Mechanisms in neurogenic stress cardiomyopathy after aneurysmal subarachnoid hemorrhage

Neurocrit Care. 2006;5(3):243-9. doi: 10.1385/NCC:5:3:243.

Abstract

Cardiac dysfunction after aneurysmal subarachnoid hemorrhage (SAH) is often referred to as "neurogenic stunned myocardium," which does not accurately reflect the suspected pathophysiology. We propose an alternative terminology, "neurogenic stress cardiomyopathy," as a more appropriate label based on our review of the current literature. This article will review the distinctive characteristics of SAH-induced cardiac dysfunction, hypotheses to explain the pathophysiology, and the supporting clinical and animal studies. Recognition of the unique features associated with SAH-induced cardiac complications allows optimal management of patients with SAH. We will also discuss the clinical and theoretical overlap of SAH-induced cardiac dysfunction with a syndrome known as tako-tsubo cardiomyopathy and explore therapeutic opportunities.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiomyopathies / diagnosis
  • Cardiomyopathies / physiopathology*
  • Cardiomyopathies / therapy
  • Coronary Vasospasm / diagnosis
  • Coronary Vasospasm / physiopathology
  • Coronary Vasospasm / therapy
  • Diagnosis, Differential
  • Humans
  • Intracranial Aneurysm / diagnosis
  • Intracranial Aneurysm / physiopathology*
  • Intracranial Aneurysm / therapy
  • Intracranial Pressure / physiology
  • Myocardial Stunning / diagnosis
  • Myocardial Stunning / physiopathology*
  • Myocardial Stunning / therapy
  • Myocardium / pathology
  • Necrosis
  • Norepinephrine / blood
  • Prognosis
  • Subarachnoid Hemorrhage / diagnosis
  • Subarachnoid Hemorrhage / physiopathology*
  • Subarachnoid Hemorrhage / therapy
  • Syndrome
  • Ventricular Dysfunction, Left / diagnosis
  • Ventricular Dysfunction, Left / physiopathology
  • Ventricular Dysfunction, Left / therapy

Substances

  • Norepinephrine