Mechanisms in neurogenic stress cardiomyopathy after aneurysmal subarachnoid hemorrhage

Vivien H Lee1, Jae K Oh, Sharon L Mulvagh

  • 1Division of Critical Care Neurology, Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.

Neurocritical Care
|February 10, 2007
PubMed

Insights

Cardiac dysfunction following aneurysmal subarachnoid hemorrhage (SAH) is better termed "neurogenic stress cardiomyopathy." This reflects the pathophysiology more accurately than "neurogenic stunned myocardium," aiding patient management.

Area of Science:

  • Neurology
  • Cardiology
  • Pathophysiology

Background:

  • Cardiac dysfunction is a common complication after aneurysmal subarachnoid hemorrhage (SAH).
  • The term "neurogenic stunned myocardium" is frequently used but may not accurately represent the underlying mechanisms.
  • Understanding SAH-induced cardiac dysfunction is crucial for effective patient care.

Purpose of the Study:

  • To propose "neurogenic stress cardiomyopathy" as a more fitting terminology for SAH-induced cardiac dysfunction.
  • To review the characteristics, pathophysiology, and supporting evidence for SAH-related cardiac complications.
  • To explore the relationship between SAH-induced cardiac dysfunction and tako-tsubo cardiomyopathy and discuss potential therapies.

Main Methods:

  • Literature review of current scientific articles and studies.
  • Analysis of clinical and animal studies related to SAH and cardiac dysfunction.
  • Comparison of SAH-induced cardiac dysfunction with tako-tsubo cardiomyopathy.

Main Results:

  • The current terminology "neurogenic stunned myocardium" may be imprecise.
  • Evidence supports a distinct pathophysiology for cardiac dysfunction following SAH.
  • SAH-induced cardiac dysfunction shares features with tako-tsubo cardiomyopathy.

Conclusions:

  • "Neurogenic stress cardiomyopathy" is a more appropriate term for cardiac dysfunction after SAH.
  • Recognizing the unique features of SAH-induced cardiac dysfunction improves patient management.
  • Further research into therapeutic strategies for SAH-related cardiac complications is warranted.

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