Biomarkers of Cardiac Stress After Generalized Convulsive Seizures Identified

13 Mar, 2019 ,
Cardiology Advisor
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Cardiology Advisor
13 Mar, 2019 ,

According to a study recently published, high‐sensitive troponin T (hsTNT), copeptin, and soluble urokinase plasminogen activator receptor can be useful in identifying cardiac stress after generalized convulsive seizures especially in patients with refractory epilepsy. The researchers also identified the approximate time of rise and decline of these biomarkers during cardiac stress. 

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Biomarkers such as high‐sensitive troponin T (hsTNT), copeptin, and soluble urokinase plasminogen activator receptor (suPAR) may be helpful to identify cardiac stress after generalized convulsive seizures (GCS) in patients with refractory epilepsy, according to study results published in Epilepsia.

A total of 36 patients with refractory epilepsy (generalized-onset tonic clonic seizures [n=6] and focal to bilateral tonic-clonic seizures [n=30]) were enrolled in the study after undergoing video-electroencephalography monitoring with simultaneous one‐lead electrocardiography recordings. At study enrollment and at various time points after GCS, researchers measured catecholamines and several cardiac biomarkers: cardiac troponin I (cTNI), hsTNT, N-terminal pro-brain natriuretic peptide, copeptin, suppression of tumorigenicity‐2, growth differentiation factor 15, suPAR, and heart-type fatty acid binding protein. In addition, the investigators analyzed heart rate, heart rate variability (HRV), and corrected QT intervals to assess periictal cardiac properties.

 

After GCS, copeptin increased by >30-fold (<.001) and fell quickly after 2 hours, returning to baseline levels ≈6 hours after the GCS. The majority of seizures (86%) resulted in copeptin levels >28.7 pmol/L, the upper limit of normal. In addition, an even greater proportion of seizures (94.4%) exceeded levels >10 pmol/L, a cutoff value used to screen for acute myocardial infarction. Increases in heart rate and corrected QT intervals were also observed during this time whereas HRV decreased. Levels of suPAR were stable throughout the study, with a trend demonstrated toward slightly higher early suPAR levels after GCS (P =.082).

In 10% and 26% of patients, elevations of cTNI and hsTNT were observed, respectively. Dopamine levels increased with elevations in cTNI (=0.53; =.001) and hsTNT (=0.58; =.001). Factors associated with elevated troponin levels included older age (mean age, 46.2 years [95% CI, 32‐60] vs 30.4 years [95% CI, 26‐34.7]; P =.006), lower HRV (5.2 [95% CI, 3.7‐6.7] msec vs 16.9 [95% CI 7.4‐ 26.3] msec; P =.033), higher dopamine (98.7 [95% CI, 33.3‐164.1] ng/L vs 38.9 [95% CI, 23.4‐54.4] ng/L; P =.009), higher levels of growth differentiation factor 15 (455.8 [95% CI, 27.9‐633.7] pg/mL vs 310.3 [95% CI, 204.5‐416.1] pg/mL; P =.047).

The small sample size, the lack of advanced cardiac imaging to assess the underlying mechanisms of troponin leaks, and the unreliable nature of blood oxygen saturation monitoring to evaluate the association between seizure-related hypoxemia and cardiac arrhythmias represented a few limitations of the study.

The investigators explained that “single GCS are unlikely to lead to acute deleterious cardiac injuries in a significant proportion of epilepsy patients without cardiac disease but may promote the development of potentially detrimental structural changes that facilitate future cardiac arrhythmias.”