in heart failure due to myocardial infarction

Objective: Patients surviving large transmural myocardial infarction (MI) are at risk for congestive heart failure with attendant alteration of ventricular geometry and scar remodeling. Altered G and G protein expression may be involved in cardiac remodeling i-2a sa associated with heart failure, however their expression in scar tissue remains unclear. Methods: MI was produced in Sprague-Dawley rats by ligation of the left coronary artery. G and G protein concentration, localization and mRNA abundance were noted in i-2a sa surviving left ventricle remote to the infarct, in border and in scar tissues from 8 week post-MI hearts with moderate heart failure. Results: We observed a 4.5- and 5.0-fold increase in immunoreactive G protein concentration occurs in the border and scar regions vs. i-2a control values, respectively, in 8-week post-MI rat hearts. Similarly, immunoreactive G protein concentration was increased 3.4- and sa 8.2-fold, respectively, in these tissues vs. controls. Double-fluorescence labeling and phenotyping studies revealed that both G and G i-2a sa proteins were localized to myofibroblasts in the infarct scar and to viable myocytes bordering the scar. Northern analysis revealed that the G / GAPDH ratio was increased in both viable and scar regions (1.24- and 1.85-fold respectively) from experimental hearts when i-2a compared to sham-operated control values when compared to noninfarcted left ventricle, the value of this ratio in scar tissue was elevated |1.5 fold. The G / GAPDH ratio was significantly increased (1.28-fold) only in the scar region vs. control. Conclusion: Our results sa indicate a marked increase in the expression of G and G from myofibroblasts of the infarct scar as well as remnant myocytes i-2a sa bordering the scar in 8-week post-MI rat hearts. We suggest that these changes may be associated with ongoing remodeling in the infarct scar in chronic post-MI phase of this experimental model. © 1999 Elsevier Science B.V. All rights reserved.