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Myocardial injury in Transient Global Amnesia: a case- control study European Journal of Neurology

Troponin Elevation in TGA, TIA and vestibular neuropathy
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  F    o   r    P    e   e   r    R    e   v   i    e   w      Myocardial injury in Transient Global Amnesia: a case-control study Journal: European Journal of Neurology  Manuscript IDEJoN-18-1146.R1Wiley - Manuscript type:Original ArticleDate Submitted by the Author:18-Dec-2018Complete List of Authors:Erdur, Hebun; Charite, Universitätsmedizin Berlin, NeurologySiegerink, B; charite universitaetsmedizin, center for stroke researchGaneshan, Ramanan; Charite, Universitätsmedizin Berlin, NeurologyAudebert, Heinrich; Charité University Hospital, Center for Stroke Research BerlinEndres, Mathias; Charite Universitatsmedizin Berlin Klinik fur Neurologie mit Experimenteller Neurologie, NeurologyNolte, Christian; Charite, Universitätsmedizin Berlin, NeurologyScheitz, Jan; Charite, NeurologyKeywords:transient global amnesia, stress, troponin, (Disorders of) Autonomic nervous system < NEUROLOGICAL DISORDERS, neurogenic cardiomyopathy, brain-heart interaction   European Journal of Neurology  F    o   r    P    e   e   r    R    e   v   i    e   w    1 Myocardial injury in Transient Global Amnesia: a case-control study Hebun Erdur a,b , MD, Bob Siegerink c , PhD, Ramanan Ganeshan a , MD, Heinrich J. Audebert a,c , MD, Matthias Endres a,b,c,d,e , MD, Christian H. Nolte a,b,c,d,e , MD, Jan F. Scheitz a,c,d , MD a Department of Neurology, Charité – Universitätsmedizin Berlin, Berlin, GermanybBerlin Institute of Health (BIH), Berlin, Germanyc Center for Stroke Research Berlin, Charité – Universitätsmedizin Berlin, Berlin, GermanydDZHK (German Centre for Cardiovascular Research), Partner Site Berlin, Berlin, GermanyeDZNE (German Center for Neurodegenerative Diseases), Partner Site Berlin, Berlin, Germany Corresponding Author :Dr. Hebun ErdurDepartment of NeurologyCharité – Universitätsmedizin Berlin, Berlin, GermanyTel.: +4930450560624. Fax: +493084454264E-mail: hebun.erdur@charite.de Word count (total):  3492. Word count (abstract):  250. Number of tables:  3. Number of figures:  0. Running title: Myocardial injury in transient global amnesia Keywords : transient global amnesia, stress, troponin, autonomic nervous system, neurogenic cardiomyopathy, brain-heart interaction Page 1 of 16 European Journal of Neurology123456789101112131415161718192021222324252627282930313233343536373839404142434445464748495051525354555657585960  F    o   r    P    e   e   r    R    e   v   i    e   w    2 AbstractBackground:  Elevation of cardiac troponin (cTn), a sensitive biomarker of myocardial injury, is observed frequently in severe acute neurological disorders. Case reports suggest that cardiac dysfunction may also occur in patients with transient global amnesia (TGA). Until now, no study has systematically assessed this phenomenon. Methods:  We performed a case-control study using data of consecutive patients presenting with TGA from 2010 to 2015. Multiple logistic regression analysis accounting for age, sex, and cardiovascular risk factors was performed to compare the likelihood of myocardial injury (defined as elevation of cTn>99 th  percentile, ≥14ng/L;  high-sensitivity cTnT assay) in TGA with three reference groups: migraine with aura, vestibular neuritis, transient ischemic attack (TIA). Results:  Of 113 patients with TGA, cTn elevation occurred in 28 (25%). TGA patients with cTn elevation were significantly older, more likely to be female and had higher blood pressure on admission compared to those without. The likelihood of myocardial injury following TGA was at least more than 2-fold higher compared to all three reference groups (adjusted OR 5.5, 95%-CI 1.2–26.4, compared with migraine with aura; aOR 2.2, 95%-CI 1.2–4.4, compared with vestibular neuritis; aOR 2.3, 95%-CI 1.3–4.2, compared with TIA). Conclusions:  One out of four patients with TGA has evidence of myocardial injury as assessed by highly sensitive cTn assays. The likelihood of myocardial injury associated with TGA was even higher than in TIA patients with a more pronounced cardiovascular risk profile. Our findings suggest presence of a TGA-related disturbance of brain-heart interaction that deserves further investigation. Page 2 of 16European Journal of Neurology123456789101112131415161718192021222324252627282930313233343536373839404142434445464748495051525354555657585960  F    o   r    P    e   e   r    R    e   v   i    e   w    3 Introduction Cardiac troponins are specific biomarkers to identify myocardial injury [1]. Using state-of-the-art highly sensitive cardiac troponin (hs-cTn) assays, myocardial injury is detectable in many patients with acute CNS disorders and following mental stress, reflecting the extensive interaction of brain and heart [1–4]. Transient global amnesia (TGA) is a neurological syndrome characterized by sudden onset of anterograde amnesia, often preceded by emotionally or physically stressful events [5–7]. Recently, case reports suggested an association between TGA and transient cardiac dysfunction with concomitant myocardial injury [8–10]. Until now, no study has systematically assessed this phenomenon.The aim of our study was (a) to assess frequency and determinants of myocardial injury (ie, hs-cTn elevation) in patients with TGA, and (b) to compare the likelihood of hs-cTn elevation in TGA with reference groups of patients with other acute but transient neurological disorders. MethodsStudy design and population We conducted a case-control study with consecutive patients with a final diagnosis of TGA between October 2010 and December 2015 at the Charité – Universitätsmedizin Berlin (Campus Benjamin Franklin). We used three reference groups: patients discharged with a final diagnosis of migraine with aura, vestibular neuritis, or transient ischemic attack (TIA). These were selected as reference groups because they too show a transient neurological Page 3 of 16 European Journal of Neurology123456789101112131415161718192021222324252627282930313233343536373839404142434445464748495051525354555657585960  F    o   r    P    e   e   r    R    e   v   i    e   w    4 dysfunction, receive a similar clinical work-up in the emergency department, and have a different cardiovascular comorbidity burden, allowing for a deeper understanding of the relation between TGA and myocardial injury.All patients were identified by searching our hospital administrative data (main ICD-10 diagnosis at discharge) for TGA (G45.4), migraine with aura (G43.1), vestibular neuritis (H81.2), and TIA (G45.0/.1/.2/.8). All patients were examined by a neurologist in the emergency department. Case files and neuroimaging of all patients were reviewed in order to confirm the diagnosis and exclude uncertain cases. TGA was defined according to established diagnostic criteria by Caplan, Hodges and Warlow [5–7]: witnessed attack; clear-cut anterograde amnesia; no clouding of consciousness and no loss of personal identity, cognitive impairment limited to amnesia; no accompanying focal neurological symptoms during the attack or significant neurological signs afterwards; absence of epileptic features; resolution of symptoms within 24h; no recent head injury or active epilepsy. Neuroimaging with 3-Tesla-MRI (DWI, ADC, FLAIR, T2*, and intracranial MR-A) was performed in 84/113 patients with TGA. Positive MRI findings for TGA included only typical small punctate DWI lesions in the hippocampus. Patients with lesions atypical for TGA (for example DWI lesions outside the hippocampus) and suggesting an ischaemic aetiology were not considered as TGA patients and not included into the study. Migraine with aura was diagnosed according to the International Headache Society criteria (ICHD-3). Patients with only one attack were included in the migraine reference group if they otherwise met the IHS criteria (probable migraine with aura). Auras were classified as visual (21/102 patients), sensory (11/102 patients), speech disturbance (4/102 patients), brainstem aura (vertigo) (10/102 patients), or a combination of at least two symptoms (mostly visual and sensory, 56/102 patients). None of the patients had a hemiplegic migraine. Every migraine patient had a brain CT (14/102 patients) or MRI (88/102 Page 4 of 16European Journal of Neurology123456789101112131415161718192021222324252627282930313233343536373839404142434445464748495051525354555657585960
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