It's a result of what is formally called an acute myocardial infarction(AMI), i.e. the loss of myocardium, aka heart muscle, from an abrupt blockage of a coronary artery.
Serum Caspase-3 p17 Fragment Is Elevated in Patients With ST-Segment Elevation Myocardial Infarction
The correlations were not tight, suggesting that both necrosis and apoptosis play a role in determining infarct size. The use of this novel assay for the first time sets the stage to investigate this critical balance. The rise and fall of p17 peptide and its correlation with peak cTnI and CK-MB suggest that serum p17 likely came from injured myocardium. A calpain (4) and stretch-mediated (5) myocyte apoptosis may have also contributed to the serum p17 level.Apoptosis is programmed cell death.Limitations include the lack of concurrent myocyte evidence of apoptosis and unknown p17 release kinetics. Designing therapies to inhibit apoptosis may provide benefit to STEMI patients.
It'd stink if you aren't already sitting in your doctor's office waiting on your lab results to know if you're going to soon be popping up daisies.
I doubt if they will be able to do this test any time soon in a doc's office. Hospital maybe, if the test has clinical utility. Most docs' offices send blood samples to outside labs.
Talking about that it takes time to get acceptance. This has been studied for some years:
(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1276.)
© 2003 American Heart Association, Inc.
Atherosclerosis and Lipoproteins
The p17 Cleaved Form of Caspase-3 Is Present Within Viable Macrophages In Vitro and in Atherosclerotic Plaque
Thomas Q. Nhan; W. Conrad Liles; Alan Chait; John T. Fallon; Stephen M. Schwartz
http://atvb.ahajournals.org/cgi/content/abstract/23/7/1276