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Cerebral Hypoperfusion in Orthostatic Hypotension with Globally Denervated Myocardium

Department of Radiology, Department of Internal Medicine, National Cardiovascular Center, Division of Tracer Kinetics, Biomedical Research Center, Osaka University Medical School, Osaka, Japan

Correspondence: For correspondence or reprints contact: Kohei Hayashida, MD, Department of Radiology, National Cardiovascular Center, 5-7-1 Fujishirodai, Suita, Osaka 565, Japan.

ABSTRACT

A 57-yr-old woman had frequent syncope when rising from a seated position. Her blood pressure fell from 140/80 mmHg to 60–70/40 mmHg while changing positions, Iodine-123-metaiodobenzylguanidine ([¹²³I]MIBG) did not accumulate in the heart, whereas ²⁰¹TI-CI (²⁰¹TI) did. Raise-up ^99mTc-hexamethyl-propyleneamine oxime (^99mTc-HMPAO) brain SPECT revealed decreased activity in the bilateral frontal areas, and subsequent supine ^99mTc-HMPAO brain SPECT revealed filling in these areas, indicating that the cerebral blood flow (CBF) was transiently decreased in the frontal areas more than others in a standing position. The plasma norepinephrine (NE) level of this patient was normal during supine rest, but when she stood up, failure to increase the plasma level of NE uncovered a sympathetic nervous dysfunction. The CBF abnormality in patients with orthostatic hypotension may be due to a "functional" hemodynamic mechanism that induces orthostatic stress. This patient had transient hypoperfusion in the frontal areas when standing, without organic cerebral arterial stenosis. Only CBF in the frontal areas revealed relative hypoperfusion. These regions might be highly susceptible to a change in blood flow. The causes of orthostatic hypotension of this patient were autonomic failure with a disturbance of the sympathetic nerve endings, which was revealed by ^99mTc-HMPAO brain SPECT and cardiac [¹²³I]MIBG imaging.

Key Words: iodine-123-MIBG • thallium-201 • technetium-99m-HMPAO • postural cerebral hypoperfusion • orthostatic hypotension-