(Circulation. 2001;103:1497.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Department of Cardiology, Papworth Hospital NHS Trust (S.C.C., P.M.S., A.A.G.), Papworth Everard, UK, and Department of Biochemistry, University of Cambridge (J.C.M., H.L.K.), Cambridge, UK.
Correspondence to James Metcalfe, Department of Biochemistry, University of Cambridge, Downing Site, Tennis Court Rd, Cambridge CB2 1QW, UK. E-mail jcm{at}mole.bio.cam.ac.uk
BackgroundTamoxifen and its analogues act as selective estrogen receptor modulators (SERMs) in women, with estrogen-like activities on some plasma cardiovascular risk factors (eg, lipoproteins). Effects of SERMs on men with coronary artery disease (CAD) have not been reported.
Methods and
ResultsThirty-one men with angiographically
proven CAD were recruited; 16 were treated with tamoxifen (40 mg/d) for
56 days, and 15 were untreated. All the CAD patients were medicated
with aspirin and an HMG-CoA reductase inhibitor for
6
weeks before entering the study. Ten men with angina-like symptoms but
normal coronary arteries by angiography (NCA group) were also
treated with tamoxifen. Blood samples were collected at days -7, 0,
7, 14, 21, 28, and 56 of treatment.
Endothelium-dependent flow-mediated dilatation (ED-FMD)
of the brachial artery was measured by high-resolution ultrasound at 5
visits. Tamoxifen caused an increase in %ED-FMD maximal at 28 days in
the CAD group (2.1±0.3% to 7.5±0.7%;
P<0.0001) and the NCA group
(3.8±0.4% to 7.9±1.0%;
P<0.0001), with no significant
change in the untreated group. Tamoxifen also caused decreases in
several plasma cardiovascular risk factors, including
total cholesterol, triglycerides,
lipoprotein(a), and fibrinogen. Except for the triglyceride
response, these effects were similar to those reported for
postmenopausal women treated with
tamoxifen.
ConclusionsTamoxifen substantially increased ED-FMD in men with CAD who were taking conventional medication. Together with the effects on risk factors, the data strongly support clinical evaluation of SERMs for the treatment of men with CAD.
Key Words: atherosclerosis endothelium hormones lipids vasodilation
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