Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1999;100:729-735

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
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 Kim, M. H.
Right arrow Articles by Starling, M. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kim, M. H.
Right arrow Articles by Starling, M. R.
Related Collections
Right arrow Cardiovascular Pharmacology
Right arrow Myocardial cardiomyopathy disease
Right arrow Coronary imaging: angiography/ultrasound/Doppler/CC

(Circulation. 1999;100:729-735.)
© 1999 American Heart Association, Inc.


Clinical Investigation and Reports

Effects of ß-Adrenergic Blocking Therapy on Left Ventricular Diastolic Relaxation Properties in Patients With Dilated Cardiomyopathy

Michael H. Kim, MD; William H. Devlin, MD; Sunil K. Das, MD; Janet Petrusha, RN; Daniel Montgomery, BS; Mark R. Starling, MD

From the University of Michigan and Veterans Affairs Medical Centers, Ann Arbor.

Background—The hemodynamic mechanism for the improvement in left ventricle (LV) end-diastolic pressure in cardiomyopathy patients treated with ß-adrenergic blocking agents is controversial. We hypothesized that the salutary effect of this kind of therapy on LV end-diastolic pressure would be indicative of an improvement in late, passive diastolic relaxation properties.

Methods and Results—We studied 14 cardiomyopathy patients in normal sinus rhythm with no arteriographic evidence of coronary artery disease and an LV ejection fraction of <=40% by radionuclide angiography both before and after 6 months of metoprolol therapy with simultaneous micromanometry and biplane cineventriculography. Four comparable patients who were not treated with metoprolol were studied in a similar fashion and served as control subjects. In those receiving metoprolol, LV end-diastolic pressure decreased (P=0.001). The isovolumic relaxation index, {tau}ln, shortened (P=0.03). In a similar fashion, the LV chamber stiffness constant, {kappa}, decreased (P=0.02), LV volume elastance improved (P=0.04), and the myocardial stiffness constant, {kappa}e, decreased (P=0.02). A multiple regression analysis revealed that the decrease in LV end-diastolic pressure was indicative of significant improvements in {tau}ln and {kappa}e with the relationship: LV end-diastolic pressure=-4.73+0.27 {tau}ln+0.54 {kappa}e (r=0.81, P<0.0001). These LV diastolic relaxation properties did not change or worsened in the control cardiomyopathy patients.

Conclusions—We conclude that the decrease in LV end-diastolic pressure in cardiomyopathy patients treated with metoprolol is an indicator of improvement in LV diastolic properties resulting from more complete myocardial relaxation.


Key Words: ventricles • cardiomyopathy • diastole • receptors, adrenergic, beta




This article has been cited by other articles:


Home page
EuropaceHome page
M. A. Perhonen, P. Haapalahti, S. Kivisto, A.-M. Hekkala, H. Vaananen, H. Swan, and L. Toivonen
Effect of physical training on ventricular repolarization in type 1 long QT syndrome: a pilot study in asymptomatic carriers of the G589D KCNQ1 mutation
Europace, October 1, 2006; 8(10): 894 - 898.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
M. A Movsesian
Altered cAMP-mediated signalling and its role in the pathogenesis of dilated cardiomyopathy
Cardiovasc Res, June 1, 2004; 62(3): 450 - 459.
[Abstract] [Full Text] [PDF]


Home page
Br J AnaesthHome page
M. Zaugg, M. C. Schaub, T. Pasch, and D. R. Spahn
Modulation of {beta}-adrenergic receptor subtype activities in perioperative medicine: mechanisms and sites of action
Br. J. Anaesth., January 1, 2002; 88(1): 101 - 123.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
M. Iwata, T. Yoshikawa, A. Baba, T. Anzai, I. Nakamura, Y. Wainai, T. Takahashi, and S. Ogawa
Autoimmunity Against the Second Extracellular Loop of {beta}1-Adrenergic Receptors Induces {beta}-Adrenergic Receptor Desensitization and Myocardial Hypertrophy In Vivo
Circ. Res., March 30, 2001; 88(6): 578 - 586.
[Abstract] [Full Text] [PDF]