Published Online
on November 14, 2005

A more recent version of this article appeared on November 22, 2005

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Submitted on May 14, 2005
Revised on August 12, 2005
Accepted on September 14, 2005

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, and 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.

^* To whom correspondence should be addressed. E-mail: zaroff{at}medicine.ucsf.edu.

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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