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Transcript of 3 Hipertensi
Bag-Bag-SMF KardiologiSMF Kardiologi & Kedokteran Vaskular & Kedokteran Vaskular
FK Universitas Cendrawasih
HipertensiHipertensi
Franklin, S.S., J Hypertens 1999; 17 (suppl 5): S29-S36
0
10
20
30
40
50
60
70
18-29 30-39 40-49 50-59 60-69 70-79 80+
SBP > 140 mm Hg DBP > 90 mm Hg
age (yrs)
pre
vale
nce
of
hyp
erte
nsi
on
(%
)
4 11
21
4454
64 65
Prevalensi HipertensiPrevalensi Hipertensi
Prevalensi :Prevalensi :
Berdasar kriteria Hipertensi WHO 1968 (tekanan darah > 160/95 mmHg), prevalensi hipertensi di dunia sekitar 5-18 %. Prevalensi hipertensi di Indonesia tidak jauh berbeda yaitu sekitar 6-15 %, walaupun dilaporkan adanya prevalensi yang rendah yaitu :
- Ungaran 1,8 %- Lembah Balim 0,6 %
serta adanya prevalensi yang tinggi :- Silungkang 19,4 %- Talang 17,8 %
Prevalensi Hipertensi di Jawa Timur hampir sama yaitu :- Sumberpucung (1976) 10 %- Lawang (1987) 11 %- Kampak (1987) 17 %
23%
16%
42%19%
Hypertensive patients who are treated but uncontrolled
Hypertensive patientswho are treated and controlled
Hypertensive patients who are unaware
Patients who are awarebut remain untreated
and uncontrolled
22 % of American adults 18 to 70 years of age have hypertension20 % of Indonesian adults have hypertension
New Criteria (WHO-ISH 1999) ≥ 140 / 90 mmHg
Source : Joffres et al. (1997) Am. J. Hypertension 10: 1097-1102
>>100100atauatau>> 160 160 Stage 2Stage 2
90-9990-99atauatau140-159140-159 Stage 1Stage 1
HipertensiHipertensi
80-8980-89atauatau120-139120-139Pre HipertensiPre Hipertensi
<80<80dandan<120<120NormalNormal
DiastolicDiastolic(mm Hg)(mm Hg)
SystolicSystolic(mm Hg)(mm Hg)CategoryCategory
Klasifikasi Hipertensi (JNC 7 - 2003)Klasifikasi Hipertensi (JNC 7 - 2003)
HipertensiHipertensi
Berdasarkan penyebabnya dapat dibedakan :
• Primer (essential)– tidak ada penyebab yang spesifik yang dapat
diidentifikasi– 90-95% dari kasus hipertensi
• Sekunder– diketahui penyebabnya– 5-10% dari kasus hipertensi– penyakit ginjal merupakan penyebab tersering
kasus hipertensi sekunder
Etiology HypertensionEtiology Hypertension• Secondary Hypertension :
– Renal disease :• Renal arterial disease• Renal parenchymal disease• Renal tumors• Arteritis (polyarteritis nodosa, neurofibromatosis)
– Endocrine Disorders• Cushing’s syndrome• Acromegaly• Primary aldosteronism• Pheochromocytoma
– Coarctation of the aorta– Neurologic disorders
• Increased intra cranial pressure (tumor)– Drug-induced hypertension
• Corticosteroids• Amphetamines• Oral contraceptives
– Psychogenic disorders
PATOPHYSIOLOGY
The factors affecting cardiac output: - sodium intake, renal function, & mineralocorticoids - the inotropic effects occur via extracellular fluid volume augmentation - an increase in heart rate and contractility
Peripheral vascular resistance is dependent upon the sympathetic nervous system, humoral factors, and local autoregulation
(Sharma, 2003)
Neurohormonal control of blood pressureBlood pressure = Cardiac output (CO) x Peripheral resistance (PR)
Hypertension = Increased CO and/or Increased PR
Preload
Fluid volume
Renal sodiumretention
Contractility
Fluid volume
Vasoconstriction
Sympatheticnervoussystem
Renin-angiotensin-aldosterone
system
Geneticfactors
Excesssodiumintake
(Adapted from Kaplan, 1994)
Hypertension :The Disease Continuum
Hypertension :The Disease Continuum
Early Paradigm
Elevated BP Target Organ Damage
Natural History of CVD ProgressionNatural History of CVD Progression
More Recent Paradigm
Vascular Dysfunction Elevated BP Target Organ Damage
A Proposed Future Paradigm
EndothelialDysfunction
LVHRenal
DamageMI Stroke
AnginaPectoris
VascularDysfunction
Elevated BP Target OrganDamage
?
Komplikasi HipertensiKomplikasi Hipertensi
Kerusakan yang disebabkan oleh hipertensi tergantung :
• Besarnya peningkatan tekanan darah
• Lamanya kondisi tekanan darah yang tidak terdiagnosis dan tidak diobati
Kerusakan Target Organ!!Eyesretinopathy
Kidneysrenal failure
Brainstroke
Heartischaemic heart disease
left ventricular hypertrophyheart failure
Peripheral arterial disease
Effects of blood pressure on the risk of cardiovascular disease
Average annual incidence rate per 10.000
Source : Framingham study (after Gorlin)
100
90
80
70
60
50
40
30
20
10
0
<100 120 140 180 >180
Systolic blood pressure (mmHg)
CHD
Stroke
CHF
SymptomsSymptoms
• Headache
• Dizziness
• Fatigue
• Pounding of the heartSymptoms are not specific and no more frequent than in patients with normotension.
• Symptoms of complications : heart failure, chest pain, claudication, vision
Evaluasi Klinis Hipertensi : Evaluasi Klinis Hipertensi :
Tujuan :
1. Konfirmasi hipertensi dan tingkatnya
2. Menyingkirkan & menemukan hipertensi sekunder
3. Menentukan kerusakan organ target
4. Mencari faktor risiko kardiovaskuler dan kondisi
klinik lain
Riwayat Klinis :Riwayat Klinis :
• Riwayat keluarga HT, DM, dislipidemia, PJK, stroke atau sakit ginjal
• Lama & tingkat TD sebelumnya & hasil Tx. serta efek
• Adanya PJK, gagal jantung, penyakit serebrovaskuler, ginjal, perifer, DM, pirai, dislipidemia, asma bronkhiale, & informasi obat
• Faktor risiko (diet lemak, Na & alkohol, rokok, aktifitas fisik, & BB)
• Riwayat obat-obatan (kontrasepsi, NSAID, kokain & amfetamin) dapat TD.
• Faktor pribadi, psikososial dan lingkungan.
Pemeriksaan Fisik :Pemeriksaan Fisik :
• Pemeriksaan fisik & TD yang teliti• Tinggi, berat, & BMI (Body mass Index) • Sistem kardiovaskuler : ukuran jantung,
gagal jantung, arteri perifer (carotis, aorta, renal)
• Paru (ronkhi & bronkhospasme), bising abdomen. • Fundus optikus & sistim syaraf (mengetahui
kerusakan serebro-vaskuler).
Technique of blood pressure measurement recommended by the British Hypertension Society
Technique of blood pressure measurement recommended by the British Hypertension Society
2.The patient should be relaxed and the arm must be supported. Ensure no tight clothing constricts the arm
3.The cuff must be level with the heart. If the circumference exceeds 33cm, a large cuff must be used (2/3 of arm). Place stethoscope diaphram over brachial artery
4.The column of mercury must be vertical. Inflate to occlude the pulse (>30 mmHg). Deflate at 2-3 mm/s. measure systolic ( first sound / Korotkoff I ) & diastolic (disappearence / Korotkoff IV or V ) to nearest 2 mmHg
(From British Hypertension Society 1985)
1.Several time, rest 5 minutes before
Recommended Technique for Measuring Blood Pressure
Standardized technique:
• Have the patient rest for 5 minutes
• Use an appropriate cuff size
• Use a mercury manometer or a recently calibrated electronic device
• Position cuff appropriately
• Increase pressure rapidly
• Support arm with antecubital fossa or heart level
• To exclude possibility of auscultatory gap, increase cuff pressure rapidly to 30 mmHg above level of diseappearance of radial pulse
• Place stethoscope over the brachial artery
Recommended Technique for Measuring Blood Pressure (cont.)
Recommended Technique for Measuring Blood Pressure (cont.)
• Drop pressure by 2 mmHg / beat:
- appearance of sound (phase I Korotkoff)
= systolic pressure
- disappearance of sound (phase V
Korotkoff) = diastolic pressure
• Take 2 blood pressure measurements, 1 minute apart
Diagnosis of Hypertension
Hypertension is defined as:
- BP 140/90 mm Hg- during 1-5 visits- with an average of 2 readings per visit
Pengukuran tekanan darah ambulatoryPengukuran tekanan darah ambulatory
Sekarang terdapat alat otomatis untuk mengukur tekanan darah selama 24 jam atau lebih.
Indikasi pemeriksaan tersebut (ABPM = Ambulatory Blood Pressure Monitoring) ialah sebagai berikut :
1. Adanya variasi tekanan darah yang besar
2. Office hypertension
3. Dicurigai adanya episode hipotensi
4. Hipertensi yang resisten terhadap pengobatan
Pemeriksaan lain-lainPemeriksaan lain-lain
• Laboratorium :• Urinalisis & mikroskopik urin• Serum kalium, kreatinin, gula darah puasa & 2 jam dan profil lemak,
asam urat• Pemeriksaan tambahan :
– Pemeriksaan hormonal seperti pengukuran aktifitas renin plasma, aldosteron plasma dan katekolamin urine atas indikasi khusus (hipertensi sekunder)
• EKG & Foto polos dada• Ekhokardiografi (curiga kerusakan organ target /LVH / lainnya)• Ultrasonografi vaskuler (curiga penyakit arteri karotis, aorta atau
perifer lain)• Ultrasonografi renal (curiga penyakit ginjal)• Angiografi
Minimal BP Goal of TherapyMinimal BP Goal of Therapy
Recommendations (SBP/DBP mmHg)
Patient Type
Uncomplicated HTN
Hypertension with diabetes mellitus
Heart failure
Hypertension with renal impairment†
JNC VI
< 140/90
< 130/85 < 130/80*
< 130/85
< 125/75
(Bakris GL, et al for the National Kidney Foundation Hypertension and Diabetes Executive Committees Working Group. Am J Kidney Dis. 2000) (JNC VI. Arch Intern Med. 1997)
*National Kidney Foundation Hypertension and Diabetes Executive Committees Working Group.†Proteinuria > 1 g/24h.
Terapi HipertensiTerapi Hipertensi
• Terapi Non-farmakologis
– Menurunkan berat badan (5-20 mmHg/10 kg)
– Latihan dan olah raga (4-9 mmHg)
– Menghindari alkohol yang berlebihan
– Mengurangi asupan garam (2-8 mmHg)
– Stop merokok
– Menurunkan asupan lemak jenuh
Lifestyle Modification
Modification Approximate SBP
reduction (range)
Weight reduction 5–20 mmHg/10 kg loss
Adopt DASH eating plan 8–14 mmHg
Dietary sodium reduction 2–8 mmHg
Physical activity 4–9 mmHg
Moderation of alcohol
consumption 2–4 mmHg
Terapi HipertensiTerapi Hipertensi
• Terapi Farmakologis– tujuan terapi antihipertensi
• Memperbaiki fungsi endothel• untuk menurunkan resistensi vaskular sistemik• mempertahankan curah jantung• mempertahankan suplai darah ke organ dan
jaringan– Pengobatan diberikan seumur hidup– Kepatuhan yang buruk merupakan penyebab
kegagalan terapi antihipertensi yang paling besar
Pilihan terapi antihipertensiPilihan terapi antihipertensi
Diuretik
Beta-blocker
Antagonis kalsium
ACE-inhibitor
Angiotensin II receptor antagonis (AIIRA / ARB)
Alpha1-blocker (sentral & perifer)
Possible combinations of different classes of antihypertensive agents. The most rational combinations are represented as thick lines.ACE, angiotensin-converting enzyme; AT1, angiotensin II type 1.
ACE inhibitorsACE inhibitors
DiureticsDiuretics
11-blockers-blockers
-blockers-blockersATAT11 receptor receptor
blockersblockers
CalciumCalciumantagonistsantagonists
Algorithm for Treatment of HypertensionAlgorithm 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.
Reasons of inadequate BP ControlReasons of inadequate BP Control
• Acceptance of inadequate control by physician
• Difficulty achieving BP control with one agent/suboptimal
regimens
• BP goals are more aggressive than in previous years
• Lack of compliance due to :
– perceived side effects of antihypertensive
medication(s)
– frequency of dosing/multiple agents to attain control
(Adapted from JNC VI. Arch Intern Med. 1997)
Presentasi pasien hipertensi yang terkontrol
Presentasi pasien hipertensi yang terkontrol
Adapted from G. Mancia / L. Ruilope
USA: JNC VI. Arch Intern Med 1997Canada: Joffres et al. Am J Hypertens 1997 England: Colhoun et al. J Hypertens 1998France: Chamontin et al. Am J Hypertens 1998
< 140/90 mmHg< 140/90 mmHg
Canada
16
USA
27
England6
France
24
Marques-Vidal P et al. J Hum Hypertens 1997
< 160/95 mmHg< 160/95 mmHg
Finland
20.5
Spain
20
Australia
19
Germany
22.5
> 65 years
Scotland
17.5
India
9
WHO-ISH (1999) WHO-ISH (1999)
Klasifikasi Derajat Tekanan Darah menurut WHO-ISH 1999 yang diadaptasi dari JNC VI 1997
Kategori Sistolik Diastolik (mmHg) (mmHg)
1 Optimal 120 80
2 Normal 130 85
3 Normal Tinggi 130 - 139 85 - 89
4 Hipertensi derajat 1 (ringan) 140 - 159 90 - 99Subgrup : perbatasan 140 - 149 90 - 94
5 Hipertensi derajat 2 (sedang) 160 - 179 100 - 109
6 Hipertensi derajat 3 (berat) 180 110
7 Hipertensi Sistolik 140 90(Isolated Systolic Hypertension)
HipertensiHipertensi• Secondary Hypertension :
Renal diseaseRenal disease Interference with renal control systems over cardiovascularInterference with renal control systems over cardiovascularsystem - activation of renin-angiotensin-aldosterone (RAA)system - activation of renin-angiotensin-aldosterone (RAA)system, leading to increased blood volume & hence hypertensionsystem, leading to increased blood volume & hence hypertension
Renal arteryRenal artery Atherosclerotic narrowing of decreased vasodilatory mechanismsAtherosclerotic narrowing of decreased vasodilatory mechanismsstenosisstenosis leading to reduced renal blood flow and activation of RAA systemleading to reduced renal blood flow and activation of RAA system
Endocrine disordersEndocrine disordersHyperaldosteronismHyperaldosteronism Excessive aldosterone production leading to salt and waterExcessive aldosterone production leading to salt and water(Conn’s syndrome)(Conn’s syndrome) retention and increased blood volumeretention and increased blood volumeCushing’s syndromeCushing’s syndrome Excessive ACTH secretion leading to salt and water retention andExcessive ACTH secretion leading to salt and water retention and
increased blood volumeincreased blood volume
PhaeochromocytomaPhaeochromocytoma Tumour of the adrenal medulla producing excessive adrenaline,Tumour of the adrenal medulla producing excessive adrenaline,causing vasoconstrictioncausing vasoconstriction
PregnancyPregnancy Complex, involving fluid volume and hormonal fluctuationsComplex, involving fluid volume and hormonal fluctuations
Coarctation of theCoarctation of the Congenital localised narrowing of the aortic lumen, causingCongenital localised narrowing of the aortic lumen, causingaortaaorta increased afterload and peripheral resistance in the upper bodyincreased afterload and peripheral resistance in the upper body
Certain drugs,Certain drugs, Complex and variousComplex and variouse.g. corticosteroids,e.g. corticosteroids,oral contraceptivesoral contraceptivesand vasoconstrictorsand vasoconstrictors
Renin inhibitorsRenin inhibitors
AII receptor blockersAII receptor blockers
Angiotensin IIAngiotensin II
ReninRenin
Converting enzymeConverting enzyme
Angiotensinreceptors
AngiotensinogenAngiotensinogen
ACE inhibitorACE inhibitor
Angiotensin IAngiotensin I
LiverLiver TissueTissueCirculatingCirculating LocalLocal
Non Renin pathways - t-PA - Cathepsin G - Tonin
Non-ACE pathways - Chymase - CAGE - Cathepsin G
The Renin-Angiotensin SystemThe Renin-Angiotensin SystemAlternate PathwayAlternate Pathway
Brown, M.J., Lancet 2000;355:653-4
Risiko Infark Miokard dan Stroke Risiko Infark Miokard dan Stroke
Systolic blood pressure (mm Hg)
5-ye
ar r
isk
(%)
0
5
10
15
0 100 200 300
StrokeStrokeMIMI
CHFCumulativeIncidence
(%)
Years From Baseline Exam
5 10 15
20
15
10
5
0
Lenfant C, Roccella EJ. J Hypertens Suppl. 1999;17:S3-S7.Data from Levy D et al. JAMA. 1996;275:1557-1562.
Stage 2+ hypertension
Stage 1+ hypertension
Normal BP
Cumulative Incidence of CHF : Normotensives and Stage 1 and 2 Hypertensives
Cumulative Incidence of CHF : Normotensives and Stage 1 and 2 Hypertensives
Effects of Angiotensin II at ATEffects of Angiotensin II at AT11 and AT and AT22 ReceptorsReceptors
Blocked by ARB s
ATAT2AT1
- Vasoconstriction- Aldosterone release- Oxidative stress- Vasopressin release- SNS activation- Inhibits renin release - Renal Na+ and H2O reabsorption- Cell growth and proliferation
- Vasodilation- Antiproliferation- Apoptosis- Antidiuresis/antinatriuresis- Bradykinin production- NO release
Siragy H. Am J Cardiol. 1999;84:3S–8S.
Role of A II in Vascular Disease
Reprinted with permission from Dzau VJ. Hypertension. 2001;37:1047-1052.
Diabetes Smoking
Oxidative Stress
Endothelial Dysfunction and Smooth Muscle Activation
Growth FactorsCytokines
Matrix
Proteolysis Inflammation
VCAM/ICAMCytokines
EndothelinCatecholamines
BP LDL
NO • ∆ Local Mediators • Tissue ACE, AII
PAI-1, Platelet Aggregation, Tissue Factor
Vasoconstriction Thrombosis Inflammation Plaque RuptureVascular Lesion and Remodeling
Clinical Sequelae
Risk Factors
Target Organ Damage 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
Khattar, R.S. et al. Circulation 1999; 100:1071-4
Assessment of the 24-hour blood pressure load isa good clinical method to identify high-risk patients
even
ts/1
00 p
t/yr
s
200+
mm Hg
< 140 140-159 160-179 180-199
1
2
3
4
5
6
7
Systolic Blood PressureSystolic Blood Pressure
Total Mortality and Continuous Ambulatory Blood Pressure
Total Mortality and Continuous Ambulatory Blood Pressure
1
2
3
4
5
Diastolic Blood PressureDiastolic Blood Pressure
mm Hg
< 80 80-89 90-99 100-109 110+
Benefits of Lowering BPBenefits of Lowering BP
Average Percent Average Percent
ReductionReduction
Stroke incidence Stroke incidence 35–40% 35–40%
Myocardial infarction Myocardial infarction 20–25% 20–25%
Heart failureHeart failure 50% 50%
Goals of Therapy(JNC-VII)
Goals of Therapy(JNC-VII)
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.
Hypertension Prevalence and Treatment :
North America and EuropePrevalence of Hypertension
0
5
10
15
20
25
30
35
40
45
50
55
Country
%
USCanada
Germany
ItalySwedenEnglandSpainFinland
0
10
20
30
40
50
60
70
80
90
100
Country
%
Wolf-Maier K et al. JAMA. 2003;289:2363-2369.
Patients on Therapy
25% 12.5%
12.5%
50%
Hypertensive patients who are treated but uncontrolled
Hypertensive patientswho are treated and controlled
Hypertensive patients who are unaware
Patients who are awarebut remain untreated
and uncontrolled
Source : Joffres et al. (1997) Am. J. Hypertension 10: 1097-1102
RULE OF HALF
BP Control Rates
Trends in awareness, treatment, and control of high blood pressure in adults ages 18–74
National Health and Nutrition Examination Survey
Percent
II
1976–80
III(Phase 1)1988–91
III(Phase 2)1991–94 1999–2000
Awareness 51 73 68 70
Treatment 31 55 54 59
Control 10 29 27 34
Sources: Unpublished data for 1999–2000 computed by M. Wolz, National Heart, Lung, and Blood Institute; JNC 6.
Antihypertensive Agents Combination
ACE INHIBITOR
DIURETIC
AT-2 RB
Ca-ANTAGONIST-BLOCKER
-BLOCKER
ESC-ESH 2003
CVD Risk FactorsCVD Risk Factors
Hypertension* Cigarette smoking Obesity* (BMI >30 kg/m2) Physical inactivity Dyslipidemia* Diabetes mellitus* Microalbuminuria or estimated GFR <60 ml/min Age (older than 55 for men, 65 for women) Family history of premature CVD
(men under age 55 or women under age 65)
* Components of the metabolic syndrome.
Classification and Management of BP for adults
Classification and Management of BP for adults
* 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.
Two-drug combination for mostTwo-drug combination for most†† (usually thiazide-type diuretic (usually thiazide-type diuretic and ACEI or ARB or BB or and ACEI or ARB or BB or CCB).CCB).
YesYes or or >>100100 >>160160 Stage 2 Stage 2 HypertensionHypertension
Drug(s) for the Drug(s) for the compelling indications.compelling indications.‡‡
Other antihypertensive Other antihypertensive drugs (diuretics, ACEI, drugs (diuretics, ACEI, ARB, BB, CCB) as ARB, BB, CCB) as needed. needed.
Thiazide-type diuretics for most. Thiazide-type diuretics for most. May consider ACEI, ARB, BB, May consider ACEI, ARB, BB, CCB, or combination.CCB, or combination.
YesYes or 90–99or 90–99 140–159140–159 Stage 1 Stage 1 HypertensionHypertension
Drug(s) for compelling Drug(s) for compelling indications. indications. ‡‡
No antihypertensive drug No antihypertensive drug indicated.indicated.
YesYes or 80–89or 80–89 120–139120–139 PrehypertensionPrehypertension
EncourageEncourage and <80and <80 <120<120 NormalNormal
With compelling With compelling indicationsindications
Without compelling Without compelling indication indication
Initial drug therapyInitial drug therapy Lifestyle Lifestyle
modificationmodification DBP* DBP*
mmHgmmHg SBP* SBP*
mmHgmmHg BP classificationBP classification
Compelling Indications for Individual Drug Classes
Compelling Indications for Individual Drug Classes
Clinical Trial BasisClinical Trial BasisInitial Therapy OptionsInitial Therapy Options Compelling IndicationCompelling Indication
ALLHAT, HOPE, ALLHAT, HOPE, ANBP2, LIFE, ANBP2, LIFE, CONVINCECONVINCE
ACC/AHA Post-MI ACC/AHA Post-MI Guideline, BHAT, Guideline, BHAT, SAVE, Capricorn, SAVE, Capricorn, EPHESUSEPHESUS
ACC/AHA Heart Failure ACC/AHA Heart Failure Guideline,Guideline, MERIT-HF, MERIT-HF, COPERNICUS, CIBIS, COPERNICUS, CIBIS, SOLVD, AIRE, TRACE, SOLVD, AIRE, TRACE, ValHEFT, RALESValHEFT, RALES
THIAZ, BB, ACE, CCBTHIAZ, BB, ACE, CCB
BB, ACEI, ALDO ANTBB, ACEI, ALDO ANT
THIAZ, BB, ACEI, ARB, THIAZ, BB, ACEI, ARB, ALDO ANTALDO ANT
High CAD riskHigh CAD risk
PostmyocardialPostmyocardialinfarctioninfarction
Heart failureHeart failure
Compelling Indications for Individual Drug Classes
Compelling Indications for Individual Drug Classes
Recurrent stroke Recurrent stroke preventionprevention
Chronic kidney diseaseChronic kidney disease
DiabetesDiabetes
Clinical Trial BasisClinical Trial BasisInitial Therapy OptionsInitial Therapy Options Compelling IndicationCompelling Indication
PROGRESSPROGRESS
NKF Guideline, NKF Guideline, Captopril Trial, Captopril Trial, RENAAL, IDNT, RENAAL, IDNT, REIN, AASKREIN, AASK
NKF-ADA Guideline,NKF-ADA Guideline, UKPDS, ALLHATUKPDS, ALLHAT
THIAZ, ACEITHIAZ, ACEI
ACEI, ARBACEI, ARB
THIAZ, BB, ACE, ARB, THIAZ, BB, ACE, ARB, CCBCCB