AI Article Synopsis
- ADAMTS13 is a metalloprotease that plays a role in cleaving von Willebrand factor (VWF), and its levels are altered in STEMI patients, raising questions about its impact on heart damage and recovery.
- In a study of 49 STEMI patients and 23 pigs, researchers monitored ADAMTS13 and VWF levels post-intervention, discovering higher VWF and lower ADAMTS13 in patients with intramyocardial hemorrhage (IMH), but no relationship to infarct size.
- The administration of recombinant ADAMTS13 in pigs did not result in reduced infarct size or IMH, suggesting that the imbalance of these proteins does not directly affect heart damage in the context of myocardial ischemia
Article Abstract
Aims: ADAMTS13, a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13, is a metalloprotease that cleaves von Willebrand factor (VWF). There is considerable evidence that VWF levels increase and ADAMTS13 levels decrease in ST-elevation myocardial infarction (STEMI) patients. It is unclear whether this contributes to no reflow, infarct size, and intramyocardial haemorrhage (IMH). We aimed to determine the role of ADAMTS13 in STEMI patients and to investigate the benefits of recombinant ADAMTS13 (rADAMTS13) in a porcine model of myocardial ischaemia-reperfusion.
Methods And Results: In 49 consecutive percutaneous coronary intervention (PCI)-treated STEMI patients, blood samples were collected directly after through 7 days following PCI. Cardiac magnetic resonance was performed 4-6 days after PCI to determine infarct size and IMH. In 23 Yorkshire swine, the circumflex coronary artery was occluded for 75 min. rADAMTS13 or vehicle was administered intracoronary following reperfusion. Myocardial injury and infarct characteristics were assessed using cardiac enzymes, ECG, and histopathology. In patients with IMH, VWF activity and VWF antigen were significantly elevated directly after PCI and for all subsequent measurements, and ADAMTS13 activity significantly decreased at 4 and 7 days following PCI, in comparison with patients without IMH. VWF activity and ADAMTS13 activity were not related to infarct size. In rADAMTS13-treated animals, no differences in infarct size, IMH, or formation of microthrombi were witnessed compared with controls.
Conclusions: No correlation was found between VWF/ADAMTS13 and infarct size in patients. However, patients suffering from IMH had significantly higher VWF activity and lower ADAMTS13 activity. Intracoronary administration of rADAMTS13 did not decrease infarct size or IMH in a porcine model of myocardial ischaemia-reperfusion. These data dispute the imbalance in ADAMTS13 and VWF as the cause of no reflow.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4957491 | PMC |
| http://dx.doi.org/10.1093/cvr/cvw097 | DOI Listing |
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