Cardiac Troponin Levels Following Complicated and Uncomplicated Epileptic Seizures

Eskandarian, Rahimeh; Asghari, Nabiolah; Darban, Mahboubeh; Ghorbani, Raheb

doi:10.1016/j.arcmed.2011.09.002

Cited by 17 publications

(20 citation statements)

References 22 publications

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“…In our study, patients with cTNI release presented more frequently with elevated CK values. This is in line with findings depicted by Eskandarian and co-workers, who demonstrated on average higher troponin levels after complicated seizers as indicated by different heart circulatory parameters [16]. In this context, supposing larger intervals of general ischemia in case of “complicated” seizures, this might also support the mechanism of a temporary ischemia behind cTNI elevation.…”

Section: Discussionsupporting

confidence: 91%

“…As general ischemia seems to be defining factor for the development of seizure-related cTNI elevation, the duration of the event is important [16]. Hence, this aspect needs verification in further examinations especially as elevated CK-levels indicating extended seizures are associated with cTNI elevation [27,28].…”

Section: Methodological Limitations Of the Studymentioning

confidence: 99%

“…Evidence on troponin elevation after seizures is based on limited data [16-20]. A better understanding on cTNI release in other conditions than an ACS is highly relevant with potential impact for the diagnostic and therapeutic management.…”

Section: Introductionmentioning

confidence: 99%

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Cardiac Troponin I elevation after epileptic seizure

et al. 2012

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Background Cardiac troponin-I (cTNI) is highly specific biomarker to prove myocardial damage, e.g. in acute coronary syndrome (ACS). However, it occurs in other conditions as well. We therefore analysed cTNI increase in patients after generalized convulsive seizure. Methods Consecutive patients admitted with acute generalized convulsive seizure were included in case of cTNI measurement on admission. Among 898 selected cases, 53 patients were referred secondary to our department; in 845 cases cTNI measurements on admission were available. In case of multiple admissions (81 cases), only the first admission entered our analysis. In 17 patients elevated cTNI was determined due to ACS; in one patient a myocarditis was found. 5 patients suffered of relevant renal insufficiency. Finally 741 patients were included in the analysis. A cTNI cut-off level of ≥ 0.1 ng/ml was considered. Factors associated with a cTNI increase were analysed subsequently. Results The mean age of the study population (n = 741) was 47.8 years (SD ± 18.6), 40.9% were female. In 50 patients (6.7%) a cTNI elevation of unknown origin was found; no obvious cardiac involvement could be detected in these patients who all remained asymptomatic. A vascular risk profile (including at least hypertension, hypercholesterolemia or diabetes) (OR = 3.62; CI: 1.59 to 8.21; p = 0.001) and elevated creatine kinase on admission (OR = 2.36; CI: 1.26 to 4.39; p = 0.002) were independent factors associated with cTNI release. Conclusion cTNI release occurs in patients with generalized convulsive seizure with predominance in patients with vascular risk profile.

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Section: Discussionsupporting

confidence: 91%

Section: Methodological Limitations Of the Studymentioning

confidence: 99%

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Cardiac Troponin I elevation after epileptic seizure

et al. 2012

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“…Patients with markers of cardiac injury were not more likely to have cardiovascular risk factors or a convulsive seizure presentation than those without markers of cardiac injury. Scant previous studies assessing troponin levels after seizures have shown that increased troponin levels are not generally seen with uncomplicated seizures (Woodruff et al., 2003), but they may occur with more severe seizures presumably causing myocardial injury or demand coronary ischemia (Parvulescu‐Codrea et al., 2006; Eskandarian et al., 2011). Troponin levels have not been previously evaluated in patients with RSE.…”

Section: Discussionmentioning

confidence: 99%

Cardiac injury in refractory status epilepticus

Hocker¹,

Prasad

Rabinstein³

2012

Epilepsia

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SUMMARYPurpose: We sought to describe the spectrum of cardiac injury in refractory status epilepticus (RSE). Methods: We reviewed all patients with RSE between 1999 and 2011 at Mayo Clinic. RSE was defined as generalized convulsive or nonconvulsive status epilepticus (SE) that continued despite initial therapies. Exclusion criteria were age <18 years, anoxic SE, psychogenic SE, simple partial SE, absence SE, and repeat RSE. Patients were divided into those with (transient left ventricular [LV] dysfunction; electrocardiography [ECG] abnormality-new T-wave inversion, ST elevation or ST depression, or QTc prolongation; and/or elevated blood troponin T levels) versus those without evidence of cardiac injury. Key Findings: We identified 59 consecutive patients with RSE. In 24 patients no cardiac-specific diagnostic studies were obtained. Twenty-two of the remaining 35 patients demonstrated markers of cardiac injury. General anesthesia was necessary for control of seizures in 31 of 35 patients for 10.5 ± 17.4 days. Twenty-three patients had troponin levels drawn at onset of SE, of which nine were abnormal. ECG findings at onset of SE included ST elevation (11.4%), ST depression (5.7%), new T-wave inversion (37.1%), and nonspecific ST changes (37.1%). Cardiac arrhythmias included ventricular tachycardia/fibrillation (11.4%), atrioventricular block (2.9%), atrial fibrillation/ flutter (20.0%), sinus bradycardia (48.6%), and sinus tachycardia (65.7%). Intervention was required for cardiac arrhythmias in 42.9%. QTc was prolonged in 22.9% of patients. One patient met criteria for non-ST-elevation myocardial infarction (NSTEMI). Three of 14 patients evaluated with ECG during SE demonstrated reversible systolic dysfunction. In-hospital mortality was 34.3%. Outcome was worse in the group with markers of cardiac injury but the difference was not statistically significant (p = 0.14). Significance: Markers of cardiac injury are common in RSE and may be underrecognized in this population. These disturbances may require specific treatment and are often reversible. Routine performance of ECG and troponin followed by an echocardiography in those with repolarization abnormalities is probably justified. This was a biased sample of patients with severe RSE who had cardiac studies performed. The prevalence of findings in this study refers to this subgroup only.

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“…In view of a multimodal treatment schedule in patients with (refractory) seizures, cardiac manifestations pre-and postseizure are considered to be usually benign. To us and as stated by Hocker et al, however, particularly tonic-clonic seizures and SE might lead to overflowing sympathetic activation potentially resulting in myocyte damage and consecutive cardiac contractile dysfunction or susceptibility to arrhythmias (Zijlmans et al, 2002;Schneider et al, 2010;Eskandarian et al, 2011;Stollberger et al, 2011). Furthermore, the neurocardio-endocrine axis has attracted attention, since acute neurologic insults (including seizures) have been reported to be associated with the so-called takotsubo cardiomyopathy (TC) several years ago (Schneider et al, 2010;Stollberger et al, 2011).…”

Section: Seizures and The Neuro-cardio-endocrine Axismentioning

confidence: 99%