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Partial status epilepticus causing a transient left ventricular apical ballooning
Seizure 20 (2011) 184–186
Contents lists available at ScienceDirect
Seizure journal homepage: www.elsevier.com/locate/yseiz
Case report
Partial status epilepticus causing a transient left ventricular apical ballooning Nadia Benyounes a,*, Michael Obadia b, Jean-Michel Devys c, Aude Thevenin c, Serge Iglesias d a
Department of Internal Medicine, Fondation Ophtalmologique Adolphe de Rothschild, 25-29, rue Manin, 75940 Paris Cedex 19, France Department of Neurology, Fondation Ophtalmologique Adolphe de Rothschild, Paris, France c Department of Anesthesiology, Fondation Ophtalmologique Adolphe de Rothschild, Paris, France d Department of Neurophysiology, Henri Mondor Hospital, Creteil, France b
A R T I C L E I N F O
A B S T R A C T
Article history: Received 3 September 2010 Received in revised form 25 October 2010 Accepted 1 November 2010
Transient left ventricular apical ballooning also called Takotsubo cardiomyopathy is a recently described cardiac syndrome. It often affects postmenopausal women having an acute physical or emotional stress, but it have also been described after convulsive status epilepticus. Although this association is rare and left ventricular function often recovers, it would be useful to the neurologist to be aware of the signs leading to this diagnosis, to improve the cardiac later care. Here we report a patient with partial status epilepticus in whom the diagnosis of transient left ventricular apical ballooning was made. We describe the diagnostic criteria and the potential complications that should be monitored. ß 2010 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.
Keywords: Seizure Partial status epilepticus Takotsubo cardiomyopathy Stress-induced cardiomyopathy
We report a patient with sudden language troubles finally related to a partial epileptic attack, who developed ECG abnormalities and a limited elevation of cardiac enzymes, diagnosed as a transient left ventricular apical ballooning. This case illustrates the link between the neurological event and the cardiovascular event, the first being a rare but possible triggering condition at the onset of the second. 1. Case report A 79-year-old woman was referred to the stroke unit of our hospital in July 2007 for a sudden onset of aphasia. The neuropsychological examination disclosed slight memory and executive disturbances. The physical examination was normal. Apart from a hypertension treated with diuretics, her medical history was unremarkable. A brain MRI performed at admission, including Flair DWI axial sequences and intracranial MR angiography was within normal, only showing some leukoaraiosis. There was no sign of infection or metabolic disorder. An EEG performed 1 day later revealed subcontinuous pseudoperiodic bi-or triphasic sharp waves over fronto-temporal lobes, with a left predominance (Fig. 1a and b). The diagnosis of partial status epilepticus was made and a medical treatment with clobazam and levetiracetam was initiated.
* Corresponding author. Tel.: +33 1 48036881; fax: +33 1 48036880. E-mail address: [email protected] (N. Benyounes).
There was a complete neurological recovery under this medication and the EEG monitoring 6 days later showed a dramatic improvement (Fig. 1c). While the first ECG at admission was normal, inverted T waves appeared in the anterior and lateral leads on the second ECG at day 1 (Fig. 1d), without chest pain, hypotension or clinical signs of heart failure. Serum troponin I levels rose until 5 mg/l the first day (reference <0.11 mg/l) and the BNP (B-type natriuretic peptide, which elevation reflects elevated left ventricular filling pressures) reached 1000 pg/ml (reference <100 pg/ml). Echocardiography at day 1 showed a dyskinesis of the left ventricular apex without thrombus (Fig. 1e) and slight midventricular wall motion abnormalities with preserved left ventricular systolic function. The coronary angiography on the same day did not show any significant coronary artery stenosis. The echocardiography at day 4 was identical to the first one. At day 10, a complete normalization of the left ventricular regional wall motion was noted (Fig. 1f). This made the diagnosis of left ventricular apical ballooning also called Takotsubo cardiomyopathy or stress-induced cardiomyopathy. 2. Discussion The Takotsubo cardiomyopathy is a fairly recently described cardiac syndrome comprising transient left ventricular apical wall motion abnormalities, a slight elevation of cardiac enzymes and ST segment and/or T waves abnormalities on the ECG, sometimes mimicking an acute coronary syndrome. Chest pain may occur.
1059-1311/$ – see front matter ß 2010 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.seizure.2010.11.001
[()TD$FIG]
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Fig. 1. (a and b) First EEG showing subcontinuous pseudoperiodic bi-or triphasic sharp waves over fronto-temporal lobes, with left predominance. (c) Second EEG showing a dramatic improvement. (d) ECG showing inverted T waves in the anterior and lateral leads. (e) First echocardiography (apical 2 chambers view stored in systole) showing a dyskinesis of the left ventricular apex (arrow). (f) Last echocardiography showing a normal left ventricular apex in systole (arrow).
However, coronary angiography is within normal, without any significant obstructive epicardial coronary disease. Postmenopausal women seem to be most at risk for developing the syndrome and an acute physical or emotional stress often triggers the onset of transient left ventricular apical ballooning.1,2
Diagnostic criteria have been proposed by the mayo clinic.3 All the four criteria must be met: (1) A transient akinesis or dyskinesis of the left ventricular apical and mid-ventricular segments, the regional wall-motion abnormalities extending beyond a single epicardial vascular distribution. (2) The absence of obstructive
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N. Benyounes et al. / Seizure 20 (2011) 184–186
coronary disease or angiographic evidence of acute plaque rupture. (3) New electrocardiographic abnormalities (either ST-segment elevation or T-wave inversion). (4) The absence of: recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis and hypertrophic cardiomyopathy. In our patient, ischemic heart disease was ruled out since the coronary angiography was normal. The left ventricular dysfunction was transitory, excluding dilated cardiomyopathy. There was no alcohol intoxication and no echographic signs of left ventricular non-compaction. Epileptic attacks have been reported as a potential trigger. Despite this, the association remains under-recognized.2,4,5 However, the diagnosis should be suspected in the setting of a neurological disease in the presence of chest pain, abnormal ECG and enzyme elevation, leading to echocardiography and coronary angiography. Indeed, patients with Takotsubo syndrome should be monitored for heart failure, arrhythmias and hemodynamic instability that may occur, even if in-hospital prognosis seems to be favourable in most patients.3 In the absence of specifically evaluated therapies, the treatment remains empirical and symptomatic. The cause of this syndrome is not yet known. Postulated mechanisms include catecholamine cardiotoxicity, myocarditis, and epicardial or microvascular coronary spasm. This phenomenon has similarities with the left ventricular dysfunction in patients with acute brain injury, also called neurogenic stunned myocardium.6 Neurogenic stunned myocardium is also possibly mediated by CNS catecholamine stimulation. It is well known in the setting of subarachnoid hemorrhage.7 Takotsubo cardiomyopathy have been reported after convulsive status epilepticus, but not after brief seizures.8 Left ventricular apex is usually affected in the apical ballooning syndrome (Takostubo cardiomyopathy),3 while it is usually spared in the neurogenic stunned myocardium (inverted or reverse Takostsubo).7
Although the diagnostic criteria proposed for Takotsubo cardiomyopathy exclude recent significant head trauma and intracranial hemorrhage, many authors believe that these are variants of a single pathology: stress-induced cardiomyopathy.9,10 Conflict of interest statement None of the authors has any conflict of interest to disclose. References 1. Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J 2006;27(13):1523–9. 2. Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina PectorisMyocardial Infarction Investigations in Japan. J Am Coll Cardiol 2001;38(1):11– 8. 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(11):858– 65. 4. Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation 2005;111(4):472–9. 5. Shin SW, Baek SH, Choi BS, Lee HJ, Kim KH, Kim ES. Takotsubo cardiomyopathy associated with nonepileptic seizure after percutaneous endoscopic lumbar discectomy under general anesthesia. J Anesth 2010;24(3):460–3. 6. 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(1):10–7. 7. Banki N, Kopelnik A, Tung P, Lawton MT, Gress D, Drew B, et al. Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg 2006;105(1):15–20. 8. Legriel S, Bruneel F, Dalle L, Appere-de-Vecchi C, Georges JL, Abbosh N, et al. Recurrent takotsubo cardiomyopathy triggered by convulsive status epilepticus. Neurocrit Care 2008;9(1):118–21. 9. Movahed MR. Transient cardiac ballooning is not best nomenclature for Takotsubo cardiomyopathy as it does not capture all variants of this syndrome. Stress cardiomyopathy is a much better term for this syndrome. Clin Cardiol 2010;33(4):241–2. 10. 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(6):539–48.
Contents lists available at ScienceDirect
Seizure journal homepage: www.elsevier.com/locate/yseiz
Case report
Partial status epilepticus causing a transient left ventricular apical ballooning Nadia Benyounes a,*, Michael Obadia b, Jean-Michel Devys c, Aude Thevenin c, Serge Iglesias d a
Department of Internal Medicine, Fondation Ophtalmologique Adolphe de Rothschild, 25-29, rue Manin, 75940 Paris Cedex 19, France Department of Neurology, Fondation Ophtalmologique Adolphe de Rothschild, Paris, France c Department of Anesthesiology, Fondation Ophtalmologique Adolphe de Rothschild, Paris, France d Department of Neurophysiology, Henri Mondor Hospital, Creteil, France b
A R T I C L E I N F O
A B S T R A C T
Article history: Received 3 September 2010 Received in revised form 25 October 2010 Accepted 1 November 2010
Transient left ventricular apical ballooning also called Takotsubo cardiomyopathy is a recently described cardiac syndrome. It often affects postmenopausal women having an acute physical or emotional stress, but it have also been described after convulsive status epilepticus. Although this association is rare and left ventricular function often recovers, it would be useful to the neurologist to be aware of the signs leading to this diagnosis, to improve the cardiac later care. Here we report a patient with partial status epilepticus in whom the diagnosis of transient left ventricular apical ballooning was made. We describe the diagnostic criteria and the potential complications that should be monitored. ß 2010 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.
Keywords: Seizure Partial status epilepticus Takotsubo cardiomyopathy Stress-induced cardiomyopathy
We report a patient with sudden language troubles finally related to a partial epileptic attack, who developed ECG abnormalities and a limited elevation of cardiac enzymes, diagnosed as a transient left ventricular apical ballooning. This case illustrates the link between the neurological event and the cardiovascular event, the first being a rare but possible triggering condition at the onset of the second. 1. Case report A 79-year-old woman was referred to the stroke unit of our hospital in July 2007 for a sudden onset of aphasia. The neuropsychological examination disclosed slight memory and executive disturbances. The physical examination was normal. Apart from a hypertension treated with diuretics, her medical history was unremarkable. A brain MRI performed at admission, including Flair DWI axial sequences and intracranial MR angiography was within normal, only showing some leukoaraiosis. There was no sign of infection or metabolic disorder. An EEG performed 1 day later revealed subcontinuous pseudoperiodic bi-or triphasic sharp waves over fronto-temporal lobes, with a left predominance (Fig. 1a and b). The diagnosis of partial status epilepticus was made and a medical treatment with clobazam and levetiracetam was initiated.
* Corresponding author. Tel.: +33 1 48036881; fax: +33 1 48036880. E-mail address: [email protected] (N. Benyounes).
There was a complete neurological recovery under this medication and the EEG monitoring 6 days later showed a dramatic improvement (Fig. 1c). While the first ECG at admission was normal, inverted T waves appeared in the anterior and lateral leads on the second ECG at day 1 (Fig. 1d), without chest pain, hypotension or clinical signs of heart failure. Serum troponin I levels rose until 5 mg/l the first day (reference <0.11 mg/l) and the BNP (B-type natriuretic peptide, which elevation reflects elevated left ventricular filling pressures) reached 1000 pg/ml (reference <100 pg/ml). Echocardiography at day 1 showed a dyskinesis of the left ventricular apex without thrombus (Fig. 1e) and slight midventricular wall motion abnormalities with preserved left ventricular systolic function. The coronary angiography on the same day did not show any significant coronary artery stenosis. The echocardiography at day 4 was identical to the first one. At day 10, a complete normalization of the left ventricular regional wall motion was noted (Fig. 1f). This made the diagnosis of left ventricular apical ballooning also called Takotsubo cardiomyopathy or stress-induced cardiomyopathy. 2. Discussion The Takotsubo cardiomyopathy is a fairly recently described cardiac syndrome comprising transient left ventricular apical wall motion abnormalities, a slight elevation of cardiac enzymes and ST segment and/or T waves abnormalities on the ECG, sometimes mimicking an acute coronary syndrome. Chest pain may occur.
1059-1311/$ – see front matter ß 2010 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.seizure.2010.11.001
[()TD$FIG]
N. Benyounes et al. / Seizure 20 (2011) 184–186
185
Fig. 1. (a and b) First EEG showing subcontinuous pseudoperiodic bi-or triphasic sharp waves over fronto-temporal lobes, with left predominance. (c) Second EEG showing a dramatic improvement. (d) ECG showing inverted T waves in the anterior and lateral leads. (e) First echocardiography (apical 2 chambers view stored in systole) showing a dyskinesis of the left ventricular apex (arrow). (f) Last echocardiography showing a normal left ventricular apex in systole (arrow).
However, coronary angiography is within normal, without any significant obstructive epicardial coronary disease. Postmenopausal women seem to be most at risk for developing the syndrome and an acute physical or emotional stress often triggers the onset of transient left ventricular apical ballooning.1,2
Diagnostic criteria have been proposed by the mayo clinic.3 All the four criteria must be met: (1) A transient akinesis or dyskinesis of the left ventricular apical and mid-ventricular segments, the regional wall-motion abnormalities extending beyond a single epicardial vascular distribution. (2) The absence of obstructive
186
N. Benyounes et al. / Seizure 20 (2011) 184–186
coronary disease or angiographic evidence of acute plaque rupture. (3) New electrocardiographic abnormalities (either ST-segment elevation or T-wave inversion). (4) The absence of: recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis and hypertrophic cardiomyopathy. In our patient, ischemic heart disease was ruled out since the coronary angiography was normal. The left ventricular dysfunction was transitory, excluding dilated cardiomyopathy. There was no alcohol intoxication and no echographic signs of left ventricular non-compaction. Epileptic attacks have been reported as a potential trigger. Despite this, the association remains under-recognized.2,4,5 However, the diagnosis should be suspected in the setting of a neurological disease in the presence of chest pain, abnormal ECG and enzyme elevation, leading to echocardiography and coronary angiography. Indeed, patients with Takotsubo syndrome should be monitored for heart failure, arrhythmias and hemodynamic instability that may occur, even if in-hospital prognosis seems to be favourable in most patients.3 In the absence of specifically evaluated therapies, the treatment remains empirical and symptomatic. The cause of this syndrome is not yet known. Postulated mechanisms include catecholamine cardiotoxicity, myocarditis, and epicardial or microvascular coronary spasm. This phenomenon has similarities with the left ventricular dysfunction in patients with acute brain injury, also called neurogenic stunned myocardium.6 Neurogenic stunned myocardium is also possibly mediated by CNS catecholamine stimulation. It is well known in the setting of subarachnoid hemorrhage.7 Takotsubo cardiomyopathy have been reported after convulsive status epilepticus, but not after brief seizures.8 Left ventricular apex is usually affected in the apical ballooning syndrome (Takostubo cardiomyopathy),3 while it is usually spared in the neurogenic stunned myocardium (inverted or reverse Takostsubo).7
Although the diagnostic criteria proposed for Takotsubo cardiomyopathy exclude recent significant head trauma and intracranial hemorrhage, many authors believe that these are variants of a single pathology: stress-induced cardiomyopathy.9,10 Conflict of interest statement None of the authors has any conflict of interest to disclose. References 1. Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J 2006;27(13):1523–9. 2. Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina PectorisMyocardial Infarction Investigations in Japan. J Am Coll Cardiol 2001;38(1):11– 8. 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(11):858– 65. 4. Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation 2005;111(4):472–9. 5. Shin SW, Baek SH, Choi BS, Lee HJ, Kim KH, Kim ES. Takotsubo cardiomyopathy associated with nonepileptic seizure after percutaneous endoscopic lumbar discectomy under general anesthesia. J Anesth 2010;24(3):460–3. 6. 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(1):10–7. 7. Banki N, Kopelnik A, Tung P, Lawton MT, Gress D, Drew B, et al. Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg 2006;105(1):15–20. 8. Legriel S, Bruneel F, Dalle L, Appere-de-Vecchi C, Georges JL, Abbosh N, et al. Recurrent takotsubo cardiomyopathy triggered by convulsive status epilepticus. Neurocrit Care 2008;9(1):118–21. 9. Movahed MR. Transient cardiac ballooning is not best nomenclature for Takotsubo cardiomyopathy as it does not capture all variants of this syndrome. Stress cardiomyopathy is a much better term for this syndrome. Clin Cardiol 2010;33(4):241–2. 10. 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(6):539–48.