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 Ͼ1.0 g/L) and the left ventricular ejection fraction (LVEF, abnormal if Ͻ50%). Six adrenoceptor polymorphisms were genotyped: ␤1AR Arg389Gly, ␤1AR Ser49Gly, ␤2AR Gly16Arg, ␤2AR Gln27Glu, ␤2AR 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 ␤1AR Arg389Gly (odds ratio [OR] 3.4, Pϭ0.030) and the CC genotype (Gln/Gln) of ␤2AR Gln27Glu (OR 3.1, Pϭ0.032) were predictive of cTi release. The presence of the ␣2AR deletion was predictive of reduced LVEF (OR 4.2, Pϭ0.023). The combination of the ␤1AR 389 CC and the ␤2AR 27 CC genotypes resulted in a marked increase in the odds of cTi release (OR 15.5, Pϭ0.012). The combination of the ␤1AR 389 CC and the ␣2AR deletion genotypes resulted in a marked increase in the odds of developing a reduced LVEF (OR 10.3, Pϭ0.033). 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.

RWMA were frequent after SAH. High-grade SAH, an elevation in cTi levels, a history of prior stimulant drug use, and tachycardia are independent predictors of RWMA.

Cardiovascular abnormalities are independent predictors of in-patient mortality after SAH. Though these effects may be explained by a reduction in cerebral perfusion pressure or other mechanisms, further research is required to determine whether or not they are causal in nature.

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