Myocarditis in patients with subarachnoid hemorrhage: A histopathologic study

Bilt, Ivo A.C. van der; Vendeville, Jean Paul; Hoef, Tim P. van de; Begieneman, Mark P.V.; Lagrand, Wim K.; Kros, Johan M.; Wilde, Arthur A.M.; Rinkel, Gabriël J.E.; Niessen, Hans W.M.

doi:10.1016/j.jcrc.2015.12.005

Cited by 25 publications

(22 citation statements)

References 22 publications

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“…There is also some evidence of cross-talk between inflammatory responses and sympathetic activation in ischemic and hemorrhagic stroke 120, 121 . The proinflammatory cytokines released by damaged neuronal and glial cells stimulate the posterior hypothalamus to increase sympathetic output and circulating catecholamine level 122–124 .…”

Section: Mechanisms Of Brain-heart Interaction After Strokementioning

confidence: 99%

“…The proinflammatory cytokines released by damaged neuronal and glial cells stimulate the posterior hypothalamus to increase sympathetic output and circulating catecholamine level 122–124 . Bilt et al found that catecholaminergic stress after brain hemorrhage coincided with influx of inflammatory cells into the heart and induced cardiac damage after SAH 121 . Neutrophils were found embedded in the inflamed myocardium along with thrombi 121 .…”

Section: Mechanisms Of Brain-heart Interaction After Strokementioning

confidence: 99%

“…Bilt et al found that catecholaminergic stress after brain hemorrhage coincided with influx of inflammatory cells into the heart and induced cardiac damage after SAH 121 . Neutrophils were found embedded in the inflamed myocardium along with thrombi 121 . The coupling of catecholamine release with parasympathetic dysfunction regulates inflammation that induces myocardial dysfunction, thrombi formation, and cardiomyocyte cell death 121 .…”

Section: Mechanisms Of Brain-heart Interaction After Strokementioning

confidence: 99%

“…Neutrophils were found embedded in the inflamed myocardium along with thrombi 121 . The coupling of catecholamine release with parasympathetic dysfunction regulates inflammation that induces myocardial dysfunction, thrombi formation, and cardiomyocyte cell death 121 . Therefore, inflammation may play an important role and as a link between brain injury and cardiac damage after ischemic stroke and SAH.…”

Section: Mechanisms Of Brain-heart Interaction After Strokementioning

confidence: 99%

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Brain–Heart Interaction

et al. 2017

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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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Section: Mechanisms Of Brain-heart Interaction After Strokementioning

confidence: 99%

Section: Mechanisms Of Brain-heart Interaction After Strokementioning

confidence: 99%

Section: Mechanisms Of Brain-heart Interaction After Strokementioning

confidence: 99%

Section: Mechanisms Of Brain-heart Interaction After Strokementioning

confidence: 99%

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Brain–Heart Interaction

et al. 2017

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“…Histopathological findings support this theory since patients presented with typical TCM showed extensive area of myocardial thinning and myocyte edema at the cardiac apex in which degenerative myocardium with histiocyte and lymphocyte infiltration, and contracture-like necrotic bands, but a less severe pathology at the base [17,18]. Oxidative stress can lead to myocardial necrosis, remodelling, and contractility disturbances [8].…”

Section: Pathophysiology Of Post-sah Tcmmentioning

confidence: 83%

Takotsubo Cardiomyopathy as a Neurocardiogenic Injury after Subarachnoid Hemorrhage: Hemodynamics and Fluid Management

Mutoh¹,

Mutoh²,

Taki³

et al. 2017

Cardiomyopathies - Types and Treatments

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Takotsubo cardiomyopathy (TCM) is a life-threatening systemic disorder that may occur early after aneurysmal subarachnoid hemorrhage (SAH), but precise hemodynamics and fluid management remain unclear. Although TCM is often regarded as a reversible or self-limited phenomenon, it contributes significantly to morbidity and mortality of SAH patients, especially when it is complicated with other neurogenic injuries such as severe left ventricular dysfunction, pulmonary edema, and pneumonia. The purpose of this chapter is to introduce the current practice in intensive hemodynamic monitoring and goal-directed fluid management of post-SAH TCM using advanced hemodynamic devices based on our institutional protocol and the relevant literature and to evaluate their effects on clinical outcomes.

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