Key result
PCSK9 inhibitors significantly lower LDL-C, triglycerides, and Lp(a) while raising HDL-C in post-MI patients.
Why the study?
Elevated LDL-C and Lp(a) represent significant residual risk and associate with inflammation and coagulation, prompting evaluation of the effect of PCSK9 inhibitors on lipid, inflammatory, and hemostatic parameters.
Do PCSK9 inhibitors improve lipid, inflammatory, and hemostatic parameters in post-MI patients with insufficiently controlled LDL-C and elevated Lp(a)?
RCT (n=100)
Do PCSK9 inhibitors improve lipid, inflammatory, and hemostatic parameters in post-MI patients with insufficiently controlled LDL-C and elevated Lp(a)?
p-value: p=<0.001
PCSK9 inhibitors effectively improve lipid profiles in post-MI patients and may decouple the relationship between LDL-C and inflammatory/fibrinolytic pathways.
Supports PCSK9 inhibitor use for lipid optimization post-MI; extends evidence to broad improvements including Lp(a) reduction.
Despite progress in treatment, elevated levels of low-density lipoprotein cholesterol (LDL-C) and lipoprotein (a) (Lp(a)), represent a significant part of the residual risk. Both are associated with inflammation and the coagulation fibrinolytic system. The purpose of our research was to evaluate the effect of proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) on lipid parameters and indicators of inflammation, coagulation and fibrinolysis. We included 100 post myocardial infarction (MI) patients with insufficiently controlled LDL-C values despite the maximum dose of statin, and highly elevated Lp(a). Patients received alirocumab or evolocumab (150 mg sc or 140 mg sc every two weeks, respectively), or placebo for 6 months. In patients receiving PCSK9i, a significant decrease in total cholesterol (TC), LDL-C, triglycerides (TG) and Lp(a), and an increase in high density lipoprotein cholesterol (p < 0.001 for all) was found. Before treatment, the concentrations of TC, LDL-C and TG correlated with the concentrations of thrombin activatable fibrinolysis inhibitor (r = 0.41, p < 0.001; r = 0.353, p < 0.001; r = 0.311, p = 0.003, respectively), and plasminogen activator inhibitor-1 (r = 0.302, p = 0.007; r = 0.218, p = 0.049; r = 0.278; p = 0.013, respectively). The concentrations of TC and LDL-C correlated with overall fibrinolytic potential (r = -0.220, p = 0.034; r = -0.207, p = 0.047, respectively). The concentration of TG was related to the concentration of interleukin 6 (r = 0.290, p = 0.004) and interleukin 8 (r = 0.332, p = 0.001). No correlations between Lp(a) and inflammatory or hemostatic variables were found. No associations were found after treatment. Our results show that inflammatory cytokines and fibrinolytic parameters are related to LDL-C and not Lp(a) in post-MI patients before and with neither of them following PCSK9i treatment. The trial registration number: NCT04613167, Date of registration: November 3, 2020.
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Likozar et al. (2023) conducted an RCT in Post myocardial infarction (n=100). PCSK9 inhibitors (alirocumab or evolocumab) vs. Placebo was evaluated on Lipid parameters and indicators of inflammation, coagulation and fibrinolysis (p=<0.001). PCSK9 inhibitors significantly decreased total cholesterol, LDL-C, triglycerides, and Lp(a), and increased HDL-C (p < 0.001 for all) in post-MI patients.
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