Decoding Atherogenic Lipoproteins: Unraveling the Role of LDL and Lp(a)

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EP: 1.Decoding Atherogenic Lipoproteins: Unraveling the Role of LDL and Lp(a)

EP: 2.Unveiling Hidden Risks: The Case for Lp(a) Testing

EP: 3.Lp(a) Genetic Patterns

EP: 4.Insights From the Lp(a) HERITAGE Study

EP: 5.Lp(a) Ethnicity and Gender Risks

EP: 6.Unveiling Cardiovascular Disparities in Lp(a)

EP: 7.Lp(a) Screening in ASCVD: Clinical Integration

EP: 8.Integration of Lp(a)Testing Across Health Care Organizations

EP: 9.A Look to The Future of Lp(a) Management

EP: 10.Actionable Insights for Health Care Decision Makers on Lp(a) Testing

This is a video synopsis/summary of an Insights involving Michael D. Shapiro, DO.

Shapiro discussed the crucial role of lipoproteins in cardiovascular risk assessment in an AJMC® segment. He emphasized the significance of apolipoprotein B–containing lipoproteins (such as LDL [low-density lipoprotein] and lipoprotein) in atherosclerotic cardiovascular disease (ASCVD) development by delivering cholesterol into arterial walls, initiating and perpetuating plaque formation. Elevated levels of LDL and lipoprotein are strongly linked to ASCVD risk, prompting the importance of assessing a patient’s lipoprotein profile, including lipoprotein(a) (Lp[a]), to guide treatment decisions and manage risk.

Lp(a) has gained prominence in cardiology due to its unique characteristics, described by Shapiro as akin to LDL but with the addition of apolipoprotein(a) (APO[a]). The LDL-like structure allows Lp(a) to transport cholesterol and contribute to plaque initiation and progression. However, the presence of APOA, resembling plasminogen, suggests its atherothrombotic potential. Moreover, APO[a] acts as a repository for highly inflammatory oxidized phospholipids, exacerbating plaque vulnerability through inflammation within arterial walls.

Regarding Lp(a)’s genetic inheritance, Shapiro explained its autosomal codominant inheritance pattern, mainly influenced by variants in the LPL gene, specifically Kringle IV subtype II copy number variants. Notably, Lp(a) levels remain remarkably stable throughout life due to genetic determination, making childhood measurements predictive of lifelong levels. Despite minimal alteration by statins or lifestyle changes, recognizing this stable trajectory is crucial in clinical assessment, guiding potential Lp(a)-lowering therapies for individuals with inherited high Lp(a) levels.

Video synopsis is AI-generated and reviewed by AJMC^® editorial staff.