Cardiovascular manifestations of neurologic disease

Dombrowski, Keith; Laskowitz, Daniel T.

doi:10.1016/b978-0-7020-4086-3.00001-1

Cited by 18 publications

(13 citation statements)

References 125 publications

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“…As both MI and NSM can be accompanied by ST segment depression and negative T waves, these ECG findings do not help to differentiate between the two etiologies. [4,5] In accordance with previous studies hsTnT elevation and stroke severity as measured by NIHSS scores were also associated [11,12,23,24]. However, in our study unlike in previous investigations, neither the size of diffusion restriction nor the size of perfusion deficit in Tmax maps, was associated with hsTnT.…”

Section: Discussionsupporting

confidence: 91%

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Baseline Troponin T level in stroke and its association with stress cardiomyopathy

et al. 2018

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BackgroundDifferential diagnosis of elevated high sensitive Troponin T (hsTnT) in acute ischemic stroke includes myocardial infarction (MI) and neurogenic stunned myocardium (NSM). The aim of this study was to identify factors associated with baseline hsTnT levels and MI or NSM in acute ischemic stroke.MethodsWe studied 204 consecutive patients of the prospective acquired Bern Stroke Database with acute ischemic stroke diagnosed by brain MR. All patient histories and cardiac examinations were reviewed retrospectively. Volumetry of lesions on diffusion and perfusion weighted brain imaging (circular singular value decomposition, Tmax >6sec) was performed. Voxel based analysis was performed to identify brain areas associated with hsTnT elevation. Linear regression analysis was used to identify predictors of baseline hsTnT levels and myocardial infarction.ResultsElevated hsTnT was observed in 58 of the 204 patients (28.4%). The mean age was 68.3 years in the normal hsTnT group and 69.7 years in the elevated hsTnT group. Creatinine (p<0.001, OR 6.735, 95% CI 58.734–107.423), baseline NIHSS score (p = 0.029, OR 2.207, 95% CI 0.675–12.096), ST segment depression (p = 0.025, OR 2.259, 95% CI 2.419–35.838), and negative T waves in baseline ECG (p = 0.002, OR 3.209, 95% CI 13.007–54.564) were associated with hsTnT elevation, while infarct location and size were not. Coronary angiography was performed in 30 of the 204 patients (14.7%) and myocardial infarction was diagnosed in 7 of them (23.3%). Predictive factors for myocardial infarction could not be identified.ConclusionElevated baseline baseline hsTnT was associated with NIHSS, creatinine, ST segment depression and inverted T waves, but not with stroke location or size. None of the factors was helpful to differentiate MI and NSM. Therefore, ancillary investigations such as coronary angiography, cardiac MRI or both may be needed to solve the differential diagnosis.

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Section: Discussionsupporting

confidence: 91%

“…[16] Beside the parts of the limbic system the rostral ventrolateral medulla [17], solitary tract nucleus, and intermediolateral cell column are thought to be brain areas that are potentially prone to produce NSM. [5]…”

Section: Introductionmentioning

confidence: 99%

Baseline Troponin T level in stroke and its association with stress cardiomyopathy

et al. 2018

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“…Apoptosis has been implicated in many heart disorders. [18] , [19] , [20] Although it is clear that myocardial injury can occur in patients with intractable epilepsy, [5] , [6] , [17] , [21] , [22] it has not previously been known whether myocardial cell apoptosis is a contributing factor. Importantly, our novel data reveal that myocardial cell apoptosis increases after induction of experimental epilepsy and suggest that this pathway may indeed be involved in epilepsy-related myocardial damage.…”

Section: Discussionmentioning

confidence: 99%

Recombinant Human Erythropoietin Protects Myocardial Cells from Apoptosis via the Janus-Activated Kinase 2/Signal Transducer and Activator of Transcription 5 Pathway in Rats with Epilepsy

et al. 2015

Current Therapeutic Research

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ObjectiveTo investigate the potential mechanisms underlying the protective effects of recombinant human erythropoietin (rhEPO) and carbamylated EPO (CEPO) against myocardial cell apoptosis in epilepsy.MethodsRats were given an intra-amygdala injection of kainic acid to induce epilepsy. Groups of rats were treated with rhEPO or CEPO before induction of epilepsy, whereas additional rats were given a caudal vein injection of AG490, a selective inhibitor of Janus kinase 2 (JAK2). At different time points after seizure onset, electroencephalogram changes were recorded, and myocardium samples were taken for the detection of myocardial cell apoptosis and expression of JAK2, signal transducer and activator of transcription 5 (STAT5), caspase-3, and bcl-xl mRNAs and proteins.ResultsInduction of epilepsy significantly enhanced myocardial cell apoptosis and upregulated the expression of caspase-3 and bcl-xl proteins and JAK2 and STAT5a at both the mRNA and protein levels. Pretreatment with either rhEPO or CEPO reduced the number of apoptotic cells, upregulated bcl-xl expression, and downregulated caspase-3 expression in the myocardium of epileptic rats. Both myocardial JAK2 and STAT5a mRNAs, as well as phosphorylated species of JAK2 and STAT5a, were upregulated in epileptic rats in response to rhEPO—but not to CEPO—pretreatment. AG490 treatment increased apoptosis, upregulated caspase-3 protein expression, and downregulated bcl-xl protein expression in the myocardium of epileptic rats.ConclusionsThese results indicate that myocardial cell apoptosis may contribute to myocardial injury in epilepsy. EPO protects myocardial cells from apoptosis via the JAK2/STAT5 pathway in rats with experimental epilepsy, whereas CEPO exerts antiapoptotic activity perhaps via a pathway independent of JAK2/STAT5 signaling.

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“…Although cardiac dysfunction has been well-documented in populations with SAH, it has also been documented after other causes of intracranial bleeding, stroke, 45 CNS infection, 46 traumatic brain injury (TBI), 42,47 brain death, 48,49 and epilepsy. 50 Other critical care syndromes (ie, sepsis) are also known to be associated to cardiac dysfunction, 51,52 with suspected similarities in mechanisms to NSM. 53…”

Section: Neurologic Disorders and Cardiac Dysfunctionmentioning

confidence: 99%

Cardiac Dysfunction After Neurologic Injury

Krishnamoorthy

Mackensen

Gibbons

et al. 2016

Chest

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Recent literature has implicated severe neurologic injuries, such as aneurysmal subarachnoid hemorrhage, as a cause of cardiac dysfunction, impaired hemodynamic function, and poor outcomes. Mechanistic links between the brain and the heart have been explored in detail over the past several decades, and catecholamine excess, neuroendocrine dysfunction, and unchecked inflammation all likely contribute to the pathophysiologic process. Although cardiac dysfunction has also been described in other disease paradigms, including septic shock and thermal injury, there is likely a common underlying pathophysiology. In this review, we will examine the pathophysiology of cardiac dysfunction after neurologic injury, discuss the evidence surrounding cardiac dysfunction after different neurologic injuries, and suggest future research goals to gain knowledge and improve outcomes in this patient population.

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Cardiovascular manifestations of neurologic disease

Cited by 18 publications

References 125 publications

Baseline Troponin T level in stroke and its association with stress cardiomyopathy

Baseline Troponin T level in stroke and its association with stress cardiomyopathy

Recombinant Human Erythropoietin Protects Myocardial Cells from Apoptosis via the Janus-Activated Kinase 2/Signal Transducer and Activator of Transcription 5 Pathway in Rats with Epilepsy

Cardiac Dysfunction After Neurologic Injury

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