Lipoprotein(a) Risk refers to the genetically determined cardiovascular risk conferred by elevated plasma concentrations of Lipoprotein(a), often abbreviated as Lp(a). This lipoprotein particle is structurally similar to LDL but contains an additional protein, apolipoprotein(a), which imparts pro-atherogenic and pro-thrombotic properties. High Lp(a) levels are considered an independent, often inherited, risk factor for heart attack and stroke, irrespective of standard cholesterol levels. Screening for this risk factor is an essential component of advanced cardiovascular diagnostics in the longevity and hormonal health space.
Origin
The term originates from the discovery of the Lipoprotein(a) particle by Kåre Berg in 1963 and the subsequent clinical realization of its potent link to premature cardiovascular disease. The concept of “Lp(a) Risk” solidified as large-scale epidemiological and genetic studies confirmed its role as a major, largely non-modifiable, inherited risk factor. It highlights a key genetic intersection with metabolic health.
Mechanism
The elevated risk is mechanistically attributed to two primary actions of the Lp(a) particle. First, its LDL-like component contributes to the accumulation of cholesterol in the arterial wall, accelerating atherosclerosis. Second, the apolipoprotein(a) component structurally resembles plasminogen, potentially interfering with the body’s natural clot-dissolving mechanism, thereby promoting thrombosis. This dual mechanism creates a uniquely aggressive form of vascular pathology.
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