Brain-Heart Interactions in Traumatic Brain Injury

Cardiol Rev. 2017 Nov/Dec;25(6):279-288. doi: 10.1097/CRD.0000000000000167.

Abstract

The cardiovascular manifestations associated with nontraumatic head disorders are commonly known. Similar manifestations have been reported in patients with traumatic brain injury (TBI); however, the underlying mechanisms and impact on the patient's clinical outcomes are not well explored. The neurocardiac axis theory and neurogenic stunned myocardium phenomenon could partly explain the brain-heart link and interactions and can thus pave the way to a better understanding and management of TBI. Several observational retrospective studies have shown a promising role for beta-adrenergic blockers in patients with TBI in reducing the overall TBI-related mortality. However, several questions remain to be answered in clinical randomized-controlled trials, including population selection, beta blocker type, dosage, timing, and duration of therapy, while maintaining the optimal mean arterial pressure and cerebral perfusion pressure in patients with TBI.

Publication types

  • Review

MeSH terms

  • Adrenergic beta-Antagonists / therapeutic use
  • Brain / physiopathology*
  • Brain Injuries, Traumatic / complications
  • Brain Injuries, Traumatic / physiopathology*
  • Cardiovascular Diseases / blood
  • Cardiovascular Diseases / drug therapy
  • Cardiovascular Diseases / etiology
  • Cardiovascular Diseases / physiopathology
  • Creatine Kinase, MB Form / blood
  • Electrocardiography
  • Heart / physiopathology*
  • Hemodynamics
  • Humans
  • Myocardial Stunning / blood
  • Myocardial Stunning / drug therapy
  • Myocardial Stunning / etiology
  • Myocardial Stunning / physiopathology*
  • Natriuretic Peptide, Brain / blood
  • Peptide Fragments / blood
  • Troponin / blood

Substances

  • Adrenergic beta-Antagonists
  • Peptide Fragments
  • Troponin
  • pro-brain natriuretic peptide (1-76)
  • Natriuretic Peptide, Brain
  • Creatine Kinase, MB Form