Document Detail


Direct effects of chronic beta-adrenergic receptor blockade on left ventricular and myocyte function in a model of tachycardia-induced congestive heart failure.
MedLine Citation:
PMID:  8989646     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Chronic beta-receptor blockade (beta-blockade) has been reported to improve symptoms and increase survival in patients with congestive heart failure (CHF); however, whether the mechanisms for the effects of beta-blockade in CHF are due to modulating chronotropy, inotropy, or both remains unknown. To address this issue, left ventricular function and isolated myocyte function were examined with chronic beta-blockade in a rapid pacing model of CHF, thereby eliminating potential chronotropic effects of beta-blockade. METHODS AND RESULTS: Pigs were randomly assigned to three groups of six pigs each: supraventricular tachycardia (SVT): 3 weeks of atrial pacing at 240 beats/min; SVT/beta-blockade: 3 weeks of rapid pacing and beta-blockade (25 mg atenolol twice daily on days 14-21 of pacing); control group, sham control animals. This dosage schedule for beta-blockade was chosen because catecholamines are persistently elevated by day 14 in this model of CHF. Left ventricular fractional shortening and end-diastolic dimension were measured by echocardiography in the conscious state with a resting ambient heart rate. Isolated left ventricular myocyte function was examined using high-speed videomicroscopy. Supraventricular tachycardia caused left ventricular dilation (5.4 +/- 0.1 vs 3.5 +/- 0.1 cm) and reduced fractional shortening (12 +/- 1% vs 35 +/- 1%) compared with control animals (P < .05). The SVT/beta-blockade group showed no significant effects on left ventricular size or function compared with the SVT group, but their ambient resting heart rate was reduced by 20% relative to the SVT group (P < .05). Myocyte shortening was reduced in the SVT group (2.2 +/- 0.1% vs 4.5 +/- 0.1%, P < .05) compared with the control group and increased from SVT-only values with beta-blockade (2.7 +/- 0.1%, P < .05). Similarly, myocyte shortening velocity was similarly reduced in the SVT and SVT/beta-blockade groups (31 +/- 1 and 32 +/- 1 microns/s) compared with the control group (51 +/- 1 microns/s, P < .05). With SVT/beta-blockade myocyte contraction duration was prolonged (525 +/- 5 ms) compared with SVT-only or control values (469 +/- 9 and 473 +/- 4 ms, P < .05). Thus, institution of beta-1-selective blockade during the development of SVT-induced CHF altered the temporal characteristics of the myocyte contraction process, which resulted in improved myocyte shortening. CONCLUSIONS: In a model of CHF due to the maintenance of a chronically elevated heart rate, institution of beta-1-selective blockade during the progression of the CHF process minimally affected left ventricular size and function. At the level of the myocyte, chronic beta-1-receptor blockade prolonged the contraction interval and thereby increased myocyte shortening. These unique results suggest that a contributory mechanism for the effects of beta-blockade in the setting of CHF is chronotropic modulation.
Authors:
F G Spinale; W S Johnson; Y Wang; Z Wang; R Mukherjee; L Hebbar; B U Jones
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of cardiac failure     Volume:  2     ISSN:  1071-9164     ISO Abbreviation:  J. Card. Fail.     Publication Date:  1996 Dec 
Date Detail:
Created Date:  1997-03-25     Completed Date:  1997-03-25     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9442138     Medline TA:  J Card Fail     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  311-8     Citation Subset:  IM    
Affiliation:
Department of Surgery and Anesthesiology, Medical University of South Carolina, Charleston 29425, USA.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Antagonists / administration & dosage,  therapeutic use*
Analysis of Variance
Animals
Atenolol / administration & dosage,  therapeutic use*
Cardiac Pacing, Artificial
Catecholamines / blood
Cell Culture Techniques
Disease Models, Animal
Heart Failure / drug therapy*,  etiology,  physiopathology
Hemodynamics / drug effects,  physiology
Myocardial Contraction / drug effects*,  physiology
Myocardium / cytology
Random Allocation
Reference Values
Swine
Tachycardia, Supraventricular / complications*
Ventricular Function, Left / drug effects*
Grant Support
ID/Acronym/Agency:
HL-45024/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic beta-Antagonists; 0/Catecholamines; 29122-68-7/Atenolol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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