Role of cardiac sympathetic nerves in preventing orthostatic hypotension in Parkinson's disease.
OBJECTIVE
Cardiac sympathetic denervation is associated with orthostatic hypotension (OH) in Parkinson's disease (PD); however, the physiological role of cardiac sympathetic nerves has yet to be elucidated. To clarify the role of the heart in orthostatic stress, we evaluated whether cardiac sympathetic nerves can alter cardiac activity and systolic blood pressure (BP) in association with elevations or depressions of total peripheral resistance during the head-up tilt test.


METHODS
Ninety-five PD patients and 17 normal controls were enrolled. Using impedance cardiography, we measured total peripheral resistance, stroke volume, heart rate, and systolic BP during the head-up tilt test. Cardiac denervation was defined as a heart-to-mediastinum ratio <1.7 for cardiac (123)I-metaiodobenzylguanidine uptake on delayed images.


RESULTS
At 60° tilt, total peripheral resistance decreased from the initial value in 49 PD patients. Among these, 36 patients exhibited cardiac denervation with severe reductions in systolic BP but little change in stroke volume; among these patients 22 had OH. The remaining 13 patients without cardiac denervation exhibited significant increases in stroke volume and well-preserved systolic BP with no OH. On the other hand, 46 patients had elevations in total peripheral resistance and reduced stroke volume, but little change in systolic BP, regardless of the presence or absence of cardiac denervation. Only one of these patients experienced OH.


CONCLUSIONS
Under orthostatic stress, cardiac sympathetic denervation with failure to increase total peripheral resistance leads to large reductions in systolic BP. However, patients without cardiac denervation exhibited a positive inotropic response against vasodilatation, which may prevent OH.
Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan; Department of Laboratory Medicine, Nagoya University Hospital, Nagoya, Japan.
Tomohiko
T
Nakamura
Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masaaki
M
Hirayama
Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan; Department of Neurology, Chutoen General Medical Center, Shizuoka, Japan.
Takashi
T
Hara
Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
Yasuaki
Y
Mizutani
Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
Junichiro
J
Suzuki
Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
Hirohisa
H
Watanabe
Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan. Electronic address: sobueg@med.nagoya-u.ac.jp.
Gen
G
Sobue
D000368:Aged; D002307:Cardiography, Impedance; D002320:Cardiovascular Physiological Phenomena; D005260:Female; D015637:Gated Blood-Pool Imaging; D006321:Heart / Q000294:innervation*; D006801:Humans; D007024:Hypotension, Orthostatic / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000150:complications* / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000502:physiology*; D018667:Tilt-Table Test; D014655:Vascular Resistance / Q000502:physiology
Cardiac (123)I-metaiodobenzylguanidine scintigraphy; Cardiac denervation; Orthostatic hypotension; Parkinson's disease; Stroke volume; Total peripheral resistance