Document Detail

Continued depression of maximal oxygen consumption and mitochondrial proteomic expression despite successful coronary artery bypass grafting in a swine model of hibernation.
MedLine Citation:
PMID:  21168030     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Clinical studies indicate incomplete functional recovery of hibernating myocardium after coronary artery bypass grafting. We hypothesized that persistent contractile abnormalities after coronary artery bypass grafting are associated with decreased mitochondrial proteins involving electron transport chain that might limit maximal oxygen consumption.
METHODS: Seven pigs with hibernating myocardium underwent off-pump revascularization with left internal thoracic artery to mid left anterior descending artery. At 4 weeks, left internal thoracic artery anastomosis was patent by multidetector computed tomography. Regional function (transthoracic echocardiography) and blood flow (microspheres) were assessed at rest and during high-dose dobutamine (40 μg/[kg · min]). Expression of electron transport chain proteins was analyzed with isobaric tags for relative and absolute quantification.
RESULTS: After revascularization, multidetector computed tomography confirmed severe left anterior descending stenosis and patent left internal thoracic artery graft. Regional function and blood flow normalized at rest; however, function in left anterior descending distribution remained depressed relative to remote regions, and myocardial blood flow in that region did not increase normally when challenged with high-work state. Concomitant with reduced maximal blood flow response in left anterior descending region was more than 40% reduction in electron transport chain proteins essential to adenosine triphosphate production.
CONCLUSIONS: Despite successful revascularization of hibernating myocardium, regional function and blood flow remained depressed during catecholamine stress. Electron transport chain proteins known to be downregulated during adaptive process within hibernating myocardium did not normalize after revascularization. These data demonstrate a potential bioenergetic cause of persistent dysfunction and heart failure within successfully revascularized hibernating myocardium.
Rosemary F Kelly; Jesús A Cabrera; Elizabeth A Ziemba; Melanie Crampton; Lorraine B Anderson; Edward O McFalls; Herbert B Ward
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  141     ISSN:  1097-685X     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-20     Completed Date:  2011-01-13     Revised Date:  2011-10-24    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  261-8     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2011 The American Association for Thoracic Surgery. All rights reserved.
Department of Surgery, University of Minnesota, Minneapolis, Minn 55417, USA.
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MeSH Terms
Adrenergic beta-1 Receptor Agonists / administration & dosage
Blood Flow Velocity
Coronary Angiography / methods
Coronary Artery Bypass*
Coronary Circulation
Disease Models, Animal
Dobutamine / administration & dosage
Electron Transport Chain Complex Proteins / metabolism*
Mitochondria, Heart / metabolism*
Mitochondrial Proteins / metabolism*
Myocardial Stunning / diagnosis,  metabolism,  physiopathology,  surgery*
Myocardium / metabolism*,  pathology
Oxygen Consumption*
Proteomics / methods
Tomography, X-Ray Computed
Vascular Patency
Ventricular Function, Left
Grant Support
R01 HL089307-01A2/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Adrenergic beta-1 Receptor Agonists; 0/Electron Transport Chain Complex Proteins; 0/Mitochondrial Proteins; 34368-04-2/Dobutamine
Comment In:
J Thorac Cardiovasc Surg. 2011 Oct;142(4):954; author reply 954-5   [PMID:  21924152 ]

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

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