efficacy of statins in primary and secondary prevention of cv events - well established...

Dr sajeerSenior Resident

Dept. of Cardiology, MCH, Calicut

Journal review of evidence

Statins for Secondary Prevention

Efficacy of statins in primary and secondary prevention of CV events - well established Meta-analyses of RCTs : - demonstrated dramatic reductions in major CV events, cardiovascular morbidity, and all-cause mortality

LDLC ↓ - reduces initial coronary events - reduces recurrent coronary events - decreases stroke - Slows progression of atherosclerosis - induce regression of atherosclerosis

- A 1% reduction in LDL-C reduces coronary events by 1%- High dose of statins→ reduces LDL-C levels and coronary events by 50%.

- Statins in Stable CAD

- Intensive Statin therapy

- Statins in Acute Coronary Syndromes

- Statin therapy before PCI

- Statins in Heart Failure

Chest 2005;128:3641-3651

•JUPITER

CAD & Statins Trials

1994 4S 2002 PROSPER

1995 WOSCOPS 2002 ALLHAT-LLA

1996 CARE 2002 ASCOT-LLA

1998 AFCAPS/TEXCAPS 2004 PROVE-IT

1998 LIPID 2004 A to Z

2001 MIRACL 2005 TNT

2002 HPS 2005 IDEAL

Statin Trials: Chronology

Primary preventionAcute coronary syndromesChronic Coronary heart disease

4S Scandinavian Simvastatin Survival Study

CARE Cholesterol and Recurrent Events study

LIPID Long-term Intervention with Pravastatin in Ischemic Disease study

HPS Heart Protection Study

Statins Secondary prevention Trials

Study Design:- Enrolled : 4444 pts

Mean Follow Up: - 4.9-6.3 yrs (median 5.4 yrs)

Mean Patient Age: 35-70 Female: 19%

Patient Population: - 35–70 years of age

- angina pectoris or - previous MI (≥6 months earlier) - serum cholesterol between 212-309 mg/dL (mean LDL 188 mg/dL).

4S Scandinavian Simvastatin Survival Study

Lancet 1994;344:1383–1389

Primary Endpoints:- all-cause mortality

Secondary Endpoints:- serum lipid levels, major coronary events

Objective :To investigate whether long-term simvastatin therapy reduces total mortality and coronary events in post-MI and or angina patients with total cholesterol between 212-309 mg/dL.

Simvastatin 40 mg v/s placebo

Scandinavian Simvastatin Survival Study (4S)

Mor

talit

y (%

)

Placebo

11.5

Simvastatin

12

8

4

0

8.2

P<0.001

30% RRR

Lancet 1994;344:1383–1389

Primary Endpoint: 4S trialPrimary Endpoint: 4S trial

80828486889092949698

100

0 1 2 3 4 5 6

Simvastatin

Placebo

Years since randomization

% S

urvi

ving

30% risk reduction

p = 0.0003

Lancet, Vol 344, November 19, 1994

• 80 centers in the US and Canada• 4159 men and women aged 21 to 75 yrs enrolled• 3 to 20 months post-MI• Total-C < 240 LDL-C between 115 – 174 mg/dl• Follow up - 5 yr

Sacks, F. et al, N Engl J Med 1996; 335:1001-9

CARE - Study Design:

(CARE) Cholesterol and Recurrent Events Study

Pravastatin 40 mg vs. placebo

(CARE) Cholesterol and Recurrent Events Study

Sacks, F. et al, N Engl J Med 1996; 335:1001-9

Cholesterol and Recurrent Events (CARE) Study

Placebo

13.2

Pravastatin

15

10

5

0

10.2

P=0.003

24% RRRRa

te o

f MI o

r CH

D

deat

h (%

)

Sacks FM et al. NEJM 1996;335:1001–1009

LIPID Long-term Intervention with Pravastatin in Ischemic Disease study

N Engl J Med 1998;339:1349-57

Baseline LDL-C (mg/dL)

Statin (n = 10,269)

Placebo (n = 10,267)

<100 282 (16.4%) 358 (21.0%)

100–129 668 (18.9%) 871 (24.7%)

130 1083 (21.6%) 1356 (26.9%)

All patients 2033 (19.8%) 2585 (25.2%)

Event Rate Ratio (95% CI)Statin Better Statin Worse

0.4 0.6 0.8 1.0 1.2 1.4

0.76 (0.72–0.81)P<0.0001

Heart Protection Study (HPS)- Simvastatin trial

HPS Collaborative Group. Lancet 2002;360:7-22

20,536 patients with CAD, other occlusive arterial disease, or DM randomized to simvastatin (40 mg) or placebo for 5.5 years

Significant benefits with simvastatin :

- 13 percent reduction in all-cause mortality (12.9 v/s 14.7 % )

- 18 percent reduction in deaths from heart disease (5.7 v/s 6.9 %)

- 24 percent reduction in major cardiovascular events (19.8 v/s 25.2 %)

- 25 percent reduction in the first event rate for stroke (4.3 v/s 5.7%)

Heart Protection Study (HPS)- Simvastatin trial

Clinical trials of statins - secondary prevention

Treating to New Targets (TNT) study

- Intensive lowering of LDL-C with high-dose atorvastatin therapy - Patients with CAD + metabolic syndrome

- prospective, double blind, parallel-group trial done at 256 sites (14 countries between 1998- 2004)- median follow-up: 4·9 yrs- 10 001 patients enrolled - aged 35–75 yrs- with clinically evident coronary heart disease.

TNT: Treating to New Targets Assessment of intensive lipid lowering on clinical outcomes

LaRosa JC et al. N Engl J Med. 2005;352:1425-35.

Design: 10,001 patients with stable CHD and LDL-C 130-250 mg/dL

Treatment: Randomized to Atorvastatin 10 mg or 80 mg

Follow-up: 4.9 years

Primary outcome: CHD death, MI, resuscitation after cardiac arrest, fatal/nonfatal stroke

TNT: Treatment effects on primary outcome

LaRosa JC et al. N Engl J Med. 2005;352:1425-35.

Major CVevents (%)

CHD death, MI, resuscitation after cardiac arrest, fatal/nonfatal stroke

Follow-up (years)

65421 3

Atorvastatin10 mg (n = 5006)

Atorvastatin 80 mg (n = 4995)

0

0.00

0.05

0.10

0.15

At 5 year: 22% Risk reductionHR = 0.78 (0.69–0.89)P < 0.001

N = 10,001

Evaluated the effect of intensive vs. moderate lipid lowering therapy in patients with a history of MI

Incremental Decrease in End Points Through Aggressive Lipid Lowering (IDEAL) Trial

8,888 patients with a history of acute MI randomized to atorvastatin (80 mg) or simvastatin (20 mg) for 5 years

Primary endpoint :- occurrence of a major coronary event

( coronary death, confirmed nonfatal acute MI, or cardiac arrest with resuscitation)

Incremental Decrease in End Points Through Aggressive Lipid Lowering (IDEAL) Trial

Cum

ulati

ve H

azar

d (%

)

Years Since Randomization

0 1 2 3 4 5

4

8

12

HR=0.89 ( 95% CI 0.78-1.01)

Simvastatin (20 mg)Atorvastatin (80 mg)

Pedersen et al. JAMA 2005;294:2437-2445

Non significant reduction in the primary endpoint (9.3 versus 10.4 percent)

No effect on : all-cause mortality ( HR 0.98 CI 0.85-1.13) : cardiovascular mortality ( HR 1.03 CI 0.85-1.24) : non cardiovascular mortality (HR 0.92 CI 0.73-1.15 )

A reduction in a number of secondary endpoints: - nonfatal myocardial infarction (6 versus 7.2 percent HR 0.83 CI 0.71-0.98) - coronary revascularization (13.0 versus 16.6 percent HR 0.77 CI 0.69-0.86)

The AVERT (Atorvastatin Versus Revascularization Treatment) trial

Compared the outcome of aggressive lipid-lowering with atorvastatin (80 mg/day) to that of angioplasty in 341 patients with 1 or 2 vessel CAD and LDL levels >115 mg/dl

18 month follow-up : - reduction in mean LDL levels was greater in the atorvastatin group - (140 to 77 mg/dL V/S 140 to 119 mg/dL in the angioplasty group)

- Atorvastatin group :- Insignificant trend toward fewer composite endpoints

(13 v/s 21 percent )- lower rate of CABG (1.2 v/s 5.1 percent) - hospitalization for worsening angina (6.7 versus 14.1 percent)

Time to the first ischemic event was significantly longer in the atorvastatin group compared with the placebo group

Non significant trend toward fewer cardiac

events (13 versus 21%).

(Death, MI , stroke, resuscitated cardiac arrest, revascularization, and hospitalization for

worsening angina)

The AVERT (Atorvastatin Versus Revascularization Treatment) trial

PROVE IT: PRavastatin Or AtorVastatin Evaluation and Infection Therapy

PROVE IT: PRavastatin Or AtorVastatin Evaluation and Infection Therapy

First major trial to compare the effects of Pravastatin versus Atorvastatin in reducing the risk of MACE

Designed to evaluate further the role of infection in cardiovascular disease

Head-to-head comparison of Pravastatin and Atorvastatin

Standard medical therapy

Pravastatin40 mg

Atorvastatin80 mg

Gatifloxacin Placebo

PROVE IT study designDouble-blind, randomised, 4,000 patients with ACS

<10 days and total cholesterol <240 mg/dL

PlaceboGatifloxacin

Follow-up visit 30 days

Minimum duration 18 months

PROVE IT-TIMI 22:

Ray KK and Cannon CP Am J Cardiol. 2005;96(suppl):54F-60F.Adapted from Cannon CP et al. N Engl J Med. 2004;350:1495-504.

30

20

3 6 9 12 30

10

0

15 18 21 24 27

40 mg Pravastatin80 mg Atorvastatin

P = 0.005

Follow-up (months)

Death or major CV event (%)

0

N = 4162 with ACS26.3%

22.4%

RRR 16%

2 years follow-up

•Within 10 days of ACS or after PCI

A to Z: Early initiation of intensive regimen v/s delayed initiation of less-intensive regimen

de Lemos JA et al. JAMA. 2004;292:1307-16.

Population: 4497 patients with ACS

Treatments: Simvastatin 40 mg/d for 1 month, followed by 80 mg/d

Placebo for 4 months, followed by simvastatin 20 mg/d

Median follow-up: 2 years (721 days)

Primary outcome: CV death, nonfatal MI, ACS readmission, stroke

de Lemos JA et al. JAMA. 2004;292:1307-16.

Primary composite outcome rate (%)

Overall study result

Randomization through month 4

Months 4–24

Simvastatin40/80 mgn = 2265

Placebo + simvastatin 20 mg n = 2232

Favorssimvastatin40/80 mg

Favors placebo + simvastatin20 mg

Hazard ratio (95% CI)

14.4 16.7

8.2 8.1

6.8 9.3

0.5 1.0 1.5

A to Z: Treatment effect on primary outcome at different time periods

CV death, MI, recurrent ACS hospitalization, stroke

N = 4497 with ACS within 2-5 days of events

Time from randomization (months)

Cum

ulati

ve e

vent

rate

(%

)*

0

5

10

15

20

0 4 8 12 16 20 24

Aggrastat to Zocor (A to Z) Trial

de Lemos JA et al. JAMA 2004;292:1307-1316

Placebo + Simvastatin 20 mg/daySimvastatin 40/80 mg/day

HR=0.89, P=0.14

- No statistical difference in the primary end point between the two treatment strategies

- Trend towards a reduced event rate in the high dose statin regimen at the end of 24 month follow-up

LaRosa JC et al. NEJM 2005;352:1425-1435

CARE=Cholesterol and Recurrent Events Trial, HPS=Heart Protection Study, LIPID=Long-term Intervention with Pravastatin in Ischaemic Disease; 4S=Scandinavian Simvastatin Survival Study, TNT=Treating to New Targets

30

25

20

15

10

5

00 70 90 110 130 150 170 190 210

LDL-C (mg/dL)

TNT (atorvastatin 80 mg/d)TNT (atorvastatin 10 mg/d)

HPSCARE

LIPIDLIPIDCARE

HPS

Even

t (%

) 4S

4SStatinPlacebo

Relationship between LDL-C Levels and Event Rates in Secondary Prevention Statin Trials of Patients with Stable CHD

CHD event rates in secondary prevention trials (5 years in duration except the PROVE-IT study, which lasted 2 years) were directly proportional to low-density lipoprotein (LDL) cholesterol levels. The event rate is predicted to approach 0 at LDL of 30 mg/dL

Cannon CP et al. JAMA 2005;294:2492-2494

RR in MI or CHD Death (%)

RR in Primary End Point (%)

LDL-C Reduction (mg/dL)

Duration (years)

PopulationTrial

1111235Stable CAD (N = 8888)

IDEAL

2122245Stable CAD (N =10,001)

TNT

1511142ACS (N = 4497)

A to Z

1616332ACS (N = 4162)

PROVE IT-TIMI 22

High-dose better High-dose worse

Odds Reduction

Event RatesNo./Total (%)

High Dose Std Dose

-17%147/2099

(7.0)172/2063

(8.3)

-15%205/2265

(9.1)235/2232

(10.5)

-21%334/4995

(6.7)418/5006

(8.3)

-12%411/4439

(9.3)463/4449

(10.4)

-16% 1097/13798 (8.0)

1288/13750 (9.4)

PROVE IT-TIMI 22

A-to-Z

TNT

IDEAL

Total

0.658451 1 1.51872

OR, 0.8495% CI, 0.77-0.91p=0.00003

Odds Ratio (95% CI)

Meta-Analysis of Intensive Statin Therapy Coronary Death or MI

High-dose statin better High-dose statin worse

Odds Reduction

Event RatesNo./Total (%)

High Dose Std Dose

-16% 3972/13798 (28.8)

4445/13750 (32.3)

-16% 1097/13798 (8.0)

1288/13750 (9.4)

-12%462/13798

(3.3)520/13750

(3.8)

+3%340/13798

(2.5)331/13750

(2.4)

-6%808/13798

(5.9)857/13750

(6.2)

-18%316/13798

(2.3)381/13750

(2.8)

Coronary Death or Any Cardiovascular Event

Coronary Death or MI

Cardiovascular Death

Non-Cardiovascular Death

Total Mortality

Stroke

0.5 1 2.5

OR 0.8295% CI, 0.71-0.96p=0.012

Odds Ratio (95% CI)

Meta-Analysis of Intensive Statin Therapy All Endpoints

OR, 0.9495% CI, 0.85-1.04P=0.20

OR, 1.0395% CI, 0.88-1.20p=0.73

OR, 0.8895% CI, 0.78-1.00p=.054

OR, 0.8495% CI, 0.77-0.91p=0.00003

OR, 0.8495% CI, 0.80-0.89p<0.0001

Cannon CP, et al. JACC 2006; 48: 438 - 445.

SATURN trial - Compared two intensive statin therapy regimens - Atorvastatin 80 mg daily v/s Rosuvastatin 40 mg daily- 1039 patients with known CAD

- No statistically-significant difference between the regimens in the primary endpoint of percent atheroma volume (↓ed with both regimens : 1.22 % V/S 0.99 % respectively)

Compared with Atorvastatin patients treated with Rosuvastatin had- lower levels of LDL-C 62 md/dl v/s 70.2 mg/dL

- higher levels of HDL-C 50 mg/dl v/s 48.6 mg/dL

Statins may decrease CVS events by a number of mechanisms( important early after MI)

- plaque stabilization- reversal of endothelial dysfunction- inhibition of monocyte recruitment

- ↓ed thrombogenicity- reduction in inflammation

Early use of statins after an ACS

Secondary prevention trials : - primarily evaluated the role of statin therapy initiated 3 to 6 months or longer after acute MI

- led to the investigation of earlier initiation of statin therapy during ACS (MI or unstable angina)

1 Pravastatin and Thrombolytic Therapy 2 Lipids in Coronary Artery Disease 3 Reduction of Cholesterol in Ischaemia and Function of the Endothelium4 FLuvastatin On RIsk Diminishing after Acute myocardial infarction5 Myocardial Ischaemia Reduction with Aggressive Cholesterol Lowering

Clinical evidence for the benefits of early statin initiation

Study Time to Statin Resultsinitiation

PTT1 6 h Pravastatin coronary events restenosis rates

L-CAD2 6 d Pravastatin Improved outcomes mean progression coronary lesion regression

RECIFE3 10 d Pravastatin Rapid improvement of

endothelial function

FLORIDA4 8 d Fluvastatin No significant benefit

MIRACL5 24–96 h Atorvastatin time to first event

Timing of statin therapy initiation after ACS in recent clinical studies

Days

Secondary prevention

0 6Months

32

PTT

L-CAD

RECIFE

CARE

LIPID

24Hours

10 6 8 1212 18 4

4S

6

Atorvastatin

Pravastatin

Simvastatin

WOSCOPS

Primary prevention

ACS

Fluvastatin

FLORIDA

MIRACL

Patients with event (%)

0

10

20

30

Non-fatal MI ** Recurrentangina **

In-hospitaldeath

Pravastatin (n=72)

Control (n=78)

† ‡

Pravastatin and Thrombolytic Therapy trial (PTT): Early therapy improves event-free survival

*Within 6 hours of MI; **6 months follow-up†p=0.01, ‡p=0.03


Days


0 6Months

32

PTT

L-CAD

RECIFE

CARE

LIPID

24Hours

10 6 8 1212 18 4

4S

6

Atorvastatin

Pravastatin

Simvastatin

WOSCOPS

Primary prevention

ACS

Fluvastatin

FLORIDA

MIRACL

L-CAD study design

L-CAD = Lipids in Coronary Artery Disease

126 men and women post acute MI and/or PTCA for UA

Pravastatin 20–40 mg (+cholestyramine and nicotinic acid) to achieve an LDL <130

mg/dL

Clinical – 2 years, Angiography – 6 months and 2 years

major CV clinical events

Baseline cholesterol130–250 mg/dL

Usual care

Pravastatin-basedintensified (n=70)

Conventional (n=56)

L-CAD: Survival without major cardiovascular events

Time (months)

0 2 4 6 8 10 12 14 16 18 20 22 240

0.2

0.4

0.6

0.8

1.0

Log rank = 0.0024Breslow = 0.0042


Days


0 6Months

32

PTT

L-CAD

RECIFE

CARE

LIPID

24Hours

10 6 8 1212 18 4

4S

6

Atorvastatin

Pravastatin

Simvastatin

WOSCOPS

Primary prevention

ACS

Fluvastatin

FLORIDA

MIRACL

(REduction of Cholesterol in Ischemia and Function of the Endothelium

Time (weeks)

*60 patients admitted for acute MI or unstable angina, enrolled before hospital discharge

Flow-mediated dilatation (%)*

4

5

6

7

8

0 6

Pravastatin 40 mg/day

Placebo

p<0.05

The RECIFE study: Pravastatin rapidly improves endothelial function after ACS


Days


0 6Months

32

PTT

L-CAD

RECIFE

CARE

LIPID

24Hours

10 6 8 1212 18 4

4S

6

Atorvastatin

Pravastatin

Simvastatin

WOSCOPS

Primary prevention

ACS

Fluvastatin

FLORIDA

MIRACL

Effects of Atorvastatin on Early Recurrent Ischemic Events in ACS: A Randomized Controlled Trial

Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL)

Objective:

“To prove that early, rapid, and intensive cholesterol lowering therapy will reduce early recurrent ischemic events in patients with unstable angina or

non-Q-wave MI”

The Hypothesis

Rapid and early cholesterol reduction

Early plaque stabilisation

Diminished incidence of recurrent ischemic

events

MIRACL study design

Prospective, randomised, multicentre, double-blind

3,086 patients

80 mg atorvastatin, commenced within 24–96 h of event

Follow up at 2, 6 and 16 weeks for endpoints

Inclusion criteriaUA or non-Q-wave MI in previous 1–4 days

Exclusion criteria• Serum cholesterol

>270 mg/dL• Concurrent or previous

interventional therapy (6 months) or surgery (3 months)

• Concurrent lipid-lowering therapy

• Any agent likely to induce rhabdomyolysis when taken with statins

Placebo, commenced within 24–96 h of event

MIRACL study outcome measures

PrimaryTime from randomisation to first occurrence of any of thefollowing:

Death (any cause) Non-fatal MI Resuscitated cardiac arrest Worsening angina pectoris with new objective evidence of

myocardial ischemia, requiring urgent rehospitalisation

SecondaryTime to occurrence and incidence of each of the primaryoutcome components, plus:

Stroke Myocardial revascularisation (CABG or PTCA) Worsening congestive heart failure Worsening angina without new objective evidence

of ischemia

0 4 8 12 16

15

10

5

0

Cumulative incidence (%)

Time since randomisation (weeks)

Atorvastatin

Placebo 17.4%

14.8%

Risk reduction = 16%p=0.048

Time to first occurrence of composite endpoint of:

Primary efficacy measure

95% CI = 0.701–0.999

Death (any cause) Non-fatal MI Resuscitated cardiac arrest Worsening angina with new

objective evidence and urgent rehospitalisation


Days


0 6Months

32

PTT

L-CAD

RECIFE

CARE

LIPID

24Hours

10 6 8 1212 18 4

4S

6

Atorvastatin

Pravastatin

Simvastatin

WOSCOPS

Primary prevention

ACS

Fluvastatin

FLORIDA

MIRACL

Comparison of Lipid-Modifying Efficacy of Rosuvastatin Versus Atorvastatin in Patients

With ACS

(LUNAR Study)

Limiting Under treatment of lipids in ACS With Rosuvastatin

Am J Cardiol 2012;109:1239 –1246

- Compared the efficacy of RSV20 and RSV40 with ATV80 in patients with ACS

- Prospective, multicenter, randomized, open-label, 3-arm, parallel-group trial.

Inclusion Criteria:1. ACS patients with in 48 hrs of ischemia - STEMI pts with intervention with in 12 hrs of symptoms (TLT or PCI) - NSTEMI/UA with conservative management - LDL-C >70 mg/dl, fasting TG < 500 mg/dl with in 72 hrs of symptom onset

Baseline characteristics of randomized

patients(n = 825)

* p <0.05; † p < 0.01; ‡ p < 0.001 versus atorvastatin 80 mg/day.

Mean percent change from baseline by weeks 2, 6, and 12 in low-density lipoprotein cholesterol (LDL-C)

Mean percent change from baseline by weeks 2, 6, and 12 in (high-density lipoprotein cholesterol (HDL-C)..

Conclusion: LUNAR study

RSV 40 more effectively decreased LDL-C , increased HDL-C and improved other blood lipid parameters when compared to RSV20 And ATV80 in patients with ACS

3.4

13

9.1

23

0

5

10

15

20

25

MACE CK-MB

% P

atien

tsARMYDA-RECAPTURE

• 30-day MACE: 3.4% vs. 9.1%, p = 0.04• CK-MB elevation: 13% vs. 23%, p = 0.02• Troponin-I elevation: 36% vs. 47%, p =

0.03• Peak CRP: 2.1 ± 6.7 vs. 3.0 ± 9.5, p =

0.12

Trial design: This study evaluated the efficacy of an atorvastatin reloading strategy in patients on chronic statin therapy undergoing PCI for stable angina or NSTEMI.

Results

Conclusions

• An 80 mg loading dose of atorvastatin followed by a 40 mg preprocedural dose may reduce the incidence of post-procedure MACE in patients on background statin therapy

• These data support a strategy of routine atorvastatin reloading prior to PCI in patients on background statin therapy

Atorvastatin(n = 177)

Placebo(n = 175)

(p = 0.02)(p = 0.04)

Daskalopoulou S, et al. European Heart Journal (2008) 29, 2083–2091

Effects of Withdrawal of Statin After AMI

starters = did not receive before AMI but started after; users = before and continuing after AMINon-users =not receiving before or after AMI; stoppers = stopped statin after AMI.

CORONA Trial:Controlled Rosuvastatin in Multinational Trial in HF

- 5011 elderly patients (age >60)- with ischemic cardiomyopathy- NYHA class II to IV HF- median follow-up of 32.8 months

- randomly assigned to Rosuvastatin 10 mg or placebo

Primary composite outcome:CVS death, nonfatal MI, or nonfatal stroke

Secondary outcomes:Death from any cause, any coronary event, death CVS

causes, number of hospitalizations.

No significant risk reduction in primary outcome- death from CVS causes - nonfatal MI - nonfatal stroke

CORONA Trial:Controlled Rosuvastatin in Multinational Trial in HF

N Engl J Med 2007;357:2252

- No effect on CVS outcome, NYHA class or quality of life.

- Fewer hospitalizations for CVS causes ( Rosuvastatin (2193) v/s placebo (n 2564) (P < .001)

Meta-analysis of Statin Use in HF

- Meta-analysis of 13 HF trials estimated survival benefit of statin use in patients with HF of ischemic and nonischemic etiologies

- Statin use in HF associated with 26% RRR in mortality (HR 0.74; 95% CI, 0.68 to 0.8)

8 trials - statin use associated with an improved survival among patients who had HF

- Effect is noted independent of etiology for HF (for ischemic etiology HR 0.73; 95% CI 0.65 to 0.82) ( for nonischemic etiology HR 0.73; 95% CI 0.61 to 0.87)

Meta-analysis of mortality among patients with heart failure HF patients using statins (n = 30,107) HF patients not using statins (n =101,323)

J Am Coll Cardiol 2008;51:422

(A) Adjusted mortality among patients with ischemic HF (n = 62,273) using statins, compared with those not using statins (B) Mortality among patients with HF of nonischemic HF (n 5 31,551) using statins

compared with those not using statins.

J Am Coll Cardiol 2008;51:423

Thank you

efficacy of statins in primary and secondary prevention of cv events - well established...

Documents

recurrent coronary events

initial coronary events

vs placebo slide

cvs death

major cv events

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death cvs causes