Related Experiment Videos
Apoptosis in human acute myocardial infarction
A Saraste1, K Pulkki, M Kallajoki
1Department of Anatomy, University of Turku, Finland.
Insights
Apoptosis, programmed cell death, occurs in human heart attacks during reperfusion injury. This finding offers a new target for developing cardioprotective therapies for acute myocardial infarction (AMI).
Area of Science:
- Cardiovascular Research
- Cellular Biology
- Pathology
Background:
- Cardiomyocytes continue to die after reperfusion in acute myocardial infarction (AMI).
- The precise mechanisms of cell death during this phase remain debated.
- This study investigated the presence of apoptosis in human AMI.
Purpose of the Study:
- To determine if apoptotic cell death occurs in human cardiomyocytes during acute myocardial infarction (AMI).
- To explore potential new targets for cardioprotection in evolving AMI.
Main Methods:
- Analysis of myocardial samples from eight patients who died of AMI with patent infarct-related arteries.
- Utilizing in situ DNA end-labeling to detect DNA strand breaks, a hallmark of apoptosis.
- Confirming internucleosomal DNA fragmentation via agarose gel electrophoresis.
Main Results:
- Extensive DNA strand breaks, indicative of apoptosis, were detected in myocardial samples.
- Apoptotic cardiomyocytes were predominantly found in the border zones of infarcted areas.
- Minimal apoptotic cells were observed in remote, non-infarcted myocardial regions.
Conclusions:
- Evidence suggests that apoptosis occurs in a subset of myocytes alongside necrosis during ischemia-reperfusion injury in human AMI.
- Targeting apoptosis presents a novel strategy for cardioprotection in evolving acute myocardial infarction.
Background:
After reopening of the infarct-related coronary artery, cardiomyocytes continue to die during reperfusion. The mechanisms of cell death have been subject to debate. We studied whether an apoptotic type of cell death occurs in human acute myocardial infarction (AMI).
Methods And Results:
We studied myocardial samples of eight patients who died of AMI and had patent infarct-related arteries at autopsy. Six of the patients had received initially successful thrombolysis. Extensive formation of DNA strand breaks, the typical biochemical feature of apoptosis, was detected with the use of the in situ DNA end-labeling method. Apoptotic cardiomyocytes were observed particularly in the border zones of histologically infarcted myocardium, whereas very few apoptotic cells were present in the remote noninfarcted myocardium. Internucleosomal fragmentation was confirmed by agarose gel electrophoresis of DNA isolated from the representative myocardial areas.
Conclusions:
This study provides evidence that in addition to overt necrosis, a subset of myocytes undergo apoptosis during ischemia-reperfusion injury. Apoptosis may provide a new target for cardioprotection during evolving AMI in humans.