Infarct-related artery occlusion, tissue markers of ischaemia, and increased apoptosis in the peri-infarct viable...

Area of Science:

• Cardiovascular Science
• Pathology
• Molecular Biology

Background:

• Unfavorable cardiac remodeling post-acute myocardial infarction (AMI) is linked to cardiomyocyte apoptosis.
• The role of ongoing or recurrent ischemia in promoting apoptosis within peri-infarct viable myocardium remains unclear.

Purpose of the Study:

• To investigate the association between infarct-related artery (IRA) occlusion, myocardial ischemia, and cardiomyocyte apoptosis in patients deceased after AMI.
• To determine if ischemia in peri-infarct viable myocardium is an independent factor for increased apoptosis.

Main Methods:

• Autopsy study of 30 patients deceased 7-120 days post-AMI and 5 controls.
• Apoptosis assessed by TUNEL and activated caspase-3 co-expression in cardiomyocytes.
• Ischemia markers (hypoxia-inducible factor-1, cyclo-oxygenase-2) evaluated in peri-infarct myocardium.

Main Results:

• Ischemia evidence was significantly more frequent in IRA occlusion cases (53%) compared to patent IRA (15%) or controls (0%).
• IRA occlusion combined with ischemia identified significantly higher apoptotic rates (12.2%) in peri-infarct myocardium.
• IRA occlusion without ischemia showed lower apoptotic rates, not significantly different from patent IRA cases.

Conclusions:

• Ischemia is prevalent in peri-infarct viable myocardium in over 50% of late post-AMI deaths with IRA occlusion.
• Myocardial ischemia in this setting is strongly associated with increased cardiomyocyte apoptosis.
• Therapeutic strategies aimed at relieving ischemia post-AMI may be beneficial in preventing apoptosis and subsequent cardiac remodeling.