in our institution's ambulatory heart failure program. Atherosclerotic plaque rupture with consecutive superimposed thrombus formation is the major cause for acute coronary syndromes including ST-elevation myocardial infarction. However, up to 7% of patients undergoing coronary angiography for this indication do not have morphological changes typical for atherosclerotic coronary
disease. In these patients, coronary embolism, usually arising from the left atrium during or after atrial fibrillation, is the most probable pathophysiological mechanism [1]. Appropriate treatment of coronary embolism remains a therapeutic challenge. The strategy of intervention varies according to the acuity of the clinical presentation. If coronary embolism results in ST-elevation myocardial infarction, various interventional procedures, including Fogarty manoeuvres, sole balloon angioplasty, stenting or thrombus aspiration, have been suggested. However, in the case of non-ST-elevation myocardial infarction (NSTEMI), there is no conclusive evidence favouring an interventional or conservative strategy [2,3]. In our patients with NSTEMI and no signs of ongoing ischemia we tried to avoid any mechanical intervention at the site of the free-floating embolus. As standard treatment had failed to cause embolus resolution within 4 days, we successfully administered bivalirudin instead of LMWH. Bivalirudin has been shown to be as effective as LMWH plus a glycoprotein IIb/IIIa inhibitor in reducing ischemic events in patients with NSTEMI [4]. Despite the fact that the histologic composition of coronary emboli differs from thrombi agglomerating on ruptured plaques bivalirudin seems to have the potential to trigger and maintain complete resolution of both types of clots [3,5,6]. Our observations may therefore draw attention to bivalirudin as conservative therapeutic strategy for coronary emboli when administration of LMWH is not effective. Appendix A. Supplementary data Supplementary data associated with this article can be found, in the online version, at doi:10.1016/j.ijcard.2007.08.032. References [1] Rigatelli G. Normal angiogram in patients with acute coronary syndrome: searching for unusual substrates of myocardial ischemia. Int J Cardiol 2005;99:25–7. [2] Hernandez F, Pombo M, Dalmau R, et al. Acute coronary embolism: angiographic diagnosis and treatment with primary angioplasty. Catheter Cardiovasc Interv 2002;50:362–70. [3] 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. [4] Stone GW, McLaurin BT, Cox DA, et al. Bivalirudin for patients with acute coronary syndromes. N Engl J Med 2006;355:2203–16. [5] Von Korn H, Ohlow M, Donev S, et al. Export aspiration system in patients with acute coronary syndrome and visible thrombus provides no substantial benefit. Catheter Cardiovasc Interv 2007;70:36–43. [6] Saito T, Tamura K, Uchida D, Saito T, Nitta T, Sugisaki Y. Histopathological evaluation of left atrial appendage thrombogenesis removed during surgery for atrial fibrillation. Am Heart J 2007;153:704–11.