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Updated: Aug 8, 2026

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
10:34

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage

Published on: August 30, 2020

Adrenoceptor polymorphisms and the risk of cardiac injury and dysfunction after subarachnoid hemorrhage

Jonathan G Zaroff1, Ludmila Pawlikowska, Jacob C Miss

  • 1Department of Medicine, University of California, San Francisco, USA. zaroff@medicine.ucsf.edu

Stroke
|May 27, 2006
PubMed

Insights

Genetic variations in adrenoceptors increase the risk of cardiac injury following subarachnoid hemorrhage. Specific gene polymorphisms are linked to higher chances of developing cardiac abnormalities, suggesting a neurocardiogenic cause.

Area of Science:

  • Cardiology
  • Genetics
  • Neuroscience

Background:

  • Subarachnoid hemorrhage (SAH) frequently leads to cardiac abnormalities.
  • Excessive catecholamine release from sympathetic nerves is a suspected cause.
  • Adrenoceptor gene variations may influence catecholamine sensitivity and cardiac risk.

Purpose of the Study:

  • To investigate the association between adrenoceptor gene polymorphisms and cardiac injury after SAH.
  • To determine if specific genetic variations increase the risk of cardiac dysfunction post-SAH.

Main Methods:

  • Prospective cohort study of 182 patients.
  • Assessed serum cardiac troponin I (cTi) and left ventricular ejection fraction (LVEF).
  • Genotyped six adrenoceptor polymorphisms: beta1AR Arg389Gly, beta1AR Ser49Gly, beta2AR Gly16Arg, beta2AR Gln27Glu, beta2AR Thr164Ile, and alpha2AR del322-325.
  • Used multivariable logistic regression to quantify risk.

Main Results:

  • Beta1AR Arg389Gly CC genotype and beta2AR Gln27Glu CC genotype predicted cTi release.
  • Alpha2AR deletion predicted reduced LVEF.
  • Combined genotypes (beta1AR 389 CC + beta2AR 27 CC) significantly increased odds of cTi release (OR 15.5).
  • Combined genotypes (beta1AR 389 CC + alpha2AR deletion) significantly increased odds of reduced LVEF (OR 10.3).

Conclusions:

  • Genetic polymorphisms in adrenoceptors are linked to increased cardiac abnormality risk after SAH.
  • Findings support the concept of neurocardiogenic injury in SAH-induced cardiac dysfunction.
Abstract

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