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(Stroke. 2007;38:2228.)
© 2007 American Heart Association, Inc.

Original Contributions

Lower Central Serotonergic Responsivity Is Associated With Preclinical Carotid Artery Atherosclerosis

Matthew F. Muldoon, MD; Rachel H. Mackey, PhD; Kim Sutton-Tyrrell, DrPH; Janine D. Flory, PhD; Bruce G. Pollock, MD, PhD Stephen B. Manuck, PhD

From Center for Clinical Pharmacology (M.F.M.), Department of Medicine, Department of Epidemiology (R.H.M., K.S.-T.), Graduate School of Public Health, and Behavioral Physiology Laboratory (S.B.M.), Department of Psychology, University of Pittsburgh, Pa; Department of Psychiatry (J.D.F.), Mount Sinai School of Medicine, New York, NY; Rotman Research Institute (B.G.P.), University of Toronto, Canada.

Correspondence to Matthew F. Muldoon, MD, Behavioral Physiology Laboratory, 506 OEH, 4015 O’Hara St, University of Pittsburgh, Pittsburgh, PA 15260. E-mail mfm10{at}pitt.edu

Background and Purpose— Central nervous system serotonergic neurotransmission appears to play a role in mood disorders, eating habits, and sleep, and also modulates blood pressure and metabolism. This investigation tested a hypothesized association between central serotonergic functioning and preclinical atherosclerosis.

Methods— Subjects were 244 adults 30 to 55 years of age and free of clinically evident vascular disease (52% men, 84% white). Central serotonergic responsivity was measured as the rise in serum prolactin concentration (area under the curve) over 2.5 hours, adjusted for baseline prolactin, after citalopram administered intravenously at 0.33 mg/kg lean body weight. Carotid artery morphology served as a marker of preclinical atherosclerosis, and carotid artery intima-media thickness and plaque occurrence were determined by B-mode ultrasonography.

Results— In linear regression models including age, gender, race, and citalopram concentration, a 1 SD lower prolactin response was associated with greater maximum intima-media thickness (+0.016 mm; P=0.006) and with greater mean intima-media thickness (+0.009 mm; P=0.03). The odds ratio for carotid artery plaque corresponding to a 1 SD decrease in prolactin response, adjusted for age, race, sex, and citalopram concentration, was 1.47 (95% CI, 0.98 to 2.19; P=0.06). The metabolic syndrome mediated (P<0.01), but did not fully account for, the association between lower prolactin response and greater maximum intima-media thickness.

Conclusions— In this young and relatively healthy sample, blunted prolactin response to citalopram was associated with carotid artery thickening, suggesting that individual differences in central serotonergic responsivity are inversely related to preclinical vascular disease.

Key Words: atherosclerosis • central nervous system • serotonin

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Lower Central Nervous System Serotonergic Function and Risk of Cardiovascular Disease: Where Are We, What’s Next?

Redford B. Williams
Stroke 2007 38: 2213-2214. [Full Text] [PDF]