Chest ACCP Member Benefits
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text (PDF) Free
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
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 Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by de Zwaan, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by de Zwaan, C.
(Chest. 1995;108:903-911.)
© 1995 American College of Chest Physicians

Changes in Wall Motion in Patients Treated for Unstable Angina

A Suggestion of the Stunned and Hibernating Myocardium in Humans

Chris de Zwaan MD1; Frits W. Bär MD1; Willem R.M. Dassen PhD1; Frank Vermeer MD1; Hein J.J. Wellens MD1; and ;UNASEM Collaborative Study Group

1 From the European Unstable Angina Study using Eminase Group, Academic Hospital Maastricht, University of Limburg, Maastricht, the Netherlands (UNASEM)

Background: A double-blind, placebo-controlled study using anistreplase was performed in 159 patients with unstable angina. All patients had a history of unstable angina combined with typical ECG changes and without evidence of a previous, recent, or ongoing myocardial infarction. The purpose of the present study was to analyze the relationship between the patency of the culprit artery and the behavior of the ischemiarelated regional left ventricular (LV) wall motion.

Methods and results: On entry to the study, all patients received conventional drug therapy: IV nitroglycerin therapy, an oral beta-blocking agent, and a calcium antagonist. Baseline angiography was carried out within 3 h after randomization, a mean of 4.2±3.0 h (range, 1 to 17 h) after the last attack of chest pain. Treatment with trial medication was withheld in 33 cases. Sixty-five patients with coronary artery disease received anistreplase (30 U/5 min)/heparin and 61 patients heparin-only therapy. Angiography was repeated 20.6±4.6 h (mean±SD; range, 12 to 39 h) after the baseline angiographic study. To assess changes in regional myocardial wall motion, the LV wall was divided into seven segments. The ischemiarelated coronary artery stenosis was calculated quantitatively and related to the quantitatively assessed mean regional left ventricular ejection fraction (RLVEF) of the ischemiarelated segments. In 118 of 126 patients who received trial medication, we found that anistreplase/heparin therapy leads to a significantly (p<0.01) greater reduction in coronary artery diameter stenosis than heparin-only therapy (n=63, mean±SD, 11±22, vs n=55, mean±SD, 3±11%). Anistreplase/heparin therapy was related to a larger significant improvement of the ischemia-related RLVEF than heparin-only therapy, although the latter association was not statistically significant (n=63, mean±SD, 7±15, vs n=55, mean±SD 5±14%). The effects of change of coronary artery stenosis on regional LV wall motion were also determined. A paradoxical finding was that a persistently occluded vessel or a vessel showing an increase in coronary artery stenosis was associated with a greater improvement of the ischemia-related RLVEF than a reopened vessel or a vessel with a reduction in coronary artery stenosis (n=15, mean±SD, 7±11, vs n=41, mean±SD, 8±13, vs n=15, mean±SD, 1±12, vs n=47, mean±SD, 5±16%, NS). One day after the last attack of chest pain, the regional LV wall motion was still abnormal in about 20% of patients.

Conclusion: In these patients with unstable angina, the LV wall motion improved both in the treated and the control group at follow-up angiography 1 day later. Improved coronary arterial anatomy was associated with a lesser improvement of the LV contractile function than when worsening of the coronary angiographic appearance occurred. There is no rational explanation of these results. This is a beginning of an effort to elucidate the clinical significance of the stunned and hibernating myocardium in humans.

Key Words: cardiac catheterization • coronary perfusion • myocardial contractility • unstable angina

Submitted on October 28, 1994
Accepted on April 12, 1995




This article has been cited by other articles:


Home page
J Am Coll CardiolHome page
B. L. Gerber, W. Wijns, J.-L. J. Vanoverschelde, G. R. Heyndrickx, B. De Bruyne, J. Bartunek, and J. A. Melin
Myocardial perfusion and oxygen consumption in reperfused noninfarcted dysfunctional myocardium after unstable angina: Direct evidence for myocardial stunning in humans
J. Am. Coll. Cardiol., December 1, 1999; 34(7): 1939 - 1946.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1995 by the American College of Chest Physicians.