| Objective: Peroxisome proliferator activated receptor y (PPAR γ ) has been implicated in several cellular pathways assumed to beneficially affect left ventricular remodeling and heart failure progression. In contrast, population-based studies demonstrate an increased incidence of heart failure in patients treated with PPAR y agonists. Therefore, we examined the effect of pioglitazone, a PPAR γ agonist, on chronic left ventricular remodeling and heart failure after experimental myocardial infarction (MI) in Sprague-Dawley mice. Short-term administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, statins, has been shown to attenuate ischemia-reperfusion injury. However, the effects of long-term administration of statins on left ventricular (LV) remodeling and failure after MI remain unknown. Methods: Mice were treated with placebo or pioglitazone (20 mg kg-1 day-1 by gavage) or atorvastatin (5mg kg-1 day-1 by gavage) or both from 6 hour to week 4 after ligation of the left anterior descending artery. A separate group of rats was randomised to: group sham-operated (SO); group sham-operated plus pioglitazone (SO+P); group sham-operated plus atorvastatin (SO+A); group sham-operated plus atorvastatin and group pioglitazone (SO+P+A); group operated (MI); group operated plus pioglitazone (MI+P); group operated plus atorvastatin (MI+A); group operated plus pioglitazone and atorvastatin(MI+P+A). Mean LV infarct sizes were similar for all groups with MI at 46.3%. Transthoracic echocardiography was performed at weeks 4. Hemodymamic parameters were measured at week 4.Results: Echocardiography showed no difference in left ventricular dilatation in group MI and group MI+P. However, hemodynamic parameters maximum rate of LV pressure rise (+dp/dtmax ) and maximum rate of LV pressure decent (-dp/dtmax) are much higher in group MI+P than mice in group MI(5363 ± 476 vs 4739 ± 621, 4383 ± 543 vs...
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