Residual risk in atherosclerotic cardiovascular disease after statin therapy: Clinical mechanisms and management strategies

Figure 1 Structural features of lipoprotein(a). Apo(a): Apolipoprotein(a); KIV: Kringles type IV; ApoB-100: Apolipoprotein B-100.

Figure 2 Mechanistic overview of residual cardiovascular risk (low-density lipoprotein-independent lipid and inflammatory pathways). TRLs: Triglyceride-rich lipoproteins; LPL: Lipoprotein lipase; eNOS: Endothelial nitric oxide synthase; LDL: Low-density lipoprotein; Lp(a): Lipoprotein(a); HDLC: High-density lipoprotein cholesterol; Apo B: Apolipoprotein B; IL: Interleukin; TNF: Tumor necrosis factor; hsCRP: High-sensitivity C-reactive protein; LDL-C: Low-density lipoprotein-cholesterol.

Figure 3 Integrated diagram of lipid and inflammation - targeting therapies. LDL: Low-density lipoprotein; PCSK9: Proprotein convertase subtilisin/kexin type 9; siRNA: Small interfering RNA; IL: Interleukin.