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Successful treatment of cerebral emboli with tissue plasminogen activator in a patient with takotsubo cardiomyopathy: A case report
Journal of Cardiology Cases 13 (2016) 117–120
Contents lists available at ScienceDirect
Journal of Cardiology Cases journal homepage: www.elsevier.com/locate/jccase
Case Report
Successful treatment of cerebral emboli with tissue plasminogen activator in a patient with takotsubo cardiomyopathy: A case report Shuntaro Ikeda (MD, PhD)*, Chika Murakami (MD), Shigehiro Miyazaki (MD), Tatsuro Hitsumoto (MD), Hisaki Kadota (MD), Hideaki Shimizu (MD), Kiyotaka Ohshima (MD, PhD), Mareomi Hamada (MD, PhD, FJCC) Department of Cardiology, Uwajima City Hospital, Uwajima, Ehime, Japan
A R T I C L E I N F O
A B S T R A C T
Article history: Received 28 October 2015 Received in revised form 8 December 2015 Accepted 16 December 2015
Takotsubo cardiomyopathy is a cardiac syndrome characterized by reversible left ventricular wall motion abnormalities. It mimics the acute coronary syndrome; however, significant obstructive coronary artery disease is absent. The prognosis is relatively favorable in many cases, but complications may occur during the acute stage. Herein, we present a case of takotsubo cardiomyopathy in a 76-yearold woman. Three days after admission for persistent chest pains, the patient suddenly developed right hemiplegia, right homonymous hemianopsia, and aphasia. By diffusion-weighted magnetic resonance imaging and magnetic resonance angiography, we diagnosed acute-phase cerebral infarction caused by abrupt occlusion of the left middle cerebral artery by a thrombus, and treated it with intravenously administered tissue plasminogen activator. Three hours afterward, the patient’s condition improved considerably. She was discharged 15 days after admission without any neurological sequelae. Thus, we show that takotsubo cardiomyopathy complicated by cerebral emboli can be successfully treated using tissue plasminogen activator. ß 2016 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
Keywords: Takotsubo cardiomyopathy Cerebral emboli Tissue plasminogen activator
Introduction Takotsubo cardiomyopathy, also called ‘stress cardiomyopathy’, is a cardiac syndrome characterized by reversible left ventricular wall motion abnormalities and the absence of significant obstructive coronary artery disease, although the symptoms and electrocardiogram changes are similar to those of the acute coronary syndrome [1]. The prognosis is relatively favorable in many cases, but sometimes complications such as cardiogenic shock, congestive heart failure, ventricular tachycardia, and sudden death are observed, especially during the acute stage of the cardiomyopathy [2–4]. Furthermore, thromboembolic phenomena such as apical thrombus formation and cerebral
* Corresponding author at: Department of Cardiology, Uwajima City Hospital, 1-1, Goten-machi, Uwajima, Ehime 798-8510, Japan. Tel.: +81 898 25 1111; fax: +81 895 25 5334. E-mail address: [email protected] (S. Ikeda).
emboli have been reported [5]. Herein, we present a case of takotsubo cardiomyopathy complicated by cerebral emboli, which we successfully treated with tissue plasminogen activator (t-PA). Case report A 76-year-old woman visited the emergency department complaining of persistent chest pain. She had taken nitroglycerin after attending the funeral of a relative, which had been particularly stressful for her. She had a medical history of hypertension. On admission, her mental status was alert, blood pressure was 92/68 mmHg, body temperature was 36.3 8C, respiratory rate was 24 min 1, peripheral capillary oxygen saturation was 92% (room air), and heart rate was 102 beats/min with a regular rhythm. A II/VI systolic murmur was heard along the left parasternal border, and fine crackles were audible at bilateral lower lung fields. Electrocardiography showed ST segment elevation in the II, III, aVF, and V2–5 leads. Laboratory tests revealed an increase in the white blood cell count (12,800 mm 3) with mild thrombocytosis
http://dx.doi.org/10.1016/j.jccase.2015.12.005 1878-5409/ß 2016 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
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S. Ikeda et al. / Journal of Cardiology Cases 13 (2016) 117–120
(47 104 mm 3) and positive heart-type fatty acid binding protein with normal levels of creatine kinase (204 IU/L). Cardiac troponin T level was slightly elevated to 2.16 ng/mL. Levels of serum C-reactive protein (1.25 mg/dL) and D-dimer (1.38 mg/l) were mildly elevated. Brain natriuretic peptide was elevated to 328 pg/mL. Echocardiography demonstrated akinesis of the left ventricular apex with augmented contraction of the basal area, leading to a suspicion of acute coronary syndrome or takotsubo cardiomyopathy. Echocardiography showed no left ventricular thrombus. Emergency coronary angiography was performed to ascertain the cause of the apical asynergy. Coronary angiography showed no significant epicardial coronary stenosis (Fig. 1A and B), while left ventriculography showed apical ballooning with basal hyperkinesis (Fig. 1C and D). Based on these angiographic findings, the patient was diagnosed with takotsubo cardiomyopathy. Three days after admission, at 11:35 am, the patient suddenly developed right hemiplegia, right homonymous hemianopsia, and aphasia. A head computed tomography scan showed no signs of early ischemia and no evidence of cerebral hemorrhage (Fig. 2A). Echocardiography showed severe apical hypokinesis with no thrombus. The National Institutes of Health Stroke Scale (NIHSS) score was 18 points. Diffusion-weighted magnetic resonance (MR) imaging showed high intensity in the left temporal lobe (Fig. 3) and MR angiography revealed proximal occlusion of the left middle cerebral artery (MCA; Fig. 2C), which was consistent with thrombotic embolism. We diagnosed acute-phase cerebral infarction on the basis of the abrupt occlusion of the left MCA by the thrombus, and intravenously administered 16 million international units of t-PA in total at 1:05 pm. Three hours after t-PA infusion, the patient could reply to questions, and the right hemiplegia improved (muscle maneuver test score 3/5, NIHSS score 8). On the next day, i.e. the fourth day after admission, the patient could answer almost clearly, and the right hemiplegia almost disappeared (NIHSS score 1). Electrocardiography or telemetry
Fig. 1.
during hospitalization demonstrated no evidence of atrial fibrillation. Follow-up echocardiography at 7 and 12 days after admission showed complete resolution of the wall motion abnormality. Computed tomography at the time of discharge revealed a lowdensity area in the left temporal lobe (Fig. 2B), and MR angiography demonstrated complete dissolution of the MCA thrombus (Fig. 2D). The patient was discharged 15 days after admission without any neurological sequelae. As post-medication, we prescribed 50 mg of oral clopidogrel per day. Discussion In the absence of significant comorbid complications, the prognosis of takotsubo cardiomyopathy is generally favorable, and left ventricular asynergy is usually resolved within several weeks. However, the disease can be associated with serious complications such as ventricular tachycardia, congestive heart failure, cardiogenic shock with severe left ventricular pressure gradient [3], cardiac rapture [4], and cerebral emboli through the formation of thrombi in the left ventricular cavity [5,6]. Despite the fact that left ventricular dysfunction in takotsubo cardiomyopathy is a transient phenomenon, it favors the formation of a thrombus through catecholamine-induced platelet activation and blood stagnation around the hypo/akinetic apical region [7]. In addition, embolic events were observed more frequently than in the acute coronary syndrome because the normalization of left ventricular contraction may promote the discharge of emboli from an apical thrombus [8]. To date, the true incidence and clinical significance of a left ventricular thrombus and related embolic outcomes in patients with takotsubo cardiomyopathy have not been fully established. The incidence of left ventricular thrombi in takotsubo cardiomyopathy varies according to researchers. Haghi and colleagues reported that a left ventricular thrombus occurred in 8% of takotsubo cardiomyopathy cases in a single center [5]. In
Emergency cine angiography and ECG. Emergency coronary angiogram images (A: left coronary artery, B: right coronary artery). There was no significant stenosis in coronary artery. Left ventriculography images (C: end-diastole, D: end-systole) showing typical ‘‘takotsubo’’ configuration. Electrocardiogram on admission (E).
S. Ikeda et al. / Journal of Cardiology Cases 13 (2016) 117–120
Fig. 2.
119
Brain computed tomography and magnetic resonance imaging angiography at acute and chronic phase. Upper panel: computed tomography scan (A: onset of stroke, B: 14 days after admission) demonstrating no signs of early ischemia and cerebral hemorrhage in acute phase. Lower panel: coronal maximum-intensity projection from magnetic resonance angiography (C: onset of stroke, D: 14 days after admission) showing abrupt occlusion of the right middle cerebral artery in acute stage (white arrow head).
their systematic review, De Gregorio et al. mentioned that the frequency of left ventricular thrombi was 2.5%, including thromboembolisms such as strokes and renal infarctions, which occurred in 0.8% of patients [6]. Thus, a left ventricular thrombus or subsequent embolism is considered to be a relatively common complication in takotsubo cardiomyopathy. Hence, physicians should be aware of this complication in the management of takotsubo cardiomyopathy. Some investigators have reported the features of left ventricular thrombi in takotsubo cardiomyopathy. Left ventricular thrombi are often discovered in the mid-apical left ventricular type of takotsubo cardiomyopathy. Kurisu et al. [9] reported that among 95 patients with takotsubo cardiomyopathy, left ventricular apical thrombi were documented in five (5.3%) patients; the thrombus was mural in two (40%) patients, and was protruding in three (60%). In one patient with a protruding thrombus, brain infarction occurred, suggesting that protruding thrombi are more likely to embolize. In the current case, the patient had a cerebral infarction three days after the onset of takotsubo cardiomyopathy. We believe that the thrombus had evolved, not from the left atrial appendage, but the ventricular cavity, because of no previous documentation of atrial fibrillation. Transthoracic echocardiography demonstrated no apparent left ventricular thrombus on the first and third day. An echocardiography-negative small thrombus may have developed during the early stage of presentation, when the apical region was still akinetic. In addition to catecholamine-induced hypercoagula-
bility, akinetic-hypokinetic ventricular segments may provide the structural basis for intra-cavity thrombus formation in takotsubo cardiomyopathy. Frequent echocardiographic observation and other modalities including MR imaging, which has a higher sensitivity, may be required to improve the detection of a left ventricular thrombus in takotsubo cardiomyopathy. To date, there are no published guidelines for the management of cerebral embolization in patients with stress-induced cardiomyopathy. Several reports showed that treatment by anticoagulation using warfarin and/or heparin was effective in patients with cerebral emboli secondary to takotsubo cardiomyopathy [5,6,9]. Our patient developed sudden-onset right hemiplegia due to a cerebral embolic stroke on the third day following hospitalization. Recently, the use of intravenous t-PA has become the first proven treatment for improving clinical outcomes in acute ischemic strokes. Administration of modified t-PA thrombolytic therapy for cerebral infarction within four and a half hours of symptom onset without contraindications has been proposed regardless of the clinical features [10]. Therefore, thrombolytic therapy with t-PA was expected to improve neurological signs in takotsubo cardiomyopathy. In the present case, administration of intravenous t-PA resulted in prompt resolution of the ischemic stroke, and thus, t-PA is a potential therapeutic option for ischemic strokes associated with takotsubo cardiomyopathy. The role of prophylactic systemic anticoagulation in takotsubo cardiomyopathy remains unclear. The determination of the precise clinical characteristics for a high risk of thrombosis may be
S. Ikeda et al. / Journal of Cardiology Cases 13 (2016) 117–120
120
Fig. 3.
Magnetic resonance image in acute phase. Upper panel: diffusion-weighted magnetic resonance image showing high intensity in the left temporal lobe. Lower panel: T2-weighted fluid-attenuated inversion recovery image showing no signs of ischemia.
important for the prevention of systemic embolization in takotsubo cardiomyopathy. Haghi et al. reported that patients with elevated serum C-reactive protein levels appear to be at a high risk of developing thrombi, as are those with thrombocytosis [5]. Mild thrombocytosis and elevation of C-reactive protein were observed in this case. Early anticoagulant therapy may prevent higher-risk patients from thromboembolic events. Further studies are required to understand the effect of prophylactic anticoagulation on cerebral embolization following development of takotsubo cardiomyopathy. Conflict of interest None. References [1] Satoh H, Tateishi H, Uchida T, Dote K, Ishihara M. Tako-tsubo-like cardiomyopathy due to multivessel spasm. In: Kodama K, Haze K, Hon M, editors. Clinical aspect of myocardial injury: from ischemia to heart failure. Tokyo: Kagakuhyoronsha Co; 1990. p. 56–64 [in Japanese]. [2] Sharkey SW, Windenburg DC, Lesser JR, Maron MS, Hauser RG, Lesser JN, Haas TS, Hodges JS, Maron BJ. Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy. J Am Coll Cardiol 2010;55:333–41.
[3] Tomofuji K, Ikeda S, Murakami C, Ochiumi Y, Nakamura M, Kadota K, Shimizu H, Ohshima K, Hamada M. Takotsubo cardiomyopathy with transient left ventricular obstruction successfully treated with cibenzoline succinate: a case report. JC Cases 2015;11:155–7. [4] Ohshima K, Ikeda S, Uga S, Murakami C, Nakamura M, Shimizu H, Ishida N, Sakao T, Tanaka S, Hamada M. A patient with takotsubo cardiomyopathy with left ventricular rupture induced by pressure gradient within the left ventricular cavity. Shinzo 2014;46:1476–82 [in Japanese]. [5] Haghi D, Papavassiliu T, Heggemann F, Kaden JJ, Borggrefe M, Suselbeck T. Incidence and clinical significance of left ventricular thrombus in tako-tsubo cardiomyopathy assessed with echocardiography. QJM 2008;101:381–6. [6] de Gregorio C, Grimaldi P, Lentini C. Left ventricular thrombus formation and cardioembolic complications in patients with Takotsubo-like syndrome: a systematic review. Int J Cardiol 2008;131:18–24. [7] Kume T, Kawamoto T, Okura H, Toyota E, Neishi Y, Watanabe N, Hayashida A, Okahashi N, Yoshimura Y, Saito K, Nezuo S, Yamada R, Yoshida K. Local release of catecholamines from the hearts of patients with tako-tsubo-like left ventricular dysfunction. Circ J 2008;72:106–8. [8] Stratton JR, Resnick AD. Increased embolic risk in patients with left ventricular thrombi. Circulation 1987;75:1004–11. [9] Kurisu S, Inoue I, Kawagoe T, Ishihara M, Shimatani Y, Nakama Y, Maruhashi T, Kagawa E, Dai K. Incidence and treatment of left ventricular apical thrombosis in Tako-tsubo cardiomyopathy. Int J Cardiol 2011;146:e58–60. [10] Minematsu K, Toyoda K, Hirano T, Kimura K, Kondo R, Mori E, Nakagawara J, Sakai N, Shiokawa Y, Tanahashi N, Yasaka M, Katayama Y, Miyamoto S, Ogawa A, Sasaki M, et al. Guidelines for the intravenous application of recombinant tissue-type plasminogen activator (alteplase), the second edition, October 2012: a guideline from the Japan Stroke Society. J Stroke Cerebrovasc Dis 2013;22:571–600.
Contents lists available at ScienceDirect
Journal of Cardiology Cases journal homepage: www.elsevier.com/locate/jccase
Case Report
Successful treatment of cerebral emboli with tissue plasminogen activator in a patient with takotsubo cardiomyopathy: A case report Shuntaro Ikeda (MD, PhD)*, Chika Murakami (MD), Shigehiro Miyazaki (MD), Tatsuro Hitsumoto (MD), Hisaki Kadota (MD), Hideaki Shimizu (MD), Kiyotaka Ohshima (MD, PhD), Mareomi Hamada (MD, PhD, FJCC) Department of Cardiology, Uwajima City Hospital, Uwajima, Ehime, Japan
A R T I C L E I N F O
A B S T R A C T
Article history: Received 28 October 2015 Received in revised form 8 December 2015 Accepted 16 December 2015
Takotsubo cardiomyopathy is a cardiac syndrome characterized by reversible left ventricular wall motion abnormalities. It mimics the acute coronary syndrome; however, significant obstructive coronary artery disease is absent. The prognosis is relatively favorable in many cases, but complications may occur during the acute stage. Herein, we present a case of takotsubo cardiomyopathy in a 76-yearold woman. Three days after admission for persistent chest pains, the patient suddenly developed right hemiplegia, right homonymous hemianopsia, and aphasia. By diffusion-weighted magnetic resonance imaging and magnetic resonance angiography, we diagnosed acute-phase cerebral infarction caused by abrupt occlusion of the left middle cerebral artery by a thrombus, and treated it with intravenously administered tissue plasminogen activator. Three hours afterward, the patient’s condition improved considerably. She was discharged 15 days after admission without any neurological sequelae. Thus, we show that takotsubo cardiomyopathy complicated by cerebral emboli can be successfully treated using tissue plasminogen activator.
Keywords: Takotsubo cardiomyopathy Cerebral emboli Tissue plasminogen activator
Introduction Takotsubo cardiomyopathy, also called ‘stress cardiomyopathy’, is a cardiac syndrome characterized by reversible left ventricular wall motion abnormalities and the absence of significant obstructive coronary artery disease, although the symptoms and electrocardiogram changes are similar to those of the acute coronary syndrome [1]. The prognosis is relatively favorable in many cases, but sometimes complications such as cardiogenic shock, congestive heart failure, ventricular tachycardia, and sudden death are observed, especially during the acute stage of the cardiomyopathy [2–4]. Furthermore, thromboembolic phenomena such as apical thrombus formation and cerebral
* Corresponding author at: Department of Cardiology, Uwajima City Hospital, 1-1, Goten-machi, Uwajima, Ehime 798-8510, Japan. Tel.: +81 898 25 1111; fax: +81 895 25 5334. E-mail address: [email protected] (S. Ikeda).
emboli have been reported [5]. Herein, we present a case of takotsubo cardiomyopathy complicated by cerebral emboli, which we successfully treated with tissue plasminogen activator (t-PA). Case report A 76-year-old woman visited the emergency department complaining of persistent chest pain. She had taken nitroglycerin after attending the funeral of a relative, which had been particularly stressful for her. She had a medical history of hypertension. On admission, her mental status was alert, blood pressure was 92/68 mmHg, body temperature was 36.3 8C, respiratory rate was 24 min 1, peripheral capillary oxygen saturation was 92% (room air), and heart rate was 102 beats/min with a regular rhythm. A II/VI systolic murmur was heard along the left parasternal border, and fine crackles were audible at bilateral lower lung fields. Electrocardiography showed ST segment elevation in the II, III, aVF, and V2–5 leads. Laboratory tests revealed an increase in the white blood cell count (12,800 mm 3) with mild thrombocytosis
http://dx.doi.org/10.1016/j.jccase.2015.12.005 1878-5409/ß 2016 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
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S. Ikeda et al. / Journal of Cardiology Cases 13 (2016) 117–120
(47 104 mm 3) and positive heart-type fatty acid binding protein with normal levels of creatine kinase (204 IU/L). Cardiac troponin T level was slightly elevated to 2.16 ng/mL. Levels of serum C-reactive protein (1.25 mg/dL) and D-dimer (1.38 mg/l) were mildly elevated. Brain natriuretic peptide was elevated to 328 pg/mL. Echocardiography demonstrated akinesis of the left ventricular apex with augmented contraction of the basal area, leading to a suspicion of acute coronary syndrome or takotsubo cardiomyopathy. Echocardiography showed no left ventricular thrombus. Emergency coronary angiography was performed to ascertain the cause of the apical asynergy. Coronary angiography showed no significant epicardial coronary stenosis (Fig. 1A and B), while left ventriculography showed apical ballooning with basal hyperkinesis (Fig. 1C and D). Based on these angiographic findings, the patient was diagnosed with takotsubo cardiomyopathy. Three days after admission, at 11:35 am, the patient suddenly developed right hemiplegia, right homonymous hemianopsia, and aphasia. A head computed tomography scan showed no signs of early ischemia and no evidence of cerebral hemorrhage (Fig. 2A). Echocardiography showed severe apical hypokinesis with no thrombus. The National Institutes of Health Stroke Scale (NIHSS) score was 18 points. Diffusion-weighted magnetic resonance (MR) imaging showed high intensity in the left temporal lobe (Fig. 3) and MR angiography revealed proximal occlusion of the left middle cerebral artery (MCA; Fig. 2C), which was consistent with thrombotic embolism. We diagnosed acute-phase cerebral infarction on the basis of the abrupt occlusion of the left MCA by the thrombus, and intravenously administered 16 million international units of t-PA in total at 1:05 pm. Three hours after t-PA infusion, the patient could reply to questions, and the right hemiplegia improved (muscle maneuver test score 3/5, NIHSS score 8). On the next day, i.e. the fourth day after admission, the patient could answer almost clearly, and the right hemiplegia almost disappeared (NIHSS score 1). Electrocardiography or telemetry
Fig. 1.
during hospitalization demonstrated no evidence of atrial fibrillation. Follow-up echocardiography at 7 and 12 days after admission showed complete resolution of the wall motion abnormality. Computed tomography at the time of discharge revealed a lowdensity area in the left temporal lobe (Fig. 2B), and MR angiography demonstrated complete dissolution of the MCA thrombus (Fig. 2D). The patient was discharged 15 days after admission without any neurological sequelae. As post-medication, we prescribed 50 mg of oral clopidogrel per day. Discussion In the absence of significant comorbid complications, the prognosis of takotsubo cardiomyopathy is generally favorable, and left ventricular asynergy is usually resolved within several weeks. However, the disease can be associated with serious complications such as ventricular tachycardia, congestive heart failure, cardiogenic shock with severe left ventricular pressure gradient [3], cardiac rapture [4], and cerebral emboli through the formation of thrombi in the left ventricular cavity [5,6]. Despite the fact that left ventricular dysfunction in takotsubo cardiomyopathy is a transient phenomenon, it favors the formation of a thrombus through catecholamine-induced platelet activation and blood stagnation around the hypo/akinetic apical region [7]. In addition, embolic events were observed more frequently than in the acute coronary syndrome because the normalization of left ventricular contraction may promote the discharge of emboli from an apical thrombus [8]. To date, the true incidence and clinical significance of a left ventricular thrombus and related embolic outcomes in patients with takotsubo cardiomyopathy have not been fully established. The incidence of left ventricular thrombi in takotsubo cardiomyopathy varies according to researchers. Haghi and colleagues reported that a left ventricular thrombus occurred in 8% of takotsubo cardiomyopathy cases in a single center [5]. In
Emergency cine angiography and ECG. Emergency coronary angiogram images (A: left coronary artery, B: right coronary artery). There was no significant stenosis in coronary artery. Left ventriculography images (C: end-diastole, D: end-systole) showing typical ‘‘takotsubo’’ configuration. Electrocardiogram on admission (E).
S. Ikeda et al. / Journal of Cardiology Cases 13 (2016) 117–120
Fig. 2.
119
Brain computed tomography and magnetic resonance imaging angiography at acute and chronic phase. Upper panel: computed tomography scan (A: onset of stroke, B: 14 days after admission) demonstrating no signs of early ischemia and cerebral hemorrhage in acute phase. Lower panel: coronal maximum-intensity projection from magnetic resonance angiography (C: onset of stroke, D: 14 days after admission) showing abrupt occlusion of the right middle cerebral artery in acute stage (white arrow head).
their systematic review, De Gregorio et al. mentioned that the frequency of left ventricular thrombi was 2.5%, including thromboembolisms such as strokes and renal infarctions, which occurred in 0.8% of patients [6]. Thus, a left ventricular thrombus or subsequent embolism is considered to be a relatively common complication in takotsubo cardiomyopathy. Hence, physicians should be aware of this complication in the management of takotsubo cardiomyopathy. Some investigators have reported the features of left ventricular thrombi in takotsubo cardiomyopathy. Left ventricular thrombi are often discovered in the mid-apical left ventricular type of takotsubo cardiomyopathy. Kurisu et al. [9] reported that among 95 patients with takotsubo cardiomyopathy, left ventricular apical thrombi were documented in five (5.3%) patients; the thrombus was mural in two (40%) patients, and was protruding in three (60%). In one patient with a protruding thrombus, brain infarction occurred, suggesting that protruding thrombi are more likely to embolize. In the current case, the patient had a cerebral infarction three days after the onset of takotsubo cardiomyopathy. We believe that the thrombus had evolved, not from the left atrial appendage, but the ventricular cavity, because of no previous documentation of atrial fibrillation. Transthoracic echocardiography demonstrated no apparent left ventricular thrombus on the first and third day. An echocardiography-negative small thrombus may have developed during the early stage of presentation, when the apical region was still akinetic. In addition to catecholamine-induced hypercoagula-
bility, akinetic-hypokinetic ventricular segments may provide the structural basis for intra-cavity thrombus formation in takotsubo cardiomyopathy. Frequent echocardiographic observation and other modalities including MR imaging, which has a higher sensitivity, may be required to improve the detection of a left ventricular thrombus in takotsubo cardiomyopathy. To date, there are no published guidelines for the management of cerebral embolization in patients with stress-induced cardiomyopathy. Several reports showed that treatment by anticoagulation using warfarin and/or heparin was effective in patients with cerebral emboli secondary to takotsubo cardiomyopathy [5,6,9]. Our patient developed sudden-onset right hemiplegia due to a cerebral embolic stroke on the third day following hospitalization. Recently, the use of intravenous t-PA has become the first proven treatment for improving clinical outcomes in acute ischemic strokes. Administration of modified t-PA thrombolytic therapy for cerebral infarction within four and a half hours of symptom onset without contraindications has been proposed regardless of the clinical features [10]. Therefore, thrombolytic therapy with t-PA was expected to improve neurological signs in takotsubo cardiomyopathy. In the present case, administration of intravenous t-PA resulted in prompt resolution of the ischemic stroke, and thus, t-PA is a potential therapeutic option for ischemic strokes associated with takotsubo cardiomyopathy. The role of prophylactic systemic anticoagulation in takotsubo cardiomyopathy remains unclear. The determination of the precise clinical characteristics for a high risk of thrombosis may be
S. Ikeda et al. / Journal of Cardiology Cases 13 (2016) 117–120
120
Fig. 3.
Magnetic resonance image in acute phase. Upper panel: diffusion-weighted magnetic resonance image showing high intensity in the left temporal lobe. Lower panel: T2-weighted fluid-attenuated inversion recovery image showing no signs of ischemia.
important for the prevention of systemic embolization in takotsubo cardiomyopathy. Haghi et al. reported that patients with elevated serum C-reactive protein levels appear to be at a high risk of developing thrombi, as are those with thrombocytosis [5]. Mild thrombocytosis and elevation of C-reactive protein were observed in this case. Early anticoagulant therapy may prevent higher-risk patients from thromboembolic events. Further studies are required to understand the effect of prophylactic anticoagulation on cerebral embolization following development of takotsubo cardiomyopathy. Conflict of interest None. References [1] Satoh H, Tateishi H, Uchida T, Dote K, Ishihara M. Tako-tsubo-like cardiomyopathy due to multivessel spasm. In: Kodama K, Haze K, Hon M, editors. Clinical aspect of myocardial injury: from ischemia to heart failure. Tokyo: Kagakuhyoronsha Co; 1990. p. 56–64 [in Japanese]. [2] Sharkey SW, Windenburg DC, Lesser JR, Maron MS, Hauser RG, Lesser JN, Haas TS, Hodges JS, Maron BJ. Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy. J Am Coll Cardiol 2010;55:333–41.
[3] Tomofuji K, Ikeda S, Murakami C, Ochiumi Y, Nakamura M, Kadota K, Shimizu H, Ohshima K, Hamada M. Takotsubo cardiomyopathy with transient left ventricular obstruction successfully treated with cibenzoline succinate: a case report. JC Cases 2015;11:155–7. [4] Ohshima K, Ikeda S, Uga S, Murakami C, Nakamura M, Shimizu H, Ishida N, Sakao T, Tanaka S, Hamada M. A patient with takotsubo cardiomyopathy with left ventricular rupture induced by pressure gradient within the left ventricular cavity. Shinzo 2014;46:1476–82 [in Japanese]. [5] Haghi D, Papavassiliu T, Heggemann F, Kaden JJ, Borggrefe M, Suselbeck T. Incidence and clinical significance of left ventricular thrombus in tako-tsubo cardiomyopathy assessed with echocardiography. QJM 2008;101:381–6. [6] de Gregorio C, Grimaldi P, Lentini C. Left ventricular thrombus formation and cardioembolic complications in patients with Takotsubo-like syndrome: a systematic review. Int J Cardiol 2008;131:18–24. [7] Kume T, Kawamoto T, Okura H, Toyota E, Neishi Y, Watanabe N, Hayashida A, Okahashi N, Yoshimura Y, Saito K, Nezuo S, Yamada R, Yoshida K. Local release of catecholamines from the hearts of patients with tako-tsubo-like left ventricular dysfunction. Circ J 2008;72:106–8. [8] Stratton JR, Resnick AD. Increased embolic risk in patients with left ventricular thrombi. Circulation 1987;75:1004–11. [9] Kurisu S, Inoue I, Kawagoe T, Ishihara M, Shimatani Y, Nakama Y, Maruhashi T, Kagawa E, Dai K. Incidence and treatment of left ventricular apical thrombosis in Tako-tsubo cardiomyopathy. Int J Cardiol 2011;146:e58–60. [10] Minematsu K, Toyoda K, Hirano T, Kimura K, Kondo R, Mori E, Nakagawara J, Sakai N, Shiokawa Y, Tanahashi N, Yasaka M, Katayama Y, Miyamoto S, Ogawa A, Sasaki M, et al. Guidelines for the intravenous application of recombinant tissue-type plasminogen activator (alteplase), the second edition, October 2012: a guideline from the Japan Stroke Society. J Stroke Cerebrovasc Dis 2013;22:571–600.