Pioglitazone, a peroxisome proliferator-activated receptor-gamma agonist, attenuates left ventricular remodeling and failure after experimental myocardial infarction

Circulation. 2002 Dec 10;106(24):3126-32. doi: 10.1161/01.cir.0000039346.31538.2c.

Abstract

Background: Peroxisome proliferator-activated receptor-gamma activators have recently been implicated as regulators of cellular proliferation and inflammatory response such as cytokine expression. Because proinflammatory cytokines play a critical role in left ventricular (LV) remodeling after myocardial infarction (MI), we examined the effects of pioglitazone treatment in an experimental model of chronic heart failure.

Methods and results: Mice with extensive anterior MI were treated with placebo or pioglitazone (3 mg x kg(-1) x d(-1)) as a dietary supplement for 4 weeks starting 6 hours after surgery. Infarct size and glucose levels were similar among all groups. LV cavity dilatation and dysfunction by echocardiography were significantly attenuated in MI mice given pioglitazone. LV end-diastolic pressure was increased in MI mice and was significantly reduced by pioglitazone treatment. Pioglitazone partially normalized LV dP/dt(max) and dP/dt(min), indices of LV contractile function, which were significantly reduced in MI mice. Improvement of LV function by pioglitazone was accompanied by a decrease in myocyte hypertrophy and interstitial fibrosis and a reduced expression of tumor necrosis factor-alpha, transforming growth factor-beta, and monocyte chemoattractant protein-1 genes in the noninfarcted LV from MI mice. LV inducible nitric oxide synthase and gelatinase B protein levels were increased in MI and were not altered by pioglitazone treatment.

Conclusions: Pioglitazone improved LV remodeling and function in mice with post-MI heart failure. This effect was associated with an attenuated LV expression of inflammatory cytokines and chemokines. Peroxisome proliferator-activated receptor-gamma ligands have promise as preventive and therapeutic agents against heart failure.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Oral
  • Animals
  • Aspartate Aminotransferases / blood
  • Blood Glucose / drug effects
  • Cytokines / genetics
  • Cytokines / metabolism
  • Disease Models, Animal
  • Disease Progression
  • Drug Administration Schedule
  • Echocardiography
  • Gene Expression / drug effects
  • Heart Failure / etiology
  • Heart Failure / prevention & control*
  • Heart Ventricles / drug effects
  • Heart Ventricles / metabolism
  • Heart Ventricles / pathology
  • Hemodynamics / drug effects
  • Male
  • Matrix Metalloproteinase 9 / genetics
  • Matrix Metalloproteinase 9 / metabolism
  • Mice
  • Myocardial Infarction / complications
  • Myocardial Infarction / drug therapy*
  • Myocardial Infarction / pathology
  • Myocardium / metabolism
  • Nitric Oxide Synthase / genetics
  • Nitric Oxide Synthase / metabolism
  • Nitric Oxide Synthase Type II
  • Observer Variation
  • Organ Size / drug effects
  • Pioglitazone
  • RNA, Messenger / metabolism
  • Receptors, Cytoplasmic and Nuclear / agonists*
  • Reproducibility of Results
  • Survival Rate
  • Thiazoles / pharmacology*
  • Thiazolidinediones*
  • Transcription Factors / agonists*
  • Ventricular Dysfunction, Left / etiology
  • Ventricular Dysfunction, Left / prevention & control
  • Ventricular Remodeling / drug effects*

Substances

  • Blood Glucose
  • Cytokines
  • RNA, Messenger
  • Receptors, Cytoplasmic and Nuclear
  • Thiazoles
  • Thiazolidinediones
  • Transcription Factors
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • Aspartate Aminotransferases
  • Matrix Metalloproteinase 9
  • Pioglitazone