TY - JOUR
T1 - Aldosterone inhibition and coronary endothelial function in women without obstructive coronary artery disease
T2 - An ancillary study of the National Heart, Lung, and Blood Institute-sponsored Women's Ischemia Syndrome Evaluation
AU - Bavry, Anthony A.
AU - Handberg, Eileen M.
AU - Huo, Tianyao
AU - Lerman, Amir
AU - Quyyumi, Arshed A.
AU - Shufelt, Chrisandra
AU - Sharaf, Barry
AU - Merz, C. Noel Bairey
AU - Cooper-Dehoff, Rhonda M.
AU - Sopko, George
AU - Pepine, Carl J.
N1 - Funding Information:
Eplerenone and matching placebo were provided by Pfizer. The Women's Ischemia Syndrome Evaluation (WISE) study was supported by contracts from the National Heart, Lung, and Blood Institute, numbers N01-HV-68161, N01-HV-68162, N01-HV-68163, and N01-HV-68164; grants U0164829 , U01 HL649141 , U01 HL649241 , T32HL69751 , and 1R03AG032631 from the National Institute on Aging ; General Clinical Research Center (GCRC) grant MO1-RR00425 from the National Center for Research Resources ; and grants from the Gustavus and Louis Pfeiffer Research Foundation, Danville, NJ; The Women's Guild of Cedars-Sinai Medical Center, Los Angeles, CA; The Ladies Hospital Aid Society of Western Pennsylvania, Pittsburgh, PA; QMED, Inc, Laurence Harbor, NJ; the Edythe L. Broad Women's Heart Research Fellowship, Cedars-Sinai Medical Center, Los Angeles, CA; the Barbra Streisand Women's Cardiovascular Research and Education Program, Cedars-Sinai Medical Center, Los Angeles; and The Society for Women's Health Research, Washington, DC. C.J.P. receives support from the National Institutes of Health/National Center for Advancing Translational Sciences Clinical and Translational Science Award to the University of Florida (UL1 TR000064).
PY - 2014/6
Y1 - 2014/6
N2 - Background Endothelial dysfunction is highly prevalent and associated with adverse outcomes among patients without obstructive coronary artery disease (CAD). Angiotensin II inhibition may improve endothelial function, but with continued treatment, "aldosterone escape" may occur. Thus, it is unknown if adding aldosterone blockade further improves endothelial function. Methods In a double-blind, parallel-group, repeated-measures study, women with symptoms and signs of ischemia, no significant CAD, and coronary endothelial dysfunction receiving an angiotensin-converting enzyme inhibitor or receptor blocker were randomized to aldosterone blockade or placebo. The primary outcome at 16 weeks was percent change in coronary diameter to acetylcholine, and secondary outcome, coronary flow reserve to adenosine, both adjusted for baseline reactivity. Results Forty-one women completed the treatment period with repeat coronary reactivity testing. Their mean age was 54 ± 10 years; body mass index, 30 ± 7.4 kg/m2; 12% had diabetes; and 15% had metabolic syndrome. There were no significant differences between treatment groups. At baseline, the percent change in reference vessel coronary diameter to acetylcholine was -5.0% in the aldosterone blockade group and -3.4% in the placebo group and, at 16 weeks, -7.2% in the aldosterone blockade group versus -14.3% in the placebo group (P =.15). At 16 weeks, the change in coronary flow reserve to intracoronary adenosine was -0.13 in the aldosterone blockade group versus -0.25 in the placebo group (P =.66). Conclusion Adding aldosterone receptor blockade to angiotensin II inhibition did not improve coronary endothelial or microvascular function among women with signs and symptoms of ischemia in the setting of nonobstructive CAD.
AB - Background Endothelial dysfunction is highly prevalent and associated with adverse outcomes among patients without obstructive coronary artery disease (CAD). Angiotensin II inhibition may improve endothelial function, but with continued treatment, "aldosterone escape" may occur. Thus, it is unknown if adding aldosterone blockade further improves endothelial function. Methods In a double-blind, parallel-group, repeated-measures study, women with symptoms and signs of ischemia, no significant CAD, and coronary endothelial dysfunction receiving an angiotensin-converting enzyme inhibitor or receptor blocker were randomized to aldosterone blockade or placebo. The primary outcome at 16 weeks was percent change in coronary diameter to acetylcholine, and secondary outcome, coronary flow reserve to adenosine, both adjusted for baseline reactivity. Results Forty-one women completed the treatment period with repeat coronary reactivity testing. Their mean age was 54 ± 10 years; body mass index, 30 ± 7.4 kg/m2; 12% had diabetes; and 15% had metabolic syndrome. There were no significant differences between treatment groups. At baseline, the percent change in reference vessel coronary diameter to acetylcholine was -5.0% in the aldosterone blockade group and -3.4% in the placebo group and, at 16 weeks, -7.2% in the aldosterone blockade group versus -14.3% in the placebo group (P =.15). At 16 weeks, the change in coronary flow reserve to intracoronary adenosine was -0.13 in the aldosterone blockade group versus -0.25 in the placebo group (P =.66). Conclusion Adding aldosterone receptor blockade to angiotensin II inhibition did not improve coronary endothelial or microvascular function among women with signs and symptoms of ischemia in the setting of nonobstructive CAD.
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U2 - 10.1016/j.ahj.2014.01.017
DO - 10.1016/j.ahj.2014.01.017
M3 - Article
C2 - 24890531
AN - SCOPUS:84901777950
SN - 0002-8703
VL - 167
SP - 826
EP - 832
JO - American heart journal
JF - American heart journal
IS - 6
ER -