title: Acute neurocardiogenic injury after subarachnoid hemorrhage.
abstract: BACKGROUND
  Left ventricular (LV) systolic dysfunction has been reported in humans with subarachnoid hemorrhage (SAH), and its underlying pathophysiology remains controversial. Possible mechanisms include myocardial ischemia versus excessive catecholamine release from sympathetic nerve terminals.
  
  
  RESULTS
  For 38 months, echocardiography and myocardial scintigraphy with technetium sestamibi (MIBI) and meta-[(123)I]iodobenzylguanidine (MIBG) were performed on 42 patients admitted with SAH to assess myocardial perfusion and sympathetic innervation, respectively. A blinded observer interpreted the scintigraphic images. Cardiac troponin I (cTI) was measured to quantify the degree of myocyte necrosis. Blinded observers calculated the LV ejection fraction and graded each LV segment as normal (score=1), hypokinetic (score=2), or akinetic (score=3). A wall-motion score was calculated by averaging the sum of the 16 segments. All subjects with interpretable scans (N=41) had normal MIBI uptake. Twelve subjects had either global (n=9) or regional (n=3) absence of MIBG uptake. In comparison with patients with normal MIBG uptake, those with evidence of functional denervation were more likely to have LV regional wall-motion abnormalities (92% versus 52%, P=0.030) and cTI levels >1 microg/L (58% versus 21%, P=0.029).
  
  
  CONCLUSIONS
  LV systolic dysfunction in humans with SAH is associated with normal myocardial perfusion and abnormal sympathetic innervation. These findings may be explained by excessive release of norepinephrine from myocardial sympathetic nerves, which could damage both myocytes and nerve terminals.
authors.affiliation: Division of Cardiology, Department of Radiology, UCSF Medical Center, San Francisco, California, USA.
authors.forename: Nader M
authors.initials: NM
authors.lastname: Banki
authors.forename: Alexander
authors.initials: A
authors.lastname: Kopelnik
authors.forename: Michael W
authors.initials: MW
authors.lastname: Dae
authors.forename: Jacob
authors.initials: J
authors.lastname: Miss
authors.forename: Poyee
authors.initials: P
authors.lastname: Tung
authors.forename: Michael T
authors.initials: MT
authors.lastname: Lawton
authors.forename: Barbara J
authors.initials: BJ
authors.lastname: Drew
authors.forename: Elyse
authors.initials: E
authors.lastname: Foster
authors.forename: Wade
authors.initials: W
authors.lastname: Smith
authors.forename: William W
authors.initials: WW
authors.lastname: Parmley
authors.forename: Jonathan G
authors.initials: JG
authors.lastname: Zaroff
mesh_terms: D019797:3-Iodobenzylguanidine; D000208:Acute Disease; D000328:Adult; D000368:Aged; D004452:Echocardiography; D005260:Female; D006801:Humans; D007457:Iodine Radioisotopes; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000378:metabolism; D011446:Prospective Studies; D011877:Radionuclide Imaging; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000378:metabolism / Q000503:physiopathology*; D017256:Technetium Tc 99m Sestamibi; D019210:Troponin I / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000209:etiology* / Q000503:physiopathology
chemical_list: D007457:Iodine Radioisotopes; D019210:Troponin I; D019797:3-Iodobenzylguanidine; D017256:Technetium Tc 99m Sestamibi; D009638:Norepinephrine