CLINICAL SPOTLIGHT
Heart, Lung and Circulation (2014) 23, e237–e239 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2014.06.007
Delayed Left Ventricular Apical Thrombus Formation Following Discontinuation of Dual Anti-Platelet Therapy Kevin Liou, MBBS, MPH *, John Lambros, MBBS, FRACP Eastern Heart Clinic, Prince of Wales Hospital, Barker Street, Randwick, 2031, NSW Received 13 March 2014; accepted 3 June 2014; online published-ahead-of-print 28 June 2014
Delayed de novo left ventricular apical thrombus following a distant antero-apical myocardial infarction has to our knowledge not been previously reported. Herein we describe a patient who developed an apical thrombus 18 months after his initial infarct following cessation of dual anti-platelet therapy for a traumatic subdural haematoma requiring surgical evacuation. Keywords
Late apical thrombus Dual anti-platelet therapy Prasugrel Myocardial infarction Subdural haematoma
Introduction Once a common complication, left ventricular (LV) apical thrombi following myocardial infarction is now a rare occurrence. While better reperfusion strategies may be the dominant mediator, the role of increasingly more potent antiplatelet therapies cannot be neglected. In this case report, we describe a 61 year-old man with late apical thrombus formation following recent cessation of his dual anti-platelet therapy (DAPT).
Case Presentation Our patient was treated for an anterior ST elevation myocardial infarction (STEMI) in June 2012 with two bare metal stents to his left anterior descending artery. He was discharged on aspirin and prasugrel with residual mild to moderate antero-apical segmental LV impairment, but no evidence of apical thrombus. While on his DAPT he suffered a traumatic subdural haematoma, which required cessation of his DAPT and surgical evacuation. His echo at this time remained unchanged. He attended an early cardiology follow-up appointment at
our institution a month later (18 months from initial STEMI) and was diagnosed with an LV apical thrombus on repeat echocardiogram (Figs. 1 and 2). Our patient was treated with intravenous heparin and subsequently warfarin after neurosurgical clearance. The patient remained well and a repeat echocardiogram showed complete resolution of the thrombus.
Discussion With better reperfusion strategies and subsequent ventricular remodelling, the incidence of LV thrombus has declined significantly [1]. Most LV thrombi form early following a myocardial infarction [2] and resolve over time with treatment [3]. A late apical thrombus formation 18 months after the initial STEMI has to our knowledge never been reported. Our patient’s persistent LV impairment provided a thrombogenic substrate [4,5], and the recent subdural haematoma may have provoked a prothrombotic state, although the cessation of his DAPT may also have played a role. While heparin has been shown to reduce LV thrombus [6] and its embolic complications [7], warfarin as a primary
*Corresponding author at: Eastern Heart Clinic, Prince of Wales Hospital, Barker Street, Randwick, 2031, NSW. Tel.: +423 778 504; fax: +9382 0799., Email: [email protected] © 2014 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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K. Liou, J. Lambros
Figure 1 Apical 4 chamber view of the apical thrombus.
Figure 2 Apical 2 chamber view of the apical thrombus.
preventative strategy against thrombus formation has never been tested. Indeed, its role may be further challenged in the era of highly potent anti-platelet therapies. Aspirin alone, and in combination with other anti-platelet agents, has been shown to be ineffective in preventing thrombus formation in low flow and low shear scenarios [8,9], and within infarcted LV [10,11]. These studies however predated the routine use of DAPT and introduction of newer antiplatelet therapies currently on the market.
Prasugrel is a more potent thienopyridine than clopidogrel [12] and it may have helped prevent a LV thrombus in our patient until the haemostatic balance was interrupted by a change in his clinical status. This is an intriguing prospect particularly in the PCI era where DAPT inclusive of more potent anti-platelet therapies such as prasugrel and ticagrelor is becoming routine, and the baseline risk of thrombus formation is low. These newer agents however have not been tested as an anti-thrombotic strategy, and as such their
Late LV thrombus
efficacy in preventing systemic thrombus formation remains largely unknown.
Conclusions Our novel case demonstrates that patients with persistent impaired LV function and wall motion abnormality are at risk of de novo thrombus formation distant from the initial myocardial infection. While warfarin is the current therapy of choice in high risk patients and patients with established LV thrombus, its role in the modern era of prompt revascularisation and highly potent anti-platelet therapies is unclear. DAPT containing either prasugrel or ticagrelor may protect against LV thrombus formation in the post-PCI era.
References [1] Kalra A, Jang IK. Prevalence of early left ventricular thrombus after primary coronary intervention for acute myocardial infarction. J Thromb Thrombolysis 2000;10(2):133. [2] Ku¨pper AJ, Verheugt FW, Peels CH, Galema T, Roos P. Left ventricular thrombus incidence and behavior studied by serial two-dimensional echocardiography in acute anterior myocardial infarction: left ventricular wall motion, systemic embolism and oral anticoagulation. J Am Coll Cardiol 1989;13(7):1514. [3] Neskovic´ A, Marinkovic´ J, Bojic´ M, Popovic A. Predictors of left ventricular thrombus formation and disappearance after anterior wall myocardial infarction. Eur Heart J 1998;19(6):908.
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[4] Asinger RW, Mikell FL, Elsperger J, Hodges M. Incidence of left-ventricular thrombosis after acute transmural myocardial infarction. Serial evaluation by two-dimensional echocardiography. N Engl J Med 1981;305(6):297. [5] Chiarella F, Santoro E, Domenicucci S, Maggioni A, Vecchio C. Predischarge two-dimensional echocardiographic evaluation of left ventricular thrombosis after acute myocardial infarction in the GISSI-3 study. Am J Cardiol 1998;81:822–7. [6] Turpie AG, Robinson JG, Doyle DJ, Mulji AS, Mishkel GJ, Sealey BJ, et al. Comparison of high-dose with low-dose subcutaneous heparin to prevent left ventricular mural thrombosis in patients with acute transmural anterior myocardial infarction. N Engl J Med 1989;320: 352–7. [7] Heik S, Kupper W, Hamm C, Bleifeld W, Koschyk DH, Waters D, et al. Efficacy of high dose intravenous heparin for treatment of left ventricular thrombi with high embolic risk. JACC 1994;24(5):1305–9. [8] Brighton T, Eikelboom J, Mann K, Mister R, Gallus A, Ockelford P, et al. Low-dose aspirin for preventing recurrent venous thromboembolism. N Engl J Med 2012;367:1979–87. [9] The ACTIVE investigators.. Effect of clopidogrel added to aspirin in patients with atrial fibrillation. N Engl J Med 2009;360:2066–78. [10] Funke A, Verhengl F, Peels C, Galema T, Den Hollander W, Roos J. Effect of low dose acetylsalicylic acid on the frequency and hematologic activity of left ventricular thrombus in anterior wall acute myocardial infarction. Am J Cardiol 1989;63:917–20. [11] Johannessen K, Stratton J, Taulow E, Osterud B, von der Lippe G. Usefulness of aspirin plus dipyridamole in reducing left ventricular thrombus formation in anterior wall acute myocardial infarction. Am J Cardiol 1989;63:101–2. [12] Wiviott SD, Braunwald E, McCabe CH, Montalescot G, Ruzyllo W, Gottlieb S, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med 2007;357:2001–15.
Heart, Lung and Circulation (2014) 23, e237–e239 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2014.06.007
Delayed Left Ventricular Apical Thrombus Formation Following Discontinuation of Dual Anti-Platelet Therapy Kevin Liou, MBBS, MPH *, John Lambros, MBBS, FRACP Eastern Heart Clinic, Prince of Wales Hospital, Barker Street, Randwick, 2031, NSW Received 13 March 2014; accepted 3 June 2014; online published-ahead-of-print 28 June 2014
Delayed de novo left ventricular apical thrombus following a distant antero-apical myocardial infarction has to our knowledge not been previously reported. Herein we describe a patient who developed an apical thrombus 18 months after his initial infarct following cessation of dual anti-platelet therapy for a traumatic subdural haematoma requiring surgical evacuation. Keywords
Late apical thrombus Dual anti-platelet therapy Prasugrel Myocardial infarction Subdural haematoma
Introduction Once a common complication, left ventricular (LV) apical thrombi following myocardial infarction is now a rare occurrence. While better reperfusion strategies may be the dominant mediator, the role of increasingly more potent antiplatelet therapies cannot be neglected. In this case report, we describe a 61 year-old man with late apical thrombus formation following recent cessation of his dual anti-platelet therapy (DAPT).
Case Presentation Our patient was treated for an anterior ST elevation myocardial infarction (STEMI) in June 2012 with two bare metal stents to his left anterior descending artery. He was discharged on aspirin and prasugrel with residual mild to moderate antero-apical segmental LV impairment, but no evidence of apical thrombus. While on his DAPT he suffered a traumatic subdural haematoma, which required cessation of his DAPT and surgical evacuation. His echo at this time remained unchanged. He attended an early cardiology follow-up appointment at
our institution a month later (18 months from initial STEMI) and was diagnosed with an LV apical thrombus on repeat echocardiogram (Figs. 1 and 2). Our patient was treated with intravenous heparin and subsequently warfarin after neurosurgical clearance. The patient remained well and a repeat echocardiogram showed complete resolution of the thrombus.
Discussion With better reperfusion strategies and subsequent ventricular remodelling, the incidence of LV thrombus has declined significantly [1]. Most LV thrombi form early following a myocardial infarction [2] and resolve over time with treatment [3]. A late apical thrombus formation 18 months after the initial STEMI has to our knowledge never been reported. Our patient’s persistent LV impairment provided a thrombogenic substrate [4,5], and the recent subdural haematoma may have provoked a prothrombotic state, although the cessation of his DAPT may also have played a role. While heparin has been shown to reduce LV thrombus [6] and its embolic complications [7], warfarin as a primary
*Corresponding author at: Eastern Heart Clinic, Prince of Wales Hospital, Barker Street, Randwick, 2031, NSW. Tel.: +423 778 504; fax: +9382 0799., Email: [email protected] © 2014 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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K. Liou, J. Lambros
Figure 1 Apical 4 chamber view of the apical thrombus.
Figure 2 Apical 2 chamber view of the apical thrombus.
preventative strategy against thrombus formation has never been tested. Indeed, its role may be further challenged in the era of highly potent anti-platelet therapies. Aspirin alone, and in combination with other anti-platelet agents, has been shown to be ineffective in preventing thrombus formation in low flow and low shear scenarios [8,9], and within infarcted LV [10,11]. These studies however predated the routine use of DAPT and introduction of newer antiplatelet therapies currently on the market.
Prasugrel is a more potent thienopyridine than clopidogrel [12] and it may have helped prevent a LV thrombus in our patient until the haemostatic balance was interrupted by a change in his clinical status. This is an intriguing prospect particularly in the PCI era where DAPT inclusive of more potent anti-platelet therapies such as prasugrel and ticagrelor is becoming routine, and the baseline risk of thrombus formation is low. These newer agents however have not been tested as an anti-thrombotic strategy, and as such their
Late LV thrombus
efficacy in preventing systemic thrombus formation remains largely unknown.
Conclusions Our novel case demonstrates that patients with persistent impaired LV function and wall motion abnormality are at risk of de novo thrombus formation distant from the initial myocardial infection. While warfarin is the current therapy of choice in high risk patients and patients with established LV thrombus, its role in the modern era of prompt revascularisation and highly potent anti-platelet therapies is unclear. DAPT containing either prasugrel or ticagrelor may protect against LV thrombus formation in the post-PCI era.
References [1] Kalra A, Jang IK. Prevalence of early left ventricular thrombus after primary coronary intervention for acute myocardial infarction. J Thromb Thrombolysis 2000;10(2):133. [2] Ku¨pper AJ, Verheugt FW, Peels CH, Galema T, Roos P. Left ventricular thrombus incidence and behavior studied by serial two-dimensional echocardiography in acute anterior myocardial infarction: left ventricular wall motion, systemic embolism and oral anticoagulation. J Am Coll Cardiol 1989;13(7):1514. [3] Neskovic´ A, Marinkovic´ J, Bojic´ M, Popovic A. Predictors of left ventricular thrombus formation and disappearance after anterior wall myocardial infarction. Eur Heart J 1998;19(6):908.
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[4] Asinger RW, Mikell FL, Elsperger J, Hodges M. Incidence of left-ventricular thrombosis after acute transmural myocardial infarction. Serial evaluation by two-dimensional echocardiography. N Engl J Med 1981;305(6):297. [5] Chiarella F, Santoro E, Domenicucci S, Maggioni A, Vecchio C. Predischarge two-dimensional echocardiographic evaluation of left ventricular thrombosis after acute myocardial infarction in the GISSI-3 study. Am J Cardiol 1998;81:822–7. [6] Turpie AG, Robinson JG, Doyle DJ, Mulji AS, Mishkel GJ, Sealey BJ, et al. Comparison of high-dose with low-dose subcutaneous heparin to prevent left ventricular mural thrombosis in patients with acute transmural anterior myocardial infarction. N Engl J Med 1989;320: 352–7. [7] Heik S, Kupper W, Hamm C, Bleifeld W, Koschyk DH, Waters D, et al. Efficacy of high dose intravenous heparin for treatment of left ventricular thrombi with high embolic risk. JACC 1994;24(5):1305–9. [8] Brighton T, Eikelboom J, Mann K, Mister R, Gallus A, Ockelford P, et al. Low-dose aspirin for preventing recurrent venous thromboembolism. N Engl J Med 2012;367:1979–87. [9] The ACTIVE investigators.. Effect of clopidogrel added to aspirin in patients with atrial fibrillation. N Engl J Med 2009;360:2066–78. [10] Funke A, Verhengl F, Peels C, Galema T, Den Hollander W, Roos J. Effect of low dose acetylsalicylic acid on the frequency and hematologic activity of left ventricular thrombus in anterior wall acute myocardial infarction. Am J Cardiol 1989;63:917–20. [11] Johannessen K, Stratton J, Taulow E, Osterud B, von der Lippe G. Usefulness of aspirin plus dipyridamole in reducing left ventricular thrombus formation in anterior wall acute myocardial infarction. Am J Cardiol 1989;63:101–2. [12] Wiviott SD, Braunwald E, McCabe CH, Montalescot G, Ruzyllo W, Gottlieb S, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med 2007;357:2001–15.
