© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Syndrome X and endothelial dysfunction
aDepartment of Cardiology, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN, UK
bDepartment of Pharmacology, Therapeutics and Toxicology, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN, UK
cDepartment of Medical Statistics and Computing, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN, UK
* Corresponding author. Tel.: +44-1222-744-430; Fax: +44-1222-743-500; E-mail: simonsw@cf.ac.uk
Objective: Syndrome X (angina, normal coronary arteriogram and positive exercise test) remains an enigma with unexplained features and apparent conflicts of evidence. The present study addressed whether (i) the Syndrome is characterised by generalised flow-related endothelial dysfunction, (ii) myocardial thallium201 defects reflect myocardial or microvascular dysfunction, (iii) endothelial dysfunction and its consequences can be improved by oral L-arginine. Methods: Flow-mediated brachial artery dilatation was measured by ultrasonic ‘wall-tracking’ in 7 Syndrome X patients, further characterised as having thallium201 defects and no known cause of endothelial dysfunction, and a normal control group. Syndrome X patients entered a 4-week randomised double-blind placebo-controlled cross-over trial of oral L-arginine (7 g twice daily), with brachial artery studies, exercise tests and technetium99 tetrafosmin scans. Results: Flow-mediated dilatation was absent in Syndrome X vs. normal. Stress technetium99 tetrafosmin and thallium201 scans showed similar defects. Flow-mediated dilatation, symptom-limited exercise duration and peak oxygen consumption (VO2 max) were increased but rate-pressure-product (RPP) and radionuclide defects were unchanged after L-arginine vs. placebo. Conclusions: The study supports coronary microvascular rather than myocardial dysfunction and shows loss of flow-mediated dilatation in systemic arteries. Oral L-arginine improved flow-mediated dilatation, exercise capacity and VO2 max (by ca. 17%) despite unchanged RPP. The findings support generalised endothelial dysfunction. The arginine effects imply NO-mediated improvement of skeletal muscle perfusion suggesting improved homogeneity of microvascular distribution.
KEYWORDS Blood flow; Coronary circulation; Endothelial function; Microcirculation; Nitric oxide; Syndrome
1 Responsible for statistical assistance.
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