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(Circulation. 2005;112:3314-3319.)
© 2005 American Heart Association, Inc.

Stroke

Acute Neurocardiogenic Injury After Subarachnoid Hemorrhage

Nader M. Banki, MD; Alexander Kopelnik, MD; Michael W. Dae, MD; Jacob Miss, BA; Poyee Tung, MD; Michael T. Lawton, MD; Barbara J. Drew, RN, PhD; Elyse Foster, MD; Wade Smith, MD, PhD; William W. Parmley, MD; Jonathan G. Zaroff, MD

From the Division of Cardiology (N.M.B., A.K., J.M., P.T., E.F., W.W.P., J.G.Z.), Department of Radiology (M.W.D.), Department of Neurosurgery (M.T.L.), Department of Physiological Nursing (B.J.D.), and Department of Neurology (W.S.), UCSF Medical Center, San Francisco, Calif.

Correspondence to Jonathan Zaroff, MD, 505 Parnassus Ave, Moffitt Suite 1177, San Francisco, CA 94143-0124. E-mail zaroff{at}medicine.ucsf.edu

Received May 14, 2005; de novo received April 25, 2005; revision received August 12, 2005; accepted September 14, 2005.

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.

Methods and Results— For 38 months, echocardiography and myocardial scintigraphy with technetium sestamibi (MIBI) and meta-[¹²³I]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 µg/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.

Key Words: echocardiography • scintigraphy • nervous system, sympathetic • hemorrhage

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