Current partner codePEPTIDESDE
NCT05408988·Not applicable·OBSERVATIONAL

Neurogenic Myocardial and Lung Injury in SAH Patients

Status

Unknown

Phase

Not applicable

Enrollment

30

Locations

1

Results

Not posted

Publications

7

Study summary

What the protocol is testing.

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.

Full detailed description

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.

Interventions

Treatment arms and agents.

DIAGNOSTIC_TEST

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

hs-TnT plasma concentration measured once every 12 hours

DIAGNOSTIC_TEST

CK-MB (creatine kinase myocardial band) plasma concentration

CK-MB plasma concentration measured every 12 hours

DIAGNOSTIC_TEST

CPK (creatine phosphokinase) plasma concentration

CPK plasma concentration measured every 12 hours

DIAGNOSTIC_TEST

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

NT-proBNP plasma concentration measured every 12 hours

DIAGNOSTIC_TEST

Metanephrine concentration in urine

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

Timeline

From registration to results.

  1. First posted

    Jun 7, 2022

  2. Study start

    Jan 22, 2022

  3. Primary completion

    Jun 30, 2024

  4. Study completion

    Dec 31, 2024

  5. Results posted

    Not reported

  6. Registry updated

    May 6, 2023

Outcomes

What the study measures.

Primary outcomes

In-hospital death (number of patients)

Time frame · 7 days

Death of the patient during the first 7 days of hospitalization.

Number of Patients with elevation in hs-TnT levels

Time frame · 7 days

hs-TnT treated as myocardial injury biomarker

Number of Patients with elevation in NT-proBNP levels

Time frame · 7 days

NT-proBNP treated as myocardial injury biomarker

Number of Patients with elevation in creatine kinase levels

Time frame · 7 days

Creatine kinase treated as myocardial injury biomarker

Number of Patients with elevation in creatine kinase MB levels

Time frame · 7 days

Creatine kinase MB treated as myocardial injury biomarker

Number of Patients with a decrease in Horowitz index

Time frame · 7 days

The decrease in Horowitz index treated as a sign of need for more invasive ventilation parameters with subsequent blood gas changes

Number of Patients with need of increased FiO2

Time frame · 7 days

Need of increased FiO2 treated as a sign of need for more invasive ventilation parameters with subsequent blood gas changes

Number of Patients with need of increased PEEP values

Time frame · 7 days

Need of increased PEEP values treated as a sign of need for more invasive ventilation parameters with subsequent blood gas changes

Secondary outcomes

Not reported in the indexed record.

Eligibility

Who can take part.

Minimum age
18 Years
Maximum age
Not reported
Sex
ALL
Healthy volunteers
No

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

Study locations

1 registered sites.

Poland. Showing up to 24 locations stored in the fast local snapshot.

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

Katowice, Silesian Voivodeship, Poland

Publications

Results and literature.

PMID 34308493Osgood 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.PMID 32545225Hofman 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.PMID 24526502Wybraniec 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.PMID 24462197Wybraniec 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.PMID 24560705Veeravagu 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.PMID 33083966Mazeraud 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.PMID 34373566Anetsberger 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.

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