CNS-disease affecting the heart: Brain–heart disorders

Finsterer, Josef; Wahbi, Karim

doi:10.1016/j.jns.2014.07.003

Cited by 56 publications

(39 citation statements)

References 82 publications

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“…Several clinical and animal studies have observed associations between IS and cardiac diseases,8, 11 such as cardiac arrhythmias,33 stress‐induced cardiomyopathy (Takotsubo syndrome),34 myocardial infarction,35 paroxysmal arterial hypertension,36 or autonomic dysfunction 9. Thereby, autonomic dysfunction is underlying the impaired physiologic regulation of heart rate and blood pressure as well as the increased secretion of catecholamines and cortisol 6, 37, 38, 39.…”

Section: Discussionmentioning

confidence: 99%

“…However, there is accumulating evidence that this relationship is not monodirectional and cerebrovascular disorders can conversely alter cardiovascular and autonomic function 4, 5, 6. IS has been associated with changes in autonomic cardiac dynamics, cardiac arrhythmias, acute myocardial damage, elevated cardiac enzymes (troponin, brain natriuretic peptide [BNP]) and plasma catecholamines, and increased susceptibility to sudden death both in humans and in laboratory animals 7, 8, 9. Within the first 3 months after IS, about 19% of patients have a fatal or serious nonfatal cardiac event, including acute myocardial infarction or ventricular tachycardia, and this mortality cannot be entirely explained by concomitant cardiac disease 5.…”

mentioning

confidence: 99%

“…Rather, cerebral ischemia may directly contribute to the generation of cardiac dysfunction via an alteration of the balance of the sympathetic and parasympathetic tone 10, 11. Whereas most of the previous studies on neurogenic heart dysfunction focused on the acute or subacute stage after stroke, with a special emphasis on myocardial infarction, cardiac arrhythmias, or the occurrence of early stress cardiomyopathy (Takotsubo syndrome), very little is known about the delayed consequences of ischemic brain damage on cardiovascular function, in particular the evolvement of chronic cardiac failure 8, 12. As potential cardiac dysfunction upon brain ischemia may prompt clinicians to perform long‐lasting cardiac monitoring or even start cardioprotective medication, a detailed mechanistic characterization of the long‐term consequences of IS on cardiac function is necessary.…”

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confidence: 99%

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Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

Bieber

Werner

Tanai

et al. 2017

Annals of Neurology

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ObjectiveCardiac diseases are established risk factors for ischemic stroke incidence and severity. Conversely, there is increasing evidence that brain ischemia can cause cardiac dysfunction. The mechanisms underlying this neurogenic heart disease are incompletely understood. Although it is established that ischemic stroke is associated with cardiac arrhythmias, myocardial damage, elevated cardiac enzymes, and plasma catecholamines in the acute phase, nothing is known about the delayed consequences of ischemic stroke on cardiovascular function.MethodsTo determine the long‐term cardiac consequences of a focal cerebral ischemia, we subjected young and aged mice to a 30‐minute transient middle cerebral artery occlusion and analyzed cardiac function by serial transthoracic echocardiography and hemodynamic measurements up to week 8 after surgery. Finally, animals were treated with metoprolol to evaluate a pharmacologic treatment option to prevent the development of heart failure.ResultsFocal cerebral ischemia induced a long‐term cardiac dysfunction with a reduction in left ventricular ejection fraction and an increase in left ventricular volumes; this development was associated with higher peripheral sympathetic activity. Metoprolol treatment prevented the development of chronic cardiac dysfunction by decelerating extracellular cardiac remodeling and inhibiting sympathetic signaling relevant to chronic autonomic dysfunction.InterpretationFocal cerebral ischemia in mice leads to the development of chronic systolic dysfunction driven by increased sympathetic activity. If these results can be confirmed in a clinical setting, treating physicians should be attentive to clinical signs of heart failure in every patient after ischemic stroke. Therapeutically, the successful β‐blockade with metoprolol in mice could also have future clinical implications. Ann Neurol 2017;82:729–743

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

Bieber

Werner

Tanai

et al. 2017

Annals of Neurology

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“…Electroconvulsive therapy is known to be associated with a marked rise in catecholamines, 195 and many of the antidepressant drugs that these patients often receive alter neuronal reuptake of plasma catecholamines, which may aggravate this surge of catecholamines. 29 Takotsubo cardiomyopathy associated with central nervous system (CNS) diseases Acute CNS diseases are often accompanied with evidence of transient cardiac dysfunction 37,196 ; however, the transient LV dysfunction associated with neurologic conditions often occurs in younger patients who experience less chest pain and less ST-segment elevation, and the regional wall motion abnormality is more often global rather than regional. A large number of cases of TTCM triggered by CNS disease have been published, 197 including cases associated with aneurysmal subarachnoid hemorrhage, ischemic stroke, and epileptic seizures.…”

Section: Takotsubo Cardiomyopathy Associated With Electroconvulsive Tmentioning

confidence: 99%

Takotsubo cardiomyopathy and its relevance to anesthesiology: a narrative review

Hessel

2016

Can J Anesth/J Can Anesth

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“…2-5) suggested the presence of arrhythmogenic substrates in Scn8a N1768D/+ mice. Previous work indicated that changes in autonomic tone may precede SUDEP in patients (35)(36)(37) and mice (24). We simulated a catecholaminergic surge by i.p.…”

Section: Bradycardia In Scn8amentioning

confidence: 99%

Cardiac arrhythmia in a mouse model of sodium channel SCN8A epileptic encephalopathy

Frasier

Wagnon

Bao

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Patients with early infantile epileptic encephalopathy (EIEE) are at increased risk for sudden unexpected death in epilepsy (SUDEP). De novo mutations of the sodium channel gene SCN8A, encoding the sodium channel Na v 1.6, result in EIEE13 (OMIM 614558), which has a 10% risk of SUDEP. Here, we investigated the cardiac phenotype of a mouse model expressing the gain of function EIEE13 patient mutation p.Asn1768Asp in Scn8a (Na v 1.6-N1768D). We tested Scn8a N1768D/+ mice for alterations in cardiac excitability. We observed prolongation of the early stages of action potential (AP) repolarization in mutant myocytes vs. controls. Scn8a N1768D/+ myocytes were hyperexcitable, with a lowered threshold for AP firing, increased incidence of delayed afterdepolarizations, increased calcium transient duration, increased incidence of diastolic calcium release, and ectopic contractility. Calcium transient duration and diastolic calcium release in the mutant myocytes were tetrodotoxin-sensitive. A selective inhibitor of reverse mode Na/Ca exchange blocked the increased incidence of diastolic calcium release in mutant cells. Scn8a N1768D/+ mice exhibited bradycardia compared with controls. This difference in heart rate dissipated after administration of norepinephrine, and there were no differences in heart rate in denervated ex vivo hearts, implicating parasympathetic hyperexcitability in the Scn8a N1768D/+ animals. When challenged with norepinephrine and caffeine to simulate a catecholaminergic surge, Scn8a N1768D/+ mice showed ventricular arrhythmias. Two of three mutant mice under continuous ECG telemetry recording experienced death, with severe bradycardia preceding asystole. Thus, in addition to central neuron hyperexcitability, Scn8a N1768D/+ mice have cardiac myoycte and parasympathetic neuron hyperexcitability. Simultaneous dysfunction in these systems may contribute to SUDEP associated with mutations of Scn8a. sodium channel | epilepsy | arrhythmia | channelopathy | mutation

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CNS-disease affecting the heart: Brain–heart disorders

Cited by 56 publications

References 82 publications

Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

Takotsubo cardiomyopathy and its relevance to anesthesiology: a narrative review

Cardiac arrhythmia in a mouse model of sodium channel SCN8A epileptic encephalopathy

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