Autonomic Effects of Intraventricular Extension in Intracerebral Hemorrhage

Sýkora, Marek; Steiner, Thorsten; Poli, Sven; Rocco, Andrea; Turčãni, Peter; Diedler, Jennifer

doi:10.1007/s12028-011-9637-1

Cited by 21 publications

(23 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Assessment of serial troponin I levels during hospital stay revealed a further increase in the rate of elevated troponin levels, a finding predominantly driven by increased ventricular involvement. As reported previously for patients with subarachnoid hemorrhage [21], elevation of troponin I levels may, on the one hand, result from intraventricular blood and, therefore, meningeal irritation, leading to strong systemic stress-responses [22,23]. As a result, an enhanced release of catecholamines and consequently higher myocardial stress may reflect a neurocardiac dysbalance, evident also after ICH, notably in those patients with intraventricular involvement [21,22,24].…”

Section: Discussionmentioning

confidence: 83%

Peak Troponin I Levels Are Associated with Functional Outcome in Intracerebral Hemorrhage

et al. 2018

View full text Add to dashboard Cite

Background: Troponin I is a widely used and reliable marker of myocardial damage and its levels are routinely measured in acute stroke care. So far, the influence of troponin I elevations during hospital stay on functional outcome in patients with atraumatic intracerebral hemorrhage (ICH) is unknown. Methods: Observational single-center study including conservatively treated ICH patients over a 9-year period. Patients were categorized according to peak troponin I level during hospital stay (≤0.040, 0.041–0.500, > 0.500 ng/mL) and compared regarding baseline and hematoma characteristics. Multivariable analyses were performed to investigate independent associations of troponin levels during hospital stay with functional outcome – assessed using the modified Rankin Scale (mRS; favorable 0–3/unfavorable 4–6) – and mortality after 3 and 12 months. To account for possible confounding propensity score (PS)-matching (1: 1; caliper 0.1) was performed accounting for imbalances in baseline characteristics to investigate the impact of troponin I values on outcome. Results: Troponin elevations (> 0.040 ng/mL) during hospital stay were observed in 308 out of 745 (41.3%) patients and associated with poorer status on admission (Glasgow Coma Scale/National Institute of Health Stroke Scale). Multivariable analysis revealed troponin I levels during hospital stay to be independently associated with unfavorable outcome after 12 months (risk ratio [95% CI]: 1.030 [1.009–1.051] per increment of 1.0 ng/mL; p = 0.005), but not with mortality. After PS-matching, patients with troponin I elevation (≥0.040 ng/mL) versus those without had a significant higher rate of unfavorable outcome after 3 and 12 months (mRS 4–6 at 3 months: < 0.04 ng/mL: 159/265 [60.0%] versus ≥0.04 ng/mL: 199/266 [74.8%]; p < 0.001; at 12 months: < 0.04 ng/mL: 141/248 [56.9%] versus ≥0.04 ng/mL: 179/251 [71.3%]; p = 0.001). Conclusions: Troponin I elevations during hospital stay occur frequently in ICH patients and are independently associated with functional outcome after 3 and 12 months but not with mortality.

show abstract

Section: Discussionmentioning

confidence: 83%

Peak Troponin I Levels Are Associated with Functional Outcome in Intracerebral Hemorrhage

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Moreover, the volume of blood within the ventricle is associated with outcome in IVH, and >20 ml of blood in the ventricle is independently associated with a worse outcome (Sumer et al 2002; Tuhrim et al 1999). Intraventricular hemorrhagic extension is more common when the focus of hemorrhage is adjacent to the ventricle, such as in the thalamus or caudate (Hallevi et al 2008; Sykora et al 2012). One study reported a 100% incidence of IVH in caudate ICH (Hallevi et al 2008).…”

Section: Therapeutic Targets and Ongoing Clinical Trialsmentioning

confidence: 99%

“…Large volume ICH and hypertension are also associated with intraventricular hemorrhagic extension (Pang et al 1986; Steiner et al 2006). In addition, the location of the hematoma in the 3 rd and 4 th ventricle may contribute to poor outcome by causing autonomic dysfunction (Hallevi et al 2012; Sykora et al 2012). …”

Section: Therapeutic Targets and Ongoing Clinical Trialsmentioning

confidence: 99%

Progress in translational research on intracerebral hemorrhage: Is there an end in sight?

Strahle

Hua

et al. 2014

Progress in Neurobiology

133

107

View full text Add to dashboard Cite

Intracerebral hemorrhage (ICH) is a common and often fatal stroke subtype for which specific therapies and treatments remain elusive. To address this, many recent experimental and translational studies of ICH have been conducted, and these have led to several ongoing clinical trials. This review focuses on the progress of translational studies of ICH including those of the underlying causes and natural history of ICH, animal models of the condition, and effects of ICH on the immune and cardiac systems, among others. Current and potential clinical trials also are discussed for both ICH alone and with intraventricular extension.

show abstract

“…Lee et al [97] also detected a higher incidence of intraventricular haemorrhage in the thalamic and basal ganglia. Intraventricular haemorrhage patients including the third and fourth ventricle or ICH patients with insular involvement are reported to have lower baroreflex sensitivity than the patients without these involvements, suggesting that involvement of these sites could contribute to impairment of autonomic blood pressure regulation [157, 158]. Hypertensive responses can be exaggerated and additive because of the impaired baroreceptor sensitivity [135].…”

Section: Acute Progressing Haemorrhagic Strokementioning

confidence: 99%

Progressing haemorrhagic stroke: categories, causes, mechanisms and managements

Chen

Zeng

2014

J Neurol

View full text Add to dashboard Cite

Haemorrhagic stroke is a severe stroke subtype with high rates of morbidity and mortality. Although this condition has been recognised for a long time, the progressing haemorrhagic stroke has not received adequate attention, and it accounts for an even worse clinical outcome than the nonprogressing types of haemorrhagic stroke. In this review article, we categorised the progressing haemorrhagic stroke into acute progressing haemorrhagic stroke, subacute haemorrhagic stroke, and chronic progressing haemorrhagic stroke. Haematoma expansion, intraventricular haemorrhage, perihaematomal oedema, and inflammation, can all cause an acute progression of haemorrhagic stroke. Specific ‘second peak’ of perihaematomal oedema after intracerebral haemorrhage and ‘tension haematoma’ are the primary causes of subacute progression. For the chronic progressing haemorrhagic stroke, the occult vascular malformations, trauma, or radiologic brain surgeries can all cause a slowly expanding encapsulated haematoma. The mechanisms to each type of progressing haemorrhagic stroke is different, and the management of these three subtypes differs according to their causes and mechanisms. Conservative treatments are primarily considered in the acute progressing haemorrhagic stroke, whereas surgery is considered in the remaining two types.

show abstract

Autonomic Effects of Intraventricular Extension in Intracerebral Hemorrhage

Abstract: Hematoma extension to the third and fourth ventricle seems to cause profound autonomic dysregulation, possibly contributing to poor outcome. Patients with IVH in this location should be monitored vigorously to prevent and treat complications of autonomic failure.

Cited by 21 publications

References 38 publications

Peak Troponin I Levels Are Associated with Functional Outcome in Intracerebral Hemorrhage

Peak Troponin I Levels Are Associated with Functional Outcome in Intracerebral Hemorrhage

Progress in translational research on intracerebral hemorrhage: Is there an end in sight?

Progressing haemorrhagic stroke: categories, causes, mechanisms and managements

Contact Info

Product

Resources

About