Familial hypercholesterolemia (FH) is an autosomal codominant genetic condition, which results in heightened levels of LDL-C in the blood. It is diagnosed by the presence of mutations in low-density lipoprotein receptor (LDLR), apolipoprotein (ApoB), or proprotein convertase subtilisin/kexin 9 (PCSK9), with the LDLR mutation most common. The LDLR variant results in the malfunction of LDLR and problems with the clearance of LDL-C from the blood.

The worldwide mortality rate of FH is between 1:200 and 1:300, and if left untreated, FH can lead to premature atherosclerosis and an elevated risk of cardiovascular events. Because lifestyle modification alone is insufficient to maintain decreased LDL-C concentrations in FH patients, lipid-lowering therapy is necessary. Newer treatment options include small-molecule- or antibody-based approaches.

How do you treat patients with heterozygous FH who need additional lowering of LDL-C levels than that conferred by maximally tolerated statin dosages and lifestyle intervention? How do you determine when and what agents to use based on patient type?

Familial hypercholesterolemia (FH) is an autosomal codominant genetic condition, which results in heightened levels of LDL-C in the blood. It is diagnosed by the presence of mutations in low-density lipoprotein receptor (LDLR), apolipoprotein (ApoB), or proprotein convertase subtilisin/kexin 9 (PCSK9), with the LDLR mutation most common. The LDLR variant results in the malfunction of LDLR and problems with the clearance of LDL-C from the blood.



The worldwide mortality rate of FH is between 1:200 and 1:300, and if left untreated, FH can lead to premature atherosclerosis and an elevated risk of cardiovascular events. Because lifestyle modification alone is insufficient to maintain decreased LDL-C concentrations in FH patients, lipid-lowering therapy is necessary. Newer treatment options include small-molecule- or antibody-based approaches.



How do you treat patients with heterozygous FH who need additional lowering of LDL-C levels than that conferred by maximally tolerated statin dosages and lifestyle intervention? How do you determine when and what agents to use based on patient type?

Familial hypercholesterolemia (FH) is an autosomal codominant genetic condition, which results in heightened levels of LDL-C in the blood. It is diagnosed by the presence of mutations in low-density lipoprotein receptor (LDLR), apolipoprotein (ApoB), or proprotein convertase subtilisin/kexin 9 (PCSK9), with the LDLR mutation most common. The LDLR variant results in the malfunction of LDLR and problems with the clearance of LDL-C from the blood.



The worldwide mortality rate of FH is between 1:200 and 1:300, and if left untreated, FH can lead to premature atherosclerosis and an elevated risk of cardiovascular events. Because lifestyle modification alone is insufficient to maintain decreased LDL-C concentrations in FH patients, lipid-lowering therapy is necessary. Newer treatment options include small-molecule- or antibody-based approaches.



How do you treat patients with heterozygous FH who need additional lowering of LDL-C levels than that conferred by maximally tolerated statin dosages and lifestyle intervention? How do you determine when and what agents to use based on patient type?

Familial hypercholesterolemia (FH) is an autosomal codominant genetic condition, which results in heightened levels of LDL-C in the blood. It is diagnosed by the presence of mutations in low-density lipoprotein receptor (LDLR), apolipoprotein (ApoB), or proprotein convertase subtilisin/kexin 9 (PCSK9), with the LDLR mutation most common. The LDLR variant results in the malfunction of LDLR and problems with the clearance of LDL-C from the blood.



The worldwide mortality rate of FH is between 1:200 and 1:300, and if left untreated, FH can lead to premature atherosclerosis and an elevated risk of cardiovascular events. Because lifestyle modification alone is insufficient to maintain decreased LDL-C concentrations in FH patients, lipid-lowering therapy is necessary. Newer treatment options include small-molecule- or antibody-based approaches.



How do you treat patients with heterozygous FH who need additional lowering of LDL-C levels than that conferred by maximally tolerated statin dosages and lifestyle intervention? How do you determine when and what agents to use based on patient type?

Familial hypercholesterolemia (FH) is an autosomal codominant genetic condition, which results in heightened levels of LDL-C in the blood. It is diagnosed by the presence of mutations in low-density lipoprotein receptor (LDLR), apolipoprotein (ApoB), or proprotein convertase subtilisin/kexin 9 (PCSK9), with the LDLR mutation most common. The LDLR variant results in the malfunction of LDLR and problems with the clearance of LDL-C from the blood.



The worldwide mortality rate of FH is between 1:200 and 1:300, and if left untreated, FH can lead to premature atherosclerosis and an elevated risk of cardiovascular events. Because lifestyle modification alone is insufficient to maintain decreased LDL-C concentrations in FH patients, lipid-lowering therapy is necessary. Newer treatment options include small-molecule- or antibody-based approaches.



How do you treat patients with heterozygous FH who need additional lowering of LDL-C levels than that conferred by maximally tolerated statin dosages and lifestyle intervention? How do you determine when and what agents to use based on patient type?