“an examination of the jupiter trial”

“An Examination of the JUPITER Trial”

Moderator

Kevin Winfield, MDMedical Director

Clear Lake Lipid CenterHouston, TX

Disclosure

• Disclosure of Unlabeled Use and Investigational Product Discussions:Dr. Winfield has indicated that his presentation will not include the discussion of unlabeled uses of commercial products or products that have not yet been approved by the FDA for use in the United States for any purpose.

• Disclosure of Affiliations and Significant Relationships:Dr. Winfield has received honoraria related to speakers’ bureau activities from Novartis, AstraZeneca, and Abbott Laboratories.


Paul Ridker, MD Director

Center for Cardiovascular Disease Prevention

Division of Preventive Medicine Brigham and Women’s Hospital

Boston, MA

Disclosure

• Disclosure of Affiliations and Significant Relationships:Dr. Ridker has received honoraria related to consulting activities from Schering-Plough, Sanofi-Aventis, AstraZeneca, Isis, Dade, Merck & Co., Novartis, Vascular Biogenics.

He has also received grant support from research activities from National Heart, Lung, and Blood Institute, National Cancer Institute, American Heart Association, Doris Duke Charitable Foundation, Leducq Foundation, Donald W. Reynolds Foundation, James and Polly Annenberg La Vea Charitable Trusts, AstraZeneca, Novartis, Pharmacia, Roche, Sanofi-Aventis, Abbott Laboratories, Amgen.

Equity: Co-inventor on patients held by Brigham and Women’s Hospital.

JUPITERAHA November 9, 2008

A Randomized Trial of Rosuvastatin in the Preventionof Cardiovascular Events Among 17,802 Apparently Healthy

Men and Women With Elevated Levels of C-Reactive Protein (hsCRP):

The JUPITER Trial

Paul Ridker*, Eleanor Danielson, Francisco Fonseca*, Jacques Genest*,Antonio Gotto*, John Kastelein*, Wolfgang Koenig*, Peter Libby*,

Alberto Lorenzatti*, Jean MacFadyen, Borge Nordestgaard*, James Shepherd*, James Willerson, and Robert Glynn*

on behalf of the JUPITER Trial Study Group

An Investigator Initiated Trial Funded by AstraZeneca, USA

* These authors have received research grant support and/or consultation fees from one or morestatin manufacturers, including Astra-Zeneca. Dr Ridker is a co-inventor on patents held by the

Brigham and Women’s Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease that have been licensed to Dade-Behring and AstraZeneca.

< 1 mg/L 1 to 3 mg/L > 3 mg/L

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What are the environmental and genetic influences on What are the environmental and genetic influences on CRP?CRP?

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“low risk”“moderate risk” “high risk”

Ridker et al Circulation 2004;109:1955-59

Inflammation, Statin Therapy, and hsCRP: Inflammation, Statin Therapy, and hsCRP: Initial ObservationsInitial Observations

Circulation. 1998;98:839–844.

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PP Trend = 0.005 Trend = 0.005

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Circulation. 1999;100:230-235.

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Clinical Relevance of Achieved LDL and Achieved hsCRP

After Treatment with Statin Therapy

Ridker et al NEJM 2005;352:20-28.

0.0 0.5 1.0 1.5 2.0 2.50.0 0.5 1.0 1.5 2.0 2.50.0 0.5 1.0 1.5 2.0 2.50.0 0.5 1.0 1.5 2.0 2.5

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LDL > 70 mg/dL, CRP > 2 mg/L

LDL < 70 mg/dL, CRP > 2 mg/LLDL > 70 mg/dL, CRP < 2 mg/L

LDL < 70 mg/dL, CRP < 2 mg/L

Clinical Relevance of Achieved LDL and Achieved hsCRP

After Treatment with Statin Therapy

Ridker et al NEJM 2005;352:20-28.

JUPITERWhy Consider Statins for Low LDL, high hsCRP Patients?

In 2001, in an hypothesis generating analysis of apparently healthy individuals in the AFCAPS / TexCAPS trial*, we observed that those with low levels of both LDL and hsCRP had extremely low vascular event rates and that statin therapy did not reduce events in this subgroup (N=1,448, HR 1.1, 95% CI 0.56-2.08). Thus, a trial of statin therapy in patients with low cholesterol and low hsCRP would not only be infeasible in terms of power and sample size, but would be highly unlikely to show clinical benefit.

In contrast, we also observed within AFCAPS/TexCAPS that among those with low LDL but high hsCRP, vascular event rates were just as high as rates among those with overt hyperlipidemia, and that statin therapy significantly reduced events in this subgroup (N=1,428, HR 0.6, 95% CI 0.34-0.98).

*Ridker et al N Engl J Med 2001;344:1959-65

JUPITERWhy Consider Statins for Low LDL, high hsCRP Patients?

However, while intriguing and of potential public health importance, the observation in AFCAPS/TexCAPS that statin therapy might be effective among those with elevated hsCRP but low cholesterol was made on a post hoc basis. Thus, a large-scale randomized trial of statin therapy was needed to directly test this hypotheses.

Ridker et al, New Engl J Med 2001;344:1959-65

Low LDL, Low hsCRP

Low LDL, High hsCRP

Statin Effective Statin Not Effective

1.0 2.00.5

[A]

[B]

Low LDL, Low hsCRP

Low LDL, High hsCRP

Statin Effective Statin Not Effective

1.0 2.00.5

AFCAPS/TexCAPS Low LDL Subgroups

RR

JUPITERPrimary Objectives

To investigate whether rosuvastatin 20 mg compared to placebo would decrease the rate of first major cardiovascularevents among apparently healthy men and women with LDL < 130 mg/dL (3.36 mmol/L) who are nonethelessat increased vascular risk on the basis of an enhanced inflammatory response, as determined by hsCRP > 2 mg/L.

To enroll large numbers of women and individuals of Black or Hispanic ethnicity, groups for whom little data on primaryprevention with statin therapy exists.

Justification for the Use of statins in Prevention: an Intervention Trial Evaluating Rosuvastatin

Ridker et al NEJM 2008

Rosuvastatin 20 mg (N=8901)Rosuvastatin 20 mg (N=8901) MIMIStrokeStroke

UnstableUnstable AnginaAngina

CVD DeathCVD DeathCABG/PTCACABG/PTCA

JUPITERJUPITERMulti-National Randomized Double Blind Placebo Controlled Trial of Multi-National Randomized Double Blind Placebo Controlled Trial of

Rosuvastatin in the Prevention of Cardiovascular EventsRosuvastatin in the Prevention of Cardiovascular EventsAmong Individuals With Low LDL and Elevated hsCRPAmong Individuals With Low LDL and Elevated hsCRP

4-week 4-week run-inrun-in

Ridker et al, Circulation 2003;108:2292-2297.

No Prior CVD or DMNo Prior CVD or DMMen Men >>50, Women 50, Women >>6060

LDL <130 mg/dL hsCRP >2 mg/L

JUPITERTrial Design

Placebo (N=8901)Placebo (N=8901)

Argentina, Belgium, Brazil, Bulgaria, Canada, Chile, Colombia, Costa Rica, Denmark, El Salvador, Estonia, Germany, Israel, Mexico, Netherlands, Norway, Panama, Poland, Romania, Russia, South Africa, Switzerland,

United Kingdom, Uruguay, United States, Venezuela

JUPITERBaseline Clinical Characteristics

Rosuvastatin Placebo(N = 8901) (n = 8901)

Age, years (IQR) 66.0 (60.0-71.0) 66.0 (60.0-71.0) Female, N (%) 3,426 (38.5) 3,375 (37.9)Ethnicity, N (%) Caucasian 6,358 (71.4) 6,325 (71.1) Black 1,100 (12.4) 1,124 (12.6) Hispanic 1,121 (12.6) 1,140 (12.8)Blood pressure, mm (IQR) Systolic 134 (124-145) 134 (124-145) Diastolic 80 (75-87) 80 (75-87)Smoker, N (%) 1,400 (15.7) 1,420 (16.0)Family History, N (%) 997 (11.2) 1,048 (11.8)Metabolic Syndrome, N (%) 3,652 (41.0) 3,723 (41.8)Aspirin Use, N (%) 1,481 (16.6) 1,477 (16.6)

All values are median (interquartile range) or N (%)

JUPITERBaseline Blood Levels (median, interquartile range)

Rosuvastatin Placebo(N = 8901) (n = 8901)

hsCRP, mg/L 4.2 (2.8 - 7.1) 4.3 (2.8 - 7.2) LDL, mg/dL 108 (94 - 119) 108 (94 - 119)

HDL, mg/dL 49 (40 – 60) 49 (40 – 60)

Triglycerides, mg/L 118 (85 - 169) 118 (86 - 169)

Total Cholesterol, mg/dL 186 (168 - 200) 185 (169 - 199)

Glucose, mg/dL 94 (87 – 102) 94 (88 – 102)

HbA1c, % 5.7 (5.4 – 5.9) 5.7 (5.5 – 5.9)

All values are median (interquartile range). [ Mean LDL = 104 mg/dL ]

JUPITER WOSCOPS AFCAPS

Sample size (n) 17,802 6,595 6,605

Women (n) 6,801 0 997

Minority (n) 5,118 0 350

Duration (yrs) 1.9 (max 5) 4.9 5.2

Diabetes (%) 0 1 6

Baseline LDL-C (mg/dL) 108 192 150

Baseline HDL-C (mg/dL) 49 44 36-40

Baseline TG (mg/dL) 118 164 158

Baseline hsCRP (mg/L) > 2 NA NA

Intervention Rosuvastatin Pravastatin Lovastatin20 mg 40 mg 10-40 mg

JUPITER Trial Study Group, Am J Cardiol 2007

Comparison of the JUPITER trial population to previous statin trialsof primary prevention

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JUPITEREffects of rosuvastatin 20 mg on LDL, HDL, TG, and hsCRP

LDL decrease 50 percent at 12 months

hsCRP decrease 37 percent at 12 months

HDL increase 4 percent at 12 months

TG decrease 17 percent at 12 months

JUPITERPrimary Trial Endpoint : MI, Stroke, UA/Revascularization, CV Death

Placebo 251 / 8901

Rosuvastatin 142 / 8901

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Placebo

8,901 8,631 8,412 6,540 3,893 1,958 1,353 983 544 157

8,901 8,621 8,353 6,508 3,872 1,963 1,333 955 534 174

JUPITERPrimary Trial Endpoint : MI, Stroke, UA/Revascularization, CV Death

Placebo 251 / 8901


HR 0.56, 95% CI 0.46-0.69P < 0.00001

Number Needed to Treat (NNT5) = 25

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8,901 8,631 8,412 6,540 3,893 1,958 1,353 983 544 157

8,901 8,621 8,353 6,508 3,872 1,963 1,333 955 534 174

JUPITERMyocardial Infarction, Stroke, Cardiovascular Death

Placebo (N = 157)

Rosuvastatin (N = 83)

HR 0.53, 95%CI 0.40-0.69P < 0.00001

- 47 %

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Placebo

8,901 8,643 8,437 6,571 3,921 1,979 1,370 998 551 159

8,901 8,633 8,381 6,542 3,918 1,992 1,365 979 550 181

JUPITERArterial Revascularization / Unstable Angina

Placebo (N = 143)

Rosuvastatin (N = 76)

HR 0.53, 95%CI 0.40-0.70P < 0.00001

- 47 %

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Rosuvastatin

Placebo

8,901 8,640 8,426 6,550 3,905 1,966 1,359 989 547 158

8,901 8,641 8,390 6,542 3,895 1,977 1,346 963 538 176

JUPITERIndividual Components of the Primary Endpoint

*Nonfatal MI, nonfatal stroke, revascularization, unstable angina, CV death

Endpoint Rosuvastatin Placebo HR 95%CI P

Primary Endpoint* 142 251 0.56 0.46-0.69 <0.00001

Non-fatal MI 22 62 0.35 0.22-0.58 <0.00001Any MI 31 68 0.46 0.30-0.70 <0.0002

Non-fatal Stroke 30 58 0.52 0.33-0.80 0.003Any Stroke 33 64 0.52 0.34-0.79 0.002

Revascularization or Unstable Angina 76 143 0.53 0.40-0.70 <0.00001

MI, Stroke, CV Death 83 157 0.53 0.40-0.69 <0.00001

JUPITERPrimary Endpoint – Subgroup Analysis I

0.25 0.5 1.0 2.0 4.0

Rosuvastatin Superior Rosuvastatin Inferior

MenWomen

Age < 65Age > 65

SmokerNon-Smoker

CaucasianNon-Caucasian

USA/CanadaRest of World

HypertensionNo Hypertension

All Participants

N P for Interaction

11,001 0.80 6,801

8,541 0.32 9,261

2,820 0.6314,975

12,683 0.57 5,117

6,041 0.5111,761

10,208 0.53 7,586

17,802

JUPITERPrimary Endpoint – Subgroup Analysis II

0.25 0.5 1.0 2.0 4.0

Rosuvastatin Superior Rosuvastatin Inferior

Family HX of CHDNo Family HX of CHD

BMI < 25 kg/m2

BMI 25-29.9 kg/mBMI > 30 kg/m

Metabolic SyndromeNo Metabolic Syndrome

Framingham Risk < 10%Framingham Risk > 10%

hsCRP > 2 mg/L Only

All Participants

N P for Interaction

2,045 0.0715,684

4,073 0.70 7,009 6,675

7,375 0.1410,296

8,882 0.99 8,895

6,375

17,802

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JUPITERAdverse Events and Measured Safety Parameters

Event Rosuvastatin Placebo P

Any SAE 1,352 (15.2) 1,337 (15.5) 0.60Muscle weakness 1,421 (16.0) 1,375 (15.4) 0.34Myopathy 10 (0.1) 9 (0.1) 0.82Rhabdomyolysis 1 (0.01)* 0 (0.0) --Incident Cancer 298 (3.4) 314 (3.5) 0.51Cancer Deaths 35 (0.4) 58 (0.7) 0.02Hemorrhagic stroke 6 (0.1) 9 (0.1) 0.44

GFR (ml/min/1.73m2 at 12 mth) 66.8 (59.1-76.5) 66.6 (58.8-76.2) 0.02ALT > 3xULN 23 (0.3) 17 (0.2) 0.34

Fasting glucose (24 mth) 98 (91-107) 98 (90-106) 0.12HbA1c (% at 24 mth) 5.9 (5.7-6.1) 5.8 (5.6-6.1) 0.01Glucosuria (12 mth) 36 (0.5) 32 (0.4) 0.64Incident Diabetes** 270 (3.0) 216 (2.4) 0.01

*Occurred after trial completion, trauma induced. All values are median (interquartile range) or N (%)**Physician reported

JUPITERStatins and the Development of Diabetes

0.25 0.5 1.0 2 4

WOSCOPS Pravastatin

HPS Simvastatin

ASCOT-LLA Atorvastatin

JUPITER Rosuvastatin

PROVE-IT Atorvastatin VS

Pravastatin

0.70 (0.50–0.98)

1.20 (0.98–1.35)

1.20 (0.91–1.44)

1.11 (0.67–1.83)

1.25 (1.05–1.54)

Statin Better Statin Worse

HR (95% CI)

PROSPER Pravastatin 1.34 (1.06–1.68)

JUPITERSecondary Endpoint – All Cause Mortality

Placebo 247 / 8901


HR 0.80, 95%CI 0.67-0.97P= 0.02

- 20 %

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RosuvastatinPlacebo

8,901 8,847 8,787 6,999 4,312 2,268 1,602 1,192 683 2278,901 8,852 8,775 6,987 4,319 2,295 1,614 1,196 684 246

JUPITERConclusions – Efficacy I

Among apparently healthy men and women with elevatedhsCRP but low LDL, rosuvastatin reduced by 47 percent incident myocardial infarction, stroke, and cardiovascular death.

Despite evaluating a population with lipid levels widely considered to be “optimal” in almost all current prevention algorithms, the relative benefit observed in JUPITER was greater than in almost all prior statin trials.

In this trial of low LDL/high hsCRP individuals who do notcurrently qualify for statin therapy, rosuvastatin significantlyreduced all-cause mortality by 20 percent.

JUPITERConclusions – Efficacy II

Benefits of rosuvastatin were consistent in all sub-groups evaluated regardless of age, sex, ethnicity, or other baseline clinical characteristic, including those with elevated hsCRP and no other major risk factor.

Rates of hospitalization and revascularization were reducedby 47 percent within a two-year period suggesting that the screening and treatment strategy tested in JUPITER is likely to be cost-effective, benefiting both patients and payers.

The Number Needed to Treat in JUPITER was 25 for the primary endpoint, a value if anything smaller than that associated with treating hyperlipidemia in primary prevention.

JUPITERConclusions - Safety

With regard to safety , the JUPITER results show no increase in serious adverse events among

thoseallocated to rosuvastatin 20 mg as compared to

placeboin a setting where half of the treated patients

achievedlevels of LDL< 55 mg/dL (and 25 percent had LDL <

44mg/dL).

show no increase in myopathy, cancer, hepaticdisorders, renal disorders, or hemorrhagic stroke

with treatment duration of up to 5 years

show no increase in systematically monitored glucose or

glucosuria during follow-up, but small increases inHbA1c and physician reported diabetes similar to

thatseen in other major statin trials

JUPITERAchieved LDLC, Achieved hsCRP, or Both?

Is the benefit observed in the JUPITERtrial associated with achieving

a low level of LDLC,a low level of hsCRP

or both?

Do we need to achieve the “dual targets”of low LDLC and low hsCRP in order to

maximize the benefit of statin therapy?

JUPITERPredicted Benefit Based on LDL Reduction vs Observed Benefit

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JUPITERPredicted Benefit Based on LDL Reduction vs Observed Benefit

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JUPITER OBSERVED


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PROVE IT – TIMI 22NEJM 2005;352:20-28.

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Follow-up (days)

A to ZCirculation 2006;114:281-8

Clinical Importance of Achieving LDL-C < 70 mg/dL and hsCRP < 2 mg/LFollowing Initiation of Statin Therapy

0 180 360 540 720 900

Follow-up (days)

LDL>70, hsCRP>2LDL<70, hsCRP>2LDL>70, hsCRP<2LDL<70, hsCRP<2

1. LDL-C is a strong, 1. LDL-C is a strong, independent predictor independent predictor of future CV eventsof future CV events

2. Statins Lower LDL-C2. Statins Lower LDL-C

3. The level of LDL-C 3. The level of LDL-C achieved after starting achieved after starting statin therapy predicts statin therapy predicts recurrent event rates (ie recurrent event rates (ie “lower is better”)“lower is better”)

1. hsCRP is a strong, 1. hsCRP is a strong, independent predictor independent predictor of future CV eventsof future CV events

2. Statins Lower hsCRP2. Statins Lower hsCRP

3. The level of hsCRP 3. The level of hsCRP achieved after starting achieved after starting statin therapy predicts statin therapy predicts recurrent event rates (ie recurrent event rates (ie “lower is better”)“lower is better”)

Dual Goals for Statin Therapy : LDL-C < 70 mg/dL and hsCRP < 2 mg/L

PROVE IT, A to Z, AFCAPS/TexCAPS, REVERSALPROVE IT, A to Z, AFCAPS/TexCAPS, REVERSALDose Correct Use of Statin Therapy Require Dose Correct Use of Statin Therapy Require

Evaluation for Evaluation for bothboth LDLC and hsCRP? LDLC and hsCRP?

JUPITERImplications for Primary Prevention

Among men over 45 and post-menopausal women:

If diabetic or family history, treatIf LDLC > 160 mg/dL, treat

If hsCRP > 3 mg/L, treat

A simple evidence based approach to statin therapyfor primary prevention.


JUPITERPublic Health Implications

Application of the simple screening and treatment strategy tested in the JUPITER trial over a five-year period could conservatively prevent more than 250,000 heart attacks, strokes, revascularization procedures, and cardiovascular deaths in the United States alone.

We thank the 17,802 patients and the >1,000 investigatorsworldwide for their personal time, effort, and commitmentto the JUPITER trial.

www.brighamandwomens.org/jupitertrial



Christie Ballantyne, MD Chief, Section of Atherosclerosis and Vascular MedicineDirector, Center for Cardiovascular Disease PreventionCo-Director, Lipid Metabolism and Atherosclerosis Clinic

Methodist DeBakey Heart CenterBaylor College of Medicine

Houston, TX

Disclosure • Disclosure of Unlabeled Use and Investigational Product

Discussions:Dr. Ballantyne has indicated that his presentation will not include the discussion of unlabeled uses of commercial products or products that have not yet been approved by the FDA for use in the United States for any purpose.

• Disclosure of Affiliations and Significant Relationships:Dr. Ballantyne has received honoraria related to speakers’ bureau activities from AstraZenece, Merck, Pfizer, Reliant, and Schering-Plough. He has also received grant support related to research activities from Abbott, ActivBiotics, Gene Logic, GlaxoSmithKline, Integrated Theraputics, Merck, Pfizer, Schering-Plough, Sanofi-Synthelabo, and Takeda. Dr. Ballantyne has also received honoraria related to consulting activities from Abbott, AstraZeneca, Atherogenics, Merck, Merck Schering-Plough, Novartis, Pfizer, Reliant, Schering-Plough, Sanfi-Synthelabo, Takeda, and GlaxoSmithKline.

“an examination of the jupiter trial”

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