Time Course and Risk Factors for Myocardial Dysfunction After Aneurysmal Subarachnoid Hemorrhage

Bilt, Ivo A. van der; Hasan, D.; Brink, R. B. van den; Cramer, Maarten J.; Jagt, Mathieu van der; Kooten, Fop van; Regtien, Joost G.; Berg, Maarten P. van den; Groen, Rob J. M.; Cate, Folkert J. Ten; Kamp, Otto; Götte, Marco J.W.; Horn, Janneke; Girbes, Armand R. J.; Vandertop, W. Peter; Algra, Ale; Rinkel, Gabriël J.E.; Wilde, Arthur A.M.

doi:10.1227/neu.0000000000000699

Cited by 18 publications

(13 citation statements)

References 23 publications

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“…The telltale sign of Takotsubo cardiomyopathy is apical ballooning, provoked by a weakening of the heart’s muscular cells. Still, Takotsubo cardiomyopathy and NSC may be the cause of ventricular wall motion abnormalities in other regions of the heart [ 108 ]. Many studies focus on the impaired systolic function of the ventricle, which results in reduced ejection fraction, but it seems that the diastolic phase of the ventricle is also involved in NSC.…”

Section: The Interaction Between Brain and Heart: Cardiac Complicamentioning

confidence: 99%

Neuroinflammatory Mechanisms in Ischemic Stroke: Focus on Cardioembolic Stroke, Background, and Therapeutic Approaches

Maida

Norrito

Daidone

et al. 2020

IJMS

324

247

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One of the most important causes of neurological morbidity and mortality in the world is ischemic stroke. It can be a result of multiple events such as embolism with a cardiac origin, occlusion of small vessels in the brain, and atherosclerosis affecting the cerebral circulation. Increasing evidence shows the intricate function played by the immune system in the pathophysiological variations that take place after cerebral ischemic injury. Following the ischemic cerebral harm, we can observe consequent neuroinflammation that causes additional damage provoking the death of the cells; on the other hand, it also plays a beneficial role in stimulating remedial action. Immune mediators are the origin of signals with a proinflammatory position that can boost the cells in the brain and promote the penetration of numerous inflammatory cytotypes (various subtypes of T cells, monocytes/macrophages, neutrophils, and different inflammatory cells) within the area affected by ischemia; this process is responsible for further ischemic damage of the brain. This inflammatory process seems to involve both the cerebral tissue and the whole organism in cardioembolic stroke, the stroke subtype that is associated with more severe brain damage and a consequent worse outcome (more disability, higher mortality). In this review, the authors want to present an overview of the present learning of the mechanisms of inflammation that takes place in the cerebral tissue and the role of the immune system involved in ischemic stroke, focusing on cardioembolic stroke and its potential treatment strategies.

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Section: The Interaction Between Brain and Heart: Cardiac Complicamentioning

confidence: 99%

Neuroinflammatory Mechanisms in Ischemic Stroke: Focus on Cardioembolic Stroke, Background, and Therapeutic Approaches

Maida

Norrito

Daidone

et al. 2020

IJMS

324

247

View full text Add to dashboard Cite

show abstract

“…The telltale sign of Takotsubo cardiomyopathy is apical ballooning, caused by a weakening of the heart’s muscular cells. Still, Takotsubo cardiomyopathy and NSC may induce ventricular wall motion abnormalities in other regions of the heart 16, 17 . Many studies focus on the impaired contraction of the ventricle which results in low ejection fraction, but it appears that the relaxation of the ventricle is also disrupted in NSC.…”

Section: Cardiac Damage As a Consequence Of Strokementioning

confidence: 99%

“…In SAH patients, the Hunt Hess grading score of severity shows that ECG changes are observed consistently at the lower grades, but echocardiography changes are found predominately in patients with higher grades 21 . It is likely that less severe ECG changes precede structural alterations, as QTc (the interval between peak contraction and repolarization) prolongation does not predict ventricular wall motion abnormalities, but more severe ECG changes like inverted T waves and elevated Troponin levels, secreted by damaged sarcomeres, can predict ventricular wall motion abnormalities 16 . Lee et al found that in spontaneous and traumatic brain hemorrhage patients 22 , 7.2% (no previous history of cardiac disease patients) show acute cardiac dysfunction and 43% have LV hypertrophy 22 .…”

Section: Cardiac Damage As a Consequence Of Strokementioning

confidence: 99%

Brain–Heart Interaction

Chen

Venkat

Seyfried

et al. 2017

Circulation Research

355

179

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Neurocardiology is an emerging specialty that addresses the interaction between the brain and the heart, i.e. the effects of cardiac injury on the brain, and the effects of brain injury on the heart. This review article focuses on cardiac dysfunction in the setting of stroke such as ischemic stroke, brain hemorrhage and subarachnoid hemorrhage (SAH). The majority of post stroke deaths are attributed to neurological damage, and cardiovascular complications are the second leading cause of post stroke mortality. Accumulating clinical and experimental evidence suggests a causal relationship between brain damage and heart dysfunction. Thus, it is important to determine whether cardiac dysfunction is triggered by stroke, is an unrelated complication, or is the underlying cause of stroke. Stroke induced cardiac damage may lead to fatality or potentially lifelong cardiac problems (such as heart failure), or to mild and recoverable damage such as neurogenic stress cardiomyopathy (NSC) and Takotsubo cardiomyopathy. The role of location and lateralization of brain lesions after stroke in brain-heart interaction, clinical biomarkers and manifestations of cardiac complications, and underlying mechanisms of brain-heart interaction following stroke, such as: the hypothalamic pituitary adrenal axis (HPA); catecholamine surge; sympathetic and parasympathetic regulation; microvesicles (MV’s); microRNAs; gut microbiome, immunoresponse and systemic inflammation are discussed.

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“…LV dysfunction can develop after 1–4 days and can persist for more than 8 days post-stroke (described in detail in Supplementary Materials, Figure 1) (143, 150). Routine echocardiography is not typically recommended for the early management of acute stroke (15, 120, 151), except among patients with suspected embolic stroke despite normal neurovascular imaging (151).…”

Section: Cardiac Considerations For Exercise and Mobilization (See Tamentioning

confidence: 99%

Aerobic Training and Mobilization Early Post-stroke: Cautions and Considerations

Marzolini

Robertson

et al. 2019

Front. Neurol.

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Knowledge gaps exist in how we implement aerobic exercise programs during the early phases post-stroke. Therefore, the objective of this review was to provide evidence-based guidelines for pre-participation screening, mobilization, and aerobic exercise training in the hyper-acute and acute phases post-stroke. In reviewing the literature to determine safe timelines of when to initiate exercise and mobilization we considered the following factors: arterial blood pressure dysregulation, cardiac complications, blood-brain barrier disruption, hemorrhagic stroke transformation, and ischemic penumbra viability. These stroke-related impairments could intensify with inappropriate mobilization/aerobic exercise, hence we deemed the integrity of cerebral autoregulation to be an essential physiological consideration to protect the brain when progressing exercise intensity. Pre-participation screening criteria are proposed and countermeasures to protect the brain from potentially adverse circulatory effects before, during, and following mobilization/exercise sessions are introduced. For example, prolonged periods of standing and static postures before and after mobilization/aerobic exercise may elicit blood pooling and/or trigger coagulation cascades and/or cerebral hypoperfusion. Countermeasures such as avoiding prolonged standing or incorporating periodic lower limb movement to activate the venous muscle pump could counteract blood pooling after an exercise session, minimize activation of the coagulation cascade, and mitigate potential cerebral hypoperfusion. We discuss patient safety in light of the complex nature of stroke presentations (i.e., type, severity, and etiology), medical history, comorbidities such as diabetes, cardiac manifestations, medications, and complications such as anemia and dehydration. The guidelines are easily incorporated into the care model, are low-risk, and use minimal resources. These and other strategies represent opportunities for improving the safety of the activity regimen offered to those in the early phases post-stroke. The timeline for initiating and progressing exercise/mobilization parameters are contingent on recovery stages both from neurobiological and cardiovascular perspectives, which to this point have not been specifically considered in practice. This review includes tailored exercise and mobilization prescription strategies and precautions that are not resource intensive and prioritize safety in stroke recovery.

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Time Course and Risk Factors for Myocardial Dysfunction After Aneurysmal Subarachnoid Hemorrhage

Abstract: NCT00123695.

Cited by 18 publications

References 23 publications

Neuroinflammatory Mechanisms in Ischemic Stroke: Focus on Cardioembolic Stroke, Background, and Therapeutic Approaches

Neuroinflammatory Mechanisms in Ischemic Stroke: Focus on Cardioembolic Stroke, Background, and Therapeutic Approaches

Brain–Heart Interaction

Aerobic Training and Mobilization Early Post-stroke: Cautions and Considerations

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