Case study Herz 2013 DOI 10.1007/s00059-013-3956-2 Received: 13 August 2013 Accepted: 15 August 2013 © Urban & Vogel 2013
J. Finsterer1 · C. Stöllberger2 · T. Pulgram3 1 Krankenanstalt Rudolfstiftung, Vienna 2 2nd Medical Department, Krankenanstalt Rudolfstiftung, Vienna 3 4th Medical Department, Krankenanstalt Rudolfstiftung, Vienna
Paraneoplastic takotsubo syndrome with ventricular thrombus and stroke Takotsubo syndrome (TTS) is categorized as unclassified cardiomyopathy by the American and European Heart Association [1]. Per definition, TTS is a reversible condition triggered by stress. Occasionally, akinesia/hypokinesia in TTS may favor intraventricular thrombus formation [2, 3, 4, 5, 6, 7, 8]. TTS triggered by stress from an initially occult neoplasm leading to intraventricular thrombus formation and consecutively to embolic, ischemic stroke has not been reported.
Case report A 66-year-old Caucasian female patient (height 174 cm, weight 51.7 kg) was admitted to hospital with acute speech disturbance, fixed gaze deviation to the left, and right-sided hemiparesis. She had a previous history of polyneuropathy, osteoporosis with a fracture of vertebral body L3, arterial hypertension, nausea, vomiting, recurrent bloody feces, weight loss, chronic alcoholism, and smoking of 40 cigarettes per day. Previous stroke or documented atrial fibrillation was not reported. Cerebral magnetic resonance imaging (MRI) revealed acute ischemic lesions within the anterior and middle territory of the left median cerebral artery, global cerebral atrophy, and old ischemic lesions in the area of the left anterior border zone. MR angiography of the intracranial arteries did not show occlusion or stenosis of the large cerebral arteries. There was marked anemia, low serum iron, folic acid deficiency, creatine
kinase (CK) elevation, a CK-MB fraction of 19.5%, elevated troponin and proBNP levels, hypoproteinemia, mild hypokalemia, and hypocalcemia (. Tab. 1). The initial electrocardiogram (ECG) showed sinus rhythm, normal PQ and QRS complex, and negative T waves in leads V3 through V6, II, III, and aVF. The QT interval was 440 ms. Bedside echocardiography revealed akinesia of the apex and the anteroseptal segments, and a thrombus within the apex. Myocardial infarction was suspected and a dual treatment with acetyl-salicylic acid and clopidogrel was initiated. Immediately after the MRI, spontaneous remission of the neurological abnormalities occurred, and therefore acute thrombolysis was withheld. On hospital day (hd) 2, two short episodes of atrial fibrillation were documented. Cerebral MRI surprisingly showed a massive hyperacute injury marker (HARM) phenomenon and almost complete regression of the diffusion deficit of the left frontal cortex. Transthoracic echocar-
diography on hd 3 was unchanged from the one recorded on hd 1 (. Fig. 1). In addition to acetyl-salicylic acid and clopidogrel, therapeutic anticoagulation with heparin was initiated on hd 3. An ECG on hd 3 and hd 4 again revealed a short episode of atrial fibrillation. Ultrasonography of the abdomen on hd 4 revealed steatosis hepatis. Coronary angiography on hd 7 showed 50–60% stenosis of the left anterior descending coronary artery. Troponin T gradually declined from the time of admission to almost normal levels within 13 days (. Tab. 1). Echocardiography on hd 17 showed normalization of the systolic function and no thrombus (. Fig. 2). ECGs on hd 18 showed negative T waves in leads II, III, aVF, and V4 through V6. The QT interval had normalized to 440 ms. An ECG on hd 28 showed negative T waves in V4 through V6 exclusively. Diagnostic work-up for anemia, hypoproteinemia, gastrointestinal bleeding, weight loss, inappetence, recurrent nausea, and vomiting by gastroscopy and
Tab. 1 Laboratory parameters Parameter CK CK-MB MB% Troponin Ery Hb Hc
Reference limits 38–174 U/l 0–24 U/l 0–6% 0–0.009 ng/ml 4–5.2 T/l 12–16 g/dl 6–20 mg/dl
hd 1 281 55 19.5 0.220 2.7 10.6 22
hd 2 237 36 15.4 0.209 2.42 9.5 27.3
hd 5 54 nd nd 0.197 2.56 9.8 28.3
hd 9 30 nd nd 0.083 2.71 10.2 29.6
hd 13 49 nd nd 0.046 2.78 10.2 30.4
hd hospital day, CK creatine-kinase, CK-MB cardiac fraction, Ery erythrocyte count, Hb hemoglobin, Hc hematocrit, nd not done Herz 2013
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Case study
Fig. 1 8 Echocardiographic apical four-chamber view showing ballooning of the left ventricular apical region and a large ventricular thrombus
colonoscopy revealed a gastric adenocarcinoma with focal infiltration of the cardia and the esophagus. Staging by CT scan of the thorax and the abdomen did not show local infiltration but liver metastasis was suspected. Liver biopsy confirmed spreading of the tumor. Under triple therapy, the ventricular thrombus resolved within 19 days, and acetyl-salicylic acid was discontinued and the anticoagulant therapy reduced to heparin and clopidogrel alone. The red blood cell counts continuously declined, as further macroscopic gastrointestinal bleedings occurred; since the cardiac abnormalities were retrospectively interpreted as TTS, heparin was reduced to the antithrombotic dosage and clopidogrel was discontinued on hd 23.
Discussion The patient presented here is an interesting case of the triggering of TTS presumably by stress from the carcinoma, the occurrence of a ventricular thrombus within the hypokinetic sack of the ventricle, and the occurrence of ischemic, embolic stroke with marked improvement after suspected spontaneous recanalization of the median cerebral artery occlusion. Concerning the triggers of TTS, neither psychological nor physical stress was reported by the patient. The only stressors that could possibly be responsible were
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Herz 2013
Fig. 2 8 Echocardiographic apical four-chamber view after 14 days shows normalization of the systolic function and no thrombus
smoking, alcohol consumption, depressive mood, or the malignancy. The previously undetected carcinoma was the most likely trigger, since malignancies have been reported as triggers of TTS [9, 10, 11, 12, 13]. Additionally, alcohol withdrawal could have played a triggering role [14]. Smoking, alcohol consumption, and depressive mood were excluded because they have not been reported as a trigger of TTS. It is also conceivable that stroke was embolic due to the atrial fibrillation and secondarily triggered TTS and that the intraventricular thrombus was not pathogenic [15]. Concerning the pathogenesis of TTS, it can be speculated that the gastric adenocarcinoma produced cortisol or another unknown triggering factor and thus induced the development of TTS, as has been previously reported [16]. Thrombi have been repeatedly reported as a complication of TTS [2, 3, 4, 5, 6, 7, 8]. Thrombus formation during TTS is attributed to stasis of the blood from akinesia/hypokinesia [2, 3, 4, 5, 6, 7, 8, 17, 18, 19]. Thrombus formation due to paraneoplastic hypercoagulability is rather unlikely, since the thrombus resolved under adequate anticoagulation and resolution of akinesia/hypokinesia. Ventricular thrombus formation may not only be a complication of early TTS but may also develop later during the course of the TTS [20]. Reported complications of intraventricular thrombus formation are
stroke [21, 22, 23], myocardial infarction [24], thromboembolism [25], cardiac arrest [25], cardiac shock [25], or death [25]. The rate of in-hospital complications is higher among old than among young patients [26]. The prognosis of a ventricular thrombus from TTS is usually fair with resolution of hypokinesia and if not additionally complicated by a thromboembolic event [27]. Various scenarios are possible in the pathogenesis of stroke. First, stroke was caused by paraneoplastic thrombophilia. Second, stroke resulted from the ventricular thrombus. Third, stroke was caused by atrial fibrillation. Arguments against the last hypothesis are that the history was negative for palpitations in particular due to atrial fibrillation, that atrial fibrillation had not been recorded prior to admission, and that atrial fibrillation was not documented on admission. Thrombophilic hypercoagulability induced by the malignancy cannot be definitively excluded, but the embolic features of the stroke make other causes more likely. Stroke in our patient was most likely due to embolization of the ventricular thrombus because such a pathogenetic scenario has been previously reported [21, 22, 23] and because TTS occurred most probably before atrial fibrillation. An atherothrombotic cause of the stroke was excluded owing to the extensive risk factor profile for embolic stroke and the mini-
mal atherosclerotic features on carotid ultrasound and coronary angiography.
Conclusion This case shows that TTS may be triggered by stress from a malignancy and that TTS may lead to intraventricular thrombus formation and consecutively embolic stroke. TTS should not be confused with an acute coronary syndrome if there are typical ECG and echocardiographic abnormalities, resolution of these abnormalities within a few days, CK and troponin elevation, but only nonsignificant coronary artery stenosis.
Corresponding address Prof. Dr. J. Finsterer Krankenanstalt Rudolfstiftung Postfach 20, 1180 Vienna Austria [email protected]
Compliance with ethical guidelines Conflict of interest. J. Finsterer, C. Stöllberger, and T. Pulgram state that there are no conflicts of interest. Consent was obtained from all patients identifiable from images or other information within the manuscript. In the case of underage patients, consent was obtained from a parent or legal guardian. All studies on humans described in the present manuscript were carried out with the approval of the responsible ethics committee and in accordance with national law and the Helsinki Declaration of 1975 (in its current, revised form). Informed consent was obtained from all patients included in studies.
References 1. Elliott P, Andersson B, Arbustini E et al (2008) Classification of the cardiomyopathies: a position statement from the European Society Of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 29:270–276 2. Correia AS, Moreno N, Gonçalves A et al (2012) Cardiac thrombus and conduction disorder in takotsubo cardiomyopathy. Rev Port Cardiol 31:513–516 3. Gregorio C de, Andò G (2012) A rare cause of Takotsubo cardiomyopathy related left ventricular apical thrombus requiring surgery. Heart Lung Circ 21:251 4. Lee PH, Song JK, Park IK et al (2011) Takotsubo cardiomyopathy: a case of persistent apical ballooning complicated by an apical mural thrombus. Korean J Intern Med 26:455–459 5. Michels G, Pfister R (2012) De novo left ventricular thrombus during tako-tsubo cardiomyopathy. Dtsch Med Wochenschr 137:2423–2426
6. Seitz MJ, McLeod MK, O’Keefe MD, Seah PW (2012) A rare cause of Takotsubo cardiomyopathy related left ventricular apical thrombus requiring surgery. Heart Lung Circ 21:245–246 7. Shin SN, Yun KH, Ko JS et al (2011) Left ventricular thrombus associated with takotsubo cardiomyopathy: a cardioembolic cause of cerebral infarction. J Cardiovasc Ultrasound 19:152–155 8. Yaguchi M, Yaguchi H, Takahashi N (2011) A case of asymptomatic Takotsubo cardiomyopathy with intraventricular thrombus associated with epileptic seizure. Brain Nerve 63:897–900 9. Burgdorf C, Kurowski V, Bonnemeier H et al (2008) Long-term prognosis of the transient left ventricular dysfunction syndrome (Tako-Tsubo cardiomyopathy): focus on malignancies. Eur J Heart Fail 10:1015–1019 10. Gingles C, Leslie S, Harvey R (2010) A case of Takotsubo’s cardiomyopathy and multiple endocrine neoplasia 2A syndrome. Clin Endocrinol (Oxf) 73:827–829 11. Mitsumori T, Nakajima K, Nozaki Y et al (2010) Multiple myeloma complicated with Takotsubo cardiomyopathy. Rinsho Ketsueki 51:291–296 12. Schweizer MT, Mehta R, Salgia R, Villaflor VM (2011) Takotsubo cardiomyopathy in a patient with squamous cell esophageal carcinoma. J Clin Oncol 29:e598–e600 13. Zeballos C, Moraca RJ, Bailey SH, Magovern GJ Jr (2012) Temporary mechanical circulatory support for Takotsubo cardiomyopathy secondary to primary mediastinal B-cell lymphoma. J Card Surg 27:119–121 14. Stout BJ, Hoshide R, Vincent DS (2012) Takotsubo cardiomyopathy in the setting of acute alcohol withdrawal. Hawaii J Med Public Health 71:193– 194 15. Scheitz JF, Mochmann HC, Witzenbichler B et al (2012) Takotsubo cardiomyopathy following ischemic stroke: a cause of troponin elevation. J Neurol 259:188–190 16. Wickboldt N, Pache JC, Dietrich PY et al (2012) Takotsubo syndrome secondary to adrenal adenocarcinoma: cortisol as a possible culprit. Am J Respir Crit Care Med 186:1061–1062 17. Kurisu S, Inoue I, Kawagoe T et al (2011) Incidence and treatment of left ventricular apical thrombosis in Tako-tsubo cardiomyopathy. Int J Cardiol 146:e58–e60 18. Mrdovic I, Perunicic J, Asanin M et al (2008) Transient left ventricular apical ballooning complicated by a mural thrombus and outflow tract obstruction in a patient with pheochromocytoma. Tex Heart Inst J 35:480–482 19. Tobar R, Rotzak R, Rozenman Y (2009) Apical thrombus associated with Takotsubo cardiomyopathy in a young woman. Echocardiography 26:575–580 20. Haghi D, Papavassiliu T, Heggemann F et al (2008) Incidence and clinical significance of left ventricular thrombus in tako-tsubo cardiomyopathy assessed with echocardiography. QJM 101:381–386 21. Mayor-Gómez S, Erro ME, Olaz-Preciado F et al (2012) Stroke and Takotsubo syndrome: a reciprocal relationship. Rev Neurol 55:475–478 22. Yaylali YT, Saricopur A (2012) Takotsubo-syndrome presenting with supraventricular tachycardia, stroke, and thrombocytopenia. Int J Cardiol 161:e39–e41 23. Kim SM, Aikat S, Bailey A, White M (2012) Takotsubo cardiomyopathy as a source of cardioembolic cerebral infarction. BMJ Case Rep. doi:pii: bcr2012006835. 10.1136/bcr-2012-006835
24. Angulo-Llanos R, Sanz-Ruiz R, Solis J, FernándezAvilés F (2013) Acute myocardial infarction: an uncommon complication of takotsubo cardiomyopathy. Catheter Cardiovasc Interv. doi:10.1002/ ccd.24846 25. Schultz T, Shao Y, Redfors B et al (2012) Stress-induced cardiomyopathy in Sweden: evidence for different ethnic predisposition and altered cardiocirculatory status. Cardiology 122:180–186 26. Citro R, Rigo F, Previtali M et al (2012) Differences in clinical features and in-hospital outcomes of older adults with tako-tsubo cardiomyopathy. J Am Geriatr Soc 60:93–98 27. Yoshida T, Hibino T, Fujimaki T et al (2009) Tako-tsubo cardiomyopathy complicated by apical thrombus formation: a case report. Int J Cardiol 132:e120–e122
Herz 2013
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J. Finsterer1 · C. Stöllberger2 · T. Pulgram3 1 Krankenanstalt Rudolfstiftung, Vienna 2 2nd Medical Department, Krankenanstalt Rudolfstiftung, Vienna 3 4th Medical Department, Krankenanstalt Rudolfstiftung, Vienna
Paraneoplastic takotsubo syndrome with ventricular thrombus and stroke Takotsubo syndrome (TTS) is categorized as unclassified cardiomyopathy by the American and European Heart Association [1]. Per definition, TTS is a reversible condition triggered by stress. Occasionally, akinesia/hypokinesia in TTS may favor intraventricular thrombus formation [2, 3, 4, 5, 6, 7, 8]. TTS triggered by stress from an initially occult neoplasm leading to intraventricular thrombus formation and consecutively to embolic, ischemic stroke has not been reported.
Case report A 66-year-old Caucasian female patient (height 174 cm, weight 51.7 kg) was admitted to hospital with acute speech disturbance, fixed gaze deviation to the left, and right-sided hemiparesis. She had a previous history of polyneuropathy, osteoporosis with a fracture of vertebral body L3, arterial hypertension, nausea, vomiting, recurrent bloody feces, weight loss, chronic alcoholism, and smoking of 40 cigarettes per day. Previous stroke or documented atrial fibrillation was not reported. Cerebral magnetic resonance imaging (MRI) revealed acute ischemic lesions within the anterior and middle territory of the left median cerebral artery, global cerebral atrophy, and old ischemic lesions in the area of the left anterior border zone. MR angiography of the intracranial arteries did not show occlusion or stenosis of the large cerebral arteries. There was marked anemia, low serum iron, folic acid deficiency, creatine
kinase (CK) elevation, a CK-MB fraction of 19.5%, elevated troponin and proBNP levels, hypoproteinemia, mild hypokalemia, and hypocalcemia (. Tab. 1). The initial electrocardiogram (ECG) showed sinus rhythm, normal PQ and QRS complex, and negative T waves in leads V3 through V6, II, III, and aVF. The QT interval was 440 ms. Bedside echocardiography revealed akinesia of the apex and the anteroseptal segments, and a thrombus within the apex. Myocardial infarction was suspected and a dual treatment with acetyl-salicylic acid and clopidogrel was initiated. Immediately after the MRI, spontaneous remission of the neurological abnormalities occurred, and therefore acute thrombolysis was withheld. On hospital day (hd) 2, two short episodes of atrial fibrillation were documented. Cerebral MRI surprisingly showed a massive hyperacute injury marker (HARM) phenomenon and almost complete regression of the diffusion deficit of the left frontal cortex. Transthoracic echocar-
diography on hd 3 was unchanged from the one recorded on hd 1 (. Fig. 1). In addition to acetyl-salicylic acid and clopidogrel, therapeutic anticoagulation with heparin was initiated on hd 3. An ECG on hd 3 and hd 4 again revealed a short episode of atrial fibrillation. Ultrasonography of the abdomen on hd 4 revealed steatosis hepatis. Coronary angiography on hd 7 showed 50–60% stenosis of the left anterior descending coronary artery. Troponin T gradually declined from the time of admission to almost normal levels within 13 days (. Tab. 1). Echocardiography on hd 17 showed normalization of the systolic function and no thrombus (. Fig. 2). ECGs on hd 18 showed negative T waves in leads II, III, aVF, and V4 through V6. The QT interval had normalized to 440 ms. An ECG on hd 28 showed negative T waves in V4 through V6 exclusively. Diagnostic work-up for anemia, hypoproteinemia, gastrointestinal bleeding, weight loss, inappetence, recurrent nausea, and vomiting by gastroscopy and
Tab. 1 Laboratory parameters Parameter CK CK-MB MB% Troponin Ery Hb Hc
Reference limits 38–174 U/l 0–24 U/l 0–6% 0–0.009 ng/ml 4–5.2 T/l 12–16 g/dl 6–20 mg/dl
hd 1 281 55 19.5 0.220 2.7 10.6 22
hd 2 237 36 15.4 0.209 2.42 9.5 27.3
hd 5 54 nd nd 0.197 2.56 9.8 28.3
hd 9 30 nd nd 0.083 2.71 10.2 29.6
hd 13 49 nd nd 0.046 2.78 10.2 30.4
hd hospital day, CK creatine-kinase, CK-MB cardiac fraction, Ery erythrocyte count, Hb hemoglobin, Hc hematocrit, nd not done Herz 2013
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Case study
Fig. 1 8 Echocardiographic apical four-chamber view showing ballooning of the left ventricular apical region and a large ventricular thrombus
colonoscopy revealed a gastric adenocarcinoma with focal infiltration of the cardia and the esophagus. Staging by CT scan of the thorax and the abdomen did not show local infiltration but liver metastasis was suspected. Liver biopsy confirmed spreading of the tumor. Under triple therapy, the ventricular thrombus resolved within 19 days, and acetyl-salicylic acid was discontinued and the anticoagulant therapy reduced to heparin and clopidogrel alone. The red blood cell counts continuously declined, as further macroscopic gastrointestinal bleedings occurred; since the cardiac abnormalities were retrospectively interpreted as TTS, heparin was reduced to the antithrombotic dosage and clopidogrel was discontinued on hd 23.
Discussion The patient presented here is an interesting case of the triggering of TTS presumably by stress from the carcinoma, the occurrence of a ventricular thrombus within the hypokinetic sack of the ventricle, and the occurrence of ischemic, embolic stroke with marked improvement after suspected spontaneous recanalization of the median cerebral artery occlusion. Concerning the triggers of TTS, neither psychological nor physical stress was reported by the patient. The only stressors that could possibly be responsible were
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Herz 2013
Fig. 2 8 Echocardiographic apical four-chamber view after 14 days shows normalization of the systolic function and no thrombus
smoking, alcohol consumption, depressive mood, or the malignancy. The previously undetected carcinoma was the most likely trigger, since malignancies have been reported as triggers of TTS [9, 10, 11, 12, 13]. Additionally, alcohol withdrawal could have played a triggering role [14]. Smoking, alcohol consumption, and depressive mood were excluded because they have not been reported as a trigger of TTS. It is also conceivable that stroke was embolic due to the atrial fibrillation and secondarily triggered TTS and that the intraventricular thrombus was not pathogenic [15]. Concerning the pathogenesis of TTS, it can be speculated that the gastric adenocarcinoma produced cortisol or another unknown triggering factor and thus induced the development of TTS, as has been previously reported [16]. Thrombi have been repeatedly reported as a complication of TTS [2, 3, 4, 5, 6, 7, 8]. Thrombus formation during TTS is attributed to stasis of the blood from akinesia/hypokinesia [2, 3, 4, 5, 6, 7, 8, 17, 18, 19]. Thrombus formation due to paraneoplastic hypercoagulability is rather unlikely, since the thrombus resolved under adequate anticoagulation and resolution of akinesia/hypokinesia. Ventricular thrombus formation may not only be a complication of early TTS but may also develop later during the course of the TTS [20]. Reported complications of intraventricular thrombus formation are
stroke [21, 22, 23], myocardial infarction [24], thromboembolism [25], cardiac arrest [25], cardiac shock [25], or death [25]. The rate of in-hospital complications is higher among old than among young patients [26]. The prognosis of a ventricular thrombus from TTS is usually fair with resolution of hypokinesia and if not additionally complicated by a thromboembolic event [27]. Various scenarios are possible in the pathogenesis of stroke. First, stroke was caused by paraneoplastic thrombophilia. Second, stroke resulted from the ventricular thrombus. Third, stroke was caused by atrial fibrillation. Arguments against the last hypothesis are that the history was negative for palpitations in particular due to atrial fibrillation, that atrial fibrillation had not been recorded prior to admission, and that atrial fibrillation was not documented on admission. Thrombophilic hypercoagulability induced by the malignancy cannot be definitively excluded, but the embolic features of the stroke make other causes more likely. Stroke in our patient was most likely due to embolization of the ventricular thrombus because such a pathogenetic scenario has been previously reported [21, 22, 23] and because TTS occurred most probably before atrial fibrillation. An atherothrombotic cause of the stroke was excluded owing to the extensive risk factor profile for embolic stroke and the mini-
mal atherosclerotic features on carotid ultrasound and coronary angiography.
Conclusion This case shows that TTS may be triggered by stress from a malignancy and that TTS may lead to intraventricular thrombus formation and consecutively embolic stroke. TTS should not be confused with an acute coronary syndrome if there are typical ECG and echocardiographic abnormalities, resolution of these abnormalities within a few days, CK and troponin elevation, but only nonsignificant coronary artery stenosis.
Corresponding address Prof. Dr. J. Finsterer Krankenanstalt Rudolfstiftung Postfach 20, 1180 Vienna Austria [email protected]
Compliance with ethical guidelines Conflict of interest. J. Finsterer, C. Stöllberger, and T. Pulgram state that there are no conflicts of interest. Consent was obtained from all patients identifiable from images or other information within the manuscript. In the case of underage patients, consent was obtained from a parent or legal guardian. All studies on humans described in the present manuscript were carried out with the approval of the responsible ethics committee and in accordance with national law and the Helsinki Declaration of 1975 (in its current, revised form). Informed consent was obtained from all patients included in studies.
References 1. Elliott P, Andersson B, Arbustini E et al (2008) Classification of the cardiomyopathies: a position statement from the European Society Of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 29:270–276 2. Correia AS, Moreno N, Gonçalves A et al (2012) Cardiac thrombus and conduction disorder in takotsubo cardiomyopathy. Rev Port Cardiol 31:513–516 3. Gregorio C de, Andò G (2012) A rare cause of Takotsubo cardiomyopathy related left ventricular apical thrombus requiring surgery. Heart Lung Circ 21:251 4. Lee PH, Song JK, Park IK et al (2011) Takotsubo cardiomyopathy: a case of persistent apical ballooning complicated by an apical mural thrombus. Korean J Intern Med 26:455–459 5. Michels G, Pfister R (2012) De novo left ventricular thrombus during tako-tsubo cardiomyopathy. Dtsch Med Wochenschr 137:2423–2426
6. Seitz MJ, McLeod MK, O’Keefe MD, Seah PW (2012) A rare cause of Takotsubo cardiomyopathy related left ventricular apical thrombus requiring surgery. Heart Lung Circ 21:245–246 7. Shin SN, Yun KH, Ko JS et al (2011) Left ventricular thrombus associated with takotsubo cardiomyopathy: a cardioembolic cause of cerebral infarction. J Cardiovasc Ultrasound 19:152–155 8. Yaguchi M, Yaguchi H, Takahashi N (2011) A case of asymptomatic Takotsubo cardiomyopathy with intraventricular thrombus associated with epileptic seizure. Brain Nerve 63:897–900 9. Burgdorf C, Kurowski V, Bonnemeier H et al (2008) Long-term prognosis of the transient left ventricular dysfunction syndrome (Tako-Tsubo cardiomyopathy): focus on malignancies. Eur J Heart Fail 10:1015–1019 10. Gingles C, Leslie S, Harvey R (2010) A case of Takotsubo’s cardiomyopathy and multiple endocrine neoplasia 2A syndrome. Clin Endocrinol (Oxf) 73:827–829 11. Mitsumori T, Nakajima K, Nozaki Y et al (2010) Multiple myeloma complicated with Takotsubo cardiomyopathy. Rinsho Ketsueki 51:291–296 12. Schweizer MT, Mehta R, Salgia R, Villaflor VM (2011) Takotsubo cardiomyopathy in a patient with squamous cell esophageal carcinoma. J Clin Oncol 29:e598–e600 13. Zeballos C, Moraca RJ, Bailey SH, Magovern GJ Jr (2012) Temporary mechanical circulatory support for Takotsubo cardiomyopathy secondary to primary mediastinal B-cell lymphoma. J Card Surg 27:119–121 14. Stout BJ, Hoshide R, Vincent DS (2012) Takotsubo cardiomyopathy in the setting of acute alcohol withdrawal. Hawaii J Med Public Health 71:193– 194 15. Scheitz JF, Mochmann HC, Witzenbichler B et al (2012) Takotsubo cardiomyopathy following ischemic stroke: a cause of troponin elevation. J Neurol 259:188–190 16. Wickboldt N, Pache JC, Dietrich PY et al (2012) Takotsubo syndrome secondary to adrenal adenocarcinoma: cortisol as a possible culprit. Am J Respir Crit Care Med 186:1061–1062 17. Kurisu S, Inoue I, Kawagoe T et al (2011) Incidence and treatment of left ventricular apical thrombosis in Tako-tsubo cardiomyopathy. Int J Cardiol 146:e58–e60 18. Mrdovic I, Perunicic J, Asanin M et al (2008) Transient left ventricular apical ballooning complicated by a mural thrombus and outflow tract obstruction in a patient with pheochromocytoma. Tex Heart Inst J 35:480–482 19. Tobar R, Rotzak R, Rozenman Y (2009) Apical thrombus associated with Takotsubo cardiomyopathy in a young woman. Echocardiography 26:575–580 20. Haghi D, Papavassiliu T, Heggemann F et al (2008) Incidence and clinical significance of left ventricular thrombus in tako-tsubo cardiomyopathy assessed with echocardiography. QJM 101:381–386 21. Mayor-Gómez S, Erro ME, Olaz-Preciado F et al (2012) Stroke and Takotsubo syndrome: a reciprocal relationship. Rev Neurol 55:475–478 22. Yaylali YT, Saricopur A (2012) Takotsubo-syndrome presenting with supraventricular tachycardia, stroke, and thrombocytopenia. Int J Cardiol 161:e39–e41 23. Kim SM, Aikat S, Bailey A, White M (2012) Takotsubo cardiomyopathy as a source of cardioembolic cerebral infarction. BMJ Case Rep. doi:pii: bcr2012006835. 10.1136/bcr-2012-006835
24. Angulo-Llanos R, Sanz-Ruiz R, Solis J, FernándezAvilés F (2013) Acute myocardial infarction: an uncommon complication of takotsubo cardiomyopathy. Catheter Cardiovasc Interv. doi:10.1002/ ccd.24846 25. Schultz T, Shao Y, Redfors B et al (2012) Stress-induced cardiomyopathy in Sweden: evidence for different ethnic predisposition and altered cardiocirculatory status. Cardiology 122:180–186 26. Citro R, Rigo F, Previtali M et al (2012) Differences in clinical features and in-hospital outcomes of older adults with tako-tsubo cardiomyopathy. J Am Geriatr Soc 60:93–98 27. Yoshida T, Hibino T, Fujimaki T et al (2009) Tako-tsubo cardiomyopathy complicated by apical thrombus formation: a case report. Int J Cardiol 132:e120–e122
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