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Evaluation of Effect of Alirocumab on Coronary Atheroma Volume in Japanese Patients Hospitalized for Acute Coronary Syndrome With Hypercholesterolemia

Phase 4
Completed
Conditions
Hypercholesterolemia
Acute Coronary Syndrome
Interventions
Registration Number
NCT02984982
Lead Sponsor
Sanofi
Brief Summary

Primary Objective:

To compare the efficacy of alirocumab (Praluent®) with standard of care (SoC) on coronary atheroma progression (percent change in normalized total atheroma volume \[TAV\]) after 9 months of treatment in participants who had acute coronary syndrome (ACS) within 4 weeks prior to randomization, with hypercholesterolemia treated with statin.

Secondary Objectives:

* To compare the efficacy of alirocumab (Praluent®) with SoC on secondary endpoints including absolute change in percent atheroma volume and normalized TAV after 9 months of treatment.

* To evaluate the efficacy of alirocumab (Praluent®) on low-density lipoprotein cholesterol (LDL-C), apolipoprotein B, triglycerides, non-high-density lipoprotein cholesterol and lipoprotein (a) after 9 months treatment.

* To evaluate the safety of alirocumab (Praluent®) including the occurrence of cardiovascular events (coronary heart disease death, non-fatal myocardial infarction, fatal and non-fatal ischemic stroke, unstable angina requiring hospitalization) throughout the study.

Detailed Description

The duration of study per participant was 9 months.

Recruitment & Eligibility

Status
COMPLETED
Sex
All
Target Recruitment
206
Inclusion Criteria

Not provided

Exclusion Criteria

Not provided

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
Standard of CareFenofibrateStatin therapy (atorvastatin or rosuvastatin) will be administered with or without non-statin lipid modifying therapies (LMTs). Non-statin LMTs will be adjusted by physicians to achieve the LDL-C target level \<100 milligrams per deciliter (mg/dL).
Standard of CareBezafibrateStatin therapy (atorvastatin or rosuvastatin) will be administered with or without non-statin lipid modifying therapies (LMTs). Non-statin LMTs will be adjusted by physicians to achieve the LDL-C target level \<100 milligrams per deciliter (mg/dL).
Standard of CareEzetimibeStatin therapy (atorvastatin or rosuvastatin) will be administered with or without non-statin lipid modifying therapies (LMTs). Non-statin LMTs will be adjusted by physicians to achieve the LDL-C target level \<100 milligrams per deciliter (mg/dL).
Standard of CareAntiplateletsStatin therapy (atorvastatin or rosuvastatin) will be administered with or without non-statin lipid modifying therapies (LMTs). Non-statin LMTs will be adjusted by physicians to achieve the LDL-C target level \<100 milligrams per deciliter (mg/dL).
Standard of CareAnticoagulantsStatin therapy (atorvastatin or rosuvastatin) will be administered with or without non-statin lipid modifying therapies (LMTs). Non-statin LMTs will be adjusted by physicians to achieve the LDL-C target level \<100 milligrams per deciliter (mg/dL).
AlirocumabAlirocumab SAR236553Alirocumab will be given subcutaneously every 2 weeks on top of stable dose statin therapy (atorvastatin or rosuvastatin) with or without stable dose non-statin LMTs.
AlirocumabAtorvastatinAlirocumab will be given subcutaneously every 2 weeks on top of stable dose statin therapy (atorvastatin or rosuvastatin) with or without stable dose non-statin LMTs.
AlirocumabRosuvastatinAlirocumab will be given subcutaneously every 2 weeks on top of stable dose statin therapy (atorvastatin or rosuvastatin) with or without stable dose non-statin LMTs.
AlirocumabFenofibrateAlirocumab will be given subcutaneously every 2 weeks on top of stable dose statin therapy (atorvastatin or rosuvastatin) with or without stable dose non-statin LMTs.
AlirocumabBezafibrateAlirocumab will be given subcutaneously every 2 weeks on top of stable dose statin therapy (atorvastatin or rosuvastatin) with or without stable dose non-statin LMTs.
AlirocumabEzetimibeAlirocumab will be given subcutaneously every 2 weeks on top of stable dose statin therapy (atorvastatin or rosuvastatin) with or without stable dose non-statin LMTs.
AlirocumabAntiplateletsAlirocumab will be given subcutaneously every 2 weeks on top of stable dose statin therapy (atorvastatin or rosuvastatin) with or without stable dose non-statin LMTs.
AlirocumabAnticoagulantsAlirocumab will be given subcutaneously every 2 weeks on top of stable dose statin therapy (atorvastatin or rosuvastatin) with or without stable dose non-statin LMTs.
Standard of CareRosuvastatinStatin therapy (atorvastatin or rosuvastatin) will be administered with or without non-statin lipid modifying therapies (LMTs). Non-statin LMTs will be adjusted by physicians to achieve the LDL-C target level \<100 milligrams per deciliter (mg/dL).
Standard of CareAtorvastatinStatin therapy (atorvastatin or rosuvastatin) will be administered with or without non-statin lipid modifying therapies (LMTs). Non-statin LMTs will be adjusted by physicians to achieve the LDL-C target level \<100 milligrams per deciliter (mg/dL).
Primary Outcome Measures
NameTimeMethod
Percent Change From Baseline in Normalized Total Atheroma Volume (TAV) at Week 36Baseline, Week 36

Least-squares (LS) means and standard errors (SE) at Week 36 were obtained from analysis of covariance (ANCOVA) model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effects, and the baseline normalized TAV as continuous fixed covariate.

Secondary Outcome Measures
NameTimeMethod
Absolute Change From Baseline in External Elastic Membrane (EEM) Volume at Week 36Baseline, Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model with treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]), as fixed categorical effects, and the baseline EEM volume value as continuous fixed covariate.

Absolute Change From Baseline in Apolipoprotein B (Apo B) at Week 36Baseline, Week 36

Adjusted LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effects, and baseline Apo B value as continuous fixed covariate.

Percent Change From Baseline in Apolipoprotein B at Week 36Baseline, Week 36

Adjusted LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effects, and baseline Apo B value as continuous fixed covariate.

Absolute Change From Baseline in Non-High-density Lipoprotein Cholesterol (Non-HDL-C) at Week 36Baseline, Week 36

Adjusted LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset \[Yes / No\]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline calculated non-HDL-C value and baseline calculated non-HDL-C value-by-time point interaction as continuous fixed covariates.

Percent Change From Baseline in Non-High-density Lipoprotein Cholesterol at Week 36Baseline, Week 36

Adjusted LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset \[Yes / No\]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline calculated non-HDL-C value and baseline calculated non-HDL-C value-by-time point interaction as continuous fixed covariates.

Absolute Change From Baseline in Total Cholesterol (TC) at Week 36Baseline, Week 36

LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset \[Yes / No\]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline calculated TC value and baseline calculated TC value-by-time point interaction as continuous fixed covariates.

Percent Change From Baseline in Total Cholesterol at Week 36Baseline, Week 36

Adjusted LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset \[Yes / No\]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline TC value and baseline TC value-by-time point interaction as continuous fixed covariates.

Absolute Change From Baseline in Lipoprotein (a) (Lp[a]) at Week 36Baseline, Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effect, and baseline Lp(a) value as continuous fixed covariate.

Absolute Change From Baseline in Percent Atheroma Volume (PAV) at Week 36Baseline, Week 36

LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effects, and the baseline PAV as continuous fixed covariate.

Absolute Change From Baseline in Normalized Total Atheroma Volume at Week 36Baseline, Week 36

LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effects, and the baseline normalized TAV as continuous fixed covariate.

Absolute Change From Baseline in Lumen Volume at Week 36Baseline, Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effects, and the baseline lumen volume value as continuous fixed covariate.

Percent Change From Baseline in Calculated Low-density Lipoprotein Cholesterol at Week 12 and Week 36Baseline, Week 12, Week 36

Adjusted LS mean and SE at Week 12 and Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset \[Yes / No\]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline calculated LDL-C value and baseline calculated LDL-C value-by-time point interaction as continuous fixed covariates.

Percent Change From Baseline in Fasting Triglycerides at Week 36Baseline, Week 36

Adjusted mean and SE were obtained by multiple imputation approach followed by robust regression model included fixed categorical effect of treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) and the continuous fixed covariate of baseline fasting TGs value.

Absolute Change From Baseline in Apolipoprotein A-1 (Apo A-1) at Week 36Baseline, Week 36

Adjusted LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effects, and baseline Apo A-1 value as continuous fixed covariate.

Percent Change From Baseline in External Elastic Membrane Volume at Week 36Baseline, Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effects, and the baseline EEM volume value as continuous fixed covariate.

Percent Change From Baseline in Lumen Volume at Week 36Baseline, Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effect, and the baseline lumen volume value as continuous fixed covariate.

Percent Change From Baseline in Apolipoprotein A-1 at Week 36Baseline, Week 36

Adjusted LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effects, and baseline Apo A-1 value as continuous fixed covariate.

Absolute Change From Baseline in Calculated Low-density Lipoprotein Cholesterol at Week 12 and Week 36Baseline, Week 12, Week 36

Adjusted LS mean and SE at Week 12 and Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset \[Yes / No\]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline calculated LDL-C value and baseline calculated LDL-C value-by-time point interaction as continuous fixed covariates.

Percent Change From Baseline in Lipoprotein (a) at Week 36Baseline, Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) as fixed categorical effect, and baseline Lp(a) value as continuous fixed covariate.

Absolute Change From Baseline in High-density Lipoprotein Cholesterol at Week 36Baseline, Week 36

Adjusted LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset \[Yes / No\]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline HDL-C value and baseline HDL-C value-by-time point interaction as continuous fixed covariates.

Percent Change From Baseline in High-density Lipoprotein Cholesterol at Week 36Baseline, Week 36

Adjusted LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset \[Yes / No\]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline HDL-C value and baseline HDL-C value-by-time point interaction as continuous fixed covariates.

Absolute Change From Baseline in Fasting Triglycerides (TGs) at Week 36Baseline, Week 36

Adjusted mean and SE were obtained from multiple imputation approach followed by robust regression model including fixed categorical effect of treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset \[Yes / No\]) and the continuous fixed covariate of baseline fasting TGs value.

Number of Participants With Cardiovascular (CV) Adverse EventsUp to 36 weeks

The suspected or confirmed CV events that occurred from randomization until end of the study visit were collected and reported. The various CV events included CV death, myocardial infarction, ischemic stroke, unstable angina requiring hospitalization , congestive heart failure requiring hospitalization, congestive heart failure requiring hospitalization, ischemia-driven coronary revascularization procedure.

Trial Locations

Locations (39)

Investigational Site Number 392008

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Gifu-shi, Japan

Investigational Site Number 392022

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Chiyoda-ku, Japan

Investigational Site Number 392039

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Hiroshima-shi, Japan

Investigational Site Number 392028

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Isehara-shi, Japan

Investigational Site Number 392036

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Itabashi-ku, Japan

Investigational Site Number 392037

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Itabashi-ku, Japan

Investigational Site Number 392013

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Izunokuni-shi, Japan

Investigational Site Number 392009

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Kitakyushu-shi, Japan

Investigational Site Number 392034

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Kitakyushu-shi, Japan

Investigational Site Number 392044

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Kochi-shi, Japan

Investigational Site Number 392003

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Kurashiki-shi, Japan

Investigational Site Number 392018

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Matsuyama-shi, Japan

Investigational Site Number 392047

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Nagaoka-shi, Japan

Investigational Site Number 392033

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Okayama-shi, Japan

Investigational Site Number 392006

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Osaka-shi, Japan

Investigational Site Number 392035

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Sapporo-shi, Japan

Investigational Site Number 392046

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Osaka-shi, Japan

Investigational Site Number 392001

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Tenri-shi, Japan

Investigational Site Number 392015

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Sagamihara-shi, Japan

Investigational Site Number 392019

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Sakai-shi, Japan

Investigational Site Number 392040

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Tsukuba-shi, Japan

Investigational Site Number 392032

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Fujisawa-shi, Japan

Investigational Site Number 392026

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Bunkyō-Ku, Japan

Investigational Site Number 392004

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Fukui-shi, Japan

Investigational Site Number 392007

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Fukuoka-shi, Japan

Investigational Site Number 392024

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Izumisano-shi, Japan

Investigational Site Number 392002

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Kumamoto-shi, Japan

Investigational Site Number 392011

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Kumamoto-shi, Japan

Investigational Site Number 392010

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Osaka-shi, Japan

Investigational Site Number 392045

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Osaka-shi, Japan

Investigational Site Number 392021

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Morioka-shi, Japan

Investigational Site Number 392005

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Wakayama-shi, Japan

Investigational Site Number 392017

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Nagakute-shi, Japan

Investigational Site Number 392025

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Tsukuba-shi, Japan

Investigational Site Number 392043

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Yokohama-shi, Japan

Investigational Site Number 392027

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Yokohama-shi, Japan

Investigational Site Number 392048

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Fukuoka-shi, Japan

Investigational Site Number 392016

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Toyoake-shi, Japan

Investigational Site Number 392020

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Kawaguchi-shi, Japan

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