An observational study in Myocardial Infarction, Ischemia and Congestive Heart Failure, sponsored by UConn Health. Recruiting at 1 site in United States. Open to participants aged 18 Years and older, including healthy volunteers. Per ClinicalTrials.gov, last updated 2026-08-17.
Sponsored by UConn Health · Observational
The purpose of this research is to determine if two proteins in the blood are increased during acute myocardial infarction and whether their levels are higher in those who develop heart failure than those who do not. These two proteins are produced and potentially released when the heart muscle is damaged. They may then be released into the blood and be detected by standard method in the research laboratory. At this time, detection of an increase in these proteins in the blood is not known to be associated with any disease or myocardial infarction.
Hypotheses, Objectives and Aims:
Hypotheses:Caspase-3, cleaved and activated, and dystrophin can be detected in human circulation. The levels of these two markers are elevated during acute myocardial infarction. Furthermore, the levels of these two proteins are greater in those who develop heart failure than those who do not.
Objectives:
Scientific Background and Significance: Apoptosis is a regulated biological process resulting in cell death (4-9). Caspases, a family of cysteine acid proteases regulate the process, and in fact, lead to apoptosis. Apoptotic trigger or signal results in the activation of proximal or initiator caspases (such caspase-8, -9, 10). These initiator caspases then cleave and in turn activate downstream effector caspases such as caspases-3, -6 and -7. These effector caspases then cleave various proteins such as those present in cytoskeletons and nucleus like lamin A, alpha-fodrin and poly (ADP-ribose) polymerase, leading to apoptosis. Caspase-3 is the key executioner in this apoptotic pathway, responsible totally or critically in the proteolytic cleavage of cellular and nuclear proteins. Activation of caspase-3 requires proteolytic processing of its inactive zymogen into active p17 and p12 fragments. The cleaved caspase-3 can be detected by antibodies specific for this cleaved enzyme (p17 fragment) in cell lysates by immunoblotting or by an ELISA assay utilizing spectrophotometric determination with a microplate reader at OD450 nm. Ischemia and reperfusion are known to cause apoptosis. Therefore, acute MI may be associated with release of the final executioner of apoptosis that is caspase-3, into the circulation.Another potential marker for acute deterioration is dystrophin. Dystrophin was originally identified as the x-linked gene whose mutations in its N-terminus cause cardiomyopathy. Dystrophin provides important structural support for the cardiac myocyte and its sarcolemmal membrane (10-11). It links actin at its N-terminus with the dystrophin-associated protein complex and sarcolemma at the C-terminus and the extracellular matrix of muscle. Mutations cause loss of support and sarcolemmal instability and myopathy. Myocardial dystrophin translocation and cleavage are associated with the progression of heart failure and contractile dysfunction. These changes are reversed following reduction of mechanical stress from ventricular assistance device (12). Since MI is associated with sarcolemmal instability, dystrophin may also be released into circulation.
2,270 studies on the registry are indexed under Myocardial Infarction; 371 are open to participants now.
This study's planned enrollment of 550 is close to the median of 568 across 814 observational studies indexed under Myocardial Infarction.
Browse Myocardial Infarction studies →UConn Health is the lead sponsor of 187 studies on the registry; 18 are open to participants now.
Of its 10 completed or terminated interventional studies of FDA-regulated products, 7 (70%) have results posted.
Counted across the registry records on this site, refreshed daily.
There are two arms to this study:
The investigators hope to enroll 350 healthy individuals, as defined by having no prior diagnosis of heart disease to determine baseline levels and diurnal variations of the markers.
Participants being evaluated for an acute Myocardial Infarction as determined by positive CK MB/troponin levels, will be asked to enroll.
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Exclusion Criteria:
Hospitalization for acute myocardial infarction, stroke or death
Time frame: 3 years
Started Jun 2007 (actual). Primary completion is estimated for Mar 2027, 237 months after the start.
Of 296 non-industry observational studies under Myocardial Infarction, half reached primary completion within 54 months of starting (the median), counting those still running; a quarter within 19 and three quarters within 140. This study's planned 237 months is above that.
Counting every sponsor, half of 333 studies reached it within 48 months; a quarter within 17 and three quarters within 114.
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