DEMA-CVN.

COM
GII THIU

GII THIU CAC TAI NGHIN CU KHOA HOC TAI HI NGHI NI KHOA TOAN QUC TAI THANH PH H CHI MINH THANG 7/ 2011

IU TR TNG HUYT P 2011:

CHNG TA ANG U ?

GS. TS. BS. ANG VAN PHC

CH TICH HI TIM MACH HOC TP. H CH MINH

BNH L TIM MCH L NGUYN NHN HNG U GY T VONG TI CC NC CNG NGHIP PHT TRIN TRN TONTH GII

BNH L TIM MCH V I THO NG GIA TNG NHANH CHNG V TR THNH NGUYN NHN QUAN TRNG GY T VONG,

BNH TT, MT SC LAO NG TI CC

NC ANG PHT TRIN TRONG C CC NC VNG CHU

Chet ot ngot

Nhoi mau c tim

Roi loan nhp

Benh mach vanh

Roi loan chc nang

Tai nh dang

X va ong mach

+ Tang huyet ap + ai thao ng + Roi loan lipid mau + + Hoi chng chuyen hoa

Suy tim
giai oan cuoi

Yeu to nguy c tim mach

T vong
5

Hin nay trn th gii c n 1,5 t ngi b THA

T suat TOAN THE GII nam 2000 do cac yeu to nguy c hang au chi phoi

T suat cao cac nc ang phat trien T suat thap cac nc ang phat trien Cac nc a phat trien

S t vong (n v ngn)
Theo thao luan gia IBLF vi WHO tai Luan on thang 10/2002

Hypertension : A Risk Factor for CV Disease

Coronary disease 50 Stroke Peripheral artery disease Heart failure

45.4
Normotensive Hypertensive 22.7 21.3 9.5 12.4 3.3 6.2 13.9 9.9 5.0 2.0 7.3 3.5 2.1 6.3

40
Biennial ageadjusted rate per 1000 patients 30

20
10 0

2.4

Risk ratio:

Men Women 2.0 2.2

Men Women 3.8 2.6

Men Women 2.0 3.7

Men Women 4.0 3.0

10

Kannel WB. JAMA. 1996;275:1571-1576.

4.00

Lien quan gia mc huyet ap vi t suat sau 25 nam nam gii

Benh ong mach vanh

Nguy c lien quan a c hieu chnh

Benh tim mach

3.00

2.00

1.00
Bnh thng

mmHg

120-129 /80-84

Bnh thng cao

130-139 /85-89

140-159 /90-99

Giai oan I

160-179 /100-109

Giai oan II

>180-110

Giai oan III

Miura K. et al.Arch Int Med 2001;161:1501-08

11

Association of SBP and CV Mortality in Men With Type 2 Diabetes

250 Nondiabetic Diabetic 200 CV mortality rate/ 10,000 person-yr 150 100 50 0

<120

120-139

140-159

160-179

180-199

200

SBP (mm Hg)

Stamler J et al. Diabetes Care. 1993;16:434-444.

12

Tan suat xay ra ot qu tren benh nhan chau A cao hn benh mach vanh
Hisayama Study
1,400 1,200 T le tren 100,000 1,000 800 600 400 200 0
196173 197486 19882000 196173 197486 19882000

ot qu Benh mach vanh

Men

Women
Kubo et al. Stroke 2003;34:234954 13

Benh ly tim mach khac han gia ngi chau A va ngi da trang: Tan suat ot qu cao hn han
16 14
T le tnh theo 1000 BN nam 12 10 8 6 4 2 0
SHEP
1

ot qu Benh mach vanh

10.4
8.8* 5.2 7.9 5.5

16 13

16

4 1.4 MRC England

2

2
3 4

2.6

Syst-Eur Europe

STONE China

Syst-China China

NICS-EH Japan

*Non-fatal MI or CHD death; MI

1SHEP

Co-operative Research Group. JAMA 1991;265:325564 2MRC Working Party. Br Med J 1985;291:97104 3Staessen et al. Lancet 1997;350:75764

et al. J Hypertens 1996;14:123745 5Liu et al. J Hypertens 1998;16:18239 6Ogihara et al. Hypertens Res 2000;23:337 14

4Gong

Huyet ap va nguy c ot qu
8.00

Ngi chau A
-10 mmHg: 40%

8.00

Da trang
-10 mmHg: 24%

4.00

4.00

Floating Absolute Risk & 95% CI

2.00

Floating Absolute Risk & 95% CI

110 120 130 140 150 160

2.00

1.00

1.00

0.50

0.50 120 130 140 150 160

Usual SBP (mmHg)

P for heterogeneity < 0.001

Usual SBP (mmHg)

J Hypertens 2003;21:707-716

15

Hypertension Management: Hypertension Awareness, Treatment & Control in Various Countries

awareness
70 60 50 % of population 40 30 20 10 0 USA Canada Italy Sweden Spain Germany England
Wolf-Maier et al 2004 16

treatment

BP control

< 140/90 mmHg

Ch c 95 BN T/1040 BN (9,1%) ang dng thuc tr THA t HA<130/80 mmHg => Phn ln cha kim sot c HA.

Kho st tnh hnh kim sot huyt p bnh nhn i tho ng ti Vit Nam

9.1% ??t HA<130/80 Khng ??t HA<130/80 90.9%

khng t HA<130/80
17

T l bnh nhn THA/ T t huyt p mc tiu rt thp (6%-13%)

HA mc tiu <130/80 mmHg
100% 90% 80% 70% 60% 50% 40% 30% 20% 10% 0% khng t HA<130/80 t HA<130/80 94% 88% 87% 87%

nhm BN n tr liu, t l t HA mc tiu: 6%. nhm BN c iu tr phi hp, t l t HA mc tiu cao hn gp 2,1 ln (1,36-3,27) vi tin cy l 95% => c ngha thng k.

6%

12%

13%
phi hp 3 thuc

13%
phi hp 4 thuc

n tr phi liu hp 2 thuc

18

CAC KHUYEN CAO QUAN TRONG VE CHAN OAN IEU TR VA PHONG NGA BENH TANG HUYET AP
Lien cac uy ban quoc gia Hoa Hoi tim mach Chau Au Ky Hoi tang huyet ap the gii Hoi tang huyet ap Chau Au
To chc y te the gii

WHO/ ISH
1993

JNC

1999

1972 JNC I 1980 JNC II 1984 JNC III 1988 JNC IV 1993 JNC V 1997 JNC VI 2003 JNC VII 2011 JNC VIII ?

ESH/ ESC
2003 2007 2009
19

S THAY OI VE PHAN LOAI TANG HUYET AP

HUYET AP (mmHg) WHO (1970S) JNC V (1991) JNC VI (1997)
WHO/ISH 1999 ESH.ESC 2003 <120 va <80 <130 va <85 130-139 hoac 85-89 140-159 hoac 90-99 HA gii han THA >160 hoac >95 180-199 hoac 110-119 200 hoac 120 THA o 3 THA o 3 THA o 4 THA o 2 Ly tng Ly tng Bnh thng Bnh thng cao THA o 1 Tien THA (Prehypertension) THA o 1 Bnh thng

JNC VII (2003)

Bnh thng

Bnh thng Bnh thng cao THA o 1

160-179 hoac 100-109

THA o 2

THA o 2

20

Cc yu t nguy c tim mch qui c

Thuc l

THA
Tng LDL.C v TC Gim HDL-C v tng TG Hi chng chuyn ho; i tho ng Bnh thn mn t vn ng, bo ph Trm cm v stress tinh thn

21

Khuyn co hi tim mch Chu u:

iu tr THA cn gim ton b

yu t nguy c

TL: Mancia G et al. European Heart Journal, June 11,2007

22

S pht trin ca cc thuc iu tr THA

Effectiveness Tolerability
1940s 1950 Direct vasodilators Peripheral sympatholytics Ganglion blockers Veratrum alkaloids Thiazides diuretics Central 2 agonists 1957 1960s 1970s -blockers 1980s 1990s 2002 Direct renin inhibitor

ARBs ACE inhibitors

Calcium antagonistsnon DHPs

-blockers

Calcium antagonistsDHPs

23

C che t ieu hoa HUYET AP = CUNG LNG TIM X SC CAN NGOAI BIEN Tang huyet ap = Tang cung lng tim va/hoac Tang sc can ngoai bien
TIEN TAI CO BOP CO THAT CHC NANG CHEN KENH Ca++ THAY OI CAU TRUC (PH AI)

C TIM

KHOI LNG DCH

TAI PHAN PHOI KHOI LNG DCH TANG HOAT TNH TK GIAO CAM

LI TIEU

HOAT TNH HE RENIN ANGIOTENSIN C CHE HE RENIN ANGIOTENSIN

CHEN BETA

24

ANGIOTENSINOGEN (Gan)
NON-ACE Chymase cathepsin G tPA, tonin, GAGE RENIN (than) ANGIOTENSIN I
ACE (Kininase II) BRADYKININ

ANGIOTENSIN II

Phan chat bat hoat

AT1
TAC ONG TREN THAN

AT2

AT3

AT4

ATn
GAY KHAT

GIAI PHONG ADH

CO MACH

ALDOSTERONE

TANG TRNG TE BAO

KCH THCH TK GIAO CAM

25

CAC CON NG TAO THANH ANGIOTENSIN II

ANGIOTENSINOGEN Renin Tissue Renin

Khong qua men chuyen (CHYMASE CATHEPSIN G)

ANGIOTENSIN I
Men chuyen (ACE)
Tissue ACE

Thuoc c che thu the Angiotensin II

ANGIOTENSIN II

Khong qua Renin (Cathepsin G Elastase TPA)

Co mach

AT1

Tai hap thu Na+/than Bai tiet Aldosterone Kch hoat he giao cam Bai tiet chat co mach Tang trng va tang sinh Dan mach

AT2
Chong tang sinh

APOPTOSIS

26

NHM THUC C CH TRC TIP RENIN: ALISKIREN

27

Classic understanding of the Renin System

Angiotensinogen Renin

Ang I

ACE

Ang II
AT1 Receptor

Aldosterone

Na+/H2O retention

Vasoconstriction Hypertension 28 Gibbons GH. 1998; Adapted from: Mller DN & Luft FC. 2006

ACEIs and ARBs cause compensatory rises in PRA

Kidney
Glomerular vasoconstriction Inflammation Fibrosis

Angiotensinogen Renin Ang I

Non ACE pathways

Heart
Hypertrophy Fibrosis Vasoconstriction

PRA Feedback Loop

ACEIs

ACE
Vessels

Ang II ARBs
AT1 Receptor

Hyperplasia hypertrophy Inflammation Oxidation Fibrosis

Brain

Biological effects

Vasoconstriction

29 Adapted from: Mller DN & Luft FC. 2006

Direct renin inhibition acts at the point of activation of the Renin System and neutralizes the PRA rise
Direct renin inhibitor
Angiotensinogen Renin Ang I
Non ACE pathways Kidney
Glomerular vasoconstriction Inflammation Fibrosis

Heart
Hypertrophy Fibrosis Vasoconstriction

PRA

ACE
Vessels

Feedback Loop
Ang II
AT1 Receptor

Hyperplasia hypertrophy Inflammation Oxidation Fibrosis

Brain

Biological effects

Vasoconstriction

30 Adapted from: Mller DN & Luft FC. 2006

Unlike ACEIs and ARBs, aliskiren reduces Ang I, Ang II and PRA
Direct renin inhibitor
Angiotensinogen Renin

Ang I
Non ACE pathways

ACE

Feedback Loop
Ang II

ACEIs ARBs
AT1 Receptor

Ang I ACEI

Ang II

Renin

PRA

ARB
Aliskiren

31 Azizi M et al. 2006; Adapted from: Mller DN & Luft FC. 2006

(Pro)renin receptor may play an important role in cardiovascular disease

Direct renin inhibitor
Angiotensinogen Renin Ang I
Non ACE pathways

(Pro)renin receptor actions: Binding of (pro)renin Increased renin catalytic activity Activates VSMC ERK1/2

ACE Feedback Loop Ang II

Direct renin inhibitor

Aliskiren binds to renin

AT1 Receptor

Heart Kidney Vessels

Target cell
(Pro)renin receptor

Vasoconstriction Remodelling

32 Nguyen G, et al. 2001

IU TRI TNG HA:

XU HNG PHI HP THUC SM

33

Nhng van e quan trong cua ieu tr ha ap theo quan iem mi

Hieu qua Ha ap

Tnh dung nap/ Tuan thu ieu tr

Bao ve C quan ch

Phong nga Benh tat va T vong

Khong xay ra bien co va duy tr Chat lng cuoc song

34

Qui trnh ieu tr tang HA (JNC VII)

Thay oi cach song Khong at HA muc tieu (<140/90 mmHg) (<130/80 mmHg cho ngi ai thao ng hoac benh than man tuh) Cac thuoc chon la au tien Khong co ch nh bat buoc Co ch nh bat buoc

(SBP 140159 hoac DBP 9099 mmHg) Thuoc li tieu loai Thiazide cho a so bn Co the xem xet ACEI, ARB, BB, CCB, hoac phoi hp

THA giai oan 1

(SBP >160 hoacDBP >100 mmHg) Phoi hp 2 thuoc cho a so bn (thng la li tieu loai thiazide va ACEI, hoac ARB, hoac BB, hoac CCB)

THA giai oan 2

Thuoc cho ch nh bat buoc

Cac thuoc ha HA khac (li tieu, ACEI, ARB, BB, CCB) khi can

Khong at HA muc tieu Tang lieu toi u hoac them thuoc khac cho en khi at HA muc tieu Nen tham van chuyen gia ve THA

35

Qui trnh ieu tr tang HA

Thuoc la chon au tien Khong co ch nh bat buoc THA giai oan 1

(SBP 140159 hoac DBP 9099 mmHg)

Thuoc li tieu loai Thiazide cho a so bn Co the xem xet ACEI, ARB, BB, CCB, hoac phoi hp
36

Qui trnh ieu tr tang HA

Thuoc la chon au tien Khong co cac ch nh bat buoc THA giai oan 2

(SBP >160 hoac DBP >100 mmHg)

Phoi hp 2 thuoc cho a so bn (thng la li tieu loai

thiazide va ACEI, hoac ARB, hoac BB, hoac CCB)

37

CAC TH NGHIEM LAM SANG VA C S HNG DAN CHO NHNG CH NH BAT BUOC OI VI TNG NHOM THUOC (7)
TNH TRNG NGUY C CAO VI CH NH BT BUC THUC C KHUYN CO
LI TIU CHN BETA CHN CANXI I KHNG ALDO

UCMC

UCTT

SUY TIM SAU NMCT BNH MCH VNH

I THO NG

BNH THN MN

PHNG NGA T QU TI PHT

38

Tng huyt p l mt bnh cnh tng th ca nhiu ri lon phi hp

THA l mt bnh cnh a yu t, do khng c g
ng ngc nhin l mi c th p ng vi iu tr rt khc nhau. Hin nay, tht khng n gin khi d on chnh xc bnh nhn no p ng tt vi loi thuc no. Cn c gii php iu tr tng th cc ri lon
- Journal of Human Hypertension 1995 ; 9 : S33-S36

39

Patient 1

Patient 2

Patient 3

Sympathetic nervous system Renin-angiotensin system Total body sodium

40

n liu php l khng tho ng Ch c 40-60% BN p ng

80

T l p ng

60

50% p ng

40

20

0 Calcium Alpha2 antagonist agonist Betablocker Diuretic Alpha1 antagonist ACEI Placebo

nh ngha p ng: HATTr < 95 mm Hg sau 1 nm iu tr Materson et al. Am J Hypertens. 1993;8:189-192. 41

Cn t nht hn mt loi thuc t c huyt p mc tiu qua cc nghin cu

Trial

Number of antihypertensive agents Target BP (mm Hg) 1 2 3 4

ALLHAT SBP <140/DBP <90 UKPDS ABCD DBP <85 DBP <75

MDRD HOT
AASK IDNT

MAP <92 DBP <80

MAP <92 SBP <135/DBP <85

DBP, diastolic blood pressure; MAP, mean arterial pressure; SBP, systolic blood pressure. Bakris GL et al. Am J Kidney Dis. 2000;36:646-661. Lewis EJ et al. N Engl J Med. 2001;345:851-860. Cushman WC et al. J Clin Hypertens. 2002;4:393-405.

42

Xu hng kt hp iu tr thuc THA

Recommendations of the Joint National Committee (JNC)
JNC I JNC II 1980 JNC III 1984
Diuretics lower dosages or betablocking angents

JNC IV 1988
Diuretics or -Blocker or ACEInhibitors Or Ca-Antag.

JNC V 1993

JNC VI

JNC VII

1977

1997

2003
Focus on sysolic Hypertension HOT-Trial : 70% of pts required Combination therapy Focus on Combination therapy

Diuretics Diuretics High high dosages dosages

Diuretics More or individulized -Blocker therapy or recommenACE-Inhibitors ded or Titration of Ca-Antag.. one (Mono)or substance -Blocker Low dose or (/ -Blocker) Combination Titration of one therapy as an substance option recommended

Monotherapy

Combinationtherapy 43

C th kt hp 6 -> 5 thuc gia cc nhm thuc h p

2003 ESH-ESC 2007 ESH-ESC

Li tiu

Thiazide diuretics ARB

Beta Blocker

Beta Blocker

ARB

Alpha Blocker

CCB
ACE inhibitor

Alpha Blocker CCB

ACE inhibitor

Thay i so vi phin bn trc 44

Ngh thut phi hp iu tr theo hng dn ca ESH/ESC

2007 ESH-ESC
Thiazide diuretics
ACEI or ARB

2008 ACC

-B

young

Beta Blocker

ARB

Alpha Blocker

CCB
ACE inhibitor

D
Diuretic

CCB

old

Adapted from European Society for Hypertension-European Society of Cardiology Guidelines Committee.J Hypertens. 2003;21:10111053.

Park JB 2008 45 Apr

Chin lc kt hp hai loi thuc h huyt p

47

Phoi hp CMC + chen canxi

ESC and ESH Guidelines 2007

Eur Heart J 2007;28:14621536.

48

CCB/ARB: Synergy of Counter-regulation

ARB
RAS blockade Congestive heart failure and renal benefits

CCB
Arteriodilation Peripheral edema Effective in low-renin patients Reduces cardiac ischemia

ARB
Venodilation Attenuates peripheral edema Effective in high-renin patients No effect on cardiac ischemia

CCB

RAS activation No renal or congestive heart failure benefits 49

Peripheral Edema Associated with CCBs

Fluid leakage

Arterial dilation

No venous dilation

Fluid leakage Capillary bed

Messerli. Am J Hypertens 2001;14:9789 Weir. J Clin Hypertens 2003;5:3305

50

Complementary Effects of a CCB/Angiotensin-receptor Blocker (ARB): Reduction of CCB-associated Edema

Arterial dilation (CCB and ARB)

Venous dilation (ARB)

Capillary bed

Messerli et al. Am J Hypertens 2001;14:9789 51

Amlodipine/Valsartan Significantly Reduces Fluid Retention versus Amlodipine Monotherapy

25 Ankle-foot volume increase (%)

23.0

n=80

20
70% difference

15

10

* 6.8

0
Amlodipine 10 mg
*p<0.01 vs. amlodipine

Amlodipine/Valsartan 10/160 mg
Fogari et al. J Hum Hypertens 2007;21:2204 52

Kha nang dung nap thuoc tot

Hieu qua bnh thng hoa c huyet ap

Che o thuoc uong n gian

S hai long cua benh nhan

Tuan thu ieu tr tng ngay

Tuan thu ieu tr lau dai

53

Anh hng toan cau cua tuoi tac

Co khoang 600 trieu ngi ln hn hay bang 60 tuoi vao nam 1999, d oan vao nam 2050, con so nay la 2 t. Vao thi iem nay, dan so vi so ngi gia se nhieu hn dan so tre (tuoi di 14).

Uy ban dan so Lien hp quoc, Khoa Kinh te va Xa hoi hoc, 1999

54

55

56

Ageing is a major risk factor for fatal stroke

fatal strokes in USA

1800 1600 1400 1200 1000 67,000 800 57,000 600 400 200 0 Age 35-44 45-54 55-64 65-74 75-84 85+ groups Number of events x 100 Rate/100,000

Stroke in USA
Leading cause of disability Third leading cause of death 275,000 deaths in 2002 72% occurred at age 65 or >

Source: www.cdc.gov

57

Heart failure is frequent in elderly patients

Incidence of heart failure
50 40 30 20 10 0

per 100 disease free persons

45-54 Age groups

55-64

65-74

75-84

85-94

Men

Women

Framingham Heart Study Adapted from Vasan et al in Hurts The Heart Mc Graw Hill 2004

58

Tuoi tho con ngi lien quan en cac ong mach cua ho
Sir William Osler 1892

Tuoi tho cua te bao noi mac trung bnh khoang 30 nam. Sau thi gian nay, tuoi tac lam cho chung mat dan va c thay the bi cac te bao xung quanh t co kha nang tao ra EDRF.
Paul M. Vanhoutte Chantal M. Boulanger 1994
59

Benh tim mach

T le t vong do benh tim mach bao gom benh tim, mach

mau nao, benh tang huyet ap, tang theo tuoi

Benh tim mach van la nguyen nhan gay t vong hang au

trong dan so gia

60

NHNG PHT HIN MI V VAI TR CA HUYT P NG MCH CH TRUNG TM

61

SBP v DBP trung bnh theo tui nam gii v ph n

(Dn s US 18 tui, NHANES III)
150 150

SBP (mm Hg)

SBP (mm Hg)

130

130

110

p lc mch ( Pulse Pressure)

110

Ap lc mch ( PP)

80

80

DBP (mm Hg)

70

DBP (mm Hg)

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

70

0
18-29

0
18-29 30-39 40-49 50-59 60-69 70-79 80+

Nam gii, tui (nm)

Ph n, tui (nm)

Burt VI, et al. Hypertension. 1995;25:305-313.

62

p lc mch (PULSE PRESSURE) tin on nguy c tt nht bnh nhn CHA ln tui A Meta-Analysis
EWPHE (N=840)

Syst-Eur (N=4695)
2-Year Risk Of End Point Syst-China (N=2394)

Diastolic Pressure (mm Hg)

Systolic Blood Pressure (mm Hg)

Blacher et al. Arch Intern Med. 2000;160.

63

64

Age and Components of Cardiac Afterload

Augmentation Component

Younger

Older

65

 The speed at which the outgoing and reflected waves travel is

dependent on the stiffness of the arteries along which they are travelling.

Central Aortic Blood Pressure: the missing link

So if a person has stiffer arteries, the reflected waves ill travel

back quicker, arriving earlier back at the heart.

Figure 1

66

Central Aortic Blood Pressure: the missing link

Conlusion: Increasing arterial stiffness independently increases the central aortic blood pressure and thus the risk of all three major cardiovascular outcomes. Central Aortic blood pressure is directly linked to CV events. All antihypertensive do not decrease central aortic blood pressure. Perindopril does.

Stroke
D LVL

PP

LVH

Figure 1

Coronary Events (MI..)

67

The Conduit Artery Functional Evaluation (CAFE) Study

Ancillary study of ASCOT
- 2073 patients - 5 centers (Leicester, Manchester, London (2), Dublin) - 96 % et 93 % under > 2 drug therapy - Radial pressure wave (Sphygmocor ) - Central pressure through a transfer function
- follow-up 3.4 years

- 305 events

68 Williams B et al. Circulation 2006

Systolic and diastolic blood pressure

180 160 140 120 100 80 60 Baseline 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5 5.5 Last visit

164.1 SBP 163.9

atenolol/thiazide amlodipine/perindopril
Mean difference 2.7
137.7 136.1

mm Hg

94.8 94.5

DBP Mean difference 1.9

79.2 77.4

Time (years)

69

All-cause mortality
%
10.0

8.0

Atenolol/thiazide (No. of events 820)

6.0

4.0

Amlodipine/perindopril (No. of events 738)

2.0

HR = 0.89 (0.810.99) p = 0.0247

0.0 1.0
9544 9532

0.0
Number at risk Amlodipine/perindopril Atenolol/thiazide

2.0
9441 9415

3.0
9332 9261

4.0
9167 9085

5.0
8078 7975

Years

9639 9618

70

Fatal and non-fatal stroke

%
5.0

4.0

Atenolol/thiazide (No. of events 422)

3.0

Amlodipine/perindopril (No. of events 327)

2.0

1.0

HR = 0.77 (0.660.89) p = 0.0003

0.0 1.0
9483 9461

0.0 2.0
9331 9274

3.0
9156 9059

4.0
8972 8843

5.0
7863 7720

Years

Number at risk Amlodipine/perindopril Atenolol/thiazide

9639 9618

71

Total CV events and procedures + development of renal impairment

Predictive value of central PP (10 mmHg)
Central PP
25.0 Cumulative Incidence (%) Amlodipine / Perindopril

HR 1.13 (1.00-1.26)

P 0.043

20.0
15.0 10.0

Atenolol / Thiazide

16%

5.0
HR=0.84 (0.79-0.90) P <.0001 0.0 0.0 1.0 9166 9115 2.0 Years 8808 8692 3.0 8455 8259 4.0 5.0 8118 7872 6965 6710

Number at risk Amlodipine + perindopril 9639 Atenolol+thiazide 9618

Williams B et al. Circulation 2005

72

In Coversyl/amlodipine patients, Central Aortic Systolic Blood Pressure is 4.3 mmHg lower than with atenolol-thiazide

140

atenolol/thiazide amlodipine/perindopril

135

mm Hg

130

Same Brachial SBP

P=.07

125

120

Different Central Aortic BP

Diff Mean (AUC) = 4.3 mm Hg
P<.0001
5.5 6 AUC

115
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5

Time (Years)
Circulation. 2006;113:1213-1225

73

VN IU TR TNG HUYT P TRN BN LN TUI V RT LN TUI

74

What do Guidelines say?

Guidelines
JNC7 2003 BHS 2004 NICE 2007

Statement
No mention of over 80s, treated as other patients For those aged over 80 at the time of diagnosis of hypertension, no clear guidance can be given offer patients over 80 years of age the same treatment as other patients over 55, taking account of any comorbidity and their existing burden of drug use, but Patients over 80 years of age are poorly represented in clinical trials and the effectiveness of treatment in this group is less certain In subjects aged 80 years or over, evidence for antihypertensive treatment is as yet inconclusive

ESH/ESC 2007

To treat or not to treat?

Increase in mortality

Reduction in strokes

This dilemma provided the rationale for the HYpertension in the Very Elderly Trial

Hypertension in the very elderly

To treat or not to treat
Which drug(s) Goal blood pressure

?
? ?

HYVET The Study Headlines

3,845 patients from Europe, China, Australasia, and Tunisia 60% female; 80 years of age or older (mean 83.6yrs); A baseline BP of 160 mm Hg or more (mean: 173.0/90.8 mm Hg); Median follow-up 1.8 years; Active treatment: The diuretic; indapamide SR the angiotensin-converting enzyme inhibitor; perindopril; Target BP of <150/80 mm Hg. The primary end point was fatal or nonfatal stroke.

Design

HYVET Headline Results

30% reduction in stroke (fatal or nonfatal); 39% reduction in death from stroke; 21% reduction in death from any cause: 23% reduction in death from cardiovascular causes; 29% reduction in death from cardiac causes 64% reduction in heart failure; Fewer serious adverse events in the activetreatment group;

Conclusion

You are never too old to start treatment for hypertension

XIN CM N S THEO DI

CA QU NG NGHIP

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