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Tight glycemic control reduces heart inflammation and remodeling during acute myocardial infarction in hyperglycemic

Raffaele Marfella1, Clara Di Filippo, Michele Portoghese

  • 1Department of Geriatrics and Metabolic Diseases, Second University of Naples, Naples, Italy. raffaele.marfella@unina2.it

Journal of the American College of Cardiology
|April 18, 2009
PubMed

Insights

Intensive glycemic control in acute myocardial infarction (AMI) patients reduced oxidative stress, inflammation, and apoptosis. This tight glycemic control may improve post-infarction heart remodeling.

Area of Science:

  • Cardiology
  • Metabolic Research
  • Molecular Biology

Background:

  • Mechanisms of tight glycemic control in acute myocardial infarction (AMI) heart remodeling remain unclear.
  • Hyperglycemia exacerbates post-infarction cardiac dysfunction and molecular damage.

Purpose of the Study:

  • To investigate the molecular mechanisms of tight glycemic control in human hearts during post-infarction remodeling.
  • To compare the effects of intensive glycemic control (IGC) versus conventional glycemic control (CGC) on cardiac molecular markers.

Main Methods:

  • Eighty-eight patients with first AMI undergoing coronary bypass surgery were studied.
  • Patients were categorized into normoglycemic, IGC (80-140 mg/dl), and CGC (180-200 mg/dl) groups.
  • Analysis included echocardiography, oxidative stress markers (nitrotyrosine, superoxide anion, iNOS), inflammation (NFkappaB, TNF-alpha), and apoptosis (caspase-3) in peri-infarcted myocardial tissue.

Main Results:

  • Hyperglycemic patients exhibited higher myocardial performance index (MPI), reduced ejection fraction, and increased oxidative stress, inflammation, and apoptosis markers compared to normoglycemic controls.
  • IGC led to greater plasma glucose reduction than CGC.
  • CGC patients showed higher MPI, lower ejection fraction, and more markers of oxidative stress, inflammation, and apoptosis than IGC patients.

Conclusions:

  • Tight glycemic control in AMI patients significantly reduces myocardial oxidative stress and inflammation.
  • These reductions may lead to decreased apoptosis in peri-infarcted areas, potentially improving post-infarction heart remodeling.
Abstract

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