In patients with a prior CV event, Praluent® demonstrated a significant reduction in the risk of MACE for the overall trial population vs placebo, HR 0.85 [95% CI 0.78 - 0.93] p=0.0003).2
A greater absolute benefit was observed in patients with baseline ≥2.6 mmol/L LDL-C (non-prespecified analysis).2
Praluent® provided consistent results across CV outcomes1
Among the main secondary endpoints, the risks of any CHD event (including CHD death, nonfatal MI, UA requiring hospitalisation, and an ischaemia-driven coronary revascularisation procedure), major CHD event (including death from CHD and nonfatal MI), CV event (including nonfatal MI and nonfatal ischaemic stroke), and a composite of death from any cause, nonfatal MI or nonfatal ischemic stroke were significantly lower among patients treated with Praluent® than those who received placebo.1
Praluent® was associated with a reduction of all-cause mortality (nominal significance by hierarchical testing) for the overall trial population vs placebo, HR 0.85 [95% CI 0.73–0.98]2,3.
In a post-hoc analysis, a greater benefit was observed in patients with baseline 100 mg/dL LDL-C for the overall trial population vs placebo, HR 0.71 [95% CI 0.56–0.90].2,3**
ACS=acute coronary syndrome; ARR=absolute risk reduction; CHD=coronary heart disease; CI=confidence interval; CV=cardiovascular; HCL-C=high-density lipoprotein cholesterol; HR=hazard ratio; LDL-C=low-density lipoprotein cholesterol; MACE=major adverse cardiac events (primary composite endpoint of CHD death, nonfatal myocardial infarction, fatal and nonfatal ischaemic stroke, or unstable angina requiring hospitalization); MI=myocardial infarction; NNT=number needed to treat; PCSK9i=proprotein convertase subtilisin/kexin type 9 inhibitor; RRR=relative risk reduction.