Document Detail


Mechanism of myocardial ischemia with an anomalous left coronary artery from the right sinus of Valsalva.
MedLine Citation:
PMID:  22564915     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: An ectopic coronary artery that courses between the aortic root and the pulmonary trunk may lead to sudden cardiac death, especially in athletes. It has been speculated that during exercise, compression of the coronary artery between the great vessels may impair coronary blood flow and produce myocardial ischemia and fatal arrhythmia. However, this hypothesis cannot be tested in humans, and little experimental data exist to explain this phenomenon. To this end, in a calf with an anomalous left coronary artery that coursed from the right sinus of Valsalva between the great vessels, we assessed for myocardial ischemia during pharmacologically induced tachycardia and hypertension.
METHODS: We identified a juvenile male calf (103 kg) with an anomalous left coronary artery from the right sinus of Valsalva that coursed between the great vessels. Via thoracotomy, the animal was instrumented for hemodynamic measurements. Intravenous dobutamine increased heart rate and myocardial metabolic demands. Intravenous phenylephrine produced arterial hypertension and increased myocardial metabolic demands. Fluorescent-labeled microspheres were used to map regional myocardial blood flow, and hemodynamics were recorded during each condition. Masson's trichrome staining for fibrosis, wheat-germ agglutinin staining for myocyte size, terminal deoxynucleotidyl transferase dUTP nick end-label staining for apoptosis, and isolectin-B4 staining for capillary density were performed.
RESULTS: For the first time, empiric data documented that an ectopic coronary artery produced myocardial ischemia during elevated myocardial metabolic demands. Left coronary artery resistance increased in a cardiac cycle-dependent pattern that was consistent with systolic compression between the great vessels. Increased cardiac fibrosis, myocyte hypertrophy, cardiac apoptosis, and capillary density indicated that regional ischemic, inflammatory-mediated myocardial remodeling was present.
CONCLUSIONS: These findings confirm the proposed mechanism of sudden death and support early surgical repair of coronary arteries that course between the aortic root and the pulmonary trunk.
Authors:
Carlo R Bartoli; William B Wead; Guruprasad A Giridharan; Sumanth D Prabhu; Steven C Koenig; Robert D Dowling
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-05-05
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  144     ISSN:  1097-685X     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-07-20     Completed Date:  2012-11-29     Revised Date:  2013-01-03    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  402-8     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2012 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.
Affiliation:
Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY 40202, USA. crbart02@louisville.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cattle
Coronary Vessel Anomalies / physiopathology*
Hemodynamics
Male
Myocardial Ischemia / chemically induced,  physiopathology*
Regional Blood Flow
Sinus of Valsalva
Comments/Corrections
Comment In:
J Thorac Cardiovasc Surg. 2012 Dec;144(6):1531; author reply 1531-3   [PMID:  23140967 ]

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


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