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

Prunet B, Basely M, D'Aranda E, Cambefort P, Pons F, Cimarelli S, Dagain A, Desse N, Veyrieres JB, Jego C, Lacroix G, Esnault P, Boret H, Goutorbe P, Bussy E, Habib G, Meaudre E - Crit Care (2014)

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

ABSTRACT

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.

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Representative PET, SPECT, and scintigraphy findings. Left ventricular transaxial slices (vertical long axis, horizontal long axis) and polar map presentation (17-segment model) of, respectively, cardiac 18F-FDG PET, 123I-mIBG SPECT, and perfusion scintigraphy performed during acute phase and follow-up in a patient with aneurysmal subarachnoid hemorrhage. We observed that the uptake of both 18F-FDG and 123I-mIBG were markedly reduced during the acute phase. The uptake of 18F-FDG was normalized two months later. The uptake of 123I-mIBG was still impaired six months after the onset of symptomatology. 123I-mIBG, 123I-meta-iodobenzylguanidine; 18F-FDG PET, 18F-fluorodesoxyglucose positron emission tomography; PET, positron emission tomography; SPECT, single-photon emission computed tomography.
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Figure 2: Representative PET, SPECT, and scintigraphy findings. Left ventricular transaxial slices (vertical long axis, horizontal long axis) and polar map presentation (17-segment model) of, respectively, cardiac 18F-FDG PET, 123I-mIBG SPECT, and perfusion scintigraphy performed during acute phase and follow-up in a patient with aneurysmal subarachnoid hemorrhage. We observed that the uptake of both 18F-FDG and 123I-mIBG were markedly reduced during the acute phase. The uptake of 18F-FDG was normalized two months later. The uptake of 123I-mIBG was still impaired six months after the onset of symptomatology. 123I-mIBG, 123I-meta-iodobenzylguanidine; 18F-FDG PET, 18F-fluorodesoxyglucose positron emission tomography; PET, positron emission tomography; SPECT, single-photon emission computed tomography.

Mentions: Another one month later, PET was performed on day 68 ± 7 for only five patients. Indeed, 10 other patients refused the follow-up or were lost to follow-up at this time. 18F-FDG LV uptake was still impaired for three patients, with a mean defect area of 25 ± 6%. Two patients exhibited normal 18F-FDG uptake. The Figure 2 illustrated the exemplary case of a patient exhibiting normal 18F-FDG uptake two months after aneurysm rupture.


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

Prunet B, Basely M, D'Aranda E, Cambefort P, Pons F, Cimarelli S, Dagain A, Desse N, Veyrieres JB, Jego C, Lacroix G, Esnault P, Boret H, Goutorbe P, Bussy E, Habib G, Meaudre E - Crit Care (2014)

Representative PET, SPECT, and scintigraphy findings. Left ventricular transaxial slices (vertical long axis, horizontal long axis) and polar map presentation (17-segment model) of, respectively, cardiac 18F-FDG PET, 123I-mIBG SPECT, and perfusion scintigraphy performed during acute phase and follow-up in a patient with aneurysmal subarachnoid hemorrhage. We observed that the uptake of both 18F-FDG and 123I-mIBG were markedly reduced during the acute phase. The uptake of 18F-FDG was normalized two months later. The uptake of 123I-mIBG was still impaired six months after the onset of symptomatology. 123I-mIBG, 123I-meta-iodobenzylguanidine; 18F-FDG PET, 18F-fluorodesoxyglucose positron emission tomography; PET, positron emission tomography; SPECT, single-photon emission computed tomography.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4230019&req=5

Figure 2: Representative PET, SPECT, and scintigraphy findings. Left ventricular transaxial slices (vertical long axis, horizontal long axis) and polar map presentation (17-segment model) of, respectively, cardiac 18F-FDG PET, 123I-mIBG SPECT, and perfusion scintigraphy performed during acute phase and follow-up in a patient with aneurysmal subarachnoid hemorrhage. We observed that the uptake of both 18F-FDG and 123I-mIBG were markedly reduced during the acute phase. The uptake of 18F-FDG was normalized two months later. The uptake of 123I-mIBG was still impaired six months after the onset of symptomatology. 123I-mIBG, 123I-meta-iodobenzylguanidine; 18F-FDG PET, 18F-fluorodesoxyglucose positron emission tomography; PET, positron emission tomography; SPECT, single-photon emission computed tomography.
Mentions: Another one month later, PET was performed on day 68 ± 7 for only five patients. Indeed, 10 other patients refused the follow-up or were lost to follow-up at this time. 18F-FDG LV uptake was still impaired for three patients, with a mean defect area of 25 ± 6%. Two patients exhibited normal 18F-FDG uptake. The Figure 2 illustrated the exemplary case of a patient exhibiting normal 18F-FDG uptake two months after aneurysm rupture.

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus