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(Hypertension. 2008;52:587.)
© 2008 American Heart Association, Inc.

Original Articles

Transtelephonic Home Blood Pressure to Assess the Monoamine Oxidase-B Inhibitor Rasagiline in Parkinson Disease

William B. White; Phyllis Salzman; Steven R. Schwid for the Parkinson’s Rasagiline: Efficacy and Safety in the Treatment of "Off" Parkinson Study Group

From the Division of Hypertension and Clinical Pharmacology (W.B.W.), Pat and Jim Calhoun Cardiology Center and Clinical Trials Unit, University of Connecticut, Farmington, Conn; Medical Affairs (P.S.), Teva Neuroscience, Inc, Horsham, Pa; and the Department of Neurology (S.R.S.), University of Rochester, Rochester, NY.

Correspondence to William B. White, Division of Hypertension and Clinical Pharmacology, Pat and Jim Calhoun Cardiology Center, University of Connecticut School of Medicine, 263 Farmington Ave, Farmington, CT 06030-3940. E-mail wwhite{at}nso1.uchc.edu

Monoamine oxidase inhibitors are associated with dietary tyramine interactions that can induce hypertensive crises. Rasagiline mesylate is a novel irreversible selective monoamine oxidase type B inhibitor for Parkinson disease that may have a low risk of interaction with dietary tyramine because of its selectivity. To study interactions of rasagiline with diets unrestricted in tyramine-containing foods, we incorporated transtelephonic, self-monitoring of the blood pressure (BP) into a randomized, placebo-controlled trial of rasagiline 0.5 and 1.0 mg daily in 414 levodopa-treated Parkinson patients with motor fluctuations. The proportion of patients with a systolic BP increase of >30 mm Hg was the primary BP end point. In 13 968 self-measured readings at baseline, the proportion of systolic BP values that increased by >30 mm Hg after a meal ranged from 9.5% to 12.9% in the 3 treatment groups. In 25 733 BPs obtained postrandomization, the proportion of values with a >30-mm Hg systolic postprandial increase was 15% in the placebo group, 15% in the rasagiline 0.5-mg group, and 11% in the rasagiline 1-mg group after 3 weeks of double-blind therapy and 13%, 14%, and 12%, respectively, after 26 weeks of treatment (P value was not significant for all of the comparisons among treatment groups). A postprandial increase in systolic BP to >180 mm Hg at any time after randomization was seen in 3.3%, 2.6%, and 2.9% of the placebo, 0.5-mg, and 1.0-mg rasagiline groups, respectively. These data demonstrate that rasagiline did not induce postprandial hypertension in patients with Parkinson disease who were on an unrestricted diet.

Key Words: rasagiline • self-monitored blood pressure • Parkinson disease • tyramine • monoamine oxidase inhibitor