Potter D Dean, Araoz Philip A, Ng Leong L, Kruger David G, Thompson Jess L, Hamner Chad E, Rysavy Joseph A, Mandrekar Jayawant N, Sundt Thoralf M
Division of Cardiovascular Surgery, University of Leicester, Leicester, United Kingdom.
J Surg Res. 2007 Aug;141(2):277-83. doi: 10.1016/j.jss.2006.12.539. Epub 2007 Jun 14.
The pacing model of heart failure produces heterogeneous changes in wall stress and myocyte diameter. The purpose of this study was to measure regional changes in cardiotrophin-1 (CT-1), a cytokine thought to play a role in LV remodeling, and regional changes in LV strain as measured with magnetic resonance imaging.
Dilated cardiomyopathy was induced in nine mongrel dogs over 4 wk by rapid pacing using a right ventricular epicardial lead. Baseline CT-1 was measured from an apical myocardial biopsy, and regional CT-1 was measured from anterior, lateral, inferior, and septal walls after the induction of heart failure and in six control dogs. Tissue tagged images were divided into similar regions and minimal principal strain (MPS), ejection fraction, and ventricular volumes were compared after induction of heart failure.
After induction of heart failure, LV ejection fraction and end-diastolic volume differed significantly from baseline (P < 0.01 and P = 0.02, respectively). Additionally, regional CT-1 and MPS were significantly different (P < 0.01 for both). Cardiotrophin-1 increased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). Minimum principal strain decreased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS).
The pacing model of heart failure produces heterogeneous changes in regional CT-1 and wall motion as measured by MPS. The greatest regional changes are closest to the pacemaker site: the inferior and septal walls. These differences in regional CT-1 may account for previously noted myocyte hypertrophy and preserved ventricular function in these regions.
