Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an expert panel of lipid specialists

Effect of Switching From Statin Monotherapy to Ezetimibe/Simvastatin Combination Therapy Compared With Other Intensified Lipid‐Lowering Strategies on Lipoprotein Subclasses in Diabetic Patients With Symptomatic Cardiovascular Disease

“…These results are in line with previous studies that showed reductions in Lp‐PLA 2 mass and activity with statins and ES were proportionate to the extent of LDL‐C lowering efficacy25, 58, 59 and that combination ezetimibe therapy with rosuvastatin and simvastatin provided additional reductions in Lp‐PLA 2 mass and activity in patients already receiving statin monotherapy 58. Ezetimibe, rosuvastatin, and fenofibrate monotherapies have been shown to primarily reduce Lp‐PLA 2 activity and mass associated with LDL lipoprotein subfractions via receptor‐mediated uptake 60.…”

“…The percent attainment of on‐treatment target levels of LDL‐C (<2.33 mmol/L, <90 mg/dL), LDL‐P (<990 nmol/L), and non–HDL‐C (<2.85 mmol/L, <110 mg/dL), defined as percentage of individuals below these levels, were assessed. These target levels for LDL‐C, non–HDL‐C, and LDL‐P corresponded to population equivalent levels (≤20th and <5th percentiles) as previously reported in the MESA (Multi‐Ethnic Study of Atherosclerosis) study cohort 25, 38. No statistical analysis was performed with respect to these percentages.…”

“…For the more‐stringent targets, equivalent to the 5th percentile based on the MESA cohort25, 38 (LDL‐C <1.8 mmol/L, 70 mg/dL, and non–HDL‐C <2.3 mmol/L, 90 mg/dL), the improvements in LDL‐C and non–HDL‐C were consistently greater for E/S 10/20 and R10 than those for doubling the statin dose (Figure 7B). With low‐dose starting statin, either simvastatin (20 mg/day) or atorvastatin (10 mg/day), the percentage of patients achieving this LDL‐C target was less than 0.6%.…”

“…Lipid and inflammatory markers, including LDL particle number (LDL‐P), HDL particle number (HDL‐P), and lipoprotein‐associated phospholipase A 2 (Lp‐PLA 2 ), may be more predictive of the atherogenic dyslipidemia present in diabetic patients with CVD 24, 25, 26. In patients with discordant LDL‐C and LDL‐P levels, LDL‐attributable atherogenic risk was shown to be more strongly correlated with LDL‐P than LDL‐C levels 27, 28.…”

“…Similarly, HDL‐P is proposed to be better correlated with CVD risk than HDL‐C 29, 30, 31, 32. Increased levels of Lp‐PLA 2 mass and activity have been shown to be associated with CVD risk and, compared with other inflammatory markers, provide an advantage as they are less subject to variability 25, 26…”