The ABCs of the AHA/ACC Prevention Guidelines Alessandra Calvo-Friedman, Andrew DeFilippis, MD, Ty Gluckman MD, Dominique Ashen, CRNP, PhD, Roger Blumenthal,

The ABC’s of the AHA/ACC Prevention Guidelines

Alessandra Calvo-Friedman, Andrew DeFilippis, MD, Ty Gluckman MD,

Dominique Ashen, CRNP, PhD, Roger Blumenthal, MD,

Johns Hopkins Ciccarone Preventive Cardiology Center

DefinitionDefinition

Primary Prevention: Modification of risk factors or prevent their development to prevent or delay the onset of CHD.

Secondary Prevention: Initiation of Rx to reduce recurrent CHD events in patients with CHD.

Primary and a Half Prevention*: As individuals with subclinical CHD are identified, the distinction between primary and secondary prevention becomes blurred.

*Celermajer DS. JACC 2005;45:1994-6

CHD=Coronary heart disease

Aspirin RecommendationsAspirin Recommendations

Aspirin (75-162 mg daily) in intermediate risk men with a 10 year risk of CHD >10%.

Aspirin (75-162 mg daily) in intermediate risk women > 65 yrs with a 10 yr risk of CHD >10%

Aspirin in low risk women with a 10 year risk of CHD <10%.

Primary Prevention

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII



CHD=Coronary heart disease

Aspirin Recommendations (Continued)Aspirin Recommendations (Continued)


Aspirin (75-325 mg daily) in those with known CHD or carotid artery or leg artery narrowings due to plaque.

Aspirin (100-325 mg daily) in those that have undergone CABG surgery*.

Secondary Prevention


CABG=Coronary artery bypass graft, CHD=Coronary heart disease

*To be administered within the first 48 hours after surgery in order to reduce the risk of saphenous vein graft failure. Doses >162 mg/day may be continued for up to one year.

Aspirin Evidence: Primary Prevention in MenAspirin Evidence: Primary Prevention in Men

Physicians’ Health Study (PHS)22,071 men randomized to aspirin (325mg every other day) followed for an

average of 5 years

Aspirin significantly reduces the risk of MI in men

End point Relative Risk (95% CI) P value Myocardial infarction Fatal 0.34 (0.15-0.75) 0.007 Nonfatal 0.59 (0.47-0.74) <0.00001 Total 0.56 (0.45-0.70) <0.00001 Stroke Fatal 1.51 (0.54-4.28) 0.43 Nonfatal 1.20 (0.91-1.59) 0.20 Total 1.22 (0.93-1.60) 0.15

Physicians’ Health Study Research Group. NEJM 1989;321:129-35

CI=Confidence interval, MI=Myocardial infarction

Aspirin Evidence: Primary Prevention in WomenAspirin Evidence: Primary Prevention in Women

Womens’ Health Study (WHS)

0.00

0.01

0.02

0 2 4 6 8 10

Cum

ulat

ive

Inci

denc

e of

MI

Placebo

Aspirin

P=0.83

Ridker P et al. NEJM 2005; 352:1293-204

MI=Myocardial infarction

Years

39,876 women randomized to aspirin (100 mg every other day) or placebo for an average of 10 years

Aspirin doesn’t reduce the risk of MI in women

Clopidogrel Evidence: Secondary PreventionClopidogrel Evidence: Secondary Prevention

Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) Trial

0.00

0.02

0.04

0.06

0.08

0.10

0.12

0.14

3 6 90 12

Rat

e of

dea

th,

myo

card

ial i

nfar

ctio

n,

or s

trok

e

P<0.001

Months of Follow Up

The CURE Trial Investigators. NEJM. 2001;345:494-502

DAP=Dual antiplatelet therapy, NSTE-ACS=Non ST-segment elevation acute coronary syndrome

Aspirin + Clopidogrel

Aspirin + Placebo

12,562 patients with a NSTE-ACS randomized to daily aspirin (75-325 mg) or clopidogrel (300 mg load, 75 mg thereafter) plus aspirin for 9 months

ACE Inhibitor RecommendationsACE Inhibitor Recommendations

An ACE inhibitor in those following a MI, regardless of EF or in those with CAD* along with hypertension (SBP >120 mmHg), LVSD (EF <0.40), heart failure, DM, or CKD.

Optional use of an ACE inhibitor in those with low risk CAD*, well controlled CV risk factors, a normal EF, and successful revascularization.


*Defined by previous MI or angiographically significant CAD.



ACE=Angiotensin converting enzyme, CAD=Coronary artery disease, CKD=Chronic kidney disease, CV=Cardiovascular, DM=Diabetes mellitus, EF=Ejection fraction, LVSD=Left ventricular systolic dysfunction, MI=Myocardial infarction, SBP=Systolic blood pressure

Days of Follow-Up

CV

dea

th, M

I, or

st

roke

(%

)

22% RRR, P<0.0010.00

0.05

0.10

0.15

0.20

0 500 1000 1500

ACE Inhibitor Evidence: Secondary PreventionACE Inhibitor Evidence: Secondary Prevention

Placebo

Ramipril

HOPE Investigators. NEJM 2000;342:145-153

Heart Outcomes Prevention and Evaluation (HOPE) Study

ACE-I=Angiotensin converting enzyme inhibitors, DM=Diabetes mellitus, CV=Cardiovascular, HF=Heart failure, LVSD=Left ventricular systolic dysfunction, MI=Myocardial infarction

9,297 patients with DM or vascular disease plus one additional CV risk factor, but without HF or known LVSD randomized to ramipril (10 mg) or

placebo for 5 years

ACE-I reduce CV events in high-risk individuals

Digitalis: RecommendationsDigitalis: Recommendations

Digitalis in those with symptomatic HF and LVSD (EF <45%) to reduce hospitalizations for HF*.

Digitalis in those with asymptomatic LVSD and normal sinus rhythm.


EF=Ejection fraction, HF=Heart failure, LVSD=Left ventricular systolic function

*Contraindications include significant sinus or atrioventricular block unless a permanent pacemaker is present.




Prevention of Events with Angiotensin Converting Enzyme Inhibition (PEACE) Trial

Prim

ary

End

Poi

nt (

%)*

30

25

20

15

10

5

00 1 2 3 4 5 6

Years After Randomization

PlaceboTrandolapril

PEACE Trial Investigators. NEJM 2004;351:2058-2068

*Includes death from cardiovascular causes, myocardial infarction, or coronary revascularization

8,290 patients with stable coronary artery disease and normal left ventricular function randomized to trandolapril (4 mg) or placebo for 5 years

ACE-I do not reduce CV events in low-risk individuals

0

5

10

15

20

0 1 2 3 4 5

HOPE, placebo

HOPE, active drug (ramipril)

PEACE, placebo


Comparison between the HOPE and PEACE trials

Patients enrolled in the PEACE trial were at lower risk*

MI,

Car

diac

dea

th,

or S

trok

e (%

)

Braunwald, E. et al., NEJM 2004;351:2058-68.

CHD=Coronary heart disease, MI=Myocardial infarction

*Reflects greater blood pressure control, revacularization, and use of other risk-reducing medications (i.e., antiplatelet therapy, -blocker, lipid-lowering medication)

Years

Years

Pro

babili

ty o

f Event

0

0.05

0.15

0.2

0.25

0.3

0 1 2 3

0.35

0.4

4

ACE-I

Placebo

OR: 0.74 (0.66–0.83)OR: 0.74 (0.66–0.83)0.1

Flather MD, et al. Lancet. 2000;355:1575–1581

SAVERadionuclideEF 40%

AIREClinical and/or radiographic signs of HF

TRACEEchocardiogramEF 35%


ACE-I=Angiotensin converting enzyme inhibitors, LVSD=Left ventricular systolic dysfunction, MI=Myocardial infarction, OR=Odds ratio

ACE-I provide substantial benefit in post-MI LVSD

Provides information on response to therapy. May help improve adherence to therapy and evaluate “white-coat” HTN.

Self-measurement

Indicated for evaluation of “white-coat” HTN. Absence of 10–20% BP decrease during sleep may indicate increased CVD risk.

Ambulatory BP monitoring

Two readings, 5 minutes apart, sitting in chair. Confirm elevated reading in contralateral arm.

In-office

Brief Description Method

JNC VII Guidelines for Measurement of BPJNC VII Guidelines for Measurement of BP

BP=Blood pressure, CVD=Cardiovascular disease, HTN=Hypertension

Chobanian AV et al. JAMA. 2003;289:2560-2572

0

20

40

60

80

Perc

en

t h

yp

ert

en

siv

e

18-29

National Health and Nutrition Examination Survey (NHANES) III

30-39 40-49 50-59 60-69 70-79 80+Age

3%9%

18%

JNC-VI. Arch Intern Med. 1997;157:2413-2446

Blood Pressure: Risk Increases with AgeBlood Pressure: Risk Increases with Age

51%

66%72%

38%

Hypertension defined as blood pressure >140/90 mmHg or treatment

Prospective Studies Collaboration. Lancet. 2002;360:1903-1913

Usual Diastolic BP (mm Hg)Usual Systolic BP (mm Hg)

Isch

emic

Hea

rt D

isea

se M

ort

alit

y

50-59

60-69

70-79

80-89Age at Risk (Y)

40-49

256

128

64

32

16

8

4

2

1

0120 140 160 180

50-59

60-69

70-79

80-89

Age at Risk (Y)

40-49

256

128

64

32

16

8

4

2

1

080 90 100 11070

Blood Pressure: Lower is BetterBlood Pressure: Lower is Better

Isch

emic

Hea

rt D

isea

se M

ort

alit

y

Ischemic Heart Disease Mortality

BP=Blood pressure

JNC VII Causes of Secondary HypertensionJNC VII Causes of Secondary Hypertension

Medical Conditions

Chronic kidney disease

Primary hyperaldosteronism

Renovascular disease

Chronic steroid therapy

Cushing’s syndrome

Pheochromocytoma

Aortic coarctation

Thyroid or parathyroid disease

Sleep apnea

Drugs

NSAIDS

Oral contraceptives

Adrenal steroids

Sympathomimetics

Cyclosporine or tacrolimus

Erythropoietin

Ephedra, mu huang, bitter orange

Cocaine or amphetamines

Alcohol


NSAIDS=Non-steroidal anti-inflammatory drugs

Modification Recommendation Approximate SBP Reduction Range

Weight reduction Maintain normal body weight (BMI=18.5-24.9)

5-20 mmHg/10 kg weight lost

Adopt DASH eating plan

Diet rich in fruits, vegetables, low fat dairy and reduced in fat

8-14 mmHg

Restrict sodium intake

<2.4 grams of sodium per day 2-8 mmHg

Physical activity Regular aerobic exercise for at least 30 minutes on most days of the week

4-9 mmHg

Moderate alcohol consumption

<2 drinks/day for men and <1 drink/day for women

2-4 mmHg

JNC VII Lifestyle Modifications for BP ControlJNC VII Lifestyle Modifications for BP Control


BMI=Body mass index, SBP=Systolic blood pressure

Two-drug combination for most† (usually thiazide-type diuretic and ACEI or ARB or BB or CCB).

Yes >100 >160 Stage 2 Hypertension

Drug(s) for the compelling indications.‡

Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed.

Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination.

Yes 90–99 140–159 Stage 1 Hypertension

Drug(s) for compelling indications. ‡

No antihypertensive drug indicated.

Yes 80–89 120–139 Prehypertension

Encourage <80 <120 Normal

With compelling indications

Without compelling indication

Initial drug therapy Lifestyle

modificationDBP* mmHg

SBP* mmHg

BP classification

JNC VII Guidelines for Management and TreatmentJNC VII Guidelines for Management and Treatment

and

or

or

or

ACEI=Angiotensin converting enzyme inhibitor, ARB=Angiotensin receptor blocker, BB=-blocker, BP=Blood pressure, CCB=Calcium channel blocker, DBP=Diastolic blood pressure, SBP=Systolic blood pressure


*Treatment determined by highest blood pressure category.†Initial combined therapy should be used cautiously in those at risk for orthostatic hypotension.‡Treat patients with chronic kidney disease or diabetes mellitus to blood pressure goal of <130/80 mmHg.

Blood Pressure RecommendationsBlood Pressure Recommendations


Initiation or maintenance of lifestyle modification in those with a BP >120/80 mmHg.

Use of an ACE inhibitor and/or -blocker in those with a BP >140/90 mmHg*. Other drugs (i.e., thiazide diuretics) should be added in order to achieve the desired BP.



ACE=Angiotensin converting enzyme, BP=Blood pressure, CKD=Chronic kidney disease, DM=Diabetes mellitus

*A BP >130/80 mmHg should be used for individuals with CKD or DM

Blood Pressure Evidence: Primary PreventionBlood Pressure Evidence: Primary Prevention

0 1 2 3 4 5 6 70

.04

.08

.12

.16

.20

RR (95% CI) P-value

A/C 0.98 (0.90-1.07) 0.65

L/C 0.99 (0.91-1.08) 0.81

Rat

e of

MI

or

fata

l CH

DAntihypertensive and Lipid-Lowering Treatment to Prevent

Heart Attack Trial (ALLHAT)

ALLHAT Investigators. JAMA. 2002;288:2981-97

Years to CHD Event

BP=Blood pressure, CHD=Coronary heart disease, HTN=Hypertension, MI=Myocardial infarction

Chlrothalidone

Amlodipine

Lisinopril

33,357 patients with HTN and >1 CHD risk factor randomized to chlorthalidone, amlodipine, or lisinopril for 5 years

There is similar efficacy among BP lowering agents

0 6 12 18 24 30 36 42 48 54 60 66

Study Month

4

8

12

16

0Pro

port

ion

with

CV

de

ath,

MI,

or s

trok

e (%

)

Blood Pressure Evidence: Primary PreventionBlood Pressure Evidence: Primary Prevention

Losartan Intervention for Endpoint (LIFE) Reduction in Hypertension Study

Dahlöf B et al. Lancet. 2002;359:995-1003.

AtenololLosartan

13% RRR, P=0.021

ARBS=Angiotensin receptor blocker strategy, CV=Cardiovascular, DBP=Diastolic blood presure, LVH=Left ventricular hypertrophy, MI=Myocardial infarction, SBP=Systolic blood pressure

*Defined by SBP=160-200 mmHg or DBP=95-115 mmHg

9,193 high-risk hypertensive* patients with LVH randomized to losartan (100 mg) or atenolol (100 mg) for 5 years

An ARB provides greater efficacy in patients with LVH

Nissen S et al. JAMA 2004;292:2217-26.

Blood Pressure Evidence: Secondary PreventionBlood Pressure Evidence: Secondary Prevention

Comparison of Amlodipine vs Enalapril to Limit Occurrences of Thrombosis (CAMELOT) Trial

*Includes CV death, MI, cardiac arrest, coronary revascularization, hospitalization for HF or angina pectoris, stroke, TIA, development of PAD

CV

eve

nt r

ate*

0

0.25

0.20

0.10

0.05

6 12 18 24

0.15

0

Placebo

AmlodipineEnalapril

Months

Follow-up BP (mmHg)

125/77124/77130/78

BP=Blood pressure, CAD=Coronary artery disease, CV=Cardiovascular, DBP=Diastolic blood pressure, HF=Heart failure, MI=Myocardial infarction, PAD=Peripheral arterial disease, TIA=Transient ischemic attack

1,991 patients with CAD and a DBP <100 mmHg randomized to amloidipine (10 mg), enalapril (20 mg), or placebo for 2 years

A BP <130/80 mmHg is associated with fewer CV events

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII A -blocker in all patients following a MI.

A beta-blocker in all patients with LVSD.

A -blocker in those with other forms of CV disease or DM, unless contraindicated.

*Relative contraindications include asthma, chronic obstructive pulmonary disease, insulin dependent diabetes mellitus, severe peripheral arterial disease, and a PR interval >0.24 seconds.

CV=Cardiovascular, DM=Diabetes mellitus, LVSD=Left ventricular systolic dysfunction, MI=Myocardial infarction

-blocker Recommendations*-blocker Recommendations*



Phase of Treatment

Acute treatment

Secondaryprevention

Overall

Total #Patients

28,970

24,298

53,268

0.5 1.0 2.0RR of death

-blockerbetter

RR (95% CI)

Placebobetter

0.87 (0.77-0.98)

0.77 (0.70-0.84)

0.81 (0.75-0.87)

-blocker Evidence: Secondary Prevention-blocker Evidence: Secondary Prevention

Antman E, Braunwald E. Acute Myocardial Infarction. In: Braunwald E, Zipes DP, Libby P, eds. Heart Disease: A textbook of Cardiovascular Medicine, 6th ed., Philadelphia, PA: W.B. Sanders, 2001, 1168.

Summary of Secondary Prevention Trials of -blocker Therapy

CI=Confidence interval, RR=Relative risk


Cholesterol Management GuidelinesCholesterol Management Guidelines


Restriction of saturated fat (<7% of total calories) and cholesterol (<200 mg/day) in all patients.

Promotion of daily physical activity and weight management in all patients.

Increase in -3 fatty acid consumption in all patients.


LDL-C=Low density lipoprotein cholesterol


Cholesterol Management Guidelines (Continued)Cholesterol Management Guidelines (Continued)

Initiation or intensification of LDL-C lowering drug therapy in those with a baseline or on-treatment LDL-C level >100 mg/dl.

Initiation of LDL-C lowering drug therapy in those with a baseline LDL-C level <100 mg/dl based on clinical judgment.



LDL-C=Low density lipoprotein cholesterol


Goals Recommendations

As set forth by the Adult Treatment

Panel III (ATP III) National Cholesterol Education Program

(NCEP)

Obtain a fasting lipid profile in all patients. For those with a myocardial infarction, a fasting lipid profile should be obtained within 24 hrs of admission.

Start therapeutic lifestyle changes in all patients, including:

• Reduced intakes of saturated fats (<7% of total calories) and cholesterol (<200 mg/day)

• Addition of plant stanols/sterols (2 g/day) and viscous fiber (10-25 g/day) to enhance LDL-C lowering

• Weight reduction

• Increased physical activity

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA 2001;285:2486.



As set forth by the Adult Treatment

Panel III (ATP III) National Cholesterol Education Program

(NCEP)

For primary and secondary prevention, HMG-coA reductase inhibitors (statins) should be first-line in order to achieve the LDL-C goal.

For those that remain above the LDL-C goal, statin therapy should be intensified along with the addition of a second LDL-C lowering agent if needed.

If the TG level is >150 mg/dl or HDL-C level is <40 mg/dl, emphasize weight management, physical activity, and smoking cessation.

If the TG level is 200-499 mg/dl after initiation of LDL-C lowering therapy, consider adding nicotinic acid or a fibrate.

If the TG level is >500 mg/dl, consider adding nicotinic acid or a fibrate before LDL-C lowering therapy.


TG=Triglyceride

0 10 20

2 RFs

0-1 RF

CAD or Risk Equivalent**

Risk Profile Assessment for LDL-C Lowering Risk Profile Assessment for LDL-C Lowering

A risk assessment tool* is needed for individuals with >2 RFs


CAD=Coronary artery disease, CHD=Coronary heart disease, DM=Diabetes mellitus, RF=Risk factor

**Includes DM, non-coronary atherosclerotic vascular disease, and >20% 10-year CHD risk by the FRS

*Such as the Framingham Risk Score (FRS)

10-year CHD Risk

Passed torch: President and Mrs. Clinton exit McDonald’s after his symbolic passage of leadership.

Years Points

20-34 -935-39 -440-44 045-49 350-54 655-59 860-64 1065-69 1170-74 1275-79 13

Step 1: Age Points

TC (mg/dl)

Age 20-39

Age 40-49

Age 50-59

Age 60-69

Age 70-79

<160 0 0 0 0 0160-199 4 3 2 1 0200-239 7 5 3 1 0240-279 9 6 4 2 1

>280 11 8 5 3 1

Framingham Risk Score: MenFramingham Risk Score: Men

Step 2: Total Cholesterol Points

HDL-C (mg/dl) Points

>60 -150-59 040-49 1<40 2

Step 3: HDL-C Points

SBP (mmHg)

If untreat

ed

If treated

<120 0 0120-129 0 1130-139 1 2140-159 1 2

>160 2 3

Step 4: SBP PointsAge

20-39Age

40-49Age

50-59Age

60-69Age

70-79

Nonsmoker 0 0 0 0 0

Smoker 8 5 3 1 1

Step 5: Smoking Status Points

AgeTotal Cholesterol

HDL-CSystolic Blood Pressure

Smoking Status

Point Total

Step 6: Sum of Points

Point Total

10-year Risk

Point Total

10-year Risk

Point Total

10-year Risk

<0 <1% 6 2% 13 12%

0 1% 7 3% 14 16%

1 1% 8 4% 15 20%

2 1% 9 5% 16 25%

3 1% 10 6% >17 >30%

4 1% 11 8%

5 2% 12 10%

Step 7: 10-year CHD Risk

Years Points

20-34 -735-39 -340-44 045-49 350-54 655-59 860-64 1065-69 1270-74 1475-79 16

Step 1: Age Points

TC (mg/dl)

Age 20-39

Age 40-49

Age 50-59

Age 60-69

Age 70-79

<160 0 0 0 0 0160-199 4 3 2 1 1200-239 8 6 4 2 1240-279 11 8 5 3 2

>280 13 10 7 4 2

Framingham Risk Score: WomenFramingham Risk Score: Women

Step 2: Total Cholesterol Points

HDL-C (mg/dl) Points

>60 -150-59 040-49 1<40 2

Step 3: HDL-C Points

SBP (mmHg)

If untreat

ed

If treated

<120 0 0120-129 1 3130-139 2 4140-159 3 5

>160 4 6

Step 4: SBP PointsAge

20-39Age

40-49Age

50-59Age

60-69Age

70-79

Nonsmoker 0 0 0 0 0

Smoker 9 7 4 2 1

Step 5: Smoking Status Points

AgeTotal Cholesterol

HDL-CSystolic Blood Pressure

Smoking Status

Point Total

Step 6: Sum of Points

Point Total

10-year Risk

Point Total

10-year Risk

Point Total

10-year Risk

<9 <1% 15 3% 22 17%

9 1% 16 4% 23 22%

10 1% 17 5% 24 27%

11 1% 18 6% >25 >30%

12 1% 19 8%

13 2% 20 11%

14 2% 21 14%

Step 7: 10-year CHD Risk

Risk Category LDL-C Goal Initiate TLCConsider

Drug Therapy

High risk: CHD or CHD risk equivalents (10-year risk >20%)

<100 mg/dL (optional goal:

<70 mg/dL)

100 mg/dL >100 mg/dL (<100 mg/dL: consider drug

options)

Moderately high risk: 2+ risk factors* (10-year risk 10% to 20%)

<130 mg/dL (optional goal: <100 mg/dL)

130 mg/dL >130 mg/dL (100-129 mg/dL: consider

drug options)

Moderate risk: 2+ risk factors* (10 year risk <10%)

<130 mg/dL 130 mg/dL >160 mg/dL

Lower risk: 0-1 risk factor*

<160 mg/dL 160 mg/dL >190 mg/dL (160-189 mg/dL: LDL-lowering drug optional)

Grundy, S. et al. Circulation 2004;110:227-39.

ATP III LDL-C Goals and Cut-points for Drug TherapyATP III LDL-C Goals and Cut-points for Drug Therapy

ATP=Adult Treatment Panel, CHD=Coronary heart disease, LDL-C=Low-density lipoprotein cholesterol, TLC=Therapeutic lifestyle changes

*Risk factors for cardiovascular disease include: cigarettes smoking, hypertension (blood pressure >140/90 mmHg or on antihypertensive medication, HDL-C <40 mg/dl (>60 mg/dl is a negative risk factor), family history of premature CHD, age >45 years in men or >55 years in women.

Primary Therapies to Lower LDL-CPrimary Therapies to Lower LDL-C

Class Drug(s)

3-Hydroxy-3-Methylglutaryl Coenzyme A (HMG-CoA) reductase inhibitors [Statins]

Atorvastatin (Lipitor)

Fluvastatin (Lescol XL)

Lovastatin (generic and Mevacor)

Pravastatin (Pravachol)

Rosuvastatin (Crestor)

Simvastatin (Zocor)

Bile acid sequestrants Cholestyramine (generic and Questran)

Colesevelam (Welchol)

Colestipol (Colestid)

Cholesterol absorption inhibitor Ezetimibe (Zetia)

Dietary Adjuncts Soluble fiber

Soy protein

Stanol esters

Illingworth DR. Med Clin North Am. 2000;84:23-42.

37

19

35

27

28

18

12

12

6

12

0 10 20 30 40 50 60

Atorvastatin 10/80

Fluvastatin 20/80

Simvastatin 20/80

Pravastatin 20/40

Lovastatin 20/80

Reduction of LDL Cholesterol (%)

HMG-CoA Reductase Inhibitor: Dose-Dependent EffectHMG-CoA Reductase Inhibitor: Dose-Dependent Effect

The Rule of 6’s

Each doubling of the statin dose produces an additional 6% reduction in the LDL-C level

HMG-CoA Reductase Inhibitor: Primary PreventionHMG-CoA Reductase Inhibitor: Primary Prevention

West of Scotland Coronary Prevention Study (WOSCOPS)

CHD=Coronary heart disease, MI=Myocardial infarction, RRR=Relative risk reduction

Shepherd J et al. NEJM 1995;333:1301-1307

Placebo

7.5

Pravastatin

9

6

3

0

5.3

P<0.001

31% RRRR

ate

of M

I or

CH

D

deat

h (%

)

6,595 men with moderate hypercholesterolemia randomized to pravastatin (40 mg) or placebo for 5 years

Statins provide significant benefit in those with average cholesterol levels

Rat

e of

MI,

unst

able

an

gina

, or

SC

D (

%)

Placebo

5.5

Lovastatin

6

4

2

0

3.5

HMG-CoA Reductase Inhibitor: Primary PreventionHMG-CoA Reductase Inhibitor: Primary PreventionAir Force/Texas Coronary Atherosclerosis Prevention Study

(AFCAPS/TexCAPS)

P<0.001

37% RRR

MI=Myocardial infarction, RRR=Relative risk reduction, SCD=Sudden cardiac death

Downs JR et al. JAMA 1998;279(20):1615–1622

6,605 patients with average LDL-C levels randomized to lovastatin (20-40 mg) or placebo for 5.2 years

Statins provide significant benefit in those with average LDL-C levels

Anglo-Scandinavian Cardiac Outcomes Trial—Lipid Lowering Arm (ASCOT-LLA)

Sever PS et al. Lancet. 2003;361:1149-1158

0

1

2

3

4

0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5

Atorvastatin 90 mg/dl*

Placebo 126 mg/dl*

P=0.0005

Cum

ulat

ive

inci

denc

e of

M

I and

fata

l CH

D (

%)

Follow-up (yr)

36% RRR

*Post-treatment LDL-C level

10,305 patients with hypertension randomized to atorvastatin (10 mg) or placebo for 5 years

Statins provide significant benefit in moderate- to high-risk individuals by lowering LDL-C levels below current goals

CHD=Coronary heart disease, RR=Relative risk


0

5

10

15

Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering Trial (MIRACL)

HMG-CoA Reductase Inhibitor: Secondary PreventionHMG-CoA Reductase Inhibitor: Secondary Prevention

17.4%

14.8%

RR=0.84, P=0.048

Com

bine

d ca

rdio

vasc

ular

ev

ent r

ate

(%)*

Weeks

*Includes death, myocardial infarction, resuscitated cardiac arrest, recurrent symptomatic myocardial ischemia requiring emergency rehospitalization.

4 8 12 160

Atorvastatin

Placebo

Schwartz GG et al. JAMA 2001;285:1711-1718

4,162 patients with an ACS randomized to atorvastatin (80 mg) or pravastatin (40 mg) for 24 months

Acute intensive therapy significantly reduces the event rate

Follow-up (months)

3 6 9 12 15 18 21 24 27 30

30

25

20

15

10

5

0

P =0.005

Rec

urre

nt M

I or

Car

diac

Dea

th

16% RRR

Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT)—TIMI 22 Study

Atorvastatin

Pravastatin

ACS=Acute coronary syndrome, CV=Cardiovascular, MI=Myocardial infarction, RRR=Relative risk reduction

Cannon CP et al. NEJM 2004;350:1495-1504





Scandinavian Simvastatin Survival Study (4S)

Mor

talit

y (%

)

Placebo

11.5

Simvastatin

12

8

4

0

8.2

P<0.001

30% RRR

4S Group. Lancet 1994;344:1383–1389

MI=Myocardial infarction, RRR=Relative risk reduction

4,444 patients with angina pectoris or previous MI randomized to simvastatin (20-40 mg) or placebo for 5.4 years



Cholesterol and Recurrent Events (CARE) Study

Placebo

13.2

Pravastatin

15

10

5

0

10.2

P=0.003

24% RRRR

ate

of M

I or

CH

D

deat

h (%

)

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


4,159 patients with a history of MI randomized to pravastatin (40 mg) or placebo for 5 years


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)


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

Statins provide significant benefit across a broad range of LDL-C levels

CAD=Coronary artery disease, CI=Confidence interval, DM=Diabetes mellitus,

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

Illingworth DR. Med Clin North Am. 2000;84:23-42.

37

19

35

27

28

18

12

12

6

12

0 10 20 30 40 50 60

Atorvastatin 10/80

Fluvastatin 20/80

Simvastatin 20/80

Pravastatin 20/40

Lovastatin 20/80

Reduction of LDL Cholesterol (%)

HMG-CoA Reductase Inhibitor: Dose-Dependent EffectHMG-CoA Reductase Inhibitor: Dose-Dependent Effect

The Rule of 6’s

Each doubling of the statin dose produces an additional 6% reduction in the LDL-C level


West of Scotland Coronary Prevention Study (WOSCOPS)


Shepherd J et al. NEJM 1995;333:1301-1307

Placebo

7.5

Pravastatin

9

6

3

0

5.3

P<0.001

31% RRRR

ate

of M

I or

CH

D

deat

h (%

)

6,595 men with moderate hypercholesterolemia randomized to pravastatin (40 mg) or placebo for 5 years


Rat

e of

MI,

unst

able

an

gina

, or

SC

D (

%)

Placebo

5.5

Lovastatin

6

4

2

0

3.5

HMG-CoA Reductase Inhibitor: Primary PreventionHMG-CoA Reductase Inhibitor: Primary PreventionAir Force/Texas Coronary Atherosclerosis Prevention Study

(AFCAPS/TexCAPS)

P<0.001

37% RRR

MI=Myocardial infarction, RRR=Relative risk reduction, SCD=Sudden cardiac death

Downs JR et al. JAMA 1998;279(20):1615–1622

6,605 patients with average LDL-C levels randomized to lovastatin (20-40 mg) or placebo for 5.2 years


Anglo-Scandinavian Cardiac Outcomes Trial—Lipid Lowering Arm (ASCOT-LLA)

Sever PS et al. Lancet. 2003;361:1149-1158

0

1

2

3

4

0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5

Atorvastatin 90 mg/dl*

Placebo 126 mg/dl*

P=0.0005

Cum

ulat

ive

inci

denc

e of

M

I and

fata

l CH

D (

%)

Follow-up (yr)

36% RRR

*Post-treatment LDL-C level

10,305 patients with hypertension randomized to atorvastatin (10 mg) or placebo for 5 years

Statins provide significant benefit in moderate- to high-risk individuals by lowering LDL-C levels below current goals

CHD=Coronary heart disease, RR=Relative risk


0

5

10

15

Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering Trial (MIRACL)


17.4%

14.8%

RR=0.84, P=0.048

Com

bine

d ca

rdio

vasc

ular

ev

ent r

ate

(%)*

Weeks

*Includes death, myocardial infarction, resuscitated cardiac arrest, recurrent symptomatic myocardial ischemia requiring emergency rehospitalization.

4 8 12 160

Atorvastatin

Placebo

Schwartz GG et al. JAMA 2001;285:1711-1718



Follow-up (months)

3 6 9 12 15 18 21 24 27 30

30

25

20

15

10

5

0

P =0.005

Rec

urre

nt M

I or

Car

diac

Dea

th

16% RRR

Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT)—TIMI 22 Study

Atorvastatin

Pravastatin

ACS=Acute coronary syndrome, CV=Cardiovascular, MI=Myocardial infarction, RRR=Relative risk reduction

Cannon CP et al. NEJM 2004;350:1495-1504





Scandinavian Simvastatin Survival Study (4S)

Mor

talit

y (%

)

Placebo

11.5

Simvastatin

12

8

4

0

8.2

P<0.001

30% RRR

4S Group. Lancet 1994;344:1383–1389

MI=Myocardial infarction, RRR=Relative risk reduction

4,444 patients with angina pectoris or previous MI randomized to simvastatin (20-40 mg) or placebo for 5.4 years



Cholesterol and Recurrent Events (CARE) Study

Placebo

13.2

Pravastatin

15

10

5

0

10.2

P=0.003

24% RRRR

ate

of M

I or

CH

D

deat

h (%

)

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


4,159 patients with a history of MI randomized to pravastatin (40 mg) or placebo for 5 years


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)


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

Statins provide significant benefit across a broad range of LDL-C levels

CAD=Coronary artery disease, CI=Confidence interval, DM=Diabetes mellitus,

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

-50

-40

-30

-20

-10

0

10

20

30

Ch

ang

e fr

om

Ba

selin

e

Goldberg A et al. Am J Cardiol 2000;85:1100-1105

500

HDL-C

LDL-C

TG

–9%–14%

–22% –21%–17%

30%30%26%

22%15%

10%

–28%

–35%

–44%–39%

–11%

–5%

Nicotinic Acid: Efficacy at Raising HDL-CNicotinic Acid: Efficacy at Raising HDL-C

1000 1500 2000 2500Dose (mg) 3000

Frick MH et al. NEJM 1987;317:1237-1245Manninen V et al. Circulation 1992;85:37-45BIP Study Group. Circulation 2000;102:21-27Rubins HB et al. NEJM 1999;341:410-418

*Post hoc analysis of subgroup with TG >200 mg/dL and HDL-C <42 mg/dL.**Post hoc analysis of subgroup with TG 200 mg/dL and HDL-C <35 mg/dL.***Difference between placebo and Rx for primary endpoint was statistically significant (p < 0.05).

0

5

10

15

20

25

30%

CH

D D

eat

h/N

onfa

tal M

I Rx

Placebo

2.72.7 4.1***4.1***

2.72.7

8.08.0

13.613.615.015.0

13.013.0

22.322.3

17.317.3

21.7***21.7***

66%66%

34%34%

9%9%

42%42% 22%22%

PRIMARY PREVENTION SECONDARY PREVENTION

HHS HHS* BIP BIP** VA-HIT

Fibrate: Primary and Secondary PreventionFibrate: Primary and Secondary Prevention

Complete cessation

No environmental tobacco smoke exposure

Cigarette Smoking Cessation GuidelinesCigarette Smoking Cessation Guidelines


Ask about tobacco use at every visit.

In a clear, strong, and personalized manner, advise the patient to stop smoking.

Urge avoidance of exposure to secondhand smoke at work and home.

Assess the patient’s willingness to quit smoking.

Develop a plan for smoking cessation and arrange follow-up.

Provide counseling, pharmacologic therapy, and referral to formal smoking cessation programs as indicated.


Smoking Cessation Pharmacotherapy*Smoking Cessation Pharmacotherapy*

Agent Caution Side Effects

Dosage Duration Instructions

Bupropion SR

(Zyban®)

Seizure disorder

Eating disorder

Taking MAO inhibitor

Pregnancy

Insomnia

Dry mouth

150 mg QAM

then

150 mg BID

3 days

Maintenance (8 weeks,

but may be used up to 6

months)

Start 1-2 weeks before quit date.

Take second dose in early afternoon or

decrease to 150 mg QAM for insomnia.

Transdermal

Nicotine

Patch**

Within 2 weeks of a MI

Unstable angina

Arrhythmias

Decompensated heart failure

Skin reaction

Insomnia

21 mg QAM

14 mg QAM

7 mg QAM

or

15 mg QAM

4 weeks

2 weeks

2 weeks

8 weeks

Apply to different hairless site

daily.

Remove before bed for insomnia.

Start at <15 mg for <10 cigs/day

*Pharmacotherapy combined with behavioral support provides the best success rate

**Other nicotine replacement therapy options include: nicotine gum, lozenge, inhaler, nasal spray

Jorenby DE et al. NEJM 1999;340:685-91

Cigarette Smoking Cessation: Primary PreventionCigarette Smoking Cessation: Primary Prevention

Placebo (n=160)

NRT (n=244)

Bupropion (n=244)

Nicotine patch and Bupropion (n=245)

Abstinence rate at 6 months

18.8% 21.3% 34.8%a,b 38.8%a,c,d

Abstinence rate at 12 months

15.6% 16.4% 30.3%a,c 35.5%a,c,e

ap<0.001 when compared to placebobp=0.001 when compared to NRTcp<0.001 when compared to NRTdp=0.37 when compared to buproprionep=0.22 when compared to buproprion

NRT=Nicotine replacement therapy

893 smokers randomized to 9 weeks of buproprion (150 mg a day for 3 days and then 150 mg twice daily), NRT (21 mg patch weeks 2-7, 14 mg patch

week 8, and 7 mg patch week 9), bupropion and NRT, or placebo

Bupropion with or without NRT provides the greatest benefit

JAMA 2006:296:47-55 and JAMA 2006;296:56-63

Smoking Cessation Pharmacotherapy: VareniclineSmoking Cessation Pharmacotherapy: Varenicline

Two trials compared treatment with varenicline, a nicotine acetylcholine receptor agonist, to treatment with buproprion or placebo.

These trials included a total of almost 700 participants. The mean duration of smoking was 25 years.

Varenicline yielded higher rates of smoking cessation than buproprion or placebo.

Study 1p<0.001 for V vs Bp<0.001 for V vs P

Study 2p<0.001 for V vs Bp<0.001 for V vs P


Calculate BMI* and measure waist circumference as part of evaluation. Monitor response of BMI and waist circumference to therapy.

BMI 18.5 to 24.9 kg/m2

Women: <35 inchesMen: <40 inches

Weight Management GuidelinesWeight Management Guidelines

Start weight management and physical activity as appropriate.

If BMI and/or waist circumference is above goal, initiate caloric restriction, measures to increase caloric expenditure, and treatment strategies for the metabolic syndrome.

BMI=Body mass index

*BMI is calculated as the weight in kilograms divided by the body surface area in meters2.

Overweight state is defined by BMI=25-30 kg/m2. Obesity is defined by a BMI >30 kg/m2.

10% weight reduction within the first year of

therapy



Prevalence of Obesity in U.S. AdultsPrevalence of Obesity in U.S. Adults

1991 1996

2003

% State Population No Data <10% 10%–14% 15%–19% 20%–24% ≥25%

Source: CDC Overweight and Obesity

Mhurchu N et al. Int J Epidemiol 2004;33:751-758

0.5

1.0

2.0

4.0

16 20 24 28 32 36

Body Mass Index (kg/m2)*

Haz

ard

Rat

io

0.5

1.0

2.0

4.0

16 20 24 28 32 36

0.5

1.0

2.0

4.0

16 20 24 28 32 36

HemorrhagicStroke

IschemicStroke

Ischemic HeartDisease

CV Risk Increases with Body Mass IndexCV Risk Increases with Body Mass Index

CV=Cardiovascular

Body mass index is calculated as the weight in kilograms divided by the body surface area in meters2.


Diabetes Mellitus GuidelinesDiabetes Mellitus Guidelines

Goal HbA1C <7% Intensive lifestyle modification to prevent the development of DM (especially in those with the metabolic syndrome)

Aggressive management of CV risk factors (i.e., tobacco use, hypertension, dyslipidemia, physical inactivity, and overweight and obese states)

Hypoglycemic therapy to achieve normal to near normal fasting plasma glucose as defined by the HbA1C (<7%)

• Weight reduction and exercise• Oral hypoglycemic agents• Insulin therapy

Coordination of diabetic care with the patient’s primary physician and/or endocrinologist.

CV=Cardiovascular, DM=Diabetes mellitus, HbA1C=Glycosylated hemoglobin



• Consists of a constellation of major risk factors, life-habit risk factors, and emerging risk factors

• Over-represented among populations with cardiovascular disease

• Often occurs in individuals with a distinctive body-type including an increased abdominal circumference

The Metabolic SyndromeThe Metabolic Syndrome

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA 2001;285:2486-2497

Risk Factor Defining Level

Waist circumference (abdominal obesity) >40 in (>102 cm) in men

>35 in (>88 cm) in women

Triglyceride level >150 mg/dl

HDL-C level <40 mg/dl in men

<50 mg/dl in women

Blood pressure >130/>85 mmHg

Fasting glucose >100 mg/dl

ATP III Definition of the Metabolic SyndromeATP III Definition of the Metabolic Syndrome

Defined by presence of >3 risk factors

HDL-C=High-density lipoprotein cholesterol

Tuomilehto J et al. NEJM 2001;344:1343-1350

0

0.05

0.1

0.15

0.2

0.25

InterventionControl

11%

23%

% with Diabetes Mellitus

Metabolic Syndrome: Risk of Developing DMMetabolic Syndrome: Risk of Developing DM

Finnish Diabetes Prevention Study

†Defined as a glucose >140 mg/dl 2 hours after an oral glucose challenge

522 overweight (mean BMI=31 kg/m2) patients with impaired fasting glucose† randomized to intervention‡ or usual care for 3.2 years

Lifestyle modification reduces the risk of developing DM

‡Aimed at reducing weight (>5%), total intake of fat (<30% total calories) and saturated fat (<10% total calories); increasing uptake of fiber (>15 g/1000 cal); and physical activity (moderate at least 30 min/day)

Metabolic Syndrome: Risk of Developing DMMetabolic Syndrome: Risk of Developing DM

Diabetes Prevention Program (DPP)

Knowler WC et al. NEJM 2002;346:393-403

0 1 2 3 4

0

10

20

30

40Placebo (n=1082)Metformin (n=1073, p<0.001 vs. Plac)Lifestyle (n=1079, p<0.001 vs. Met , p<0.001 vs. Plac )

Percent developing diabetes

All participants

All participants

Years from randomization

Cu

mu

lativ

e in

cid

en

ce (

%)

*Includes 7% weight loss and at least 150 minutes of physical activity per week

Placebo

Metformin

Lifestyle modification

Inci

denc

e of

DM

(%

)

0

20

30

10

40

00 1 42 3

Years

3,234 patients with elevated fasting and post-load glucose levels randomized to placebo, metformin (850 mg twice daily), or lifestyle

modification* for 2.8 years

Lifestyle modification reduces the risk of developing DM

Assess risk, preferably with exercise test, to guide prescription.

Encourage aerobic activity (e.g., walking, jogging, cycling) supplemented by an increase in daily activities (e.g., walking breaks at work, gardening, household work).

Encourage resistance training (e.g., weight machines, free weights) 2 days a week (Class IIb, Level C)

Encourage cardiac rehabilitation for patients with chronic stable angina, recent myocardial infarction, left ventricular systolic dysfunction, or recent coronary artery bypass graft surgery.

Minimum: 30 minutes,5 days per week

Optimal: 30 minutes daily


Exercise GuidelinesExercise Guidelines


Ejection Fraction GuidelinesEjection Fraction Guidelines


Echocardiography in those following a STEMI to re-evaluate ventricular function when results are used to guide therapy*.

Echocardiography or radionuclide angiography in those following a NSTE-ACS when results are used to guide therapy*.

*Includes use of an aldosterone antagonist, digitalis, and/or an implantable cardioverter defibrillator

NSTE-ACS=Non-ST-segment elevation acute coronary syndrome, STEMI=ST-segment elevation myocardial infarction


Digitalis: RecommendationsDigitalis: Recommendations

Digitalis in those with symptomatic HF and LVSD (EF <45%) to reduce hospitalizations for HF*.

Digitalis in those with asymptomatic LVSD and normal sinus rhythm.


EF=Ejection fraction, HF=Heart failure, LVSD=Left ventricular systolic function

*Contraindications include significant sinus or atrioventricular block unless a permanent pacemaker is present.



80706050403020

54-60 >60

50

40

30

20

10

0

<30

31-35

36-45

46-53

Car

diac

Mor

talit

y %

Brodie B et al. Am J Cardiol 1992;69:1113

Relationship Between EF* and MortalityRelationship Between EF* and Mortality

Ejection Fraction (%)

*Post myocardial infarction

EF=Ejection fraction

Pitt B et al. NEJM 1999;341:709-717

RR = 0.70, P<0.001

Months

Sur

viva

l (%

)

3633302724211815129630

1.00

.90

.80

.70

.60

.50

0

Aldosterone Antagonist: Secondary PreventionAldosterone Antagonist: Secondary Prevention

Randomized Aldactone Evaluation Study (RALES)

EF=Ejection fraction, HF=Heart failure, LVSD=Left ventricular systolic dysfunction, NYHA=New York Heart Association

SpironolactonePlacebo

1,663 patients with NYHA Class III or IV HF and LVSD (EF <0.35) randomized to spironolactone (25 mg) or placebo (50 mg) for 24 months

Aldosterone inhibition provides significant benefit in patients with advanced heart failure

RR = 0.85, P=0.008

6 12 18 24 30 360

5

10

15

20

25

0

All

Cau

se M

orta

lity

(%)

Month

Aldosterone Antagonist: Secondary PreventionAldosterone Antagonist: Secondary Prevention

Eplerenone Poct-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS)

EplerenonePlacebo

3,313 patients with evidence of heart failure and LVSD (EF <0.40) after a MI randomized to eplerenone (50 mg) or placebo for 16 months

Aldosterone inhibition provides significant benefit in patients with post-MI heart failure and LVSD

Pitt B et al. NEJM 2003;348:1309-21

EF=Ejection fraction, LVSD=Left ventricular systolic dysfunction, MI=Myocardial infarction

ICD Algorithm

EF < 30%

EPS

Yes

+

NEJM 349:1836,2003

EF 31-40%

No

No ICD.Medical Rx

EF > 40%

-

Additional Marker of Electrical Instability?

At least one month following a myocardial infarction

EF=Ejection fraction, EPS=Electrophysiology study, ICD=Implantable cardioverter defibrillator, Rx=Treatment, SCD=Sudden cardiac death,

1 Moss AJ. N Engl J Med. 1996;335:1933-19402 Buxton AE. N Engl J Med. 1999;341:1882-18903 Moss AF. N Engl J Med. 2002;346:877-883

0

20

40

60

80

MADIT MUSTT MADIT-II1 2 3

54%

75%

55%

73%

31%

61%

27 Months 39 Months 20 Months

% M

ort

alit

y R

edu

ctio

n w

/ IC

D R

xICD: Secondary Prevention*ICD: Secondary Prevention*

*Primary prevention of sudden cardiac death

Overall death

Arrhythmic death

EF <35% EF <40% EF <30%

Prevention Pyramid

Physical activityHealthy eatingIdeal weight

Psychosocial factorsFamilial predisposition

LipidsHypertension

Smoking cessationDiabetes

+Primordial

ASAACE-IRehab

β-blockers+Primary

ACE-1 = angiotensin converting enzyme inhibitor; ASA = aspirin

Secondary

Primary

Primordial

Documents

The ABCs of the AHA/ACC Prevention Guidelines Alessandra Calvo-Friedman, Andrew DeFilippis, MD, Ty Gluckman MD, Dominique Ashen, CRNP, PhD, Roger Blumenthal,