PCSK9 Polymorphism and Risk of Cardiac Rupture

Gene Polymorphism, Post-Infarction Heart Rupture

PCSK9, Cardiac rupture

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.

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