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Cardiac Sympathetic Denervation in Parkinson Disease

David S. Goldstein, MD, PhD; Courtney Holmes, CMT; Sheng-Ting Li, MD; Simon Bruce, MD; Leo Verhagen Metman, MD; and Richard O. Cannon III, MD
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Copyright ©2004 by the American College of Physicians


Ann Intern Med. 2000;133(5):338-347. doi:10.7326/0003-4819-133-5-200009050-00009
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Background: In Parkinson disease, orthostatic hypotension can result from L-dopa treatment or from sympathetic neurocirculatory failure. The latter is detected by abnormal blood pressure responses to the Valsalva maneuver and can be associated with loss of functional cardiac sympathetic nerve terminals.

Objective: To determine the frequency of cardiac sympathetic denervation in Parkinson disease, with or without sympathetic neurocirculatory failure, and its association with disease duration, severity, and L-dopa treatment.

Design: Intergroup comparisons in resting patients.

Setting: National Institutes of Health Clinical Center, Bethesda, Maryland.

Patients: 29 patients with Parkinson disease (9 with sympathetic neurocirculatory failure, 10 who had stopped receiving or had never been treated with L-dopa), 24 patients with multiple-system atrophy (17 with sympathetic neurocirculatory failure, 8 receiving L-dopa), 7 patients with pure autonomic failure, 33 controls with episodic or persistent orthostatic intolerance without sympathetic neurocirculatory failure, and 19 normal volunteers.

Measurements: Beat-to-beat blood pressure responses to the Valsalva maneuver, interventricular septal 6-[18F]fluorodopamine–derived radioactivity, cardiac extraction fraction of [3H]norepinephrine, appearance rate of norepinephrine in coronary sinus plasma (cardiac norepinephrine spillover) and venous–arterial differences in levels of dihydroxyphenylglycol (DHPG) and endogenous L-dopa.

Results: Of the 29 patients with Parkinson disease, 9 with sympathetic neurocirculatory failure and 11 without had low septal 6-[18F]fluorodopamine–derived radioactivity (2861 ± 453 Bq/mL per MBq/kg and 5217 ± 525 Bq/mL per MBq/kg, respectively). All 6 patients with Parkinson disease and decreased 6-[18F]fluorodopamine–derived radioactivity who underwent right-heart catheterization had a decreased cardiac extraction fraction of [3H]norepinephrine and virtually no cardiac norepinephrine spillover or venous–arterial increments in plasma levels of DHPG and L-dopa. Sympathetic neurocirculatory failure and decreased 6-[18F]fluorodopamine–derived radioactivity were unrelated to disease duration, disease severity, or L-dopa treatment.

Conclusions: Many patients with Parkinson disease—including all those with sympathetic neurocirculatory failure—have evidence of cardiac sympathetic denervation. This suggests that loss of catecholamine innervation in Parkinson disease occurs in the nigrostriatal system in the brain and in the sympathetic nervous system in the heart.

Figures

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Figure 1.
Heart rate and blood pressure responses to the Valsalva maneuver in a control patient with a history of neurocardiogenic syncope (left) and a patient with Parkinson disease and orthostatic hypotension (right).

Arrows indicate blood pressure near the end of phase II, and the broad line indicates the baseline systolic pressure. The patient with Parkinson disease has a progressive decrease in blood pressure during phase II and absence of an “overshoot” in blood pressure during phase IV.

Grahic Jump Location
Grahic Jump Location
Figure 2.
Individual values for septal myocardial 6-[ 18 F]fluorodopamine–derived radioactivity.

The scanning interval was 5 to 10 minutes after initiation of injection of the imaging agent. The dashed line indicates the mean value in 19 normal volunteers. MSA = multiple-system atrophy; PAF = pure autonomic failure; PD = Parkinson disease; SNF = sympathetic neurocirculatory failure.

Grahic Jump Location
Grahic Jump Location
Figure 3.
Relationships between septal myocardial 6-[ 18 F]fluorodopamine–derived radioactivity and cardiac fractional extraction of [ 3 H]norepinephrine (top) and cardiac norepinephrine spillover (bottom).

White triangles represent patients with Parkinson disease, black diamonds represent patients with multiple-system atrophy, black circles represent patients with pure autonomic failure, and white diamonds represent patients with chronic orthostatic intolerance.

Grahic Jump Location
Grahic Jump Location
Figure 4.
Relationships between septal myocardial 6-[18 F]fluorodopamine–derived radioactivity and the cardiac venous–arterial difference in plasma levels of dihydroxyphenylglycol (DHPG) (top) and the cardiac venous–arterial difference in plasma levels of L-dopa (bottom).

White triangles represent patients with Parkinson disease, black diamonds represent patients with multiple-system atrophy, black circles represent patients with pure autonomic failure, and white diamonds represent patients with chronic orthostatic intolerance.

Grahic Jump Location

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Summary for Patients

The Effect of Parkinson Disease on the Nerves of the Heart

Copyright ©2004 by the American College of Physicians

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