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Cardiac Injury After Traumatic Brain Injury: Clinical Consequences and Management.

Authors :
Coppalini, Giacomo
Salvagno, Michele
Peluso, Lorenzo
Bogossian, Elisa Gouvêa
Quispe Cornejo, Armin
Labbé, Vincent
Annoni, Filippo
Taccone, Fabio Silvio
Source :
Neurocritical Care. Apr2024, Vol. 40 Issue 2, p477-485. 9p.
Publication Year :
2024

Abstract

Traumatic brain injury (TBI) is a significant public health issue because of its increasing incidence and the substantial short-term and long-term burden it imposes. This burden includes high mortality rates, morbidity, and a significant impact on productivity and quality of life for survivors. During the management of TBI, extracranial complications commonly arise during the patient's stay in the intensive care unit. These complications can have an impact on both mortality and the neurological outcome of patients with TBI. Among these extracranial complications, cardiac injury is a relatively frequent occurrence, affecting approximately 25–35% of patients with TBI. The pathophysiology underlying cardiac injury in TBI involves the intricate interplay between the brain and the heart. Acute brain injury triggers a systemic inflammatory response and a surge of catecholamines, leading to the release of neurotransmitters and cytokines. These substances have detrimental effects on the brain and peripheral organs, creating a vicious cycle that exacerbates brain damage and cellular dysfunction. The most common manifestation of cardiac injury in TBI is corrected QT (QTc) prolongation and supraventricular arrhythmias, with a prevalence up to 5 to 10 times higher than in the general adult population. Other forms of cardiac injury, such as regional wall motion alteration, troponin elevation, myocardial stunning, or Takotsubo cardiomyopathy, have also been described. In this context, the use of β-blockers has shown potential benefits by intervening in this maladaptive process. β-blockers can limit the pathological effects on cardiac rhythm, blood circulation, and cerebral metabolism. They may also mitigate metabolic acidosis and potentially contribute to improved cerebral perfusion. However, further clinical studies are needed to elucidate the role of new therapeutic strategies in limiting cardiac dysfunction in patients with severe TBI. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
15416933
Volume :
40
Issue :
2
Database :
Academic Search Index
Journal :
Neurocritical Care
Publication Type :
Academic Journal
Accession number :
176221227
Full Text :
https://doi.org/10.1007/s12028-023-01777-3