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

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Abstract
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−1 · min−1, PConclusions—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.