RESUMEN
INTRODUCTION: Although aneurysmal subarachnoid hemorrhage (SAH) is often complicated by myocardial injury, whether this neurogenic cardiomyopathy is associated with the modification of cardiac metabolism is unknown. This study sought to explore, by positron emission tomography/computed tomography, the presence of altered cardiac glucose metabolism after SAH. METHODS: During a 16-month period, 30 SAH acute phase patients underwent myocardial (18)F- fluorodesoxyglucose positron emission tomography ((18)F-FDGPET), (99m)Tc-tetrofosmin and (123)I-meta-iodobenzylguanidine ((123)I-mIBG) scintigraphy, respectively, assessing glucose metabolism, cardiac perfusion, and sympathetic innervation. Patients with initial abnormalities were followed monthly for two months for (18)F-FDG, and six months later for (123)I-mIBG. RESULTS: In this SAH population, acute cardiac metabolic disturbance was observed in 83% of patients (n = 25), and sympathetic innervation disturbance affected 90% (n = 27). Myocardial perfusion was normal for all patients. The topography and extent of metabolic defects and innervation abnormalities largely overlapped. Follow-up showed rapid improvement of glucose metabolism in one or two months. Normalization of sympathetic innervation was slower; only 27% of patients (n = 8) exhibited normal (123)I-mIBG scintigraphy after six months. Presence of initial altered cardiac metabolism was not associated with more unfavorable cardiac or neurological outcomes. CONCLUSIONS: These findings support the hypothesis of neurogenic myocardial stunning after SAH. In hemodynamically stable acute phase SAH patients, cardiomyopathy is characterized by diffuse and heterogeneous (18)F-FDG and (123)I-mIBG uptake defect. TRIAL REGISTRATION: Clinicaltrials.gov NCT01218191. Registered 6 October 2010.