¿Cómo mitigar el riesgo residual?: manejo de factores de riesgo, estrategia holística de abordaje del riesgo cardiovascular y objetivos de tratamiento diferentes a LDL (c-no-HDL, Lp(a), TG, apoB).

Triglycerides are associated with cardiovascular risk largely mediated by their final product of catabolism, the cholesterol-rich remnant, which may come from the liver or the intestine. There is a direct association between fasting and postprandial triglycerides and cardiovascular risk. ApoB is associated with the number of particles and the amount of RC, which explains its determining role in CVD. Non-HDL cholesterol represents atherogenic lipoproteins, with correlation and concordance with apoB; both are cardiovascular risk markers. Lipoprotein (a) is a cardiovascular risk factor not only because of the cholesterol and apoB it contributes, but also because of its proinflammatory and prothrombotic activity. Viewing these factors holistically, it is important to note that it is primarily a reduction in apoB, remnant cholesterol and non-HDL cholesterol that reduces cardiovascular events. A 10% weight loss improves TG levels without reducing apoB or cardiovascular risk. Of the classic lipid-lowering agents, high-dose statins and ethyl eicosapentanoate reduce cardiovascular risk through apoB, RC, and non-HDL reduction. To date, we do not have lipid-lowering agents aimed at reducing Lp(a), which is only slightly reduced by PCSK9 inhibitors and markedly reduced by LDL apheresis. These residual risk markers serve not only to stratify cardiovascular risk but also to establish follow-up goals. [ABSTRACT FROM AUTHOR]