Lp(a), or Lipoprotein(a), is a distinct, genetically determined lipoprotein particle in the blood plasma, structurally similar to low-density lipoprotein (LDL) but containing an additional protein called apolipoprotein(a). Elevated concentrations of Lp(a) are a significant, independent, and causal risk factor for atherosclerotic cardiovascular disease, including myocardial infarction and stroke, regardless of conventional lipid panel results. Clinical evaluation of Lp(a) is essential for a comprehensive cardiovascular risk assessment, particularly in individuals with a family history of premature heart disease or those with unexplained elevated LDL-C. It is a critical, often overlooked, marker in preventative cardiology and longevity medicine.
Origin
Lp(a) was first identified in 1963 by the Norwegian physician Kåre Berg, who noted its genetic variability and association with coronary artery disease. The particle’s unique structure and clinical significance have been the subject of extensive research since its discovery, highlighting a genetic component to cardiovascular risk. Its naming reflects its lipid and protein components, emphasizing its distinct biological identity from other lipoproteins.
Mechanism
The pathogenic mechanism of Lp(a) is dual-pronged: it promotes atherogenesis and thrombogenesis. Similar to LDL, Lp(a) can infiltrate the arterial wall, where its lipid component contributes to plaque formation. Crucially, the apolipoprotein(a) component structurally mimics plasminogen, a key enzyme in fibrinolysis, but it lacks fibrinolytic activity. This molecular mimicry interferes with the body’s natural clot-dissolving mechanism, promoting a prothrombotic state and increasing the risk of acute cardiovascular events.
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