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

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.

Stress-Induced Cardiomyopathy

“…Sympathectomy, but not adrenalectomy, prevents cardiac dysfunction in animal studies of SAH, further supporting the role of local catecholamines in the pathogenesis of this disease (26). Cardiac metabolism may be altered in the absence of abnormal perfusion as well (32). Catecholamines may lead to cardiac dysfunction via microvascular dysfunction or direct toxicity.…”

The role of nuclear cardiac imaging in redefining neurogenic stunned myocardium in subarachnoid hemorrhage: a deeper look into the heart

“…However, data regarding acute myocardial metabolic alterations in SAH are sparse. The recent article by Prunet and colleagues in Critical Care deals with this poorly studied area [ 1 ].…”

“…In their recent article, Prunet and coworkers assessed myocardial glucose metabolism and sympathetic innervation in SAH by means of scintigraphy, and investigated the possible associations with left ventricular (LV) systolic and diastolic dysfunction, troponin elevation and SAH outcomes [ 1 ]. The authors provide scintigraphic evidence of impaired glucose metabolism (assessed by 18 F-fluorodesoxyglucose positron emission tomography) and sympathetic innervation (studied by 123 I-meta-iodobenzylguanidine scintigraphy) in 83.3% (25/30) and 90% (27/30), respectively, of 30 patients with acute SAH.…”

“…Follow-up studies showed improvement of glucose metabolism in 50% (15/30) of SAH patients in 1 to 2 months. Normalization of sympathetic innervation was slower, however; only 26.7% (8/30) exhibited normal 123 I-meta-iodobenzylguanidine scintigraphy 6 months later [ 1 ]. These data provide novel insight into the metabolic consequences and their evolution over time in SAH, an issue that was until now largely undetermined.…”

“…SAH-induced neurocardiogenic injury demonstrates comparable scintigraphic features [ 4 , 5 ] with TTC, which is also attributed to massive release of catecholamines [ 6 ]. However, the topography of these regional abnormalities differs significantly between SAH, which diffusely affects LV myocardium [ 1 ], and TTC, in which LV apical myocardium is predominantly affected [ 4 , 5 ]. Furthermore, myocardial scintigraphic defects showed no association to echocardiography in SAH [ 1 ], whereas impaired glucose uptake in TTC is closely related with LV apical ballooning on echocardiography.…”