Teragawa H, Mitsuba N, Nishioka K, Ueda K, Kono S, Higashi Y, Chayama K, Kihara Y. Impaired coronary microvascular endothelial function in men with metabolic syndrome. World J Cardiol 2010; 2(7): 205-210 [PMID: 21160752 DOI: 10.4330/wjc.v2.i7.205]
Corresponding Author of This Article
Hiroki Teragawa, MD, PhD, FACC, FAHA, Department of Cardiovascular Medicine, Hiroshima General Hospital of West Japan Railway Company, 3-1-36 Futabanosato, Higashi-ku, Hiroshima 732-0057, Japan. hteraga@gmail.com
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Brief Article
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Hiroki Teragawa, Department of Cardiovascular Medicine, Hiroshima General Hospital of West Japan Railway Company, 3-1-36, Futabanosato, Higashi-ku, Hiroshima 732-0057, Japan
Naoya Mitsuba, Kenji Nishioka, Kentaro Ueda, Yasuki Kihara, Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan
Shingo Kono, Department of Radiology, Hiroshima University Hospital, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan
Yukihito Higashi, Department of Cardiovascular Physiology and Medicine, Hiroshima University Graduate School of Biomedical Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan
Kazuaki Chayama, Department of Molecular Medicine, Hiroshima University Graduate School of Biomedical Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan
Author contributions: Teragawa H designed the study, collected data and wrote the manuscript; Mitsuba N, Nishioka K, Ueda K and Kono S collected data; Higashi Y performed the evaluation of the study data and revised the manuscript; Chayama K and Kihara Y approved the final version.
Correspondence to: Hiroki Teragawa, MD, PhD, FACC, FAHA, Department of Cardiovascular Medicine, Hiroshima General Hospital of West Japan Railway Company, 3-1-36 Futabanosato, Higashi-ku, Hiroshima 732-0057, Japan. hteraga@gmail.com
Telephone: +81-82-2621170 Fax: +81-82-2621499
Received: May 9, 2010 Revised: June 11, 2010 Accepted: June 18, 2010 Published online: July 26, 2010
Abstract
AIM: To assess coronary endothelial function of conduit and resistance vessels in patients with metabolic syndrome (MS).
METHODS: Seventy-eight men (mean age, 57 years) with chest pain and angiographically normal coronary arteries were included in the study. Patients with coronary spastic angina were excluded. Changes in coronary artery diameter and coronary blood flow (CBF) in response to acetylcholine (ACh) were determined using quantitative coronary angiography and Doppler velocity measurements. Coronary flow reserve was calculated as the ratio of coronary blood velocity after adenosine triphosphate infusion relative to baseline values. Patients were divided into two groups based on the presence or absence of MS.
RESULTS: There were 24 patients in the MS group (31%). The increase in CBF in response to ACh infusion was impaired in the MS group (P < 0.0001) compared to the non-MS group, whereas changes in coronary artery diameter in response to ACh infusion did not differ between the two groups. Multivariate regression analysis revealed that MS was a significant factor associated with the lesser change in CBF induced by ACh infusion at 30 μg/min (P < 0.0001, r2 = 0.46).
CONCLUSION: Coronary endothelial dysfunction was present at the level of resistance vessels but not conduit vessels in the MS patients included in our study.
