Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
« Previous Article | Table of Contents | Next Article »
Arteriosclerosis, Thrombosis, and Vascular Biology. 1998;18:294-299

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yokoyama, I.
Right arrow Articles by Omata, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yokoyama, I.
Right arrow Articles by Omata, M.
(Arteriosclerosis, Thrombosis, and Vascular Biology. 1998;18:294-299.)
© 1998 American Heart Association, Inc.

Original Contributions

Altered Myocardial Vasodilatation in Patients With Hypertriglyceridemia in Anatomically Normal Coronary Arteries

Ikuo Yokoyama; Tohru Ohtake; Shin-ichi Momomura; Katsunori Yonekura; Naoshi Kobayakawa; Teruhiko Aoyagi; Seiryo Sugiura; Yasuhito Sasaki; ; Masao Omata

From the Second Department of Internal Medicine (I.Y., S.M., K.Y., N.K., T.A., S.S., M.O.) and the Department of Radiology (T.O., Y.S.), University of Tokyo, Japan.

Abstract—Reduced myocardial vasodilatation (MVD) in hypercholesterolemics without overt coronary stenosis has been reported. However, the status of MVD in hypertriglyceridemics has not yet been clarified. The aim of this study was to investigate whether MVD is impaired in patients with hypertriglyceridemia without overt coronary stenosis. Twenty-three hypertriglyceridemics (10 normocholesterolemic hypertriglyceridemics [HTGs] and 13 mixed combined hyperlipidemics [MCHLs]) and 13 age-matched controls were studied. All patients were proven to have more than one normal coronary artery, as diagnosed by coronary angiography, and those segments that were perfused by anatomically normal coronary arteries were used in the study. Myocardial blood flow (MBF) during dipyridamole (DP) loading and baseline MBF were measured by using positron emission tomography and [13N]ammonia, after which MVD was calculated. Baseline MBF (mL · min-1 · 100 g-1) was comparable among HTG (76.0±26.1), MCHL (77.0±26.1), and controls (80.3±38.5). However, MBF during DP loading was significantly lower in MCHL (159±52.5) than in control subjects (292±166, P<.01), while it was comparable in HTG (202±104) and controls. MVD was significantly reduced in both HTG (2.70±1.09, P<.05) and MCHL (2.07±.70, P<.01) compared with controls (3.73±1.14). MVD in MCHLs tended to be reduced compared with that in HTGs, but the difference was statistically insignificant (P=.08). There was a significant relationship between MVD and both plasma triglycerides (r=-.47, P<.01) and plasma total cholesterol (r=-.55, P<.01). When controls and HTGs were combined, the relationship between MVD and plasma total triglycerides became more prominent (r=-.55, P<.05), and the significant relationship between cholesterol level and MVD disappeared. Multivariate regression analysis has revealed that the triglyceride level (F=5.2, P<.05) was independently related to MVD (r=.69, P<.01). In conclusion, MVD was reduced in hypertriglyceridemics in anatomically normal coronary arteries. Hypertriglyceridemia is an independent factor for this abnormality.


Key Words: hyperlipidemia • hypertriglyceridemia • atherosclerosis • myocardial vasodilatation • PET




This article has been cited by other articles:


Home page
 ANGIOLOGYHome page
M. Saglam, O. Karakaya, I. Barutcu, A. M. Esen, M. Turkmen, R. Kargin, O. Esen, N. Ozdemir, and C. Kaymaz
Identifying Cardiovascular Risk Factors in a Patient Population With Coronary Artery Ectasia
Angiology, January 1, 2008; 58(6): 698 - 703.
[Abstract] [PDF]

Home page
 ANGIOLOGYHome page
A. T. Sezgin, I. Barutcu, N. Sezgin, H. Gullu, A. M. Esen, N. Acikgoz, E. Topal, and R. Ozdemir
Contribution of Plasma Lipid Disturbances to Vascular Endothelial Function in Patients With Slow Coronary Flow
Angiology, January 1, 2007; 57(6): 694 - 701.
[Abstract] [PDF]

Home page
 Eur Heart JHome page
I. Yokoyama, Y. Inoue, T. Moritan, K. Ohtomo, and R. Nagai
Impaired myocardial vasodilatation during hyperaemic stress is improved by simvastatin but not by pravastatin in patients with hypercholesterolaemia
Eur. Heart J., April 2, 2004; 25(8): 671 - 679.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
P. J. Nestel, H. Shige, S. Pomeroy, M. Cehun, and J. Chin-Dusting
Post-prandial remnant lipids impair arterial compliance
J. Am. Coll. Cardiol., June 1, 2001; 37(7): 1929 - 1935.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
J. J. P. Kastelein, J. W. Jukema, A. H. Zwinderman, S. Clee, A. J. van Boven, H. Jansen, T. J. Rabelink, R. J. G. Peters, K. I. Lie, G. Liu, et al.
Lipoprotein Lipase Activity Is Associated With Severity of Angina Pectoris
Circulation, October 3, 2000; 102(14): 1629 - 1633.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
I. Yokoyama, S.-i. Momomura, T. Ohtake, K. Yonekura, W. Yang, N. Kobayakawa, T. Aoyagi, S. Sugiura, N. Yamada, K. Ohtomo, et al.
Improvement of Impaired Myocardial Vasodilatation Due to Diffuse Coronary Atherosclerosis in Hypercholesterolemics After Lipid-Lowering Therapy
Circulation, July 13, 1999; 100(2): 117 - 122.
[Abstract] [Full Text] [PDF]


ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search
Copyright © 1998 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.