Epilepsy and ultra-structural heart changes: The role of catecholaminergic toxicity and myocardial fibrosis. What can we learn from cardiology?

Fialho, Guilherme Loureiro; Wolf, Peter; Walz, Roger; Lin, Kátia

doi:10.1016/j.seizure.2019.07.002

Cited by 30 publications

(24 citation statements)

References 61 publications

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“…We believe that chronic and repeated seizures promote subtle myocardial aggressions and that could explain a heart failure with preserved ejection fraction (HEFPEF)-like phenotype in PWE. 33 This cardiovascular continuum has been called "the epileptic heart" by other authors, 38 and this could be related to worse functional class in PWE and their increased risk of sudden death. In contrast, the present study argues against the presence of a heart failure with reduced ejection fraction (HEFREF)-like phenotype.…”

Section: Discussionmentioning

confidence: 99%

“…16,31,32 TA B L E 1 End-systolic elastance, effective arterial elastance, and ventricular-arterial coupling in PWE and controls Epilepsy has been compared with a stress-related cardiomyopathy model. 33 Seizures elicit repeated sympathetic over-stimulation, and this could lead to catecholaminergic toxicity to the heart with myofilament damage, extracellular matrix deposition, and myocardial fibrosis. 33,34 Troponin, a cardiac biomarker of myocyte injury, is elevated in up to 25% of PWE after tonic-clonic seizures.…”

Section: Discussionmentioning

confidence: 99%

“…33 Seizures elicit repeated sympathetic over-stimulation, and this could lead to catecholaminergic toxicity to the heart with myofilament damage, extracellular matrix deposition, and myocardial fibrosis. 33,34 Troponin, a cardiac biomarker of myocyte injury, is elevated in up to 25% of PWE after tonic-clonic seizures. 35 Recently, we showed that young PWE without cardiovascular disease had higher left ventricle stiffness measured non-invasively by echocardiography compared to a control group, and such finding was related to autonomic dysfunction.…”

Section: Discussionmentioning

confidence: 99%

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Left ventricle end‐systolic elastance, arterial‐effective elastance, and ventricle‐arterial coupling in Epilepsy

et al. 2020

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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

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Left ventricle end‐systolic elastance, arterial‐effective elastance, and ventricle‐arterial coupling in Epilepsy

et al. 2020

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“…Autonomic dysfunction is also more common in WD-neuro + patients [ 12 ]. Increased autonomic dysfunction in patients with neurological disorders of the brain can lead to cardiac fibrosis via catecholaminergic toxicity [ 56 , 58 ]. Thus the brain–heart interaction via autonomic dysfunction might be an additional factor resulting in cardiac alterations in WD patients, particularly in those with neurological symptoms.…”

Section: Discussionmentioning

confidence: 99%

The impact of Wilson disease on myocardial tissue and function: a cardiovascular magnetic resonance study

Salatzki

Mohr

Heins

et al. 2021

Journal of Cardiovascular Magnetic Resonance

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Background Systemic effects of altered serum copper processing in Wilson Disease (WD) might induce myocardial copper deposition and consequently myocardial dysfunction and structural remodeling. This study sought to investigate the prevalence, manifestation and predictors of myocardial tissue abnormalities in WD patients. Methods We prospectively enrolled WD patients and an age-matched group of healthy individuals. We applied cardiovascular magnetic resonance (CMR) to analyze myocardial function, strain, and tissue characteristics. A subgroup analysis of WD patients with predominant neurological (WD-neuro+) or hepatic manifestation only (WD-neuro−) was performed. Results Seventy-six patients (37 years (27–49), 47% women) with known WD and 76 age-matched healthy control subjects were studied. The prevalence of atrial fibrillation in WD patients was 5% and the prevalence of symptomatic heart failure was 2.6%. Compared to healthy controls, patients with WD had a reduced left ventricular global circumferential strain (LV-GCS), and also showed abnormalities consistent with global and regional myocardial fibrosis. WD-neuro+ patients presented with more severe structural remodeling and functional impairment when compared to WD-neuro− patients. Conclusions In a large cohort, WD was not linked to a distinct cardiac phenotype except CMR indexes of myocardial fibrosis. More research is warranted to assess the prognostic implications of these findings. Trial registration: This trial is registered at the local institutional ethics committee (S-188/2018).

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“…The epileptic heart is defined as “a heart and coronary vasculature damaged by chronic epilepsy as a result of repeated surges in catecholamines and hypoxemia leading to electrical and mechanical dysfunction, and of adverse effects of certain antiseizure medications (ASMs), which may predispose to hyperlipidemia or arrhythmias. In some patients, acquired cardiac channelopathies in response to recurrent seizures may be involved.” Although the contemporary definition of sudden unexpected death in epilepsy (SUDEP; Table 1) excludes cardiac causes, 2–5 this semantic construct should not be interpreted as ruling out the involvement of heart disease as a factor in premature sudden death in individuals with chronic epilepsy 1,6–8 . Epidemiologic studies show that the incidence of sudden cardiac death (SCD) in individuals with chronic epilepsy is threefold greater than in the general population 9–12 and is 4.5‐fold greater than SUDEP as typically defined (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

Epileptic heart: A clinical syndromic approach

et al. 2021

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Prevention of premature death in patients with chronic epilepsy remains a major challenge. Multiple pathophysiologic factors have been implicated, with intense investigation of cardiorespiratory mechanisms. Up to four in five patients with chronic epilepsy exhibit cardiovascular comorbidities. These findings led us to propose the concept of an “epileptic heart,” defined as “a heart and coronary vasculature damaged by chronic epilepsy as a result of repeated surges in catecholamines and hypoxemia leading to electrical and mechanical dysfunction.” Among the most prominent changes documented in the literature are high incidence of myocardial infarction and arrhythmia, altered autonomic tone, diastolic dysfunction, hyperlipidemia, and accelerated atherosclerosis. This suite of pathologic changes prompted us to propose for the first time in this review a syndromic approach for improved clinical detection of the epileptic heart condition. In this review, we discuss the key pathophysiologic mechanisms underlying the candidate criteria along with standard and novel techniques that permit evaluation of each of these factors. Specifically, we present evidence of the utility of standard 12‐lead, ambulatory, and multiday patch‐based electrocardiograms, along with measures of cardiac electrical instability, including T‐wave alternans, heart rate variability to detect altered autonomic tone, echocardiography to detect diastolic dysfunction, and plasma biomarkers for assessing hyperlipidemia and accelerated atherosclerosis. Ultimately, the proposed clinical syndromic approach is intended to improve monitoring and evaluation of cardiac risk in patients with chronic epilepsy to foster improved therapeutic strategies to reduce premature cardiac death.

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Epilepsy and ultra-structural heart changes: The role of catecholaminergic toxicity and myocardial fibrosis. What can we learn from cardiology?

Cited by 30 publications

References 61 publications

Left ventricle end‐systolic elastance, arterial‐effective elastance, and ventricle‐arterial coupling in Epilepsy

Left ventricle end‐systolic elastance, arterial‐effective elastance, and ventricle‐arterial coupling in Epilepsy

The impact of Wilson disease on myocardial tissue and function: a cardiovascular magnetic resonance study

Epileptic heart: A clinical syndromic approach

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