HTN and Dyslipidemia.pptx - RussoCME - Primary Care Medical ...

Slide Source:Lipids Online Slide Librarywww.lipidsonline.org

How to Succeed at Hypertension

without really trying

Or how to normalize CAD Risk in Most of Your Patients with Essential Hypertension

Thomas E. Richtsmeier MD FACC

Wenatchee Valley Medical Center

Moses Lake Clinic


What I propose to do in the next hour Put Atherosclerosis in context of RISK FACTORS,

especially HTN & DYSLIPIDEMIA.

Review the pathobiology of HTN, HTN Tx/Rx, and how to design effective, well tolerated, and affordable therapy

Review the pathobioloby of DYSLIPIDEMIA, lipid lowering Tx/Rx, and how to design well tolerated, and affordable therapy

This hour can not cover all the details; familiarize yourself with good reviews [JNC 7/8, NCEP 3/4]


U.S. Department of Health and Human

Services

National Institutes of Health

National Heart, Lung, and Blood Institute

The Seventh Report of the Joint National Committee onPrevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7)

The Seventh Report of the Joint National Committee onPrevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7)

National Heart, Lung, and Blood InstituteNational High Blood Pressure Education ProgramNational Heart, Lung, and Blood InstituteNational High Blood Pressure Education Program

JNC 8 WILL SOON BE COMING TO

A Medical JOURNAL

And @nhlbi.gov NEAR YOU!!


For persons over age 50, SBP is a more important than DBP as CVD risk factor.

Starting at 115/75 mmHg, CVD risk doubles with each increment of 20/10 mmHg throughout the BP range.

Persons who are normotensive at age 55 have a 90% lifetime risk for developing HTN.

Those with SBP 120–139 mmHg or DBP 80–89 mmHg should be considered prehypertensive who require health-promoting lifestyle modifications to prevent CVD.

New Features and Key Messages


HYPERTENSION AND CARDIOVASCULAR DISEASE RISK

HTN prevalence ~ 50 million people in the United States.

The BP relationship to risk of CVD is continuous, consistent, and independent of other risk factors.

Each increment of 20/10 mmHg doubles the risk of CVD across the entire BP range starting from 115/75 mmHg.

Prehypertension signals the need for increased education to reduce BP in order to prevent hypertension.


Blood Pressure Classification

Normal <120 and <80

Prehypertension 120–139 or 80–89

Stage 1 Hypertension 140–159 or 90–99

Stage 2 Hypertension >160 or >100

BP Classification SBP mmHg DBP mmHg


Complications of Hypertension: End-Organ Damage

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

Peripheral Vascular Disease Renal Failure,

Proteinuria

LVH, CHD, CHFHemorrhage,Stroke

Retinopathy

CHD = coronary heart diseaseCHF = congestive heart failureLVH = left ventricular hypertrophy

HypertensionHypertension


Lewington S, et al. Lancet. 2002;360:1903-1913;Chobanian AV, et al. JAMA. 2003;289:2560-2572.

Cardiovascular Mortality RiskIncreases as Blood Pressure Rises*

Card

iovascu

lar

Mort

ality

Ris

k

Systolic/Diastolic Blood Pressure (mm Hg)

0

1

2

3

4

5

6

7

8

115/75 135/85 155/95 175/105

2x

4x

8x

*Measurements taken in individuals aged 40–69 years, beginning with a blood pressure of 115/75 mm Hg.


*Defined as death due to cardiovascular disease or as having recognized myocardial infarction, stroke, or congestive heart failure.

Cu

mu

lati

ve I

ncid

en

ce o

f M

ajo

r C

ard

iovascu

lar

Even

ts (

%) 16

12

10

8

6

4

2

0

14

0 2 4 6 8 10 12

Time (Years)

Optimal<120/80 mm Hg

Normal120–129/80–84 mm Hg

High-Normal130–139/85–89 mm Hg

Impact of High-Normal Blood Pressure on Risk of Major Cardiovascular Events* in Men

Vasan RS. N Engl J Med. 2001;345:1291-1297.

Blood Pressure:


Relationship of Hypertension to Its Comorbidities

Comorbidity Relationship to Hypertension

Coronary artery disease50% of patients with coronary artery disease have hypertension

Left ventricular hypertrophy15% to 20% of hypertensive adults have an increased left ventricular mass

Ischemic stroke77% of patients who have a first stroke have a blood pressure >140/90 mm Hg

Chronic kidney disease8% to 15% of hypertensive adults have decreased renal function

Diabetes75% of added cardiovascular risk in diabetic patients is attributable to hypertension

Peripheral artery disease74% of patients with peripheral artery disease have hypertension

Diamond JA, Phillips RA. Hypertens Res. 2005;28:191-202;El-Atat F, et al. Curr Hypertens Rep. 2004;6:215-223; Pepine CJ. Am J Cardiol. 1998;82(3A):21H-24H; Rosamond W, et al. Circulation. 2007;115:69-171; Segura J, et al. Curr Opin Nephrol Hypertens. 2004;13:495-500; Selvin E, Erlinger P. Circulation. 2004;110:738-743.


Prevalence of Hypertensionin the United States by Age Group*

†

Hyp

ert

en

sio

nP

revale

nce

Age

*Based on data from the 19992000 National Health and Nutrition Examination Survey. Hypertension is defined as blood pressure 140/90 mm Hg or as receiving antihypertensive treatment.

†Low reliability due to large relative error.Fields LE, et al. Hypertension. 2004;44:398-404.


The VA Cooperative Study, 1967:Assessable Morbid/Fatal Events

Placebo

n=70

Active Rx*

n=73

Accelerated hypertension

12 0

Stroke 4 1

Coronary event 2 0

CHF 2 0

Renal damage 2 0

Deaths 4 0

VA Cooperative Study Group. JAMA. 1967;202:1028-1034.

*P<0.001 active drug therapy vs placebo

[Tx:Hctz, Reserpine, Hydralaz]


Landmark Clinical TrialsHypertension Treatment and Cardiovascular Disease Outcomes

1967 – VA Cooperative Study on DBP 115-129

1970 – VA Cooperative Study on DBP 90-114

1979 – HDFP

1980 – Australian Trial, Oslo Trial

1985 – MRC I, EWPHE

1991 – SHEP, STOP-Hypertension

1992 – MRC II in the elderly

1997 – Syst-Eur

2002 – LIFE

2002 – ALLHAT


Veterans Administration, 1967


Hypertension Stroke Study, 1974

USPHS Study, 1977

EWPHE Study, 1985

Coope and Warrender, 1986

SHEP Study, 1991

STOP-Hypertension Study, 1991

MRC Study, 1992

Syst-Eur Study, 1997

Total

Relative Risk for Stroke

0 0.5 1 1.5 20.63(0.55 to 0.72)

Odds ratios and95% confidence intervals

Active treatment better than placebo

Active treatment worse than placeboReprinted from He J, et al. Am Heart J. 1999;

138:211-219, with permission from Elsevier.




Hypertension Stroke Study, 1974

USPHS Study, 1977

EWPHE Study, 1985

Coope and Warrender, 1986

SHEP Study, 1991

STOP-Hypertension Study, 1991

MRC Study, 1992

Syst-Eur Study, 1997

Total

Relative Risk for Coronary Heart Disease

Odds ratios and95% confidence intervals

0 0.5

1 1.5 2

0.79(0.69 to 0.90)

Reprinted from He J, et al. Am Heart J. 1999; 138:211-219, with permission from Elsevier.

Active treatment better than

placebo

Active treatment worse than

placebo


Benefits of Lowering BP

Average Percent Reduction

Stroke incidence 35–40%

Myocardial infarction 20–25%

Heart failure 50%


Office BP Measurement

Use auscultatory method with a properly calibrated and validated instrument.

Patient should be seated quietly for 5 minutes in a chair (not on an exam table), feet on the floor, and arm supported at heart level.

Appropriate-sized cuff should be used to ensure accuracy.

At least two measurements should be made. Consider ABI

Clinicians should provide to patients, verbally and in writing, specific BP numbers and BP goals.


Patient Evaluation

Evaluation of patients with documented HTN has three objectives:

1. Assess lifestyle and identify other CV risk factors or concomitant disorders that affects prognosis and guides treatment.

2. Reveal identifiable causes of high BP. [95-98 % will be “Essential”]

3. Assess the presence or absence of target organ damage and CVD.


Laboratory Tests Routine Tests

• Electrocardiogram • Urinalysis • Blood glucose, and hematocrit • Serum potassium, creatinine, or the corresponding estimated

GFR, and calcium• Lipid profile, after 9- to 12-hour fast, that includes high-

density and low-density lipoprotein cholesterol, and triglycerides

Optional tests • Measurement of urinary albumin excretion or

albumin/creatinine ratio

More extensive testing for identifiable causes is not generally indicated unless BP control is not achieved


Easily Identifiable (“Primary”) Causes of Hypertension

High Sodium Diet ………….[Use of salt shaker and convenience

foods, high urinary sodium] Sleep apnea………………………….……..….[Obesity, typical Sx] Drug-induced or related causes………………[BCP, NSAIDs, etc] Chronic kidney disease ………...…..[CC< 60cc/min, Proteinuria] Primary aldosteronism ……………………..………[Hypokalemia] Reno vascular disease……..…. [Abdominal bruit in m.a. woman] Coarctation of the aorta…….. [Widened radial-pedal pulse inter- val; measure pedal systolic BP. ABI>1]


Classification and Management of BP for adults

BP classification

SBP* mmHg

DBP* mmHg

Lifestyle modification

Initial drug therapy Without compelling

indication With compelling

indicationsNormal <120 and <80 Encourage

Prehypertension 120–139 or 80–89 Yes No antihypertensive drug indicated.

Drug(s) for compelling indications. ‡

Stage 1 Hypertension

140–159 or 90–99 Yes Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination.

Drug(s) for the compelling indications.‡

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

Stage 2 Hypertension

>160 or >100 Yes Two-drug combination for most† (usually thiazide-type diuretic and ACEI or ARB or BB or CCB).

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


BP Measurement and Clinical Evaluation

Classification of BP Tobacco CVD Risk [e.g. Framingham 10 year or 30 year RISK] Lipids DM

BP Measurement Techniques FHx

• In-office• Ambulatory BP Monitoring• Self-measurement

Patient EvaluationLaboratory Tests and Other Diagnostic Procedures Patient Centered: Dx, Overall Risk, Education, and compact for

care


0.5

1

1.5

2

2.5

3

Rela

tive R

isk

Microalbuminuria Compared To Traditional Risk Factors For Ischemic Heart Disease

N=2,085; 10 year follow-up

Borch-Johnsen K, et al. Arterioscler Thromb Vasc Biol. 1999;19(8):1992-1997.

A/C ra

tio >

0.65

mg/

mm

ol

> 2

40 m

g/dL

or 7

.0 m

mol/L

> 1

60 m

mHg


Target Organ Damage

Heart• Left ventricular hypertrophy• Angina or prior myocardial infarction• Prior coronary revascularization• Heart failure

Brain• Stroke or transient ischemic attack

Chronic kidney disease

Peripheral arterial disease Retinopathy


mm Hg

UncomplicatedHypertension

Chronic Kidney Disease

Coronary Artery Disease Diabetes

≤140

≤90

≤130

≤80

Systolic Blood Pressure

Diastolic Blood Pressure

Current Blood Pressure Targets for Various Chronic Conditions

American Diabetes Association. Diabetes Care. 2003;26:S80-S82; Hansson L, et al. Lancet. 1998;351:1755-1762; National Kidney Foundation. Am J Kidney Dis. 2002;39(2 Suppl 1):S1-S266;Rosendorff C, et al. Circulation. 2007;115:2761-2788.


-36 -33

-50

-32

-42

-30 -29 -31

-60

-50

-40

-30

-20

-10

0

*P=0.0003; †P=0.003.BB=β-blocker; DHP CCB=dihydropyridine calcium channel blocker.SHEP Cooperative Research Group. JAMA. 1991;265:3255-3264; Staessen et al. Lancet. 1997;350:757-764; Kostis et al. JAMA. 1997;278:212-216.

Major Trials in Isolated Systolic Hypertension

SHEP Syst-Eur

Agent N Age Entry BP (mm Hg)Diuretic BB 4736 60

171/77DHP CCB 4695 60174/86

Stroke CHD CHF All CVD

Rela

tive R

isk

Red

ucti

on

(%

)

*†


Goals of Therapy

Reduce CVD and renal morbidity and mortality.

Treat to BP <140/90 mmHg or BP <130/80 mmHg in patients with diabetes or chronic kidney disease.

Achieve SBP goal especially in persons >50 years of age.

However, do not lower Diastolic BP < 60 mmHg to protect Coronary Perfusion


Recommended Lifestyle Modifications and Their Individual Effects on Blood Pressure

Chobanian AV, et al. JAMA. 2003;289:2560-2572;Blumenthal JA, et al. Arch Intern Med. 2000;160:1947-1958.

Modifications* RecommendationApproximate SBP Reduction

Reduce weight Maintain normal body weight

(BMI of 18.524.9 kg/m2)320 mm Hg

Adopt DASH dietRich in fruit, vegetables, and

low-fat dairy; reduced saturated and total fat content

814 mm Hg

Reduce dietary sodium

<100 mmol (2.4 g)/day 28 mm Hg

Increase physical activity

Aerobic activity >30 min/day most days of the week

49 mm Hg

Moderate alcohol consumption

Men: ≤ 2 drinks/dayWomen: ≤ 1 drink/day

24 mm Hg

*Combining 2 or more of these modifications may or may not have an additive effect on blood pressure reduction.

SBP = systolic blood pressure; BMI = body mass index; DASH = Dietary Approaches to Stop Hypertension


THEMEDITERRANEANDIET:

SIMPLENOT EXPENSIVETASTYEFFICACIOUS

Details at nih.hlbi.gov


Effects of Diet on Blood PressureDietary Approaches to Stop Hypertension Sodium Trial

Appel LJ, et al. N Engl J Med. 1997;336:1117-1124. Copyright © 1997, Massachusetts Medical Society. All rights reserved.

Fruits-and- Vegetables Diet

CombinationDiet*

Systo

lic B

lood

Pre

ssu

re

(mm

Hg

)

Control Diet

122

124

126

128

130

132

Dia

sto

lic B

lood

Pre

ssu

re

(mm

Hg

)

Week of Intervention

0 1 2 3 4 5 6 7 878

80

82

84

86

88

0 1 2 3 4 5 6 7 8

Week of Intervention

*Rich in fruits and vegetables, and rich in low-fat dairy products and low in saturated and total fat. 0 = baseline.


Decreasing Dietary Salt Intake Reduces Systolic Blood PressureDietary Approaches to Stop Hypertension Trial

*Error bars represent standard deviation; †140 mmol/day; ‡62 mmol/day.

Reprinted from Obarzanek E, et al. Hypertension. 2003;42:459-467, with permission from Lippincott Williams & Wilkins.

High-Salt

Diet†

124

126

128

130

132

134

136

Systo

lic B

lood

Pre

ssu

re (

mm

Hg

)

1 2 3 4

Weeks on Low-Salt Diet‡

*

*

**

*


Ask about tobacco use status at every visit Advise every tobacco user to quit Assess the tobacco user’s willingness to quit Assist by counseling and developing a plan

for quitting Arrange follow-up, referral to special

programs, or pharmacotherapy (including nicotine replacement and bupropion)

Urge avoidance of exposure to environmental tobacco smoke at work and home

Cigarette Smoking: Recommendations

GOAL Complete Cessation and No Exposure to Environmental Tobacco Smoke

l lla llb lll

B

Smith SC Jr et al. Circulation 2006;113:2363–2372.

NEVER GIVE UP HELPING THEM TO QUIT


a--Blockers

ACE Inhibitors

AT1 Blockers

Direct renin inhibitors

1-Blockers

2-Agonists

All CCBs

Diuretics

Sympatholytics

Vasodilators

-Blockers

Non-DHPCCBs

Diuretics

BloodPressure = Cardiac

Output

ACE = angiotensin-converting enzyme; AT1 = angiotensin type 1;CCBs = calcium channel blockers; DHP = dihydropyridine

Antihypertensive Drug Classes: Action Sites

Total PeripheralResistance

An

tih

yp

ert

en

siv

e

Dru

g C

lasses


Classes of Antihypertensive Drugs

Aldosterone receptor antagonists (blockers)

Angiotensin II antagonists/RB

Angiotensin-converting enzyme inhibitors

-Blockers– 1-Selective– Nonselective

-Blockers– -1/-2– -1 predominant– / vasodilators– Intrinsic

sympathomimetic activity

Calcium channel antagonists – Nondihydropyridine– Dihydropyridine

Central 2 agonists

Direct renin inhibitors

Direct vasodilators

Hydralizine, Minoxidil

Diuretics– Thiazide-type– Loop-type– Potassium-sparing

Ganglionic blockers


Reductions in Diastolic Blood Pressure Among All Patients VA Cooperative Study of Responses to Single-Drug Therapy

Materson BJ, et al. N Engl J Med. 1993;328:914-921.

-20

-16

-12

-8

-4

0

Ch

an

ge in

DB

P (

mm

Hg

) fr

om

Baselin

e

*P ≤ 0.05 vs. all drugs except clonidine; †P ≤ 0.05 vs. captoprilDBP = diastolic blood pressure

† †*

182 177 176 186 188 188 186

AtenololClonidine

DiltiazemPrazosin

HydrochlorothiazideCaptopril

Placebo

n =


Reductions in Systolic Blood Pressure Among All Patients VA Cooperative Study of Responses to Single-Drug Therapy

Materson BJ, et al. N Engl J Med. 1993;328:914-921.

Ch

an

ge in

SB

P (

mm

Hg

)fr

om

Baselin

e

-35

-30

-25

-20

-15

-10

-5

0

*P ≤ 0.05 vs. captopril**

*

177 188 182 186 176 188 186

Clonidine

CaptoprilHydrochlorothiazide

Diltiazem

Prazosin

Atenolol Placebo

n =

SBP = systolic blood pressure


Diuretics Used to Treat HypertensionT½ (hours)

Thiazide and Thiazide-like Diuretics

Hydrochlorothiazide* 65 – 75 3.0 – 10.0 6 – 12

Chlorothiazide 30 – 50 15.0 – 25.0 6 – 12

Chlorthalidone ** 65 24.0 – 55.0 24 – 72

Bendroflumethiazide 90 2.5 – 5.0 18 – 24

Indapamide 90 6.0 – 15.0 24 – 36

Metolazone 65 14 12 – 24

Loop Diuretics

Bumetanide 80 – 90 0.3 – 1.5 4-6

Furosemide * 10 – 100 0.3 – 3.4 6-8

Torsemide 80 – 100 3.0 – 4.0 6-8

Potassium-SparingDiuretics

Amiloride 15-20 17.0 – 26.0 24

Triamterene * 83 (55)* 3.0 (3.0)* 7-9

Spironolactone * >90 1.5 – 15.0† 48-72

Eplerenone 69 2.2 – 9.4 NA

*Parentheses denote active metabolite. †The half-life of one active metabolite, potassium canrenoate, is 15 h. BA = bioavailability; T½ = half-life; DOA = duration of action: NA = unknown.

BA (%) DOA (hours)

Reprinted from Brater DC. In: Principles of Pharmacology: Based Concepts andClinical Applications. 1995:657-672, with permission from Springer Science and Business Media; Delyani JA, et al. Cardiovasc Drug Rev. 2001;19:185-200; Rosenberg J, et al. Cardiovasc Drug Ther. 2005;19:301-306; Sica DA. Congest Heart Fail. 2003;9:100-105.


Diuretics Are as Effective as ACE Inhibitors and CCBs in Reducing Coronary Events: ALLHAT

ALLHAT Collaborative Research Group. JAMA. 2002;288:2981-2997.Copyright © 2002 American Medical Association. All rights reserved.

0

4

8

12

16

20

Cu

mu

lati

ve R

ate

for

Fata

l C

on

gesti

ve H

eart

Dis

ease

an

d N

on

fata

l M

yocard

ial

Infa

rcti

on

Even

ts (

%)

Time to Event (yrs)0 1 2 3 4 5 6

1525590489054

7Numberat Risk

1447785768535

1382082188123

1310278437711

1136268246662

634038703832

295618781770

209215195

Chlorthalidone (Diuretic)

Amlodipine (Calcium Channel Blocker)

Lisinopril (Angiotensin-Converting Enzyme Inhibitor)

ALLHAT = Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial;CCBs = calcium channel blockers


Change in Mean 24-Hour Systolic Blood Pressure The Systolic Evaluation of Lotrel Efficacy and Comparative Therapies Trial*

*Ambulatory monitoring was used to measure blood pressure.†P < 0.0001 for combination vs. amlodipine besylate alone and combination vs. benazepril hydrochloride (HCl) alone.

Reprinted from Neutel JM, et al. J Clin Hypertens. 2005;7:641-646, with permission from Blackwell Publishing.

-25

-20

-15

-10

-5

0

Red

ucti

on

in

Systo

lic

Blo

od

Pre

ssu

re (

mm

Hg

)

-10.8

-21.1†

-12.4

Amlodipine Besylate+ Benazepril HCl(5+20 mg/day)

AmlodipineBesylate

(10 mg/day)Benazepril HCl

(40 mg/day)


Recommended Drug Classes for Adults with Hypertension and a Related Comorbidity

CompellingIndicator* Diuretic -Blocker

ACE Inhibitor ARB CCB

AldosteroneAntagonist

Heart failure

Prior myocardial infarction

High risk of coronary disease

Diabetes

Chronic kidney disease

Prior stroke †

Chobanian AV, et al. JAMA. 2003;289:2560-2572. Copyright © 2003 American Medical Association. All rights reserved.

*Based on documented benefits from outcome studies or on existing clinical guidelines; each compelling indicator is managed in parallel with hypertension.† When used in conjunction with a diuretic.ACE = angiotensin-converting enzyme; ARB = angiotensin receptor blocker;CCB = calcium channel blocker


Average Number of Anti-Hypertensive Agents Used to Achieve Target BP

MDRD ABCD HOT UKPDS

Goal BP<92

mmHgMAP*

<75 mmHgDBP

<80 mmHgDBP

<85 mmHgDBP

Achieved BP

93 ~75 81 82

Avg # of drugs per

patient

3.6 2.7 3.3 2.8

*The goal mean arterial pressure (MAP) of <92 mmHg specified in the MDRD trial corresponds to a systolic/diastolic blood pressure of approximately 125/75 mmHg.


0%

20%

40%

60%

80%

100%

6 mon 1 yr 3 yr 5 yr

ALLHAT Medication Use and BP Control*P

ati

en

ts (

%)

# o

f Dru

gs/P

atie

nt

ALLHAT = Antihypertensive Lipid-Lowering Treatmentto Prevent Heart Attack Trial; BP = blood pressure*Percentage controlled to <140/90 mm Hg. Cushman WC, et al. J Clin Hypertens. 2002;4:393-404.

21.81.61.41.210.80.60.40.20

1 Drug 2 Drugs 3 Drugs Average #

of Drugs

≥4 Drugs

72

2227

3236

181464

1

2

3

6

63

4837


Algorithm for Treatment of Hypertension

Not at Goal Blood Pressure (<140/90 mmHg) (<130/80 mmHg for those with diabetes or chronic kidney disease)

Initial Drug Choices

Drug(s) for the compelling indications

Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB)

as needed.

With Compelling Indications

Lifestyle Modifications

Stage 2 Hypertension (SBP >160 or DBP >100 mmHg)

2-drug combination for most (usually thiazide-type diuretic and

ACEI, or ARB, or BB, or CCB)

Stage 1 Hypertension(SBP 140–159 or DBP 90–99 mmHg)

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

or combination.

Without Compelling Indications

Not at Goal Blood Pressure

Optimize dosages or add additional drugs until goal blood pressure is achieved.

Consider consultation with hypertension specialist.


Step-wise therapy to control Essential Hypertension

Outline DIET and LIFE-STYLE therapies that patient can reasonably begin and maintain.

Encourage DASH diet and HBPM

Begin Rx with ACE-I (e.g. LISINOPRIL 10-20 mg) or ARB (e.g. LOSARTAN 25-50 mg) or Diuretic (Chlorthalidone 12.5 mg)

Add D-CCB (e.g. Amlodipine 5 mg)


Escalating therapy in Essential Hypertension

Next add low dose diuretic (e.g. Chlorthalidone 12.5-25 or HCTZ 12.5- 25 mg) Use loop diuretic if edema, CHF, or KKD present: (e.g. Furosemide 20-40 mg QD-BID)

Next uptitrate ACE-I and/or D-CCB to full dose

(e.g. Lisinopril 40 mg and Amlodipine 10 mg)

Next add vasodilator-BB (e.g. Carvedilol 6.25 mg BID)

Uptitrate all Rx to full dose and/or add Spironalactone


Hypertension Control Rates AreSlowly Improving (NHANES Data)

*Controlled blood pressure was defined as <140/90 mm Hg and expressed as a % of all hypertensives. NHANES = National Health and Nutrition Examination Survey.

Chobanian AV, et al. JAMA. 2003;289:2560-2572; Ong KL, et al. Hypertension. 2007;49:69-75; Ostchega Y, et al. NCHS Data Brief. 2008;(3):1-8.

1976-1980

1988-1991

2001-2002

2003-2004

2005-2006

1991-1994

1999-2000

Ad

ult

s (%

)


Monthly Cost of 4 Drug Therapy

BASED ON GENERIC DRUGS AT DISCOUNT PHARMACIES FOR 30 DAYS OF THERAPY

Diet and life style…………………….… ….….…$0.00

Chlorthalidone 25 mg QD………… ….….….$3.00

Lisinopril 40 mg QD…………………….....…...$6.00

Amlodipine 10 mg ½ QD……… …..........$14.00

Carvedilol 25 mg ½ BID……………….....….$3.00

TOTAL COST FOR 1 MONTH Rx....$26.00


Treatment Objectives to Prevent Macrovascular Disease in Diabetic Patients

Hypertension– BP < 130/80 mmHg

Hypercholesterolemia– LDL < 100 mg/dL, HDL > 40 mg/dL

Hyperglycemia– HbA1c ~ 7.0 %

American Diabetes Association Clinical Practice Recommendations. Diabetes Care. 2001;24(suppl1):S1-S133.


Causes of Resistant Hypertension

1. Excess dietary sodium intake (Diet must be < 2 Grams Sodium)2. Medication prescription issues a. Inadequate diuretic therapy b. Inadequate doses of vasodilator meds c. Drug actions and interactions (e.g., nonsteroidal anti-inflamm.

drugs (NSAIDs), cocaine, sympathomimetics, oral contraceptives) d. Non-adherence (Not refilling Rx or not taking Rx)3. Excessive alcohol intake (Often >5 oz/day)4. Obesity, esp. Abnormal Sleep Breathing/Obstructive Sleep Apnea5. Primary causes of HTN (KKD, B RAS, Pheo, Aldost, Coarct, etc) Circulation 2008;117:e510-526


How to Succeed at Treating

Dyslipidemia without really tryingOr how to normalize CAD Risk in Most of Your Patients

Thomas E. Richtsmeier MD FACC

Wenatchee Valley Medical Center

Moses Lake Clinic

Adult Treatment Panel III and Update(ATP III) Guidelines

National Cholesterol Education Program

NCEP ATP IV is coming soon to

a Journal of web site near you!!

NCEP III: Update 2004NCEP III 2001 JAMA 2001 285:2486-97

5 New Clinical Trials MRC HPS*, PROSPER, ALLHAT-LLT, ASCOT-LLA*, PROVE IT*. 2 Additional Trials: REVERSAL*, CARDS

Confirmation of “CAD Risk Equivalents” including Type 2 Diabetes and Continued emphasis on the Metabolic Syndrome.

New LDL Goal for “very high risk patients” LDL-C goal < 70 mg/dL, or Non-HDL < 100 mg/dL and LDL lowering of at least 30% Circulation 2004; 110:227-39 Or www.nhlbi.nih.gov/guidelines/cholesterol


ORIGIN OF BLOOD LIPIDSTriglyceridesSaturated Fat

&

CHOLESTEROL IS ESSENTIAL FOR LIFE


Risk Factors for CHD MODIFIABLE

– DYSLIPIDEMIA* Elevated LDL* Low HDL Raised TGs (esp.

remnants)– SMOKING* – HYPERTENSION*– DIABETES MELLITUS*– Novel Risk Factors: Alb-uria hs-CRP, Metabolic Syndrome– Thrombogenic factors– Sedentary lifestyle

Wood D, et al. Atherosclerosis. 1998;140:199-270. & TR.

NON-MODIFIABLE • AGE

• SEX

• FAMILY HISTORY of

Premature CAD

HIGHEST RISK: PRESENCE OF ASCVD

CAD, CVD, PAD Indicates more rigorous

Secondary Prevention


Initiation of Atherosclerosis

Healthy Endothelium Function:• Vasodilatory• Non-Thrombogenic• Non-Adhesive of Mono. and Plat.

n

Endothelium


Atherosclerosis Is an Inflammatory

Disease

Libby et al. Circulation 2002;105:1135-1143.

E-Selectin, P-Selectin

LDL

OxLDL

L-Selectin, Integrins

VCAM-1, ICAM-1

M-CSF

MCP-1

MacrophageActivation & Division

Monocyte

Intima

Media

Smooth Muscle CellMigration

Other inflammatory triggers

Libby P. Circulation. 1995;91:2844-2850.

Characteristics of Plaques Prone to Rupture

– T lymphocyte

– Macrophagefoam cell (tissue factor+)

– “Activated” intimal SMC (HLA-DR+)

– Normal medial SMC“Stable” plaque

“Vulnerable” plaque

Lumen

area ofdetail

MediaFibrous cap

Lumen

Lipidcore

Lipidcore


0.0

1.0

2.0

3.0

Low HDL-C Predicts Coronary Heart Disease Risk Independent of LDL-C:The Framingham Heart Study

100

Relative Risk of Coronary

Heart Disease

After 4 Years

25

LDL-C (mg/dL)

160 22085

6545

HDL-C(mg/dL)

Data for men aged 50–70 years

Reproduced with permission from Castelli WP. Can J Cardiol. 1988;4(Suppl A):5A-10A. Copyright © 1988 Pulsus Group Inc.

HDL-C = high-density lipoprotein cholesterol; LDL-C = low-density lipoprotein cholesterol

59

ATP III Lipid and

Lipoprotein Classification LDL Cholesterol (mg/dL)

50-70…………Normal in all mammals

70-100………..“Normal,” Optimal

100–129………Near optimal

130–159………Borderline high

160–189………High

190…………...Very high


Classification of Serum Triglycerides

Triglyceride Category

ATP II LevelsATP III Levels

Normal <200 mg/dL <150 mg/dL

Borderline-high 200–399 mg/dL150–199 mg/dL

High400–1000

mg/dL200–499 mg/dL

Very high >1000 mg/dL 500 mg/dL

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA 1993;269:3015-3023. | Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA 2001;285:2486-2497.

61

HDL-C ATP III Lipid and Lipoprotein Classification (continued)

• HDL Cholesterol (mg/dL)

<40 = Low 60 = High • HDL>60 is a negative risk factor.

• Non-HDL Cholesterol is 2nd target for Tx. Example: T-C=200 HDL-C=50 NonHDL-C=150

• T-Chol/HDL ratio remains the single • best predictor of risk on lipid profile Example: T-C=200 HDL-C=50 T-C/HDL= 4


Atherogenic LipoproteinsAtherogenic Lipoproteins Non-HDL-Cholesterol = TC – HDL-C

Total=VLDL + LDL+ OxLDL+IDL +Remnants

Can be accurately measured in nonfasting state

Apo B concentration represents total number of lipoprotein particles (LDL + IDL + VLDL)

This may be called the “atherogenic cholesterol”

Goal Non-HDL-C < 130 or High Risk Pts <100

Grundy SM. Circulation 1997;95:1-4.


Oxidized LDL

Saturated Fat

Visceral Adiposity

CHOOSING THERAPY GOALS

RISK ASSESSMENT in Primary Prevention TO DEFINE CAD RISK AND ASSESS FOR Rx: USE FRAMINGHAM RISK .

Framingham Heart Study 10 year CAD risk. <10% Low. 10-20% Intermediate. >20% High

**

** *

*

***

**


0.0

1.0

2.0

3.0

4.0

5.0

High Medium Low LowMedium

High

hs-CRP Adds to Predictive Value of TC:HDL Ratio in Risk of First MI

Ridker PM et al. Circulation 1998;97:2007-2011.1998 Lippincott Williams & Wilkins.

Total Cholesterol:HDL Ratio

hs-CRP

67

ATP III CHD Risk Equivalents• Patients with Clinical Coronary Artery Disease (MI,

PCI, Angina, etc) have a 10 year risk >20 % MACE• Other clinical forms of atherosclerotic disease

(peripheral arterial disease, abdominal aortic aneurysm, and symptomatic carotid artery disease)

• Diabetes Mellitus• Multiple risk factors that confer a 10-year risk for

CHD >20%

• THIS MANDATES MORE AGGRESSIVE TX

SUMMARY OF NEW LIPID LOWERING GUIDELINES.

Low 0-1 < 5% < 160 > 190

Moderate 1- 2 < 10% < 130 > 160

Moderate- High

> 2, DM-2 Met. Synd.

10-20% < 70-130 > 130

High

CAD, CAD=,DM-2, Met. Syndrome

> 20%

< 70-100 > 100

Very High Recent ACS, DM-CAD

> 20-50% < 70-100 > 100

CAD Risk Risk 10 Year CAD Goal LDL LDL Level Indic-Category Factors Risk Level for TLC ating Rx

www.nhlbi.nih.gov/guidelines/cholesterol

69

0.0

1.0

2.0

3.0

100

Framingham Study

Risk of CHD after 4 Years*

25

LDL-C (mg/dL)

160 22085

6545

HDL-C(mg/dL)

FUTURE

Reprinted in adapted form from Castelli WP. Can J Cardiol. 1988;4(Suppl A):5A–10A, with permission from Pulsus Group Inc.

*Risk of coronary heart disease (CHD) over 4 years of follow-up for men ages 50 to 70

THE DIET DELEMMMA:FINDING A RATIONALRESOLTION

DIET AND LIFESTYLE THERAPY Is The CORNERSTONE for ALL PATIENTS. DIETARY THERAPY TO PREVENT CAD: WHICH ONE?? ADA? AHA? ATKINS? LOW CARB? LOW GLYCEMIC INDEX FOODS? WHATEVER?

100 to150 minutes/wk

Simple Non-expensive, Tasty Efficacious


Dietary Adjuncts

TLC for patients with LDL-C = 160

Walden CE, et al. Arterioscler Thromb Vasc Biol. 1997;17:375-382.Jenkins DJ, et al. Curr Opin Lipidol. 2000;11:49-56.Cato N. Stanol meta-analysis. Personal communication, 2000.

Dietary Component LDL-C (mg/dL)

Low saturated fat/dietary cholesterol –12

Viscous fiber (10–25 g/d) –8

Plant stanols/sterols (2 g/d) –16

Total –36


Ask about tobacco use status at every visit Advise every tobacco user to quit Assess the tobacco user’s willingness to quit Assist by counseling and developing a plan

for quitting Arrange follow-up, referral to special

programs, or pharmacotherapy (including nicotine replacement and bupropion)

Urge avoidance of exposure to environmental tobacco smoke at work and home

Cigarette Smoking: Recommendations

GOAL Complete Cessation and No Exposure to Environmental Tobacco Smoke

l lla llb lll

B


Try to get everyone to quit.


Assess risk with a physical activity history and/or an exercise test, to guide prescription

Physical Activity: Recommendations

l lla llb lll

B

l lla llb lll

BEncourage 30 to 60 minutes of moderate intensity aerobic activity such as brisk walking, on most, preferably all days of the week, supplemented by an increase in daily lifestyle activities

l lla llb lll

BAdvise medically supervised programs for high-risk patients (e.g. recent acute coronary syndrome or revascularization, HF)

GOAL 30 minutes/day, 7 days/week; Minimum 5 days/week


Almost every one can walk, even if its only to shop at Walmart. Park your car as far from the entrance as possible. These alone will count as 20 minutes.


Cholesterol Management Pharmacotherapy

*Daily dose of 40 mg of each drug, excluding rosuvastatin

TC = Total cholesterol, LDL-C = Low-density lipoprotein cholesterol, HDL-C = High-density lipoprotein cholesterol, TG = Triglycerides

Therapy TC LDL-C HDL-C TGPatient

tolerability

Statins* 19 – 37% 25 – 50% 4 – 12% 14 – 29% Good

Ezetimibe 13% 18% 1% 9% Good

Bile acid sequestrants

7 – 10% 10 – 18% 3% Neutral or Poor

Nicotinic acid 10 – 20% 10 – 20% 14 – 35% 30 – 70% Reasonable to poor

Fibrates 19% 4 – 8% 11 – 13% 30% Good

Yeshurun D et al. South Med J 1995;88:379–391. | NCEP. Circulation 1994;89:1333–1445. | Knopp RH. N Engl J Med 1999;341:498–511. | Gupta EK et al. Heart Dis 2002;4:399–409.

75

-70

-60

-50

-40

-30

-20

-10

0

4S Group. Lancet 1994;334:1383–1389.

Simvastatin Reduced the Risk of Major Coronary Events: Subgroup Analyses from the Scandinavian Simvastatin

Survival Study

Perc

en

t R

isk

Red

uct

ion

Men

P=0.002

Women Older Smokers Hyper-tension

Diabetes

n=1814

-55

-37-31

-34-35-34

n=407 n=1156 n=542 n=573 n=105

P<0.002P<0.002P<0.0005P=0.01P<0.00001

76

HMG CoA Reductase Inhibitors (Statins)

Statin Dose Range

Lovastatin 20–80 mg …Least Expen.Pravastatin 20–40 mg….Best toleratedSimvastatin 20–80 mg….Best genericFluvastatin 20–80 mgAtorvastatin/ Lipitor 10–80 mg ….Overall bestCerivastatin 0.4–0.8 mg Rousuvastatin/ Crestor 10--40 mg…..Most potent

78

HMG CoA Reductase Inhibitors (Statins) (continued)

Demonstrated Therapeutic Benefits

• Reduce MACE (major coronary events)• Reduce CHD mortality• Reduce coronary procedures

(PTCA PCI-S CABG)• Reduce stroke• Reduce total mortality


Atorvastatin10/20/40/80 mg

211 mg/dl*

Simvastatin10/20/40 mg†

219 mg/dl*

Mean

ch

an

ge f

rom

base

line

Majority of LDL-C Lowering Occurs at the Lowest Statin Dose

Adapted from Jones P et al. Am J Cardiol 1998;81:582-587.

*Mean baseline LDL-C.†At the time of this study, the maximum dose for simvastatin was 40 mg.

Daily Dose

10 mg

20 mg

40 mg

80 mg

-60%

-50%

-40%

-30%

-20%

-10%

0%

16% with3 titrations

13%

54%

38%

46%

51%

28%

35%

41%

80

0

5

10

15

20

25

30

HMG-CoA Reductase Inhibitor:Secondary PreventionRelationship between LDL-C Levels and Event Rates in

Secondary Prevention Trials of Patients with Stable CHD

Event

(%)

LDL-C (mg/dL)

3 70 90 110 130 150 170 190

StatinPlacebo

4S

LaRosa et al. N Engl J Med 2005;352:1425–1435.

LDL-C=low-density lipoprotein cholesterol; CHD=coronary heart disease; TNT=Treating to New Targets; HPS=Heart Protection Study; CARE=Cholesterol and Recurrent Events Trial; LIPID=Long-term Intervention with Pravastatin in Ischaemic Disease; 4S=Scandinavian Simvastatin Survival Study.

210

4S

LIPIDLIPIDCARE

HPS

CAREHPS

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


Components of Secondary Prevention

• Cigarette smoking cessation

• Blood pressure control

• Lipid management to goal

• Physical activity

• Weight management to goal

• Diabetes management to goal

• Antiplatelet agents / anticoagulants

• Renin angiotensin aldosterone system blockers

• Beta blockers

• Influenza vaccination



CHD All PatientsHigh RiskPati

en

ts a

chie

vin

g g

oal

(%)

Inadequate Achievement of NCEP ATP III Treatment Goals, Especially among Patients at Highest CHD Risk

70%

Adapted from Pearson TA et al. Arch Intern Med 2000;160;459-467.Copyright © 2000 American Medical Association. All rights reserved.

Low Risk

Drug therapy included statins (fluvastatin, lovastatin, pravastatin, simvastatin), gemfibrozil, bile acid sequestrants, niacin, psyllium fiber, and combination drug therapy.

1,352 4,1371,924861

40%

18%

39%

n =

0%

20%

40%

60%

80%

100%


Limitations of Statin Monotherapy on CHD Events

Trial Drug N

Events,* n

Risk Reduction,

%†

Events not

Avoided, %

ControlGroup

StatinGroup

4SWOSCOPSCAREAFCAPSLIPID

SimvastatinPravastatinPravastatinLovastatinPravastatin

30,817 2,042 1,490 26 74

HPS Simvastatin 20,586 1,212 898 26 74

PROSPER Pravastatin 5,804 356 292 19 81

ASCOT-LLA Atorvastatin 10,305 154 100 36 64

Total 67,462 3,764 2,780 27 73

Reprinted from Bays H. Expert Rev Cardiovasc Ther 2004;2:89-105, with permissions from Future Science Group.

* Nonfatal MI and CHD death; AFCAPS also included unstable angina† Weighted average

84

Combined Dyslipidemias: Low HDL & Elevated Triglycerides

Non-HDL Cholesterol: Secondary Target

• Primary target of therapy: LDL cholesterol

Try to achieve LDL goal before treating

non-HDL cholesterol• Therapeutic approaches to elevated non-HDL

cholesterol– Intensify therapeutic lifestyle changes– Intensify LDL-lowering drug therapy– Nicotinic acid or fibrate therapy to lower VLDL


Combination Lipid-Altering Drug Therapy with StatinsNeed for combination lipid-altering

drug therapy To achieve ATP III goals. Ezetimibe and statins Bile acid sequestrants and statins PPAR agonists and statins Fish oils and statins

Niacin and statins Investigational lipid-altering drug

combinations (CETP inhibition)

86

Lipid Monotherapy Options:Clinical and Lipid

Expectations

Compiled by Brown BG, December 2006.

Drug Class

CV EventReduction

(%)

LDL-CDecrease

(%)

HDL-CIncrease

(%)

TGDecrease

(%)

LDLSize/

Buoyancy

Statins 25% - 35%(4S, CARE,

LIPID)

++++ +5%

+ +

Niacin 16% - 35%(CDP,

Stockholm)

++ ++++30%

++++ +++

Fibrates 11% - 24%(FIELD,VA-HIT)

+ ++10%

++++ +

Torcetrapib 61%(??????)

+ ++++40%

+ +

CV=cardiovascular; LDL-C=low-density lipoprotein cholesterol; HDL-C=high-density lipoprotein cholesterol; TG=triglyceride


Combination Niacin Extended-Release/ Lovastatin vs Monotherapy with Atorvastatin or Simvastatin

Percent Change from Baseline

Week 8 Week 12

Niacin ER/L1000/40 mg A 10 mg

Niacin ER/L1000/40 mg S 20 mg

LDL-C –39%* –38% –42%* –35%

HDL-C +20%** +3% +19%** +8%

Triglyceride –30%** –20% –36%** –15%

Lipoprotein(a) –16%** +5% –20%** –1%

Bays H et al. Am J Cardiol 2003;91:667-672.

*P<0.01 versus simvastatin**P<0.001 versus atorvastatin and simvastatin

88

-2

-1

0

1

2

3

4

Change f

rom

Base

line in M

ean

Pro

xim

al %

Ste

nosi

s (

%S)

0

Angiographic Effects of Lipid Drug Classes Meta-Analysis, 12 Trials

755025

% Change in LDL-C in Rx(%) Placebo-Adjusted

Placebo (6)

Fibrates (1)

Statins (6)

Statin+Resin (1)

Niacin Combos (4)

Progression

Regression

Compiled by Brown BG, August 2006.

STATIN and NIACIN Combination

NEJM 2001. 345:1583-92. 160 pts with CAD and low HDL and WNL LDL. Angiogr. Regression occurred only in Sim + Niacin pts


Placebo S + N + AVS + N

0

5

10

15

20

25

Com

posi

te E

ven

t R

ate

, %

HDL-Atherosclerosis Treatment Study (HATS)Niacin and Statin Outcome Trial

Brown BG et al. N Engl J Med 2001;345:1583-1592.

AV

Coronary Death, MI, Stroke, or Revascularization

89%Reduction

21.4

2.6*

14.3

*P<.05vs Placebo23.7

ASSESSING LIPID THERAPY AFTER ADEQUATE STATIN Tx.

Is glycemic therapy adequate?Is patient on TZD or Metformin?

Is patient on high dose BB or diuretic or smoking?Can patient exercise?

Is patient’s glycemic control adequate?Is pt on TZD or Metformin?

Fibrate is Rx of choice for Trig> 500.

#

# Each doubling of statin dose lowers LDL by about 6%.

Lower dietary carb. and Saturated fats.

*

92

Summary: Niacin plus Statin

• Exceeds statin effects on LDL, HDL, TG, and LDL particle size/density

• Stops stenosis progression in its tracks (small regression)

• Magnitude of benefits predicted by epidemiology, (% HDL-C and % LDL-C change), and supported by 23-trial meta-analysis

• Clinical proof: “AIM HIGH” trial release 2011 or 2012

LDL=low-density lipoprotein; HDL=high-density lipoprotein; TG=triglyceride; HDL-C= high-density lipoprotein cholesterol; LDL-C=low-density lipoprotein cholesterol

93

HOW TO USE STATIN & NIACIN

VARIETIES• Niacin XR-Lovastatin

Niacin XR-Simvastatin

Advicor, Simcor

• Any Statin with OTC Niacin XR (“SloNiacin”)

• Any Statin with Niaspan

ADMINISTRATION1. Start Niacin XR 500 mg

with ASA 81 and Statin

with supper or H.S.

2. Slowly titrate to goal

Do not exceed 2000mg Niacin XR

3. Monitor FBS, LFTs,

Pyrosis, flushing , gout


Bile Acid Sequestrants: Colesevelam and Statins

Colesevelam HCl Statin

TC (%)

LDL-C (%)

HDL-C (%)

TG (%)

0 mg(no tablets)

Atorvastatin80 mg

–43 –56 +2 –43

3750 mg(6 tablets)

Atorvastatin10 mg

–35 –51 +7 –11

Bays H et al. Expert Opin Pharmacother 2003;4:779-790.Hunninghake D et al. Atherosclerosis 2001;158:407-416.


0

10

20

30

40

50

Haffner SM et al. N Engl J Med 1998;339:229-234.

Incidence of MI during a 7-Year Follow-up in a Finnish Population

Fat a

l or

Nonfa

tal M

I (

%)

Prior MI

18.8

3.5

45.0

20.2

P<0.001

P<0.001

Prior MINo prior MI No prior MINondiabetic subjects Diabetic subjects

(n=1373) (n=1059)

National Diabetes Data Group. Diabetes in America. 2nd ed. NIH;1995 & TR

Atherosclerosis in Diabetes~80% of all diabetic mortality– 75% from coronary atherosclerosis and/or CHF– 25% from cerebral or peripheral vascular

disease>75% of all hospitalizations for diabetic complications>50% of patients with newly diagnosed type 2 diabetes have CHD

Most common cause of ESRD and Blindness which are micro-vascular diseases.

DM-2 is as much or more a Vascular Disease as a Metabolic Disease.

Stepwise Selection of Risk Factors* in 2693 White Patients with Type 2 Diabetes with Dependent Variable as Time to First

Event: UKPDS

Variable

Low-Density Lipoprotein Cholesterol

High-Density Lipoprotein Cholesterol

Hemoglobin A1c

Systolic Blood Pressure

Smoking

P Value

<0.0001

0.0001

0.0022

0.0065

0.056

Coronary Artery Disease (n=280)

Position in Model

First

Second

Third*

Fourth*

Fifth

*Adjusted for age and sex.Turner RC et al. BMJ 1998;316:823-828.


Intensive Multiple Risk Factor Management in Patients with Type 2 Diabetes: STENO-2

0

10

20

30

40

50

60

Pri

mary

Com

posi

te E

ndpoin

t* (

%)

Months of Follow-up

N=160; follow-up = 7.8 years

Primary composite endpoint: conventional therapy (44%) and intensive therapy (24%). *Death from CV causes, nonfatal MI, CABG, PCI, nonfatal stroke, amputation, or surgery for peripheral

atherosclerotic artery disease. †Behavior modification and pharmacologic therapy.

Adapted from Gaede P et al. N Eng J Med 2003;348:383–393.

0 12 24 36 48 72 9660 84

Aggressive treatment of†:

– Microalbuminuria with ACEIs, ARBs, or combination– Hypertension– Hyperglycemia– Dyslipidemia– Secondary prevention of CVD

Conventional Therapy

Intensive Therapy†

20% Absolute Risk Reduction

99

Components of Secondary Prevention

• Cigarette smoking cessation

• Blood pressure control

• Lipid management to goal

• Physical activity

• Weight management to goal

• Diabetes management to goal

• Antiplatelet agents / anticoagulants

• Renin angiotensin aldosterone system blockers

• Beta blockers

• Influenza vaccination


HTN and Dyslipidemia.pptx - RussoCME - Primary Care Medical ...

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Transcript of HTN and Dyslipidemia.pptx - RussoCME - Primary Care Medical ...