Cardiac structural and molecular alterations in rodent models of temporal lobe epilepsy

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Abstract Objective Cardiac structural and molecular changes are prevalent in people with chronic epilepsy, possibly contributing to an increased risk of premature mortality. However, understanding of the underlying pathophysiological mechanisms is limited. Here, we investigated the subacute and chronic changes in cardiac structure and ion channel/exchanger expression in different rodent models of temporal lobe epilepsy (TLE). Methods Two models of TLE were used: the kainic acid‐induced post‐status epilepticus (KASE) model in Wistar rats and the electrical self‐sustained status epilepticus (SSSE) model in C57BL/6J mice. Heart tissue was collected at subacute (7 days post‐SE) and chronic (12–16 weeks post‐SE) timepoints from both models. Histological analysis for cardiac fibrosis and qPCR of ion channel/exchanger mRNA expression was performed. Results Increased cardiac fibrosis was found in the KASE rats at the subacute (p = 0.016) and chronic (p = 0.003) timepoints compared with sham rats. In chronically epileptic KASE rats, mRNA expression analyses showed that NaV1.5 and NCX1 were reduced in the septum (p = 0.026 and p = 0.020, respectively) compared with shams. In SSSE mice, NaV1.5 was decreased in the right atrium (p = 0.039), and CaV3.2 and NCX1 were increased in the left ventricle subacutely (p = 0.033 and p = 0.003, respectively), and NaV1.5 was increased in the septum at the chronic timepoint (p = 0.008), compared with the non‐epileptic sham group. Significance Cardiac alterations at structural and molecular levels were found in both experimental rodent epilepsy models, subacutely post‐SE and during the chronically epileptic timepoint. The presence of similar cardiac changes across the models, despite being different species and having different modes of epilepsy indication, suggests that these changes are a direct or indirect result of the seizures. Plain Language Summary Epilepsy may lead to heart problems, which could raise the risk of early death, but the exact causes are unclear. This study examined heart changes in two rodent models of epilepsy. In rats, heart scarring and stiffness (fibrosis) increased both shortly after seizures and during chronic epilepsy, and the ability to produce key heart proteins was altered. In mice, similar changes in heart proteins appeared in different heart areas. These findings suggest seizures can directly or indirectly cause harmful heart changes. Understanding these effects might help improve care for people with epilepsy and reduce related heart risks.

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