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Circulation. 1999;99:1795-1801

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(Circulation. 1999;99:1795-1801.)
© 1999 American Heart Association, Inc.


Clinical Investigation and Reports

Endothelium-Dependent and -Independent Perfusion Reserve and the Effect of L-arginine on Myocardial Perfusion in Patients With Syndrome X

Morten Bøttcher, MD, ; Hans Erik Bøtker, MD, PhD, ; Helle Sonne, MD, ; Torsten Toftegaard Nielsen, MD, ; Johannes Czernin, MD,

From the Department of Cardiology B (M.B., H.E.B., H.S., T.T.N.), and The PET Center (M.B.), Aarhus University Hospital, Aarhus N, Denmark; and Division of Nuclear Medicine (J.C.), Department of Molecular and Medical Pharmacology, UCLA School of Medicine, Los Angeles, Calif.

Correspondence to Morten Bøttcher, MD, Department of Cardiology B, Aarhus University Hospital, DK-8200 Aarhus N, Denmark. E-mail skejmb{at}aau.dk

Background—Impaired vasodilatation capacity in patients with angina pectoris and a normal coronary arteriogram (syndrome X [SX]) has been reported. Most studies report on the response in epicardial vessels. This does not necessarily reflect compromised myocardial microcirculation. Lack of the NO precursor L-arginine has been suggested as a possible cause.

Methods and Results—Myocardial blood flow (MBF) was measured, using PET, at rest (MBF-rest) and during intravenous dipyridamole (MBF-DIP) in 25 women (mean age 53±7 years) with SX. Thirty healthy volunteers served as controls. One group (A) consisted of 15 age-matched female volunteers (54±10 years). The other control group consisted of 15 young healthy women (B; 24±5 years). In 12 SX patients, MBF-rest and MBF during cold pressor testing were also measured after infusion of L-arginine (6.7 g/min for 45 minutes). The increase in MBF after cold pressor testing was similar in the SX group compared with controls. L-arginine did not affect MBF-rest (0.83±0.14 versus 0.89±0.13 mL · g-1 · min-1) or MBF after cold pressor test (0.95±0.10 versus 1.03±0.17 mL · g-1min-1). In contrast, the hyperemic response to DIP was blunted compared with the group A controls (1.68±0.49 versus 2.34±0.45 mL · g-1 · min-1, P<0.05); this resulted in a significant reduction of the coronary flow reserve in SX patients relative to controls (2.03±0.53 versus 2.96±0.63 mL · g-1 · min-1, P<0.01).

Conclusions—In patients with SX, the microcirculatory response to cold, reflecting the endothelium function, is normal and unaltered by intravenous L-arginine. This suggests preserved microcirculatory endothelial function. However, a markedly attenuated hyperemic flow and flow reserve after DIP suggest a dysfunction of the adenosine-mediated endothelium-independent vasodilatation at the microcirculatory level in these patients.


Key Words: blood flow • l-arginine • angina • syndrome X • tomography




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