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GS. TS. BS. ANG VAN PHC


CH TCH HI TIM MCH HC TP. H CH MINH
IU TR TNG HUYT P 2011:
CHNG TA ANG U ?
2
BNH L TIM MCH L NGUYN NHN
HNG U GY TVONG
TI CC NC CNG NGHIP
PHT TRIN TRN TONTH GII
3
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
4
Yeu to nguy
c tim mach
X va
ong mach
Roi loan chc nang
Tai nh dang
Nhoi mau c tim
Chet ot ngot
Roi loan nhp
Benh
mach vanh
T
vong
Suy tim
giai oan cuoi
+ Tang huyet ap
+ ai thao ng
+ Roi loan lipid mau
+
+ Hoi chng chuyen hoa
5
Hin nay trn th gii c
n 1,5 t ngi b THA
6
T suat TOAN THE GII nam 2000
do cac yeu to nguy c hang au chi phoi
Theo thao luan gia IBLF vi WHO tai Luan on thang 10/2002
Cac nc a phat trien
T suat thap cac nc ang
phat trien
T suat cao cac nc ang
phat trien
S t vong (n v ngn)
8
9
Kannel WB. JAMA. 1996;275:1571-1576.
Hypertension : A Risk Factor for CV Disease
22.7
9.5
3.3
2.4
5.0
2.0
3.5
2.1
45.4
21.3
12.4
6.2
9.9
7.3
13.9
6.3
0
10
20
30
40
50
Men
2.0
Women
2.2
Men
3.8
Women
2.6
Men
2.0
Women
3.7
Men
4.0
Women
3.0
Normotensive
Hypertensive
Coronary
disease Stroke
Peripheral artery
disease
Heart
failure
Risk ratio:
Biennial
age-
adjusted
rate per
1000
patients
10
Lien quan gia mc huyet ap vi t suat
sau 25 nam nam gii
Benh o ng ma ch va nh
Benh tim ma ch
120-129
/80-84
130-139
/85-89
140-159
/90-99
160-179
/100-109
>180-110
1.00
2.00
3.00
4.00
Miura K. et al.Arch Int Med 2001;161:1501-08
N
g
u
y

c


l
i
e
n

q
u
a
n

c

h
i
e
u

c
h

n
h
mmHg
Bnh thng cao Giai oan I Giai oan II Giai oan III Bnh thng
11
Association of SBP and CV Mortality
in Men With Type 2 Diabetes
250
200
150
100
50
0
<120 120-139 140-159 160-179 180-199
SBP (mm Hg)
CV
mortality
rate/
10,000
person-yr
Nondiabetic
Diabetic
Stamler J et al. Diabetes Care. 1993;16:434-444.
200
12
1un sout xuy ru dot qo tron bonh nhun
chuo A cuo hon bonh much vunh
Kobo ot u. Stroko 2003,34:234954
Hisayama Stody
T


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c
n

1
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1,400
1,200
1,000
800
600
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Mcn Womcn
196173 197486 19882000 196173 197486 19882000
ot qo|
cnb macb vanb
13
l
SHLl Co-oporutvo kosourch Croop. AMA l99l,265:325564
2
MkC \orkng lurty. r Mod l985,29l:97l04
3
Stuosson ot u. Luncot l997,350:75764
cnb Iy tim macb kbac ban gioa ngooi cbao A
va ngooi da trang: Tan soat dot qo| cao bon ban
FngIand Foropc Cbina Cbina )apan
SHFF
1
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13
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16
4
4
Cong ot u. Hyportons l996,l4:l23745
5
Lo ot u. Hyportons l998,l6:l8239
6
Oghuru ot u. Hyportons kos 2000,23:337
*Non-utu Ml or CHD douth,

Ml
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8
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l
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0.S0
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2.00
4.00
8.00
120 130 140 1S0 160
Hoyct ap va ngoy co dot qo|
-10 mmHg: 40%
-10 mmHg: 24%
) Hypcrtcns 2003,21:707-716
l or hotorogonoty < 0.00l
15
0
10
20
30
40
50
60
70
USA
awareness
England Italy Sweden Canada Germany
treatment BP control
Spain
%

o
f

p
o
p
u
l
a
t
i
o
n
< 140/90 mmHg
Wolf-Maier et al 2004
Hypertension Management: Hypertension Awareness,
Treatment & Control in Various Countries
16
khng t HA<130/80
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
90.9%
9.1%
??t
HA<130/80
Khng ??t
HA<130/80
17
HA mc tiu <130/80 mmHg
6%
12%
13% 13%
94%
88%
87% 87%
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
n tr
liu
phi
hp 2
thuc
phi
hp 3
thuc
phi
hp 4
thuc
khng t HA<130/80
t HA<130/80
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.
T l bnh nhn THA/ T t huyt p
mc tiu rt thp (6%-13%)
18
CAC KHUYEN CAO QUAN TRONG VE
CHAN OAN IEU TR VA PHONG NGA
BENH TANG HUYET AP
To chc y te the gii
Hoi tang huyet ap the gii
WHO/ ISH
1993
1999
Lien cac uy ban quoc
gia Hoa Ky
JNC
1972 JNC I
1980 JNC II
1984 JNC III
1988 JNC IV
1993 JNC V
1997 JNC VI
2003 JNC VII
2011 JNC VIII ?
Hoi tim mach Chau Au
Hoi tang huyet ap Chau Au
ESH/ ESC
2003
2007
2009
19
h0YET kF (mmhg) Wh0 (19708) 1h6 V (1991) 1h6 VI (1997)
Wh0lI8h 1999
E8h.E86 Z008
JhC v (2OO8)
<1Z0 va <80
8nh Ihuong
Ly Iuong Ly Iuong Binh thuJng
<180 va <86 8nh Ihuong 8nh Ihuong
Tien ThA
(FrahyparIansIon)
180189 hoar 8689 8nh Ihuong
rao
8nh Ihuong rao
140169 hoar 9099 hk gIoI han Thk do 1 Thk do 1 ThA do 1
160179 hoar 100109
Thk >160 hoar
>96
Thk do Z Thk do Z
ThA do 2 180199 hoar 110119 Thk do 8
Thk do 8
Z00 hoar 1Z0 Thk do 4
S THAY OI VE PHAN LOAI
TANG HUYET AP
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
Direct
vasodilators
-blockers
Peripheral
sympatholytics
Ganglion
blockers
Veratrum
alkaloids
Central
2
agonists
Calcium
antagonists-
non DHPs
-blockers
Thiazides
diuretics
Calcium
antagonists-
DHPs
ARBs
1940s 1950 1957 1960s 1970s 1980s 1990s 2002
ACE
inhibitors
Effectiveness
Tolerability
Direct
renin
inhibitor
23
6o rha Iu dIau hoa
h0YET kF = 60h L00h TIM X 806 6kh h0kI 8IEh
Tang huyaI ap = Tang rung Iuong IIm valhoar Tang sur ran ngoaI bIan
6hEh kEhh
6a
++
L0I TIE0
6hEh 8ETk
06 6hE hE
EhIh khI0TEh8Ih
60 ThkT ThkY 0I 6k0
6h06 hkh T06 (Fh kI)
TIEh TkI 60 80F
60 TIM
kh0I L00h TkI Fhkh Fh0I
[6h kh0I L00h
[6h
Tkh h0kT Thh
Tk Ik0 6kM
h0kT Thh hE EhIh
khI0TEh8Ih
24
Tk6 0h
TEh Thkh
IkI Fh0h
kh
Tkh T00h
TE 8k0
60 Mk6h
k6h Th6h Tk
Ik0 6kM
kY khkT
kL08TE0hE
Fhan rhaI
baI hoaI
khI0TEh8Ih0Eh (an)
khI0TEh8Ih I
khI0TEh8Ih II
EhIh (Ihan)
8kYkIhIh
k6E
(kInInasa II)
h0hk6E
6hymasa
raIhapsIn
IFk, IonIn,
kE
AT
1
AT
2
AT
3
AT
4
ATn
25
6k6 60h 00h Tk0 Thkhh khI0TEh8Ih II
ANGIOTENSINOGEN
Renin
ANGIOTENSIN I
Tissue Renin
ANGIOTENSIN II
Khong qua men
chuyen
(CHYMASE
CATHEPSIN
G)
Khong qua Renin
(Cathepsin G Elastase
TPA)
Dan mach
Chong tang sinh
APOPTOSIS
Thuoc c che thu the
Angiotensin II
Co mach
Tai hap thu Na
+
/than
Bai tiet Aldosterone
Kch hoat he giao cam
Bai tiet chat co mach
Tang trng va tang sinh
AT
1
AT
2
Men chuyen
(ACE)
Tissue ACE
26
NHM THUC C CH TRC TIP RENIN:
ALISKIREN
27
Classic understanding of the Renin System
Gibbons GH. 1998; Adapted from: Mller DN & Luft FC. 2006
ACE
Na
+
/H
2
O retention
Vasoconstriction
Hypertension
Aldosterone
Renin
Angiotensinogen
Ang I
AT
1
Receptor
Ang II
28
ACEIs and ARBs cause
compensatory rises in PRA
Glomerular
vasoconstriction
Inflammation
Fibrosis
Kidney
Hypertrophy
Fibrosis
Vasoconstriction
Heart
Vasoconstriction
Brain
Hyperplasia hypertrophy
Inflammation
Oxidation
Fibrosis
Vessels Feedback Loop
AT
1
Receptor
Renin
Ang I
Angiotensinogen
Ang II
Biological effects
ACE
Non ACE pathways
ARBs
ACEIs
PRA
Adapted from: Mller DN & Luft FC. 2006
29
Direct renin inhibition acts at the point of activation
of the Renin System and neutralizes the PRA rise
Feedback Loop
AT
1
Receptor
Renin
Ang I
Angiotensinogen
Ang II
Direct renin inhibitor
Biological effects
ACE
Non ACE pathways
PRA
Adapted from: Mller DN & Luft FC. 2006
Glomerular
vasoconstriction
Inflammation
Fibrosis
Kidney
Hypertrophy
Fibrosis
Vasoconstriction
Heart
Vasoconstriction
Brain
Hyperplasia hypertrophy
Inflammation
Oxidation
Fibrosis
Vessels
30
Unlike ACEIs and ARBs, aliskiren reduces
Ang I, Ang II and PRA

Aliskiren
ARB
ACEI
PRA Renin Ang II Ang I
Feedback Loop
AT
1
Receptor
Renin
Ang I
Angiotensinogen
Ang II
Direct renin inhibitor
ARBs
ACE
Non ACE pathways
ACEIs
Azizi M et al. 2006; Adapted from: Mller DN & Luft FC. 2006
31
(Pro)renin receptor may play an important role
in cardiovascular disease
(Pro)renin
receptor
Vasoconstriction
Remodelling
Vessels
Kidney
Heart
(Pro)renin receptor actions:
Binding of (pro)renin
Increased renin catalytic activity
Activates VSMC ERK1/2
Aliskiren binds
to renin
Target cell
Feedback Loop
AT
1
Receptor
Renin
Angiotensinogen
Ang II
Non ACE pathways
Ang I
ACE
Direct renin inhibitor
Nguyen G, et al. 2001
Direct renin inhibitor
32
IU TR TNG HA:
XU HNG PHI HP THUC SM
33
Nhong vun do qoun trong cou doo tr
hu up thoo qoun dom mo
Hoo qou
Hu up
Tnb dong
nap/
Toan tbo
dico tr|
uo vo
Co qoun
dch
lhong ngou
onh tut vu
1o vong
kbong xay ra bicn co va doy
tr Cbat Ioong cooc song
34
Qui trnh ieu tr tang HA (JNC VII)
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
Thuoc cho ch nh bat buoc
Cac thuoc ha HA khac (li tieu, ACEI,
ARB, BB, CCB)
khi can
Co ch nh bat buoc
Thay oi cach song
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
THA giai oan 2
(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 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
Khong co ch nh bat
buoc
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
TNH TRNG NGUY C
CAO VI CH NH BT
BUC
THUC C KHUYN CO
LI TIU CHN BETA UCMC UCTT CHN CANXI I KHNG
ALDO
SUY TIM
SAU NMCT
BNH MCH VNH
I THO NG
BNH THN MN
PHNG NGA T QU
TI PHT
CAC TH NGHIEM LAM SANG VA C S
HNG DAN CHO NHNG CH NH BAT
BUOC OI VI TNG NHOM THUOC (7)
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
Sympathetic nervous system
Renin-angiotensin system
Total body sodium
Patient 1 Patient 2 Patient 3
40
Materson et al. Am J Hypertens. 1993;8:189-192.
0
20
40
60
80
Calcium
antagonist
Beta-
blocker
Diuretic Alpha
1
antagonist
ACEI Alpha
2
agonist
Placebo
50% p ng
nh ngha p ng: HATTr < 95 mm Hg
sau 1 nm iu tr
T

n
g
n liu php l khng tho ng
Ch c 40-60% BN p ng
41
Target BP (mm Hg)
Number of antihypertensive agents
1 Trial 2 3 4
AASK MAP <92
UKPDS DBP <85
ABCD DBP <75
MDRD MAP <92
HOT DBP <80
IDNT SBP <135/DBP <85
ALLHAT SBP <140/DBP <90
Cn t nht hn mt loi thuc t c
huyt p mc tiu qua cc nghin cu
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
Diuretics
high
dosages
Diuretics
lower
dosages
or beta-
blocking
angents
Diuretics
or
-Blocker
or
ACE-
Inhibitors
Or
Ca-Antag.
Diuretics
or
-Blocker
or
ACE-Inhibitors
or
Ca-Antag..
or
-Blocker
or
(/ -Blocker)
Titration of one
substance
recommended
More
individulized
therapy
recommen-
ded
Titration of
one (Mono)-
substance
Low dose
Combination
therapy as an
option
Focus on
sysolic
Hypertension
HOT-Trial
: 70% of pts
required
Combination
therapy
Focus on
Combination
therapy
JNC I
1977
JNC II
1980
JNC III
1984
JNC IV
1988
JNC V
1993
JNC VI
1997
Monotherapy
Combination-
therapy
JNC VII
2003
Diuretics
High
dosages
Recommendations of the Joint National Committee (JNC)
43
C th kt hp 6 -> 5 thuc gia cc
nhm thuc h p
Thay i so vi
phin bn trc
2003 ESH-ESC 2007 ESH-ESC
CCB
ARB
Thiazide
diuretics
Alpha Blocker
ACE inhibitor
Beta Blocker
CCB
ARB
Li tiu
Beta Blocker
Alpha Blocker
ACE inhibitor
44
Ngh thut phi hp iu tr theo hng dn
ca ESH/ESC
Adapted from European Society for
Hypertension-European Society of
Cardiology Guidelines Committee.J
Hypertens. 2003;21:10111053.
2008 ACC 2007 ESH-ESC
Park JB 2008 Apr
CCB
ARB
Thiazide
diuretics
Beta Blocker
Alpha Blocker
ACE inhibitor
ACEI
or
ARB
Diuretic CCB
-B
young
old
A
B
C
D
46
Chin lc kt hp hai loi
thuc h huyt p
47
Phoi hp CMC + chen canxi
Eur Heart J 2007;28:14621536.
ESC and ESH Guidelines 2007
48
CCB
Arteriodilation
Peripheral edema
Effective in low-renin patients
Reduces cardiac ischemia
CCB
RAS activation
No renal or
congestive heart
failure benefits
CCB/ARB: Synergy of Counter-regulation
ARB
Venodilation
Attenuates peripheral edema
Effective in high-renin patients
No effect on cardiac ischemia
ARB
RAS blockade
Congestive heart
failure and renal
benefits
49
Messerli. Am J Hypertens 2001;14:9789
Weir. J Clin Hypertens 2003;5:3305
Arterial
dilation
No venous
dilation
Fluid leakage
Fluid leakage
Capillary bed
Peripheral Edema Associated with CCBs
50
Complementary Effects of a CCB/Angiotensin-receptor Blocker
(ARB): Reduction of CCB-associated Edema
Messerli et al. Am J Hypertens 2001;14:9789
Arterial
dilation
(CCB and
ARB)
Venous
dilation
(ARB)
Capillary bed
51
*p<0.01 vs. amlodipine Fogari et al. J Hum Hypertens 2007;21:2204
Amlodipine/Valsartan Significantly Reduces Fluid Retention
versus Amlodipine Monotherapy
*
6.8
23.0
25
20
15
10
5
0
A
n
k
l
e
-
f
o
o
t

v
o
l
u
m
e

i
n
c
r
e
a
s
e

(
%
)
Amlodipine 10 mg Amlodipine/Valsartan
10/160 mg
n=80
70%
difference
52
Kha nang dung nap thuoc tot
Hieu qua bnh thng
hoa c huyet ap
Tuan thu ieu
tr tng ngay
Tuan thu ieu
tr lau dai
Che o thuoc
uong n gian
S hai long cua
benh nhan
53
Anh huJng toan cau cua tuoi tac
6o khoang 600 IrIau nguoI Ion hon hay bang 60
IuoI vao nam 1999, du doan vao nam Z060, ron
so nay Ia Z I. Vao IhoI dIam nay, dan so voI so
nguoI gIa sa nhIau hon dan so Ira (IuoI duoI 14).
Uy ban dan so Lien hp quoc,
Khoa Kinh te va Xa hoi hoc, 1999
54
55
56
fatal strokes in USA
0
200
400
600
800
1000
1200
1400
1600
1800
35-44 45-54 55-64 65-74 75-84 85+
Number of events x 100 Rate/100,000
Age
groups
Source: www.cdc.gov
Ageing is a major risk factor
for fatal stroke
57,000
67,000
Stroke in USA
Leading cause of disability
Third leading cause of death
275,000 deaths in 2002
72% occurred at age 65 or >
57
Incidence of heart failure
per 100 disease free persons
0
10
20
30
40
50
45-54 55-64 65-74 75-84 85-94
Men Women
Heart failure is frequent in
elderly patients
Framingham Heart Study
Adapted from Vasan et al in Hurts The Heart Mc Graw Hill 2004
Age
groups
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
18-29 30-39 40-49 50-59 60-69 70-79 80+
0
70
80
110
130
150
D
B
P
(
m
m

H
g
)
S
B
P
(
m
m

H
g
)
Nam gii, tui (nm)
p lc mch ( Pulse Pressure)
18-29 30-39 40-49 50-59 60-69 70-79 80+
0
70
80
110
130
150
D
B
P
(
m
m

H
g
)
S
B
P
(
m
m

H
g
)
Ph n, tui (nm)
p lc mch ( PP)
SBP v DBP trung bnh theo tui nam gii
v ph n
(Dn s US 18 tui, NHANES III)
Burt VI, et al. Hypertension. 1995;25:305-313.
62
Blacher et al. Arch Intern Med. 2000;160.
p lc mch (PULSE PRESSURE) tin on nguy c tt nht
bnh nhn CHA ln tui
A Meta-Analysis
2
-
Y
e
a
r

R
i
s
k

O
f

E
n
d

P
o
i
n
t
Systolic Blood Pressure (mm Hg)
Diastolic
Pressure
(mm Hg)
EWPHE (N=840)
Syst-Eur (N=4695)
Syst-China (N=2394)
63
64
Age and Components of Cardiac Afterload
Younger
Older
Augmentation
Component
65
Figure 1
Central Aortic Blood Pressure: the missing link
The speed at which the outgoing and reflected waves travel is
dependent on the stiffness of the arteries along which they are
travelling.
So if a person has stiffer arteries, the reflected waves ill travel
back quicker, arriving earlier back at the heart.
66
Figure 1
D LVL
PP
Central Aortic Blood Pressure: the missing link
Central Aortic blood pressure is directly linked to CV events. All antihypertensive
do not decrease central aortic blood pressure. Perindopril does.
Stroke
LVH
Coronary
Events (MI..)
Conlusion: Increasing arterial stiffness independently increases the central aortic
blood pressure and thus the risk of all three major cardiovascular outcomes.
67
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
Williams B et al. Circulation 2006
The Conduit Artery Functional Evaluation
(CAFE) Study
68
Systolic and diastolic blood pressure
m
m

H
g
60
80
100
120
140
160
180
Time (years)
Baseline 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5 5.5
atenolol/thiazide
amlodipine/perindopril
137.7
136.1
79.2
77.4
Mean difference 1.9
Last
visit
Mean difference 2.7
SBP
DBP
163.9
164.1
94.8
94.5
69
All-cause mortality
Number at risk
Amlodipine/perindopril 9639 9544 9441 9332 9167 8078
Atenolol/thiazide 9618 9532 9415 9261 9085 7975
0.0 1.0 2.0 3.0 4.0 5.0
Years
0.0
2.0
4.0
6.0
8.0
10.0
HR = 0.89 (0.81-0.99)
p = 0.0247
%
Amlodipine/perindopril
(No. of events 738)
Atenolol/thiazide
(No. of events 820)
70
Fatal and non-fatal stroke
Number at risk
Amlodipine/perindopril 9639 9483 9331 9156 8972 7863
Atenolol/thiazide 9618 9461 9274 9059 8843 7720
0.0 1.0 2.0 3.0 4.0 5.0 Years
0.0
1.0
2.0
3.0
4.0
5.0
Amlodipine/perindopril
(No. of events 327)
Atenolol/thiazide
(No. of events 422)
HR = 0.77 (0.66-0.89)
p = 0.0003
%
71
Total CV events and procedures
+ development of renal impairment
Williams B et al. Circulation 2005
Number at risk
Amlodipine + perindopril 9639 9166 8808 8455 8118 6965
Atenolol+thiazide 9618 9115 8692 8259 7872 6710
Atenolol / Thiazide
Amlodipine / Perindopril
25.0
20.0
15.0
10.0
5.0
0.0
0.0 1.0 2.0 3.0 4.0 5.0
Years
C
u
m
u
l
a
t
i
v
e

I
n
c
i
d
e
n
c
e

(
%
)
HR=0.84 (0.79-0.90) P <.0001
16%
Predictive value of central PP (10 mmHg)
HR P
Central PP 1.13 (1.00-1.26) 0.043
72
In Coversyl/amlodipine patients, Central Aortic Systolic Blood Pressure is
4.3 mmHg lower than with atenolol-thiazide
115
120
125
130
135
140
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5 5.5 6
Time (Years)
m
m

H
g
Diff Mean (AUC) = 4.3 mm Hg
AUC
P=.07
P<.0001
Circulation. 2006;113:1213-1225
Same
Brachial SBP
Different
Central Aortic BP
atenolol/thiazide
amlodipine/perindopril
73
VN IU TR TNG HUYT P TRN BN
LN TUI V RT LN TUI
What do Guidelines say?
Guidelines Statement
JNC7 2003
No mention of over 80s, treated as other patients
BHS 2004
For those aged over 80 at the time of diagnosis of
hypertension, no clear guidance can be given
NICE 2007
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
ESH/ESC
2007
In subjects aged 80 years or over, evidence for
antihypertensive treatment is as yet inconclusive
This dilemma provided the rationale for the
HYpertension in the Very Elderly Trial
To treat or not to treat?
Increase in
mortality
Reduction in
strokes
To treat or not to treat
Which drug(s)
Goal blood pressure
Hypertension in the very elderly
?
?
?
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 active-
treatment group;
Conclusion
You are never too old to start
treatment for hypertension
82
XIN CM N S THEO DI
CA QU NG NGHIP

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