Document Detail

Differential modulation of right ventricular strain and right atrial mechanics in mild vs. severe pressure overload.
MedLine Citation:
PMID:  21926343     Owner:  NLM     Status:  MEDLINE    
Increased right atrial (RA) and ventricular (RV) chamber volumes are a late maladaptive response to chronic pulmonary hypertension. The purpose of the current investigation was to characterize the early compensatory changes that occur in the right heart during chronic RV pressure overload before the development of chamber dilation. Magnetic resonance imaging with radiofrequency tissue tagging was performed on dogs at baseline and after 10 wk of pulmonary artery banding to yield either mild RV pressure overload (36% rise in RV pressure; n = 5) or severe overload (250% rise in RV pressure; n = 4). The RV free wall was divided into three segments within a midventricular plane, and circumferential myocardial strain was calculated for each segment, the septum, and the left ventricle. Chamber volumes were calculated from stacked MRI images, and RA mechanics were characterized by calculating the RA reservoir, conduit, and pump contribution to RV filling. With mild RV overload, there were no changes in RV strain or RA function. With severe RV overload, RV circumferential strain diminished by 62% anterior (P = 0.04), 42% inferior (P = 0.03), and 50% in the septum (P = 0.02), with no change in the left ventricle (P = 0.12). RV filling became more dependent on RA conduit function, which increased from 30 ± 9 to 43 ± 13% (P = 0.01), than on RA reservoir function, which decreased from 47 ± 6 to 33 ± 4% (P = 0.04), with no change in RA pump function (P = 0.94). RA and RV volumes and RV ejection fraction were unchanged from baseline during either mild (P > 0.10) or severe RV pressure overload (P > 0.53). In response to severe RV pressure overload, RV myocardial strain is segmentally diminished and RV filling becomes more dependent on RA conduit rather than reservoir function. These compensatory mechanisms of the right heart occur early in chronic RV pressure overload before chamber dilation develops.
Rochus K Voeller; Abdulhameed Aziz; Hersh S Maniar; Nneka N Ufere; Ajay K Taggar; Noel J Bernabe; Brian P Cupps; Marc R Moon
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-09-16
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  301     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2011-12-06     Completed Date:  2012-01-23     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H2362-71     Citation Subset:  IM    
Division of Cardiothoracic Surgery, Washington University School of Medicine, Saint Louis, Missouri, USA.
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MeSH Terms
Adaptation, Physiological
Atrial Function, Right*
Blood Pressure
Disease Models, Animal
Hypertension, Pulmonary / complications*,  physiopathology
Hypertrophy, Right Ventricular / etiology,  physiopathology
Magnetic Resonance Imaging
Pulmonary Artery / physiopathology,  surgery
Severity of Illness Index
Stress, Mechanical
Stroke Volume
Time Factors
Ventricular Dysfunction, Right / etiology*,  physiopathology
Ventricular Function, Right*
Ventricular Pressure*
Grant Support

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

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