Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1997;95:2607-2609

This Article
Right arrow Full Text
Right arrow Alert me when this article is cited
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 arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Oosterga, M.
Right arrow Articles by van Gilst, W. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Oosterga, M.
Right arrow Articles by van Gilst, W. H.

(Circulation. 1997;95:2607-2609.)
© 1997 American Heart Association, Inc.


Articles

Plasma Angiotensin-Converting Enzyme Activity and Left Ventricular Dilation After Myocardial Infarction

Margreeth Oosterga, MD; Adriaan A. Voors, MD; Pieter-Jan de Kam, MSc; Heribert Schunkert, MD; Yigal M. Pinto, MD, PhD; J. Herre Kingma, MD, PhD; Wiek H. van Gilst, PhD

From the Department of Clinical Pharmacology (M.O., A.A.V., Y.M.P., W.H. van G.), University of Groningen, the Netherlands; Department of Cardiology (M.O., A.A.V., P.-J. de K., Y.M.P., W.H. van G.), University Hospital Groningen, the Netherlands; Department of Cardiology (A.A.V., J.H.K.), St Antonius Hospital Nieuwegein, the Netherlands; and Department of Cardiology (H.S.), University Hospital Regensburg, Germany.

Correspondence to Margreeth Oosterga, MD, Department of Clinical Pharmacology, University of Groningen, A. Deusinglaan 1, 9713 AV Groningen, Netherlands.

Background Left ventricular dilation after acute myocardial infarction (MI) is mainly determined by infarct size. In addition, this detrimental structural adaptation seems to be augmented in patients with the ACE DD genotype. The ACE DD genotype is associated with increased ACE activity. The aim of the present study was to evaluate whether ACE activity per se may carry prognostic significance for subsequent left ventricular dilation as assessed by echocardiography during 1-year follow-up after acute MI.

Methods and Results Left ventricular end-systolic and end-diastolic volume indexes were assessed by two-dimensional echocardiography. In 102 consecutive patients, plasma ACE activity was determined 3.7±0.1 hours after the onset of MI. In 64 of these patients, left ventricular volume indexes obtained at baseline and 1 year after MI were used for the present analysis. Patients were divided into a group having low ACE activity (<=12 IU/L, n=15) and a group having high ACE activity (>12 IU/L, n=49). Infarct size was a significant predictor of the increase in left ventricular volume indexes (P=.0001) in these patients. Multivariate regression analysis, after correction for infarct size, demonstrated that elevated plasma ACE activity is a significant predictor of the increase in left ventricular end-diastolic and end-systolic volume indexes (P=.0006 and P=.02, respectively) 1 year after MI.

Conclusions Elevated plasma ACE activity determined soon after the onset of MI may be a significant predictor of the development of left ventricular dilation and may identify patients at risk.


Key Words: myocardial infarction • angiotensin • enzymes • remodeling • genes




This article has been cited by other articles:


Home page
Circ. Res.Home page
I. Fleming
Signaling by the Angiotensin-Converting Enzyme
Circ. Res., April 14, 2006; 98(7): 887 - 896.
[Abstract] [Full Text] [PDF]


Home page
Mol. Pharmacol.Home page
K. Kohlstedt, R. Kellner, R. Busse, and I. Fleming
Signaling via the Angiotensin-Converting Enzyme Results in the Phosphorylation of the Nonmuscle Myosin Heavy Chain IIA
Mol. Pharmacol., January 1, 2006; 69(1): 19 - 26.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
K. Kohlstedt, F. Shoghi, W. Muller-Esterl, R. Busse, and I. Fleming
CK2 Phosphorylates the Angiotensin-Converting Enzyme and Regulates Its Retention in the Endothelial Cell Plasma Membrane
Circ. Res., October 18, 2002; 91(8): 749 - 756.
[Abstract] [Full Text] [PDF]


Home page
Eur Heart JHome page
H. Montgomery, S. Humphries, and S. Danilov
Is genotype or phenotype the better tool for investigating the role of ACE in human cardiovascular disease?
Eur. Heart J., July 2, 2002; 23(14): 1083 - 1086.
[Full Text] [PDF]


Home page
Eur Heart JHome page
A Jeron, C Hengstenberg, S Engel, H Lowel, G.A.J Riegger, H Schunkert, and S Holmer
The D-allele of the ACE polymorphism is related to increased QT dispersion in 609 patients after myocardial infarction
Eur. Heart J., April 2, 2001; 22(8): 663 - 668.
[Abstract] [PDF]


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
B. Agerholm-Larsen, B. G. Nordestgaard, and A. Tybjarg-Hansen
ACE Gene Polymorphism in Cardiovascular Disease : Meta-Analyses of Small and Large Studies in Whites
Arterioscler. Thromb. Vasc. Biol., February 1, 2000; 20(2): 484 - 492.
[Abstract] [Full Text] [PDF]