Cardiovascular and neurological causes of sudden death after ischaemic stroke

Sörös, Peter; Hachinski, Vladimir

doi:10.1016/s1474-4422(11)70291-5

Cited by 226 publications

(137 citation statements)

References 101 publications

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“…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. The insular cortex has been identified as a crucial area within the central nervous system relevant for autonomic regulation 11, 30, 40, 41, 42.…”

Section: Discussionmentioning

confidence: 99%

“…In population‐based studies, about 30% of IS are caused by cardiac diseases 2, 3. 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.…”

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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%

Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

Bieber

Werner

Tanai

et al. 2017

Annals of Neurology

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“…The exact mechanisms leading to sudden death remain incompletely understood. Further research is needed to investigate the autonomic consequences of acute stroke and to identify patients at high risk of sudden death" [8].…”

Section: From Literaturementioning

confidence: 99%

New pharmacological strategies in some metabolic endocrine disorder under a toxicological approach

Luisetto¹

2017

Ann Clin Endocrinol Metabol

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In this review After Observing biomedical literature (starting from some heart disease) results that some pathological phenomena are deeply involved in some metabolic endocrine condition: Kinetics and gradients in metabolism, catabolism, time related, toxic like effect, electrical cell membrane status, smooth vascular muscle cell hyper-reactivity, platelet iperactivations, central autonomic control after acute stroke, great electrolytes unbalances et other factors as pro-hypertrophic signaling and oxidative stress. Observing actual current therapy in some metabolic endocrine therapy often is used association of drugs (in example in type II diabetes). In Many other pathologies effi cacy drug therapy exist, and often only 1 pharmacological molecule resolve the pathological condition. But in many disease even associating 2-3-4 drugs the % of cure not increase (effi cacy, effectiveness). It mean that this drugs strategies are not the really best? Or it mean a low active level? Why for this pathological condition this association drugs in currently use not do the right works as really needed? There is the need for new really effi cacy drugs strategy that show a profi le of effi cacy as requested in order to resolve the pathological condition? Or to be added to the actual therapy? The actual pharmacological strategies in some metabolic endocrine disorder is really the best? Or other strategies can be introduced?

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“…Островковая доля, возможно, яв-ляется частью нейрональной системы, связывающей су-прамаргинальную извилину и зону Брока, и может уча-ствовать (наряду с премоторной корой) в фонетическом планировании речи [15][16][17].…”

Section: функция островковой доли мозгаunclassified