- Email: [email protected]
Acute global cardiac decompensation due to inverted takotsubo cardiomyopathy after skull–brain trauma—A case report
Injury Extra 42 (2011) 54–57
Contents lists available at ScienceDirect
Injury Extra journal homepage: www.elsevier.com/locate/inext
Case report
Acute global cardiac decompensation due to inverted takotsubo cardiomyopathy after skull–brain trauma—A case report Alexander Samol a,*, Matthias Grude a, Jo¨rg Stypmann a, Alexander Christian Bunck b, David Maintz b, Holger Reinecke a, Pia Lebiedz a a b
Department of Cardiology and Angiology, University Hospital of Muenster, Albert-Schweitzer-Str. 33, 48149 Muenster, Germany Department of Radiology, University Hospital of Muenster, Germany
A R T I C L E I N F O
Article history: Accepted 24 January 2011
1. Introduction Takotsubo cardiomyopathy (TTC) usually occurs in postmenopausal women after acute physical or mental stress and typically presents with apical ballooning of the left ventricle. TTC manifests with symptoms similar to acute coronary syndrome and may be accompanied by ECG changes, so coronary angiography is mandatory to exclude acute coronary syndrome.6,3 Other forms of TTC with atypical mid-ventricular ballooning have been described.5 Severe cerebral damage may also go along with ECG changes such as ST segment elevation, release of cardiac enzymes and/or cardiac dysfunction and often presents similar to TTC.5,2 For that reason a recent review postulates a pathophysiological relationship between TTC and cardiac dysfunction after cerebral bleeding.7 2. Case report We report on the case of a 56 year old female who was suffering from skull–brain trauma after bike accident. Shortly after the accident the patient grew comatose and was orotracheally intubated and transferred to the trauma department of our hospital. CCT revealed a minimal parenchymatous and subarachnoidal cerebral bleeding of the right frontal brain and a left-sided petrous bone fracture (Fig. 1). Two attempts of extubation failed due to quick respiratory insufficiency caused by cardiac decompensation. Therefore, cardiac enzymes were assessed and echocardiography was performed. Whereas creatine kinase was normal, troponine I was elevated up
* Corresponding author. Tel.: +49 251 8347641; fax: +49 251 8346190. E-mail address: [email protected] (A. Samol). 1572-3461/$ – see front matter ß 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.injury.2011.01.023
to 6.8 ng/ml (norm < 0.04 ng/ml). Transthoracal echocardiography revealed high-grade global and regional reduction of the left ventricular function. ECG was without pathological findings of the ST-segment apart from discrete preterminal T-wave negativity in leads V3 to V6 but showed a modest prolonged QTc-time of 450 ms (Fig. 2). Acute myocardial infarction was suggested and the patient was transferred to our department of cardiology and underwent an emergency coronary angiography. Herein we did not find any significant coronary stenosis (Fig. 3A and B) but levocardiography confirmed severe left ventricular hypokinesia in the midventricular area with well-preserved contraction in apical and basal regions (Fig. 3C). We considered the tentative diagnosis of ‘‘inverted’’ takotsubo cardiomyopathy (iTTC). After control CCT that revealed no progress in bleeding, the patient was transferred to our intensive care unit. During the next hours the patient required high dosage of catecholamines. On the next day a cardiac magnetic resonance imaging (MRI) exam was performed. The scan confirmed the diagnosis of severe impairment of left ventricular function with akinesia of the midportion of the left ventricle (ejection fraction 25%). In line with echocardiographic findings, apical and basal contractility of the left ventricle was preserved (Fig. 3D and E). On late enhancement imaging no signs of myocardial necrosis or inflammation were found (Fig. 3F). In summary, cardiac MRI provided conclusive evidence of the diagnosis of iTTC. After 48 h patient’s condition improved, catecholamines were ceased and termination of mechanical ventilation was possible. Neurological examination showed no signs of sensoric or motoric impairment and no amnesia. Control echocardiography confirmed an improvement of left ventricular ejection fraction to 45% and after another surveillance period of 48 h at our intensive care unit the patient was transferred to another hospital after introduction of a heart failure medication with an ACE-Inhibitor and a beta-blocker. None of the daily ECGs showed any pathological signs except of the modest QTc-prolongation. The course of troponine, creatine kinase (CK) and myocardial band fraction of CK (CKMB) are illustrated in Fig. 4. Brain natriuretic peptide (NT-pro BNP) was measured two times and was elevated up to 10,895 pg/ml at the time of transfer to our ICU and 10,156 pg/ml 48 h later.
[()TD$FIG]
A. Samol et al. / Injury Extra 42 (2011) 54–57
55
ventricle in levocardiography resembling a Japanese octopus trapping pot. By now, several cases of this syndrome have also been reported in Western populations. In 2004 Bybee et al. proposed the following clinical characteristics for the diagnosis of takotsubo cardiomyopathy3: (1) Transient akinesis or dyskinesis of the left ventricular wall with chest pain; (2) New electrocardiographic changes; (3) No significant coronary artery disease; (4) Absence of recent significant head trauma, intracerebral bleeding, phaeochromocytoma, myocarditis, and hypertrophic cardiomyopathy.
Fig. 1. CCT at hospital admission revealed a minimal parenchymatous and subarachnoidal cerebral bleeding of the right frontal brain (black arrows).
3. Discussion Several years ago, a new syndrome with transient left ventricular dysfunction has first been described in Japanese patients. This new entity was called takotsubo cardiomyopathy or apical ballooning due to the typical endsystolic shape of the left
Although the aetiology of this disease is unknown, the available evidence is consistent with the concept that extreme emotional (33–45%) and/or physical stress (17–22%) may trigger it.8 A predominance of postmenopausal women has been reported but the increased susceptibility of women and the potential genderrelated differences in the response to catecholamines is not well understood.11 Multivessel coronary spasms and catecholamine cardiotoxicity are suspected as underlying mechanism of TTC.4,1 Another type of transient left ventricular myocardial dysfunction has been reported in patients after subarachnoid haemorrhage. Already 50 years ago myocardial-ischaemia-like ECG changes have been reported after subarachnoid haemorrhage.9 Several studies report a reversible myocardial dysfunction with enzyme release after brain injury or cerebrovascular events2 in the absence of coronary artery disease.7 In summary, this transient myocardial dysfunction seems also to be catecholamine induced. TTC with, neurogenic stunning of the myocardium occurs
[()TD$FIG]
Fig. 2. Baseline ECG after admission to our hospital shows no pathological findings of the ST-segment apart from discrete preterminal T-wave negativity in leads V3 to V6 but a modest prolonged QTc-time of 450 ms.
[()TD$FIG]
56
A. Samol et al. / Injury Extra 42 (2011) 54–57
Fig. 3. Coronary angiography (A: left coronary artery and B: right coronary artery) 24 h after the accident reveals no significant stenosis. (C) Levocardiography shows severe hypokinesia of the mid-ventricular region with well-preserved contraction in apical and basal regions (white arrows). bFFE cine sequence of MRI (D: enddiastolic and E: endsystolic) shows severe impairment of left ventricular function with akinesia of the midportion of the left ventricle (white arrows) and preserved apical and basal contractility of the left ventricle. (F) Late enhancement imaging shows no signs of myocardial inflammation, acute infarction or scarring.
especially in postmenopausal women. TTC frequently affects apical segments of the left ventricle and normalizes within in a few days or weeks.7 Proposed criteria for the diagnosis of TTC3 postulate the exclusion of acute brain injury. However, the cardiotoxic mechanism in both disease patterns seems to be catecholamine induced. Implementing these criteria, our patient does not meet the diagnostic criteria of takotsubo. Nevertheless, the parenchymatous and subarachnoidal cerebral bleeding of the right frontal brain in our patient was small and without neurological impairment. We hypothesize that this minimal lesion could not solely cause the severe ventricular dysfunction in our case and that the midven-
tricular contraction impairment was induced by acute psychic stress during the accident. In accordance to Trio et al. we propagate that acute brain injury should not exclude the diagnosis of TTC.10 In fact, a new stress induced temporary myocardial dysfunction entity including patients after acute brain injury should be defined. This case especially emphasizes the impact of early interdisciplinary cooperation in trauma patients. Especially in prior healthy patients without cardiovascular risk factors after physical or mental stress, TTC is a potential differential diagnosis in patients with ECG-changes or elevated biomarkers of myocardial necrosis. Nevertheless, the early transfer of these patients to a department of cardiology is essential to exclude the main differential diagnosis of
[()TD$FIG]
A. Samol et al. / Injury Extra 42 (2011) 54–57
57
References
Fig. 4. Course of biomarkers of myocardial necrosis during the first five days after bike accident: troponine increased at day 2 with a maximum of 6.8 ng/ml, CK was elevated up to 480 U/l at day 4 with no significant increase of myocardial band fraction of CK (CKMB).
acute myocardial infarction by coronary angiography. Echocardiography in the hands of an experienced examiner is an additional useful tool to evaluate the left ventricular function and regional contraction abnormalities, especially at the ICU bedside, but is solely not sufficient to exclude significant coronary stenosis.
1. Akashi YJ, Nakazawa K, Sakakibara M, Miyake F, Sasaka K. Reversible left ventricular dysfunction ‘‘takotsubo’’ cardiomyopathy related to catecholamine cardiotoxicity. J Electrocardiol 2002;35:351–6. 2. Ako J, Sudhir K, Farouque HM, Honda Y, Fitzgerald PJ. Transient left ventricular dysfunction under severe stress: brain–heart relationship revisited. Am J Med 2006;119:10–7. 3. Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics STsegment elevation myocardial infarction. Ann Intern Med 2004;141:858–65. 4. Girod JP, Messerli AW, Zidar F, Tang WH, Brener SJ. Images in cardiovascular medicine. Tako-tsubo-like transient left ventricular dysfunction. Circulation 2003;107:e120–1. 5. Hurst RT, Askew JW, Reuss CS, Lee RW, Sweeney JP, Fortuin FD, et al. Transient midventricular ballooning syndrome: a new variant. J Am Coll Cardiol 2006;48:579–83. 6. Kawai S, Kitabatake A, Tomoike H. Guidelines for diagnosis of takotsubo (ampulla) cardiomyopathy. Circ J 2007;71:990–2. 7. Kono T, Morita H, Kuroiwa T, Onaka H, Takatsuka H, Fujiwara A. Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium. J Am Coll Cardiol 1994;24:636–40. 8. Nef HM, Mollmann H, Elsasser A. Tako-tsubo cardiomyopathy (apical ballooning). Heart 2007;93:1309–15. 9. Shuster S. The electrocardiogram in subarachnoid haemorrhage. Br Heart J 1960;22:316–20. 10. Trio O, de GC, Ando G. Myocardial dysfunction after subarachnoid haemorrhage and tako-tsubo cardiomyopathy: a differential diagnosis? Ther Adv Cardiovasc Dis 2010;4:105–7. 11. Wittstein IS, Thiemann DR, Lima JA, Baughman KL, Schulman SP, Gerstenblith G, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539–48.
Contents lists available at ScienceDirect
Injury Extra journal homepage: www.elsevier.com/locate/inext
Case report
Acute global cardiac decompensation due to inverted takotsubo cardiomyopathy after skull–brain trauma—A case report Alexander Samol a,*, Matthias Grude a, Jo¨rg Stypmann a, Alexander Christian Bunck b, David Maintz b, Holger Reinecke a, Pia Lebiedz a a b
Department of Cardiology and Angiology, University Hospital of Muenster, Albert-Schweitzer-Str. 33, 48149 Muenster, Germany Department of Radiology, University Hospital of Muenster, Germany
A R T I C L E I N F O
Article history: Accepted 24 January 2011
1. Introduction Takotsubo cardiomyopathy (TTC) usually occurs in postmenopausal women after acute physical or mental stress and typically presents with apical ballooning of the left ventricle. TTC manifests with symptoms similar to acute coronary syndrome and may be accompanied by ECG changes, so coronary angiography is mandatory to exclude acute coronary syndrome.6,3 Other forms of TTC with atypical mid-ventricular ballooning have been described.5 Severe cerebral damage may also go along with ECG changes such as ST segment elevation, release of cardiac enzymes and/or cardiac dysfunction and often presents similar to TTC.5,2 For that reason a recent review postulates a pathophysiological relationship between TTC and cardiac dysfunction after cerebral bleeding.7 2. Case report We report on the case of a 56 year old female who was suffering from skull–brain trauma after bike accident. Shortly after the accident the patient grew comatose and was orotracheally intubated and transferred to the trauma department of our hospital. CCT revealed a minimal parenchymatous and subarachnoidal cerebral bleeding of the right frontal brain and a left-sided petrous bone fracture (Fig. 1). Two attempts of extubation failed due to quick respiratory insufficiency caused by cardiac decompensation. Therefore, cardiac enzymes were assessed and echocardiography was performed. Whereas creatine kinase was normal, troponine I was elevated up
* Corresponding author. Tel.: +49 251 8347641; fax: +49 251 8346190. E-mail address: [email protected] (A. Samol). 1572-3461/$ – see front matter ß 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.injury.2011.01.023
to 6.8 ng/ml (norm < 0.04 ng/ml). Transthoracal echocardiography revealed high-grade global and regional reduction of the left ventricular function. ECG was without pathological findings of the ST-segment apart from discrete preterminal T-wave negativity in leads V3 to V6 but showed a modest prolonged QTc-time of 450 ms (Fig. 2). Acute myocardial infarction was suggested and the patient was transferred to our department of cardiology and underwent an emergency coronary angiography. Herein we did not find any significant coronary stenosis (Fig. 3A and B) but levocardiography confirmed severe left ventricular hypokinesia in the midventricular area with well-preserved contraction in apical and basal regions (Fig. 3C). We considered the tentative diagnosis of ‘‘inverted’’ takotsubo cardiomyopathy (iTTC). After control CCT that revealed no progress in bleeding, the patient was transferred to our intensive care unit. During the next hours the patient required high dosage of catecholamines. On the next day a cardiac magnetic resonance imaging (MRI) exam was performed. The scan confirmed the diagnosis of severe impairment of left ventricular function with akinesia of the midportion of the left ventricle (ejection fraction 25%). In line with echocardiographic findings, apical and basal contractility of the left ventricle was preserved (Fig. 3D and E). On late enhancement imaging no signs of myocardial necrosis or inflammation were found (Fig. 3F). In summary, cardiac MRI provided conclusive evidence of the diagnosis of iTTC. After 48 h patient’s condition improved, catecholamines were ceased and termination of mechanical ventilation was possible. Neurological examination showed no signs of sensoric or motoric impairment and no amnesia. Control echocardiography confirmed an improvement of left ventricular ejection fraction to 45% and after another surveillance period of 48 h at our intensive care unit the patient was transferred to another hospital after introduction of a heart failure medication with an ACE-Inhibitor and a beta-blocker. None of the daily ECGs showed any pathological signs except of the modest QTc-prolongation. The course of troponine, creatine kinase (CK) and myocardial band fraction of CK (CKMB) are illustrated in Fig. 4. Brain natriuretic peptide (NT-pro BNP) was measured two times and was elevated up to 10,895 pg/ml at the time of transfer to our ICU and 10,156 pg/ml 48 h later.
[()TD$FIG]
A. Samol et al. / Injury Extra 42 (2011) 54–57
55
ventricle in levocardiography resembling a Japanese octopus trapping pot. By now, several cases of this syndrome have also been reported in Western populations. In 2004 Bybee et al. proposed the following clinical characteristics for the diagnosis of takotsubo cardiomyopathy3: (1) Transient akinesis or dyskinesis of the left ventricular wall with chest pain; (2) New electrocardiographic changes; (3) No significant coronary artery disease; (4) Absence of recent significant head trauma, intracerebral bleeding, phaeochromocytoma, myocarditis, and hypertrophic cardiomyopathy.
Fig. 1. CCT at hospital admission revealed a minimal parenchymatous and subarachnoidal cerebral bleeding of the right frontal brain (black arrows).
3. Discussion Several years ago, a new syndrome with transient left ventricular dysfunction has first been described in Japanese patients. This new entity was called takotsubo cardiomyopathy or apical ballooning due to the typical endsystolic shape of the left
Although the aetiology of this disease is unknown, the available evidence is consistent with the concept that extreme emotional (33–45%) and/or physical stress (17–22%) may trigger it.8 A predominance of postmenopausal women has been reported but the increased susceptibility of women and the potential genderrelated differences in the response to catecholamines is not well understood.11 Multivessel coronary spasms and catecholamine cardiotoxicity are suspected as underlying mechanism of TTC.4,1 Another type of transient left ventricular myocardial dysfunction has been reported in patients after subarachnoid haemorrhage. Already 50 years ago myocardial-ischaemia-like ECG changes have been reported after subarachnoid haemorrhage.9 Several studies report a reversible myocardial dysfunction with enzyme release after brain injury or cerebrovascular events2 in the absence of coronary artery disease.7 In summary, this transient myocardial dysfunction seems also to be catecholamine induced. TTC with, neurogenic stunning of the myocardium occurs
[()TD$FIG]
Fig. 2. Baseline ECG after admission to our hospital shows no pathological findings of the ST-segment apart from discrete preterminal T-wave negativity in leads V3 to V6 but a modest prolonged QTc-time of 450 ms.
[()TD$FIG]
56
A. Samol et al. / Injury Extra 42 (2011) 54–57
Fig. 3. Coronary angiography (A: left coronary artery and B: right coronary artery) 24 h after the accident reveals no significant stenosis. (C) Levocardiography shows severe hypokinesia of the mid-ventricular region with well-preserved contraction in apical and basal regions (white arrows). bFFE cine sequence of MRI (D: enddiastolic and E: endsystolic) shows severe impairment of left ventricular function with akinesia of the midportion of the left ventricle (white arrows) and preserved apical and basal contractility of the left ventricle. (F) Late enhancement imaging shows no signs of myocardial inflammation, acute infarction or scarring.
especially in postmenopausal women. TTC frequently affects apical segments of the left ventricle and normalizes within in a few days or weeks.7 Proposed criteria for the diagnosis of TTC3 postulate the exclusion of acute brain injury. However, the cardiotoxic mechanism in both disease patterns seems to be catecholamine induced. Implementing these criteria, our patient does not meet the diagnostic criteria of takotsubo. Nevertheless, the parenchymatous and subarachnoidal cerebral bleeding of the right frontal brain in our patient was small and without neurological impairment. We hypothesize that this minimal lesion could not solely cause the severe ventricular dysfunction in our case and that the midven-
tricular contraction impairment was induced by acute psychic stress during the accident. In accordance to Trio et al. we propagate that acute brain injury should not exclude the diagnosis of TTC.10 In fact, a new stress induced temporary myocardial dysfunction entity including patients after acute brain injury should be defined. This case especially emphasizes the impact of early interdisciplinary cooperation in trauma patients. Especially in prior healthy patients without cardiovascular risk factors after physical or mental stress, TTC is a potential differential diagnosis in patients with ECG-changes or elevated biomarkers of myocardial necrosis. Nevertheless, the early transfer of these patients to a department of cardiology is essential to exclude the main differential diagnosis of
[()TD$FIG]
A. Samol et al. / Injury Extra 42 (2011) 54–57
57
References
Fig. 4. Course of biomarkers of myocardial necrosis during the first five days after bike accident: troponine increased at day 2 with a maximum of 6.8 ng/ml, CK was elevated up to 480 U/l at day 4 with no significant increase of myocardial band fraction of CK (CKMB).
acute myocardial infarction by coronary angiography. Echocardiography in the hands of an experienced examiner is an additional useful tool to evaluate the left ventricular function and regional contraction abnormalities, especially at the ICU bedside, but is solely not sufficient to exclude significant coronary stenosis.
1. Akashi YJ, Nakazawa K, Sakakibara M, Miyake F, Sasaka K. Reversible left ventricular dysfunction ‘‘takotsubo’’ cardiomyopathy related to catecholamine cardiotoxicity. J Electrocardiol 2002;35:351–6. 2. Ako J, Sudhir K, Farouque HM, Honda Y, Fitzgerald PJ. Transient left ventricular dysfunction under severe stress: brain–heart relationship revisited. Am J Med 2006;119:10–7. 3. Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics STsegment elevation myocardial infarction. Ann Intern Med 2004;141:858–65. 4. Girod JP, Messerli AW, Zidar F, Tang WH, Brener SJ. Images in cardiovascular medicine. Tako-tsubo-like transient left ventricular dysfunction. Circulation 2003;107:e120–1. 5. Hurst RT, Askew JW, Reuss CS, Lee RW, Sweeney JP, Fortuin FD, et al. Transient midventricular ballooning syndrome: a new variant. J Am Coll Cardiol 2006;48:579–83. 6. Kawai S, Kitabatake A, Tomoike H. Guidelines for diagnosis of takotsubo (ampulla) cardiomyopathy. Circ J 2007;71:990–2. 7. Kono T, Morita H, Kuroiwa T, Onaka H, Takatsuka H, Fujiwara A. Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium. J Am Coll Cardiol 1994;24:636–40. 8. Nef HM, Mollmann H, Elsasser A. Tako-tsubo cardiomyopathy (apical ballooning). Heart 2007;93:1309–15. 9. Shuster S. The electrocardiogram in subarachnoid haemorrhage. Br Heart J 1960;22:316–20. 10. Trio O, de GC, Ando G. Myocardial dysfunction after subarachnoid haemorrhage and tako-tsubo cardiomyopathy: a differential diagnosis? Ther Adv Cardiovasc Dis 2010;4:105–7. 11. Wittstein IS, Thiemann DR, Lima JA, Baughman KL, Schulman SP, Gerstenblith G, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539–48.