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(Stroke. 2006;37:1680.)
© 2006 American Heart Association, Inc.

Original Contributions

Adrenoceptor Polymorphisms and the Risk of Cardiac Injury and Dysfunction After Subarachnoid Hemorrhage

Jonathan G. Zaroff, MD; Ludmila Pawlikowska, PhD; Jacob C. Miss, BA; Sirisha Yarlagadda, MD; Connie Ha, BS; Achal Achrol, BS; Pui-Yan Kwok, MD, PhD; Charles E. McCulloch, PhD; Michael T. Lawton, MD; Nerissa Ko, MD; Wade Smith, MD, PhD William L. Young, MD

From the Departments of Medicine/Cardiology Division (J.Z., J.M., S.Y.), Cardiovascular Research Institute (L.P., C.H., P.K.), Epidemiology and Biostatistics (C.M.), Neurology (N.K., W.S.), Neurosurgery (M.L.), and The Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care (A.A., W.Y.), University of California, San Francisco.

Correspondence to Jonathan G. Zaroff, MD, 505 Parnassus Avenue, Moffitt Suite 1176, San Francisco, CA 94143-0124. E-mail zaroff{at}medicine.ucsf.edu

Background and Purpose— Cardiac abnormalities occur commonly after subarachnoid hemorrhage (SAH) and may be caused by excessive release of catecholamines from the myocardial sympathetic nerves. We hypothesized that adrenoceptor polymorphisms resulting in greater catecholamine sensitivity would be associated with an increased risk of cardiac injury.

Methods— This was a prospective cohort study. The primary outcome variables were the serum level of cardiac troponin I (cTi, abnormal if >1.0 µg/L) and the left ventricular ejection fraction (LVEF, abnormal if <50%). Six adrenoceptor polymorphisms were genotyped: ß1AR Arg389Gly, ß1AR Ser49Gly, ß2AR Gly16Arg, ß2AR Gln27Glu, ß2AR Thr164Ile, and 2AR del322-325. The effect of each polymorphism on the risk of developing cardiac abnormalities was quantified using multivariable logistic regression.

Results— The study included 182 patients. The CC genotype (Arg/Arg) of ß1AR Arg389Gly (odds ratio [OR] 3.4, P=0.030) and the CC genotype (Gln/Gln) of ß2AR Gln27Glu (OR 3.1, P=0.032) were predictive of cTi release. The presence of the 2AR deletion was predictive of reduced LVEF (OR 4.2, P=0.023). The combination of the ß1AR 389 CC and the ß2AR 27 CC genotypes resulted in a marked increase in the odds of cTi release (OR 15.5, P=0.012). The combination of the ß1AR 389 CC and the 2AR deletion genotypes resulted in a marked increase in the odds of developing a reduced LVEF (OR 10.3, P=0.033).

Conclusions— Genetic polymorphisms of the adrenoceptors are associated with an increased risk of cardiac abnormalities after SAH. These data support the hypothesis that cardiac dysfunction after SAH is a form of neurocardiogenic injury.

Key Words: cerebral hemorrhage • congestive heart failure • echocardiography

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