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CLINICAL STUDY

Plasma asymmetric dimethylarginine and hyperemic myocardial blood flow in young subjects with borderline hypertension or familial hypercholesterolemia

Hannu Päivä, MD^*, Juha Laakso, MSc, Hanna Laine, MD, PhD, Reijo Laaksonen, MD, PhD^*, Juhani Knuuti, MD, PhD and Olli T. Raitakari, MD, PhD^||,*

^* Department of Medicine, University of Tampere, Tampere, Finland
Department of Clinical Pharmacology, University of Helsinki, Helsinki, Finland
Department of Medicine, University of Turku, Turku, Finland
Turku PET Centre, Turku University Central Hospital, Turku, Finland
^|| Department of Clinical Physiology, University of Turku, Turku, Finland

Manuscript received June 20, 2000; revised manuscript received May 20, 2002, accepted June 27, 2002.

^* Reprint requests and correspondence: Dr. Olli T. Raitakari, Turku PET Centre, Turku University Central Hospital, FIN-20520 Turku, Finland.
olli.raitakari{at}utu.fi

OBJECTIVES: The goal of this study was to examine the relationship between plasma asymmetric dimethylarginine (ADMA) level and hyperemic myocardial blood flow (MBF) in subjects with borderline hypertension (BHT) and familial hypercholesterolemia (FH).

BACKGROUND: Asymmetric dimethylarginine is an endogenous competitive inhibitor of nitric oxide synthase that may modulate vascular function.

METHODS: We measured plasma ADMA levels and myocardial flow in 77 young men (mean age 35 ± 5 years), including 47 healthy controls, 16 men with BHT, and 14 men with FH. Basal and dipyridamole-induced myocardial flow was measured using positron emission tomography. Plasma ADMA levels were measured using high-pressure liquid chromatography.

RESULTS: Asymmetric dimethylarginine levels were significantly elevated in the BHT group compared with controls (0.59 ± 0.13 µmol/l vs. 0.43 ± 0.12 µmol/l, p < 0.001), and they had significantly lower dipyridamole flow (2.85 ± 1.20 ml/min/g vs. 3.69 ± 1.68 ml/min/g, p < 0.05). In a multivariate regression model adjusted for the study group, dipyridamole flow was inversely associated with ADMA (p < 0.05), age (p < 0.05), and apolipoprotein B concentration (p < 0.05).

CONCLUSIONS: We conclude that plasma ADMA concentration is related to dipyridamole-induced vasodilatory function in young men, independently of blood pressure elevation and hypercholesterolemia. Subjects with BHT have significantly increased plasma ADMA levels, which may partly explain the impaired hyperemic MBF in this condition.

Abbreviations and Acronyms   ADMA   asymmetric dimethylarginine   BHT   borderline hypertension   BP   blood pressure   FH   familial hypercholesterolemia   HDL   high-density lipoprotein   HPLC   high-performance liquid chromatography   IMT   intima-media thickness   LDL   low-density lipoprotein   LV   left ventricle/ventricular   MBF   myocardial blood flow   NO   nitric oxide   OPA   o-pthalaldehyde   PET   positron emission tomography   ROI   region of interest   SDMA   symmetrical dimethylarginine

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