Dual assessment of abnormal cardiac electrical dispersion and diastolic dysfunction for early detection of the epileptic heart condition

The neural and cardiovascular systems interact to foster homeostasis. However, in disease states, there are three main ways to alter these interactions and overall health. First, common risk factors such as age, hypertension, diabetes, or diseases, such as neurocardiogenic syncope or genetic diseases related to ion channels leading to epilepsy and arrhythmic syndromes, can affect both organs. Second, some heart diseases can lead to diseases of the brain, as in cases of cardio-embolic stroke or cognitive impairment in patients with atrial fibrillation or heart failure [1,2]. Third, brain insults can lead to heart disorders, such as neurogenic heart disease or stress-associated heart disease [1,2].

Epilepsy is the second most common neurological problem in primary care, affecting approximately 65 million individuals worldwide [3]. People with epilepsy (PWE) are at increased risk for premature death due to falls, drowning, suicide, automobile accidents, and pneumonia [3,4]. Sudden unexpected death in epilepsy (SUDEP) is among the most important causes of death in epilepsy, being responsible for 1.2 deaths in every 1000 patients-years in that population [5]. SUDEP can be defined as a sudden, unexpected, nontraumatic and nondrowning death in PWE, with or without evidence of a seizure preceding the event and excluding documented status epilepticus or a toxicologic or anatomic cause of death in postmortem examination [5]. Possibly, sudden cardiac death (SCD) in epilepsy is also as important, since PWE have a 3-to-6-fold increased risk and a 10-year earlier age of incidence of this type of death, compared to the general population [6,7]. Since SUDEP, by its definition, is an exclusion diagnosis, the search for biomarkers that could further explain the possible causes of sudden death in PWE is of utmost importance.

In 2020, Verrier et al. coined the term “Epileptic Heart” to explain the pathways of poorly controlled epilepsy leading to chronic and subtle heart and vascular damage [8]. This “neurocardiovascular continuum” of neurological insult to the heart and vessels in PWE could involve autonomic dysfunction with catecholaminergic toxicity, myocardial inflammation and fibrosis, atherosclerosis and ischemia, predisposing to an electrical substrate that may evolve to lethal arrhythmias [2,9]. As observed in post-myocardial infarction, reactive or reparative myocardial fibrosis can lead to abnormal electrical conduction in the heart, promoting unidirectional block and reentry circuits, electrical dispersion, and arrhythmias [10].

In cardiology, electrical dispersion or heterogeneity is defined as the non-uniformity in depolarization and repolarization of the heart. It can be categorized as temporal (related to variations over time), spatial (variations among different regions) or, more commonly, spatiotemporal [10]. Electrical dispersion has been linked to increased risk for sudden cardiac death, arrhythmias, implantable cardioverter-defibrillator (ICD) discharge, and adverse outcomes [10]. Interestingly, electrical dispersion is also related to diastolic compromise or speckle tracking strain alterations, reflecting electromechanical coupling [11,12].

In the current study, we hypothesized that there is a linkage between abnormal cardiac electrical dispersion and early diastolic dysfunction in patients with chronic epilepsy. Accordingly, we analyzed electrical repolarization dispersion indices and QT interval in PWE compared to a control group as well as the electromechanical relationship between echocardiographic parameters, including myocardial stiffness, a marker of fibrosis, and electrical dispersion, measured as T-wave peak to T-wave end (TpTe), QT dispersion (QTd), and QT interval corrected for heart rate (QTc) in PWE.

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