Lipoprotein(a)

Abstract

Lipoprotein(a) (LP(a))-discovered by Kare Berg [1] in 1963-is of increasing importance in clinical routine as reflected by the ESC/EAS Guidelines for the Management of Dyslipidaemias and the recent AHA Guideline [2, 3]. These guidelines provide detailed recommendations for screening and lipid analyses in the assessment of cardiovascular risk. A consensus paper of the European Society of Cardiology summarizes basic principles, background as well as diagnostic and therapeutic principles [4]. Structure-physiochemical characteristics LP(a) is a lipid protein complex with a structure compared to that of LDL (low density lipoprotein). Another apoprotein, glycoprotein apoprotein(a) (Apo(a)) is bonded to the apoprotein B-100 (Apo B-100) of the LDL cholesterol via a disulphide bridge [5]. The presence of Apo(a) impairs the bond between Lp(a) and the LDL receptor. An independent Lp(a) receptor has not been identified so far. Corresponding to the LDL cholesterol (LDL-C), the Lp(a) molecule is coated by a layer of simple phospholipids, free cholesterol, and apoproteins. Its core consists of triglycerides and esterified cholesterol [6]. Due to its structural similarity, Lp(a) competes with plasminogen for bindings sites on endothelial cells thus blocking the development of plasmin [7]. This leads to a delay of fibrinolysis. Similar to plasminogen, Apo(a) contains a kringle domain [8].

Assessment of Serum Lipoprotein(a) Status in Type 2 Diabetes Mellitus

“…Lp(a) has thrombogenic and atherogenic characteristics, and in the blood circulation, it constitutes an antagonist of plasminogen which is the inactive precursor of plasmin, a major enzyme of the fibrinolytic system. It competes with plasminogen at the binding sites of endothelial cells, thus blocking the formation of plasmin, leading to a delay in fibrinolysis and its deposition on the vascular wall [5,6]. High levels of Lp(a) therefore lead to a high thrombotic risk due to inhibition of fibrinolytic mechanisms [6].…”

“…It competes with plasminogen at the binding sites of endothelial cells, thus blocking the formation of plasmin, leading to a delay in fibrinolysis and its deposition on the vascular wall [5,6]. High levels of Lp(a) therefore lead to a high thrombotic risk due to inhibition of fibrinolytic mechanisms [6]. Elevated serum Lp(a) concentrations have long been reported to be associated with increased risk of ischemic cardiovascular disease and, in particular, coronary heart disease [7].…”

Infarto agudo de miocardio en paciente con bajo riesgo cardiovascular y lipoproteína (a) elevada. Reporte de caso

“…Desde su descubrimiento en 1963, la lipoproteína (a) (Lp (a)) presenta mayor relevancia en la práctica clínica debido a la sólida asociación entre el aumento de Lp (a) y la enfermedad cardiovascular (ECV)/ enfermedad coronaria y estenosis valvular aórtica calcificada (1) . Esta lipoproteína está compuesta por una partícula similar a la LDL con una molécula de apolipoproteína B-100 (ApoB-100) y la apolipoproteína (a) (Apo (a)) (2,3) .…”

“…Se han propuesto mecanismos fisiopatológicos subyacentes a su potencial efecto aterotrombótico, entre ellos destacan: 1) su infiltración directa en la íntima, uniéndose a la matriz extracelular a través de la ApoB-100 y la Apo (a); 2) aumenta la expresión de moléculas de adhesión y citoquinas proinflamatorias; 3) la Lp (a) es más propensa a oxidarse, promoviendo la formación de células espumosas y el depósito de colesterol; 4) la inhibición de la cascada fibrinolítica; la Apo (a) inhibe la activación del plasminógeno bloqueando la formación de plasmina, y estimula la trombogénesis al bloquear la función del inhibidor de la vía del factor tisular (1,3,4,5) . La Lp (a) es más aterogénica que la LDL porque contiene los componentes proaterogénicos de LDL, y la Apo (a), que potencia la aterotrombosis (4,5,6,7) .…”

Relação entre a lipoproteína (a) e a aterosclerose carotídea subclínica em indivíduos assintomáticos

“…Somado a isso, Tsimikas e colaboradores (64) relataram a presença de apo (a) em placas ateroscleróticas. Portanto, um número razoável de estudos sugerem que a Lp(a) pode estar envolvida no processo de aterosclerose (64,(104)(105)(106)(107)(108).…”