Neurogenic Myocardial and Lung Injury in SAH Patients

NCT ID: NCT05408988

Last Updated: 2023-05-06

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

UNKNOWN

Total Enrollment

30 participants

Study Classification

OBSERVATIONAL

Study Start Date

2022-01-22

Study Completion Date

2024-12-31

Brief Summary

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Up to this day, little is known whether the extent of brain damage in patients with SAH correlates with the degree neurogenic myocardial injury and neurogenic lung injury.

This is a prospective observational study designed to asses relationship between catecholamine surge and development of myocardial and lung injury in subarachnoid haemorrhage patients.

Detailed Description

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Multiple forms of brain damage, primarily, subarachnoid haemorrhage (SAH) are frequently accompanied by neurogenic myocardial injury with changes in the electrocardiogram, accompanied by the release of markers of myocardial injury. This form of cardiac dysfunction is thought to be mediated by cellular toxicity associated with catecholamine release. Central nervous system damage in the course of intracranial haemorrhage may, in a similar pathogenic pathway, lead to neurogenic lung injury. Up to this day, little is known whether the extent of brain damage in patients with SAH correlates with the degree of neurogenic myocardial injury. Moreover, it remains unknown what is the full clinical picture and duration of this type of myocardial injury and how often it co-occurs with neurogenic lung injury. Such analysis is a fundamental and most important step in optimising the treatment of these patients.

Methods: In this prospective observational study the authors aim to recruit 30 patients with subarachnoid haemorrhage, requiring hospitalization in the Intensive Care Unit. The patients will be monitored for elevation in cardiac damage markers (hs-TnT, CPK, CK-MB, NT-proBNP) and worsening of respiratory conditions, defined by need for more invasive ventilation parameters, and subsequent changes in arterial blood gas. The above mentioned parameters will be assessed every 12 hours. Additionally, the patients will be screened for an elevation in catecholamine metabolite (metanephrine) concentration in 12-hour urine collection.

Hypothesis to be tested: Myocardial and lung injury in SAH patients is timely-associated with an increase in metanephrine concentration in urine.

Conditions

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Myocardial Injury Lung Injury Subarachnoid Hemorrhage

Study Design

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Observational Model Type

COHORT

Study Time Perspective

PROSPECTIVE

Study Groups

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Patients with subarachnoid haemorrhage

Patients aged 18 or older hospitalized in the Intensive Care Unit with Subarachnoid Haemorrhage.

hs-TnT (high-sensitive cardiac troponin T) plasma concentration

Intervention Type DIAGNOSTIC_TEST

hs-TnT plasma concentration measured once every 12 hours

CK-MB (creatine kinase myocardial band) plasma concentration

Intervention Type DIAGNOSTIC_TEST

CK-MB plasma concentration measured every 12 hours

CPK (creatine phosphokinase) plasma concentration

Intervention Type DIAGNOSTIC_TEST

CPK plasma concentration measured every 12 hours

NT-proBNP (N-terminal prohormone of brain natriuretic peptide) plasma concentration

Intervention Type DIAGNOSTIC_TEST

NT-proBNP plasma concentration measured every 12 hours

Metanephrine concentration in urine

Intervention Type DIAGNOSTIC_TEST

Metanephrine concentration measured in 12-hour urine collection using spectrophotometry.

Interventions

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hs-TnT (high-sensitive cardiac troponin T) plasma concentration

hs-TnT plasma concentration measured once every 12 hours

Intervention Type DIAGNOSTIC_TEST

CK-MB (creatine kinase myocardial band) plasma concentration

CK-MB plasma concentration measured every 12 hours

Intervention Type DIAGNOSTIC_TEST

CPK (creatine phosphokinase) plasma concentration

CPK plasma concentration measured every 12 hours

Intervention Type DIAGNOSTIC_TEST

NT-proBNP (N-terminal prohormone of brain natriuretic peptide) plasma concentration

NT-proBNP plasma concentration measured every 12 hours

Intervention Type DIAGNOSTIC_TEST

Metanephrine concentration in urine

Metanephrine concentration measured in 12-hour urine collection using spectrophotometry.

Intervention Type DIAGNOSTIC_TEST

Eligibility Criteria

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Inclusion Criteria

* patients with subarachnoid haemorrhage (both aneurysmal and non-aneurysmal) with acute consciousness disturbances (Glasgow Coma Scale \< 8 pts) requiring intubation and mechanical ventilation, hospitalized in the ICU for over 24 hours

Exclusion Criteria

* severe prior pulmonary diseases
* severe prior cardiac diseases
* death in the first 72 hours of ICU stay
* need for any extracorporeal life-saving techniques
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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Medical University of Silesia

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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Łukasz Krzych, PhD

Role: STUDY_CHAIR

University Clinical Center prof. K. Gibiński of the Medical University of Silesia in Katowice

Locations

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University Clinical Center prof. K. Gibiński of the Medical University of Silesia in Katowice

Katowice, Silesian Voivodeship, Poland

Site Status RECRUITING

Countries

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Poland

Central Contacts

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Natalia Rachfalska

Role: CONTACT

+48 32 789 42 01

Facility Contacts

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Łukasz Krzych, PhD

Role: primary

32 789 4201

References

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Osgood ML. Aneurysmal Subarachnoid Hemorrhage: Review of the Pathophysiology and Management Strategies. Curr Neurol Neurosci Rep. 2021 Jul 26;21(9):50. doi: 10.1007/s11910-021-01136-9.

Reference Type BACKGROUND
PMID: 34308493 (View on PubMed)

Hofman M, Hajder N, Duda I, Krzych LJ. A Questionnaire Survey of Management of Patients with Aneurysmal Subarachnoid Haemorrhage in Poland. Int J Environ Res Public Health. 2020 Jun 11;17(11):4161. doi: 10.3390/ijerph17114161.

Reference Type BACKGROUND
PMID: 32545225 (View on PubMed)

Wybraniec MT, Mizia-Stec K, Krzych L. Neurocardiogenic injury in subarachnoid hemorrhage: A wide spectrum of catecholamin-mediated brain-heart interactions. Cardiol J. 2014;21(3):220-8. doi: 10.5603/CJ.a2014.0019. Epub 2014 Feb 14.

Reference Type BACKGROUND
PMID: 24526502 (View on PubMed)

Wybraniec M, Mizia-Stec K, Krzych L. Stress cardiomyopathy: yet another type of neurocardiogenic injury: 'stress cardiomyopathy'. Cardiovasc Pathol. 2014 May-Jun;23(3):113-20. doi: 10.1016/j.carpath.2013.12.003. Epub 2013 Dec 27.

Reference Type BACKGROUND
PMID: 24462197 (View on PubMed)

Veeravagu A, Chen YR, Ludwig C, Rincon F, Maltenfort M, Jallo J, Choudhri O, Steinberg GK, Ratliff JK. Acute lung injury in patients with subarachnoid hemorrhage: a nationwide inpatient sample study. World Neurosurg. 2014 Jul-Aug;82(1-2):e235-41. doi: 10.1016/j.wneu.2014.02.030. Epub 2014 Feb 20.

Reference Type BACKGROUND
PMID: 24560705 (View on PubMed)

Mazeraud A, Robba C, Rebora P, Iaquaniello C, Vargiolu A, Rass V, Bogossian EG, Helbok R, Taccone FS, Citerio G. Acute Distress Respiratory Syndrome After Subarachnoid Hemorrhage: Incidence and Impact on the Outcome in a Large Multicenter, Retrospective Cohort. Neurocrit Care. 2021 Jun;34(3):1000-1008. doi: 10.1007/s12028-020-01115-x. Epub 2020 Oct 20.

Reference Type BACKGROUND
PMID: 33083966 (View on PubMed)

Anetsberger A, Jungwirth B, Blobner M, Ringel F, Bernlochner I, Heim M, Bogdanski R, Wostrack M, Schneider G, Meyer B, Graessner M, Baumgart L, Gempt J. Association of Troponin T levels and functional outcome 3 months after subarachnoid hemorrhage. Sci Rep. 2021 Aug 9;11(1):16154. doi: 10.1038/s41598-021-95717-w.

Reference Type BACKGROUND
PMID: 34373566 (View on PubMed)

Other Identifiers

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PCN/0022/KB/206/20

Identifier Type: -

Identifier Source: org_study_id

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