Clinical Trial Summary
Protein convertase subtilisin/kexin type 9 (PCSK9) plays a regulatory role in cholesterol
homeostasis by promoting low-density lipoprotein receptor (LDLr) degradation. Although the
vast majority of the studies have focused on the role of PCSK9 in LDLr expression in the
liver, an increasing body of evidence suggests that PCSK9 gene is also present in
extra-hepatic tissues. A recent publication showed for the first time that PCSK9 is expressed
in the ischemic heart and the expression is highest in the zone bordering the infarcted
areas. Furthermore, the expression of PCSK9 is maximal early, at 1 week of ischemia.
Mechanical complications (or cardiac ruptures) are uncommon but potentially lethal sequelae
of acute myocardium infarction (AMI) and are commonly associated with early mortality without
appropriate surgical intervention. It's unknown why some patients develop these devasting
complications following AMI, while others not. Interestingly, studies have shown that
post-infarction cardiac rupture affect the border zone between the ischemic and normal area
and occur within the first 3 to 5 days after AMI.
Based on the aforementioned observations, it's likely to assume a relationship between PCSK9
expression and the development of post-AMI cardiac rupture. Therefore, the main purpose of
the this project is to study the PCSK9 gene polymorphism and its association with cardiac
rupture. Investigators hypothesize that PCSK9 expression/secretion and development of
post-AMI cardiac rupture may be a part of the dynamic changes at cellular levels occurring in
the ischemic heart of genetically predisposed patients.
