International Journal of Cardiology 182 (2015) 377–378
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Giant biventricular thrombi in a patient with heart failure and heparin-induced thrombocytopenia Johannes Rigger, Niklas F. Ehl, Reto Nägele, Hans Rickli, Micha T. Maeder ⁎ Cardiology Division, Kantonsspital St. Gallen, Switzerland
a r t i c l e
i n f o
Article history: Received 21 December 2014 Accepted 31 December 2014 Available online 3 January 2015 Keywords: Thrombus Heparin Thrombocytopenia Heart failure
To the Editor A 59-year-old man with a two month history of progressive dyspnea was admitted with biventricular decompensated heart failure. Echocardiography on admission revealed dilatation of all cardiac chambers and severe biventricular systolic dysfunction (left ventricular ejection fraction 15%, right ventricular fractional area change 9%) as well as thrombi in both the left (Fig. 1, Panel A, showing apical four chamber view, and Panel B, showing parasternal short axis view) and right ventricle. Treatment with heparin and aspirin as well as heart failure medication were established. Cardiac magnetic resonance imaging showed full viability of the left ventricular myocardium and confirmed the large thrombi (Panel F, T1-weighted images, arrows). Coronary angiography revealed severe triple vessel disease. Coronary bypass surgery was planned but primarily deferred because of the presence of the thrombi. A followup echocardiogram 13 days later revealed a massive growth of the thrombi in the left (Panel C, apical four chamber view, panel D, parasternal short axis view) and right (panel E, apical four chamber view) ventricle. At the same time, a significant fall of the thrombocyte count was observed (46 G/l; initially 202 G/l, nadir 26 G/l), and anti-PF4 antibodies were detected. Thus, a diagnosis of heparininduced thrombocytopenia (HIT) with thrombus (HITT) was made. Anticoagulation was switched from heparin to argatroban given that
⁎ Corresponding author at: Cardiology Division, Kantonsspital St. Gallen, Rorschacherstrasse 95, 9007 St. Gallen, Switzerland. E-mail address: [email protected] (M.T. Maeder).
http://dx.doi.org/10.1016/j.ijcard.2014.12.160 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
the patient also had renal failure (estimated glomerular filtration rate 35 ml/min/1.73 m2). Another follow-up echocardiogram two days later revealed a slight regression of the size of the thrombi. On the next day, the patient collapsed and was found to be in ventricular fibrillation. Multiple attempts of defibrillation and prolonged reanimation were unsuccessful. Autopsy revealed a massively hypertrophied heart with multiple small zones of necrosis. Large biventricular thrombi were still present. (See Fig. 1.) This case represents an exceptional example of a fatal complication of HIT. Up to 5% of patients receiving heparin will develop HIT [1]. Risk factors for the occurrence of HIT include the use of unfractioned heparin, a longer duration of heparin exposure, female gender, and other patient characteristics [1]. Two types of HIT exist including the mild type I and, like in our case the type II with positive platelet-activating anti-PF4 antibodies and a more pronounced fall in the thrombocyte count. As a result of these antibody-mediated reaction affected patients will have a decrease of platelets (N 50%) within 5 to 10 days after initiation of heparin. The typical clinical presentation is a venous thrombosis (17–55%) or, however significantly less common, an arterial thrombotic event (3–10%) [1,2]. HIT-associated cardiac thrombotic complications have rarely been described [3]. Our patient had a predisposition for the development of ventricular thrombi, i.e., a severely depressed LVEF in the presence of severe coronary artery disease but no intracardiac device where HIT-associated left ventricular thrombi have been reported previously [3]. The massive growth of the thrombi after establishing an adequate therapy with heparin was very unusual and represents a dramatic clinical course of HIT. Although antithrombotic therapy was appropriately switched to the direct thrombin inhibitor argatroban, which represents the treatment of choice in patients with renal failure [1], the patient did not survive. The exact cause of death remains unknown. An embolization of a thrombus into the left ventricular outflow tract would have been a possible scenario but could not be proven. Global myocardial ischemia due to diffuse coronary thrombosis in the context of HIT on the background of severe diffuse coronary artery disease and left ventricular hypertrophy is the most likely scenario. The present case highlights the fact that despite the availability of alternatives to heparin HIT remains a disease with high mortality. In fact, approximately 5% to 10% of patients with HIT die, usually as a result of thrombotic complications [1]. References [1] L.A. Linkins, A.L. Dans, L.K. Moores, R. Bona, B.L. Davidson, S. Schulman, M. Crowther, Treatment and prevention of heparin-induced thrombocytopenia. antithrombotic
378
J. Rigger et al. / International Journal of Cardiology 182 (2015) 377–378 Figure 1
A
B
C
E
D
F
Fig. 1. Panel A: apical four chamber view showing the left ventricular thrombus on admission. Panel B: parasternal short axis view showing the left ventricular thrombus on admission. Panel C: apical four chamber view showing two large left ventricular thrombi (53 × 19 mm and 49 × 27 mm) at follow-up 13 days later. Panel D: parasternal short axis view showing the left ventricular thrombi at follow-up 13 days later. Panel E: apical four chamber view showing thrombi in the right ventricle at follow-up (60 × 31 mm). Panel F: cardiac magnetic resonance imaging showing large left ventricular thrombi (T1-weighted images, arrows).
therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines, Chest 141 (2012) e495S–e530S. [2] T.E. Warkentin, J.G. Kelton, A 14-year study of heparin-induced thrombocytopenia, Am. J. Med. 101 (1996) 502–507.
[3] T. Kuhl, S. Wendt, G. Langenbartels, A. Kröner, T. Wahlers, Recurrent left atrial and left ventricular thrombosis due to heparin-induced thrombocytopenia: case report and short review, Thorac. Cardiovasc. Surg. 61 (2013) 537–540.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Giant biventricular thrombi in a patient with heart failure and heparin-induced thrombocytopenia Johannes Rigger, Niklas F. Ehl, Reto Nägele, Hans Rickli, Micha T. Maeder ⁎ Cardiology Division, Kantonsspital St. Gallen, Switzerland
a r t i c l e
i n f o
Article history: Received 21 December 2014 Accepted 31 December 2014 Available online 3 January 2015 Keywords: Thrombus Heparin Thrombocytopenia Heart failure
To the Editor A 59-year-old man with a two month history of progressive dyspnea was admitted with biventricular decompensated heart failure. Echocardiography on admission revealed dilatation of all cardiac chambers and severe biventricular systolic dysfunction (left ventricular ejection fraction 15%, right ventricular fractional area change 9%) as well as thrombi in both the left (Fig. 1, Panel A, showing apical four chamber view, and Panel B, showing parasternal short axis view) and right ventricle. Treatment with heparin and aspirin as well as heart failure medication were established. Cardiac magnetic resonance imaging showed full viability of the left ventricular myocardium and confirmed the large thrombi (Panel F, T1-weighted images, arrows). Coronary angiography revealed severe triple vessel disease. Coronary bypass surgery was planned but primarily deferred because of the presence of the thrombi. A followup echocardiogram 13 days later revealed a massive growth of the thrombi in the left (Panel C, apical four chamber view, panel D, parasternal short axis view) and right (panel E, apical four chamber view) ventricle. At the same time, a significant fall of the thrombocyte count was observed (46 G/l; initially 202 G/l, nadir 26 G/l), and anti-PF4 antibodies were detected. Thus, a diagnosis of heparininduced thrombocytopenia (HIT) with thrombus (HITT) was made. Anticoagulation was switched from heparin to argatroban given that
⁎ Corresponding author at: Cardiology Division, Kantonsspital St. Gallen, Rorschacherstrasse 95, 9007 St. Gallen, Switzerland. E-mail address: [email protected] (M.T. Maeder).
http://dx.doi.org/10.1016/j.ijcard.2014.12.160 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
the patient also had renal failure (estimated glomerular filtration rate 35 ml/min/1.73 m2). Another follow-up echocardiogram two days later revealed a slight regression of the size of the thrombi. On the next day, the patient collapsed and was found to be in ventricular fibrillation. Multiple attempts of defibrillation and prolonged reanimation were unsuccessful. Autopsy revealed a massively hypertrophied heart with multiple small zones of necrosis. Large biventricular thrombi were still present. (See Fig. 1.) This case represents an exceptional example of a fatal complication of HIT. Up to 5% of patients receiving heparin will develop HIT [1]. Risk factors for the occurrence of HIT include the use of unfractioned heparin, a longer duration of heparin exposure, female gender, and other patient characteristics [1]. Two types of HIT exist including the mild type I and, like in our case the type II with positive platelet-activating anti-PF4 antibodies and a more pronounced fall in the thrombocyte count. As a result of these antibody-mediated reaction affected patients will have a decrease of platelets (N 50%) within 5 to 10 days after initiation of heparin. The typical clinical presentation is a venous thrombosis (17–55%) or, however significantly less common, an arterial thrombotic event (3–10%) [1,2]. HIT-associated cardiac thrombotic complications have rarely been described [3]. Our patient had a predisposition for the development of ventricular thrombi, i.e., a severely depressed LVEF in the presence of severe coronary artery disease but no intracardiac device where HIT-associated left ventricular thrombi have been reported previously [3]. The massive growth of the thrombi after establishing an adequate therapy with heparin was very unusual and represents a dramatic clinical course of HIT. Although antithrombotic therapy was appropriately switched to the direct thrombin inhibitor argatroban, which represents the treatment of choice in patients with renal failure [1], the patient did not survive. The exact cause of death remains unknown. An embolization of a thrombus into the left ventricular outflow tract would have been a possible scenario but could not be proven. Global myocardial ischemia due to diffuse coronary thrombosis in the context of HIT on the background of severe diffuse coronary artery disease and left ventricular hypertrophy is the most likely scenario. The present case highlights the fact that despite the availability of alternatives to heparin HIT remains a disease with high mortality. In fact, approximately 5% to 10% of patients with HIT die, usually as a result of thrombotic complications [1]. References [1] L.A. Linkins, A.L. Dans, L.K. Moores, R. Bona, B.L. Davidson, S. Schulman, M. Crowther, Treatment and prevention of heparin-induced thrombocytopenia. antithrombotic
378
J. Rigger et al. / International Journal of Cardiology 182 (2015) 377–378 Figure 1
A
B
C
E
D
F
Fig. 1. Panel A: apical four chamber view showing the left ventricular thrombus on admission. Panel B: parasternal short axis view showing the left ventricular thrombus on admission. Panel C: apical four chamber view showing two large left ventricular thrombi (53 × 19 mm and 49 × 27 mm) at follow-up 13 days later. Panel D: parasternal short axis view showing the left ventricular thrombi at follow-up 13 days later. Panel E: apical four chamber view showing thrombi in the right ventricle at follow-up (60 × 31 mm). Panel F: cardiac magnetic resonance imaging showing large left ventricular thrombi (T1-weighted images, arrows).
therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines, Chest 141 (2012) e495S–e530S. [2] T.E. Warkentin, J.G. Kelton, A 14-year study of heparin-induced thrombocytopenia, Am. J. Med. 101 (1996) 502–507.
[3] T. Kuhl, S. Wendt, G. Langenbartels, A. Kröner, T. Wahlers, Recurrent left atrial and left ventricular thrombosis due to heparin-induced thrombocytopenia: case report and short review, Thorac. Cardiovasc. Surg. 61 (2013) 537–540.
