Document Detail


Right ventricular pacing improves right heart function in experimental pulmonary arterial hypertension: a study in the isolated heart.
MedLine Citation:
PMID:  19734361     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Right heart failure in pulmonary arterial hypertension (PH) is associated with mechanical ventricular dyssynchrony, which leads to impaired right ventricular (RV) function and, by adverse diastolic interaction, to impaired left ventricular (LV) function as well. However, therapies aiming to restore synchrony by pacing are currently not available. In this proof-of-principle study, we determined the acute effects of RV pacing on ventricular dyssynchrony in PH. Chronic PH with right heart failure was induced in rats by injection of monocrotaline (80 mg/kg). To validate for PH-related ventricular dyssynchrony, rats (6 PH, 6 controls) were examined by cardiac magnetic resonance imaging (9.4 T), 23 days after monocrotaline or sham injection. In a second group (10 PH, 4 controls), the effects of RV pacing were studied in detail, using Langendorff-perfused heart preparations. In PH, septum bulging was observed, coinciding with a reversal of the transseptal pressure gradient, as observed in clinical PH. RV pacing improved RV systolic function, compared with unpaced condition (maximal first derivative of RV pressure: +8.5 + or - 1.3%, P < 0.001). In addition, RV pacing markedly decreased the pressure-time integral of the transseptal pressure gradient when RV pressure exceeds LV pressure, an index of adverse diastolic interaction (-24 + or - 9%, P < 0.01), and RV pacing was able to resynchronize time of RV and LV peak pressure (unpaced: 9.8 + or - 1.2 ms vs. paced: 1.7 + or - 2.0 ms, P < 0.001). Finally, RV pacing had no detrimental effects on LV function or coronary perfusion, and no LV preexcitation occurred. Taken together, we demonstrate that, in experimental PH, RV pacing improves RV function and diminishes adverse diastolic interaction. These findings provide a strong rationale for further in vivo explorations.
Authors:
M Louis Handoko; Regis R Lamberts; Everaldo M Redout; Frances S de Man; Christa Boer; Warner S Simonides; Walter J Paulus; Nico Westerhof; Cornelis P Allaart; Anton Vonk-Noordegraaf
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Validation Studies     Date:  2009-09-04
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  297     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2009 Nov 
Date Detail:
Created Date:  2009-10-27     Completed Date:  2009-11-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1752-9     Citation Subset:  IM    
Affiliation:
Department of Physiology, VU University Medical Center, Institute for Cardiovascular Research, Amsterdam, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiac Pacing, Artificial*
Chronic Disease
Disease Models, Animal
Heart Failure / chemically induced,  pathology,  physiopathology,  therapy*
Heart Septum / pathology,  physiopathology
Hypertension, Pulmonary / chemically induced,  complications,  pathology,  physiopathology,  therapy*
Magnetic Resonance Imaging
Male
Monocrotaline
Myocardial Contraction
Perfusion
Rats
Reproducibility of Results
Time Factors
Ventricular Dysfunction, Right / chemically induced,  pathology,  physiopathology,  therapy*
Ventricular Function, Left
Ventricular Function, Right*
Ventricular Pressure
Chemical
Reg. No./Substance:
315-22-0/Monocrotaline

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


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