Key result
Adding ezetimibe to rosuvastatin cuts LDL-C by ~20% versus monotherapy and reduces inflammatory markers in AMI.
Why the study?
The effect of adding ezetimibe to rosuvastatin on reductions in LDL-C, hsCRP, and Lp-PLA2 in patients with acute myocardial infarction was not well established.
Does the addition of ezetimibe to rosuvastatin reduce LDL-C, hsCRP, and Lp-PLA2 in patients with acute myocardial infarction?
RCT (n=113)
Computer-generated sequence of random numbers
No
Does the addition of ezetimibe to rosuvastatin reduce LDL-C, hsCRP, and Lp-PLA2 in patients with acute myocardial infarction?
Absolute Event Rate: 1.19% vs 1.49%
p-value: p=<0.05
The addition of ezetimibe to rosuvastatin in patients with acute myocardial infarction further reduces LDL-C and inflammatory markers (hsCRP and Lp-PLA2) compared to rosuvastatin monotherapy.
May further lower Lp-PLA2 when ezetimibe is added to rosuvastatin in acute MI; leaves open outcome benefits.
Statins lower low‑density lipoprotein cholesterol (LDL‑C) and high‑sensitivity C‑reactive protein (hsCRP), and the addition of ezetimibe to statins further reduces LDL‑C and hsCRP. Lipoprotein‑associated phospholipase A2 (Lp‑PLA2) is a potentially important pathogenic factor participating in the progression of atherosclerosis. The aim of current study was to investigate how the addition of ezetimibe to rosuvastatin treatment affects reductions in LDL‑C, hsCRP and Lp‑PLA2 in patients with acute myocardial infarction (AMI). A total of 135 patients were enrolled in the study within 24 h of AMI, and were randomized to receive 10 mg rosuvastatin or 10 mg rosuvastatin plus 10 mg ezetimibe daily. HsCRP, Lp‑PLA2, total cholesterol (TC), triglycerides (TG), LDL‑C and high‑density lipoprotein cholesterol (HDL‑C) were determined at baseline and after 1, 3, 6 and 12 months of treatment. The addition of ezetimibe to rosuvastatin led to greater reduction of LDL‑C compared with rosuvastatin monotherapy (from 3.00 to 1.19 mmol/l vs. 2.93 to 1.49 mmol/l, respectively; P<0.05), as well as reduced levels of hsCRP (from 5.15 to 0.68 mg/l vs. 4.33 to 1.49 mg/l, respectively; P<0.05) and Lp‑PLA2 (from 333.13 to 79.07 mg/l vs. 327.95 to 123.62 mg/l, respectively; P<0.05). A positive association was identified between reductions of Lp‑PLA2 and the changes of LDL‑C (r=0.367; P=0.002). However, no significant correlation was observed between changes in Lp‑PLA2 and hsCRP (r=0.264; P=0.512). The values of hsCRP and Lp‑PLA2 appeared to increase during the first week after randomization, but dropped steeply to a lower level and remained stable thereafter. In conclusion, the addition of ezetimibe to rosuvastatin was demonstrated to further reduce LDL‑C, hsCRP and Lp‑PLA2 compared with rosuvastatin monotherapy in patients with AMI.
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Ren et al. (2017) conducted an RCT in Acute myocardial infarction (n=113). Rosuvastatin plus ezetimibe vs. 10 mg rosuvastatin daily was evaluated on LDL-C level at 12 months (mmol/l) (p=<0.05). The addition of ezetimibe to rosuvastatin significantly reduced LDL-C to 1.19 mmol/l compared to 1.49 mmol/l with rosuvastatin alone, and further reduced hsCRP and Lp-PLA2 levels in patients with AMI.
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