Impairment of cardiac metabolism and sympathetic innervation after aneurysmal subarachnoid hemorrhage: a nuclear medicine imaging study.

Bertrand Prunet,Frédéric Pons,Sébastien Cimarelli,Mathieu Basely,Eric Meaudre,Henry Boret,Arnaud Dagain,Gilbert Habib,Guillaume Lacroix,Jean-Brice Veyrieres,Nicolas Desse,Christophe Jego,Pierre Cambefort,Erwan D’Aranda,Emmanuel Bussy,Philippe Goutorbe,Pierre Esnault

doi:10.1186/cc13943

Abstract

IntroductionAlthough 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.MethodsDuring a 16-month period, 30 SAH acute phase patients underwent myocardial 18 F- fluorodesoxyglucose positron emission tomography (18F-FDGPET), 99mTc-tetrofosmin and 123I-meta-iodobenzylguanidine (123I-mIBG) scintigraphy, respectively, assessing glucose metabolism, cardiac perfusion, and sympathetic innervation. Patients with initial abnormalities were followed monthly for two months for 18F-FDG, and six months later for 123I-mIBG.ResultsIn 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 123I-mIBG scintigraphy after six months. Presence of initial altered cardiac metabolism was not associated with more unfavorable cardiac or neurological outcomes.ConclusionsThese findings support the hypothesis of neurogenic myocardial stunning after SAH. In hemodynamically stable acute phase SAH patients, cardiomyopathy is characterized by diffuse and heterogeneous 18F-FDG and 123I-mIBG uptake defect.Trial registrationClinicaltrials.gov NCT01218191. Registered 6 October 2010.

Highlights

Aneurysmal subarachnoid hemorrhage (SAH) is often complicated by myocardial injury, whether this neurogenic cardiomyopathy is associated with the modification of cardiac metabolism is unknown
In hemodynamically stable acute phase SAH patients, cardiomyopathy is characterized by diffuse and heterogeneous 18F-FDG and 123I-mIBG uptake defect
Patient characteristics During the study period, 40 patients were admitted to our intensive care unit (ICU) with acute-phase aneurysmal SAH

Summary

Introduction

Aneurysmal subarachnoid hemorrhage (SAH) is often complicated by myocardial injury, whether this neurogenic cardiomyopathy is associated with the modification of cardiac metabolism is unknown. Methods: During a 16-month period, 30 SAH acute phase patients underwent myocardial 18 F- fluorodesoxyglucose positron emission tomography (18F-FDGPET), 99mTc-tetrofosmin and 123I-meta-iodobenzylguanidine (123I-mIBG) scintigraphy, respectively, assessing glucose metabolism, cardiac perfusion, and sympathetic innervation. Subarachnoid hemorrhage (SAH) following aneurysm rupture remains a devastating condition with high mortality and poor outcome among survivors [1,2]. The primary objective of this study was to observe the impairment of cardiac glucose metabolism and to quantify its incidence and reversibility in a population of SAH patients. The duration and reversibility of cardiac neurogenic sympathetic injury after SAH remain unknown, and were evaluated as a secondary objective during the acute period and six months later

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