Time course of right ventricular remodeling in rats with experimental myocardial infarction

1  Department of Internal Medicine, 97080 Würzburg; and 2  Department of Biophysics Experimentelle Physik, University of Würzburg, 97074 Würzburg, Germany Right ventricular (RV) weight increases dependent on time after myocardial infarction (MI) and on MI size. The sequential changes in RV volume an...

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Bibliographic Details
Published in:American journal of physiology. Heart and circulatory physiology 2003-01, Vol.284 (1), p.H241-H248
Main Authors: Nahrendorf, Matthias, Hu, Kai, Fraccarollo, Daniela, Hiller, Karl-Heinz, Haase, Axel, Bauer, Wolfgang R, Ertl, Georg
Format: Article
Language:English
Subjects:
Animals
Biomarkers - analysis
Body Weight
Cardiomegaly - metabolism
Hemodynamics
Magnetic Resonance Imaging
Male
Myocardial Infarction - complications
Myocardial Infarction - diagnosis
Myocardial Infarction - physiopathology
Myocardium - pathology
Organ Size
Rats
Time Factors
Ventricular Dysfunction, Left - etiology
Ventricular Function, Right
Ventricular Remodeling
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Summary:1  Department of Internal Medicine, 97080 Würzburg; and 2  Department of Biophysics Experimentelle Physik, University of Würzburg, 97074 Würzburg, Germany Right ventricular (RV) weight increases dependent on time after myocardial infarction (MI) and on MI size. The sequential changes in RV volume and hemodynamics and their relations to left ventricular (LV) remodeling after MI are unknown. We therefore examined the time course of RV remodeling in rats with LV MI. MI was produced by left coronary artery ligation. Four, eight, and sixteen weeks later, LV and RV hemodynamic measurements were performed and pressure-volume curves were obtained. For serial measurement of RV volumes and performance, cine-MRI was performed 2 and 8 wk after MI. The ratios of -myosin heavy chain (MHC) to -MHC and skeletal to cardiac -actin were determined for the RV and LV after large MI or sham operation. RV weight increased in rats with MI, as did RV volume. RV pressure-volume curves were shifted toward larger volumes 16 wk after large MI. RV systolic pressure increased gradually over time; however, the gain in RV weight was always in excess of RV systolic pressure. The ratios of skeletal to cardiac -actin and -MHC to -MHC were increased after MI in both ventricles in a similar fashion. Because RV wall stress was not increased after infarction, mechanical factors may not conclusively explain hypertrophy, which maintained balanced loading conditions for the RV even after large LV infarction. rat heart; magnetic resonance imaging
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.00537.2002