No abstract

No abstract

Autonomic dysfunction is linked to sudden death regardless of the presence of structural heart disease. The pathway from autonomic dysfunction to sudden death is not fully understood, but myocardial sympathetic stimulation leading to arrhythmia and/or cardiac fibrosis might play a role. Our goal was to evaluate cardiac stiffness by echocardiography and its association with clinical, structural, and autonomic variables in people with epilepsy (PWE) compared to healthy controls. A 12-lead electrocardiogram, treadmill testing, and transthoracic echocardiography from 30 patients with temporal lobe epilepsy (TLE) without any known cardiovascular disorders were compared to 30 individuals without epilepsy matched by sex, age, and body mass index. Distribution of cardiovascular risk factors was similar in both groups. PWE had a higher left ventricle stiffness, left ventricle filling pressure, and greater left atrial volume as well as markers of autonomic dysfunction such as impaired chronotropic index and percentage achieved of predicted peak heart rate at effort. In multiple regressions, autonomic dysfunction explained 52% of stiffness and carbamazepine treatment and polytherapy with antiepileptic drugs (AEDs) explained, additionally, 6% each. Stiffness is increased in young patients with TLE and is related to autonomic dysfunction and to a lesser extent, carbamazepine use and polytherapy with AEDs.

Working in the ER on a 24-h shift leads to abnormal BP behavior in medical residents, thus suggesting that this type of work may be a risk factor for cardiovascular disease.

In this article, we explore the interaction of brain and heart in patients with epilepsy (PWE), focusing on new insights into possible pathways from epilepsy, catecholaminergic toxicity, subtle cardiac changes and sudden death. Initial evidence and biological plausibility point to an interaction between autonomic dysfunction, higher sympathetic drive, myocardial catecholaminergic toxicity and cardiac fibrosis resulting in subtle myocardial changes in structure, function, arrhythmogenesis and/or a heart failure-like phenotype in PWE. Non invasive imaging and biomarkers of cardiac injury and fibrosis are emerging as possible diagnostic tools to better stratify the risk of such individuals. Translational lessons from cardiac models of disease and ultra-structural lesions are used to support these considerations.

No abstract

Sudden death can occur to anyone and Myerburg Paradox refers to the observation that healthy or mildly affected individuals compose most of the victims of this devastating event. 1-3 Fifty to 65 million people suffer from epilepsy worldwide. 4 Patients with epilepsy (PWE) have two-to threefold increased mortality risk compared with the general population due to falls, automobile accidents, drowning, suicide, pneumonia, status epilepticus, or sudden death. 5,6 However, the main cause of death in PWE is sudden unexpected death (SUDEP), with 1 in every 1000 adult patients progressing to this outcome. 7 Younger individuals (20-40 years old), namely those who we would not expect

ObjectiveIdentification of epilepsy patients with elevated risk for atrial fibrillation (AF) is critical given the heightened morbidity and premature mortality associated with this arrhythmia. Epilepsy is a worldwide health problem affecting nearly 3.4 million people in the United States alone. The potential for increased risk for AF in patients with epilepsy is not well appreciated, despite recent evidence from a national survey of 1.4 million hospitalizations indicating that AF is the most common arrhythmia in people with epilepsy.MethodsWe analyzed inter‐lead heterogeneity of P‐wave morphology, a marker reflecting arrhythmogenic nonuniformities of activation/conduction in atrial tissue. The study groups consisted of 96 patients with epilepsy and 44 consecutive patients with AF in sinus rhythm before clinically indicated ablation. Individuals without cardiovascular or neurological conditions (n = 77) were also assessed. We calculated P‐wave heterogeneity (PWH) by second central moment analysis of simultaneous beats from leads II, III, and aVR (“atrial dedicated leads”) from standard 12‐lead electrocardiography (ECG) recordings from admission day to the epilepsy monitoring unit (EMU).ResultsFemale patients composed 62.5%, 59.6%, and 57.1% of the epilepsy, AF, and control subjects, respectively. The AF cohort was older (66 ± 1.1 years) than the epilepsy group (44 ± 1.8 years, p < .001). The level of PWH was greater in the epilepsy group than in the control group (67 ± 2.6 vs. 57 ± 2.5 μV, p = .046) and reached levels observed in AF patients (67 ± 2.6 vs. 68 ± 4.9 μV, p = .99). In multiple linear regression analysis, PWH levels in individuals with epilepsy were mainly correlated with the PR interval and could be related to sympathetic tone. Epilepsy remained associated with PWH after adjustments for cardiac risk factors, age, and sex.SignificancePatients with chronic epilepsy have increased PWH comparable to levels observed in patients with AF, while being ~20 years younger, suggesting an acceleration in structural change and/or cardiac electrical instability. These observations are consistent with emerging evidence of an “epileptic heart” condition.