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OpenTrials
Completed

NCT Number: NCT02984982

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

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.

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Key information

Conditions

Hypercholesterolemia Acute Coronary Syndrome Cardiovascular Diseases Dyslipidemias Heart Diseases Hyperlipidemias Lipid Metabolism Disorders Metabolic Diseases Myocardial Ischemia Nutritional and Metabolic Diseases Vascular Diseases

Age range

20 year and older

Sex eligibility

All sexes

Study type

Interventional

Phase

Phase 4

Primary location

Investigational Site Number 392026, Bunkyō City, Japan

Loading trial locations.

About this study

The duration of study per participant was 9 months.

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • Participants hospitalized for ACS (Acute ST-segment elevation myocardial infarction [STEMI], Acute non-ST-segment elevation myocardial infarction [NSTEMI], and unstable angina.
  • LDL-C >=100 mg/dL at ACS diagnosis.
  • Participants who has stenosis with at least >50% stenosis angiographically within 1 week after the ACS onset, and has analyzable coronary intravascular Ultrasound image.
  • Participants aged >=20 years old at ACS diagnosis.
  • Negative Hepatitis B surface antigen, negative Hepatitis B core antibody, and negative Hepatitis C antibody. Or, negative Hepatitis B surface antigen, positive Hepatitis B core antibody, negative Hepatitis B deoxyribonucleic acid, and negative Hepatitis C antibody.
  • Written informed consent.

Exclusion criteria

  • Participants who had previously treated with at least one dose of any anti-proprotein convertase subtilisin/kexin type 9 monoclonal antibody.
  • Uncontrolled hypertension (multiple reading with systolic blood pressure >180 mmHg or diastolic blood pressure >110 mmHg) between ACS diagnosis and randomization visit.
  • Known history of hemorrhagic stroke.
  • Currently under treatment for cancer.
  • Participants on LDL apheresis.
  • Any clinically significant abnormality identified that in the judgment of the Investigator or any sub-Investigator would preclude safe completion of the study or constrain endpoints assessment such as major systemic diseases, participants with short life expectancy.
  • Considered by the Investigator or any sub-Investigator as inappropriate for this study for any reason, including:
  • Unable to meet specific protocol requirements, such as scheduled visits;
  • Investigator or any sub-Investigator, pharmacist, study coordinator, other study staff or relative thereof directly involved in the conduct of the protocol, etc;
  • Presence of any other conditions (eg, geographic, social, etc.) actual or anticipated, that the Investigator feels would restrict or limit the participant's participation for the duration of the study.
  • Laboratory findings measured within 4 weeks after the ACS diagnosis (positive serum or urine pregnancy test in females of childbearing potential).

The above information was not intended to contain all considerations relevant to a participant's potential participation in a clinical trial.

Treatment and study plan

Alirocumab SAR236553

Drug

Pharmaceutical form: Solution for injection

Route of administration: Subcutaneous

Other names: Praluent

atorvastatin

Drug

Pharmaceutical form: tablet

Route of administration: oral

Rosuvastatin

Drug

Pharmaceutical form: tablet

Route of administration: oral

fenofibrate

Drug

Pharmaceutical form: tablet

Route of administration: oral

Bezafibrate

Drug

Pharmaceutical form: tablet

Route of administration: oral

ezetimibe

Drug

Pharmaceutical form: tablet

Route of administration: oral

Antiplatelets

Drug

Pharmaceutical form: tablet or capsule

Route of administration: oral

Anticoagulants

Drug

Pharmaceutical form: tablet or capsule

Route of administration: oral

Primary outcomes

  1. Percent Change From Baseline in Normalized Total Atheroma Volume (TAV) at Week 36

    Time frame: Baseline, 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 outcomes

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

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

  3. Absolute Change From Baseline in External Elastic Membrane (EEM) Volume at Week 36

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

  5. Absolute Change From Baseline in Lumen Volume at Week 36

    Time frame: Baseline, 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.

  6. Percent Change From Baseline in Lumen Volume at Week 36

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

  10. Percent Change From Baseline in Apolipoprotein B at Week 36

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

  14. Percent Change From Baseline in Total Cholesterol at Week 36

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

  20. Percent Change From Baseline in Fasting Triglycerides at Week 36

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

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

    Time frame: Baseline, 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.

  23. Number of Participants With Cardiovascular (CV) Adverse Events

    Time frame: Up 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.

Sponsors and collaborators

Lead sponsor

Sanofi

Industry

Collaborators

  • Regeneron Pharmaceuticals

Registry information

Official study title

A Randomized, Open-label, Blinded Intravascular Ultrasound Analysis, Parallel Group, Multicenter Study to Evaluate the Effect of Praluent® (Alirocumab) on Coronary Atheroma Volume in Japanese Patients Hospitalized for Acute Coronary Syndrome With Hypercholesterolemia Not Adequately Controlled With Statin

Acronym: ODYSSEY J-IVUS

Important dates

Study start
2016
Primary completion
2018
Study completion
2018
First posted
Dec 7, 2016
Registry last updated
Sep 9, 2019

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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