AS H PAPE R

Clinical
Practice
Guidelin
es for
the
Manage
ment of
Hyperten
sion in
the
Commun
ity
A
Stateme
nt by the
America
n Society
of
Hyperten
sion and
the
Internati
onal
Society
of
Hyperten
sion
Michael A. Weber,
1
MD; Ernesto L.
2
Schiffrin, MD;
William B. White,
3
MD; Samuel
4
Mann, MD; Lars
5
H. Lindholm, MD;
John G.
6
Kenerson, MD;
John M. Flack,
7
MD; Barry L.
8
Carter, Pharm D;
Barry J. Materson,

MD; C. Venkata
10
S. Ram, MD;
Debbie L. Cohen,
11
MD; JeanClaude Cadet,
12
MD; Roger R.
Jean-Charles,
13
MD; Sandra
14
Taler, MD; David
15
Kountz, MD;
Raymond R.
16
Townsend, MD;
John Chalmers,
17
MD; Agustin J.
18
Ramirez, MD;
George L. Bakris,
19
MD; Jiguang
20
Wang, MD;
Aletta E. Schutte,
21
MD; John D.
22
Bisognano, MD;
Rhian M. Touyz,
23
MD; Dominic
24
Sica, MD;
Stephen B.
25
Harrap, MD
State University of
New York,
Downstate College
of Medicine,
1
Brooklyn, NY;
Department of
Medicine, Sir
Mortimer B. Davis
Jewish General
Hospital, McGill
University, Montreal,
2
Canada; Calhoun
Cardiology Center,
University of
Connecticut,
3
Farmington, CT;
Department of
Medicine, Weil
Cornell College of
Medicine, New York,
4
NY; Department of
Public Health and
Clinical Medicine,
Umea University,
5
Umea, Sweden;
Cardiovascular
Associates, Virginia
6
Beach, VA;
Department of
Medicine, Wayne
State University,
7
Detroit, MI;
Department of
Pharmacy Practice
and Science,
University of Iowa,
8
Iowa City, IA;
Department of
Medicine, University
of Miami Miller
School of Medicine,
9
Miami, FL; MediCiti
Institutions,
10
Hyderabad, India;

Department of
Medicine, University
of Pennsylvania
School of Medicine,
11
Philadelphia, PA;
State University
School of Medicine,
Port Au Prince,
12
Haiti; Hypertension
Center of Haiti, Port
13
Au Prince, Haiti;
Department of
Medicine, Mayo
Clinic, Rochester,
14
MN; Jersey Shore
University Medical
Center, Neptune,
15
NJ; Hypertension
Center, University of
Pennsylvania,
16
Philadelphia, PA;
George Institute for
Global Health,
University of Sydney,
Sydney, NSW,
17
Australia; Arterial
Hypertension and
Metabolic Unit,
University Hospital,
Favaloro
Foundation, Buenos
18
Aires, Argentina;
ASH Comprehensive
Hypertension
Center, University of
Chicago Medicine,
19
Chicago, IL; The
Shanghai Institute of
Hypertension,
Shanghai Jiaotong
University School of
Medicine, Shanghai,
20
China;
Hypertension in
Africa Research
Team, North West
University,
Potchefstroom,
21
South Africa;
Department of
Medicine, University
of Rochester
Medical Center,
22
Rochester, NY;
Institute of
Cardiovascular and
Medical Sciences,
University of
Glasgow, Glasgow,
23
UK; Virginia
Commonwealth
University,
24
Richmond, VA;
and Department of
Physiology,
University of
Melbourne,
Melbourne, Vic,
25
Australia

POS
E
STA
TEM
ENT
OF
PUR

Thes
e
guide
lines

have
been
writte
n to
provi
de a
straig
htforwa
rd
appro
ach
to
mana
ging
hyper
tensi
on in
the
com
munit
y. We
have
inten
ded
that
this
brief
curric
ulum
and
set of
reco
mme
ndati
ons
be
usefu
l not
only
for
prima
ry
care
physi
cians
and
medi
cal
stude
nts,
but
for
all
profe
ssion
als
who
work
as
hands
-on
practi

tioner
s.
We
are
awar
e that
there
is
great
varia
bility
in
acces
s to
medi
cal
care
amon
g
com
munit
ies.
Even
in socalle
d
wealt
hy
count
ries
there
are
sizabl
e
com
munit
ies in
whic
h
econ
omic,
logist
ic,
and
geogr
aphic
issue
s put
const
raints
on
medi
cal
care.
And,
at the
same
time,
we
are
remin
ded

that
even
in
count
ries
with
highl
y
limite
d
resou
rces,
medi
cal
leade
rs
have
assig
ned
the
highe
st
priori
ty to
supp
ortin
g
their
colle
agues
in
confr
ontin
g the
growi
ng
toll
of
devas
tating
strok
es,
cardi
ovasc
ular
event
s, and
kidne
y
failur
e
cause
d by
hyper
tensi
on.
Our
goal
has
been
to
give

suffic
ient
infor
matio
n to
enabl
e
healt
h
care
practi
tioner
s,
wher
ever
they
are
locat
ed, to
provi
de
profe
ssion
al
care
for
peopl
e
with
hyper
tensi
on.
All
the
same,
we
recog
nize
that it
will
often
not
be
possi
ble to
carry
out
all of
our
sugge
stions
for
clinic
al
evalu
ation,
tests,
and
thera
pies.
Indee
d,
there

are
situat
ions
wher
e the
most
simpl
e and
empir
-ical
care
for
hyper
tensi
on
simpl
y
distri
butin
g

Addres
s for
corresp
ondenc
e:
Michae
l A.
Weber,
MD,
Divisio
n of
Cardio
vascul
ar
Medici
ne,
State
Univer
sity of
New
York,
Downst
ate
Colleg
e of
Medici
ne, 450
Clarks
on
Avenue
, Box
97,
Brookly
n, NY
11203

E-mail:
micha
elweb
ermd
@cs.c
om
DOI:
10.111
1/jch.1
2237

what
ever
antih
ypert
ensiv

e
drugs
might
be
avail
able
to
peopl
e
with
high
blood
press
ure
is
better
than
doing
nothi
ng at
all.
We
hope
that
we
have
allow
ed
suffic
ient
flexib
ility
in
this
state
ment
to
enabl
e
respo
nsibl
e
clinicians
to
devis
e
work
able
plans
for
provi
ding
the
best
possi
ble
care
for
patie
nts
with
hyper

tensi
on in
their
com
munit
ies.
We
have
divid
ed
this
brief
docu
ment
into
the
follo
w-ing
sectio
ns:
Intro
ducti
on
Epide
miolo
gy
Speci
al
Issues
With
Black
Patie
nts
(Afric
an
Ance
stry)

How
is
Hype
rtensi
on
Defin
ed?
How
is
Hype
rtensi
on
Class
ified?
Caus
es of
Hype
rtensi
on
Maki
ng
the
Diag
nosis

of
Hype
rtensi
on
Evalu
ating
the
Patie
nt
Physi
cal
Exam
inatio
n
Tests
Goals
of
Treati
ng
Hype
rtensi
on
Nonp
harm
acolo
gic
Treat
ment
of
Hype
rtensi
on
Drug
treat
ment
for
Hype
rtensi
on
Brief
Com
ment
s on
Drug
Class
es
Treat
mentResis
tant
Hype
rtensi
on

INT
RO
DU
CTI
ON
Abou
t one

third
of
adult
s in
most
com
munit
ies in
the
devel
oped
and
devel
oping
world
have
hyper
tensi
on.

the
most
com
mon
chron
ic
condi
tion
dealt
with
by
prima
ry
care
physi
cians
and
other
healt
h
practi
tioner
s.

Hype
rtensi
on is

Official Journal of the

American Society of
Hypertension, Inc.
The Journal
of Clinical Hypertension

1
ASH/IS
H
Hypert
ension
Guideli
nes |
Weber
et al.

Most
patie
nts
with
hyper
tensi
on
have
other
risk
factor
s as
well,
inclu
ding
lipid
abnor
maliti
es,
gluco
se
intole
rance
, or
diabe

tes; a
famil
y
histor
y of
early
cardiova
scula
r
event
s;
obesi
ty;
and
cigar
ette
smok
ing.
The
succe
ss of
treati
ng
hyper
tensi
on
has
been
limited,
and

despi
te
wellestabl
ished
appro
aches
to
diagn
osis
and
treat
ment,
in
many
com
munit
ies
fewer
than
half
of all
hyper
tensi
ve
patie
nts
have
adeq
uatel
y
contr
olled
blood
press
ure.

EPI
DE
MIO
LOG
Y
There
is a
close
relati
onshi
p
betw
een
blood
press
ure
levels
and
the
risk
of
cardi
ovasc
ular

event
s,
strok
es,
and
kidne
y
disea
se.
The
risk
of
these
outco
mes
is
lowes
t at a
blood
press
ure of
aroun
d
115/7
5 mm
Hg
Abov
e
115/7
5 mm
Hg,
for
each
incre
ase of
20
mm
Hg in
systol
ic
blood
press
ure or
10
mm
Hg in
diast
olic
blood
press
ure,
the
risk
of
major
cardi
ovascu

lar
and
strok
e
event
s
doubl
es.
The
high
preva
lence
of
hyper
tensi
on in
the
com
munity
is
curre
ntly
being
drive
n by
two
phen
omen
a: the
incre
ased
age
of
our
popul
ation
and
the
growi
ng
preva
lence
of
obesi
ty,
whic
h is
seen
in
devel
oping
as
well
as
devel
oped
count
ries.
In
many
com

munit
ies,
high
dietar
y salt
intak
e is
also a
major
factor
.
The
main
risk
of
event
s is
tied
to an
incre
ased
systol
ic
blood
press
ure;
after
age
50 or
60
years,
diast
olic
blood
press
ure
may
actua
lly
start
to
decre
ase,
but
systol
ic
press
ure
conti
nues
to
rise
throu
ghout
life.
This
incre
ase in
systol
ic
blood

press
ure
and
decre
ase in
diast
olic
blood
press
ure
with
aging
reflec
ts the
progressi
ve
stiffe
ning
of the
arteri
al
circul
ation.
The
reaso
n for
this
effect
of
aging
is not
well
under
stood
, but
high
systol
ic
blood
press
ures
in
older
peopl
e
repre
sent a
major
risk
factor
for
cardi
ovasc
ular
and
strok
e
event
s and
kidne
y
disea

se
progr
essio
n.

SPE
CIA
L
ISS
UES
WIT
H
BLA
CK
PATI
ENT
S
(AF
RIC
AN
ANC
EST
RY)
Hype
rtensi
on is
a
partic
ularly
com
mon
findi
ng in
black
peopl
e.
Hype
rtensi
on
occur
s at a
youn
ger
age
and is
often
more
sever
e in
terms
of
blood
press
ure
levels
in
black
patie

nts
than
in
white
s.
A
highe
r
propo
rtion
of
black
peopl
e are
sensit
ive to
the
blood
press
ure
raisin
g
effect
s of
salt
in the
diet
than
white
patie
nts,
and
this

toget
her
with
obesi
ty,
espec
ially
amon
g
wom
en
may
be
part
of the
expla
natio
n for
why
youn
g
black
peopl
e
tend
to
have
earlie

r and
more
sever
e
hyper
tensi
on
than
other
group
s.
Black
patie
nts
with
hyper
tensi
on
are
partic
ularly
vulne
rable
to
strok
es
and
hyper
tensi
ve
kidne
y disease.
They
are 3
to 5
times
as
likely
as
white
s to
have
renal
comp
licati
ons
and
endstage
kidne
y
disea
se.
There
is a
tende
ncy
for
black

patie
nts to
have
differ
ing
blood
press
ure
respo
nses
to the
avail
able
antih
ypert
ensiv
e
drug
class
es:
they
usual
ly
respo
nd

well
to
treat
ment
with
calci
um
chan
nel
block
ers
and
diuret
ics
but
have
small
er
blood
press
ure
reduc
tions
with
angio
tensi
nconv
erting
enzy
me
inhibi

tors,
angio
tensi
n
recep
tor
block
ers,
and
bblock
ers.
However,
appro
priate
comb
inatio
n
thera
pies
provi
de
powe
rful
antih
ypert
ensiv
e
respo
nses
that
are
simil
ar in
black
and
white
patie
nts.
Most
patie
nts
will
requi
re
more
than
one
antih
ypert
ensiv
e
drug
to
maint
ain
blood
press
ure
contr
ol.

HO
W
IS
HYP
ERT
ENS
ION
DEF
INE
D?

and

Most
major
guide
lines
reco
mme
nd
that
hyper
tensi
on be
diagn
osed
when
a
perso
ns
systol
ic
blood
press
ure is
140
mm
Hg or
their
diast
olic
blood
press
ure is
90
mmH
g, or
both,
on
repea
ted
exam
inatio
n.
The
systol
ic
blood
press
ure is
partic
ularly
impo
rtant

Thes
e
numb
ers
apply
to all
adult
s
older
than
18
years,
altho
ugh
for
patie
nts
aged
80 or
older
a
systol
ic
blood
press
ure
up to
150
mm
Hg is
now

is the
basis
for
diagn
osis
in
most
patie
nts.

regar
ded
as
accep
table.
The
goal
of
treati
ng
hyper
tensi
on is
to
reduc
e
blood

press
ure to
levels
belo
w the
numb
ers
used
for

evide
nce
to
justif
y
treati
ng
hyper
-

maki
ng
the
diagn
osis.

tensi
on
down
to
such
a low
level.

Thes
e
defini
tions
are
based
on
the
result
s of
major
clinic
al
trials
that
have
show
n the
benef
its of
treati
ng
peopl
e to
these
levels
of
blood
press
ure.
Even
thoug
ha
blood
press
ure of
115/7
5 mm
Hg is
ideal,
as
discu
ssed
earlie
r,
there
is no

We
do
not
have
suffic
ient
infor
matio
n
about
youn
ger
adult
s
(betw
een
18
and
55
years
) to
know
whet
her
they
might
benef
it
from
defini
ng
hyper
tensi
on at
a
level
<140/
90
mmH
g (eg,
130/8
0 mm
Hg)
and
treati

ng
them
more
aggre
ssivel
y
than
older
adult
s.
Thus,
guide
lines
tend
to use
140/9
0 mm
Hg
for
all
adult
s (up
to 80
years
).
Even
so, at
a
practi
tioner
s
discr
etion,
lower
blood
press
ure
target
s may
be
consi
dered
in
youn
g
adult
s,
provi
ded
the
thera
py is
well
tolera
ted.
Some
recen
t
guide
lines
have

reco
mme
nded
diagn
os-tic
value
s of
130/8
0 mm
Hg
for
patie
nts
with
diabe
tes or
chron
ic
kidne
y
disea
se.
How
ever,
the
clinic
al
benef
its of
this
lower
target
have
not
been
establ
ished
and
so
these
patie
nts
shoul
d be
treate
d to
<140/
90
mm
Hg.

HO
W
IS
HYP
ERT
ENS
ION
CLA
SSI
FIE
D?

For
patie
nts
with
systol
ic
blood
press
ure
betw
een
120
mm
Hg
and
139
mm
Hg,
or
diast
olic
press
ures
betw
een
80
and
89
mm
Hg,
the
term
prehy
perte
nsion
can
be
used.
Patie
nts
with
this
condi
tion
shoul
d not
be
treate
d
with
blood
press
ure
medi
catio

ns;
howe
ver,
they
shoul
d be
enco
urage
d to
make
lifest
yle
chan
ges in
the
hope
of
delay
ing or
even
preve
nting
progr
essio
n to
hyper
tensi
on.
Stage
1
hyper
tensi
on:
patie
nts
with
systol
ic
blood
press
ure
140
to
159
mm
Hg or
diast
olic
blood
press
ure
90 to
99
mm
Hg.

The Journal
of Clinical Hypertension
Official
Journal of the American
Society of Hypertension,
Inc.

tial

Stage
2
hyper
tensi
on:
systol
ic
blood
press
ure
160
mm
Hg or
diast
olic
blood
press
ure
100
mm
Hg.

CAU
SES
OF
HYP
ERT
ENS
ION
Prim
ary
Hype
rtens
ion
Abou
t 95%
of
adult
s
with
high
blood
press
ure
have
prima
ry
hyper
tensi
on
(som
etime
s
calle
d
essen

hyper
tensi
on).
The
cause
of
prima
ry
hyper
tensi
on is
not
know
n,
altho
ugh
genet
ic
and
envir
onme
ntal
factor
s that
affect
blood
press
ure
regul
ation
are
now
being
studi
ed.
Envir
onme
ntal
factor
s
inclu
de
exces
s
intak
e of
salt,
obesi
ty,
and
perha
ps
seden
tary
lifest
yle.

Some
genet
ically
relate
d
factor
s
could
inclu
de
inappropr
iately
high
activi
ty of
the
renin
angio
tensi
naldos
teron
e
syste
m
and
the
symp
atheti
c
nervo
us
syste
m
and
susce
ptibil
ity to
the
effect
s of
dietar
y salt
on
blood
press
ure.
Anot
her
com
mon
cause
of
hyper
tensi
on is
stiffe
ning
of the

aorta
with
incre
asing
age.
This
cause
s
hyper
tensi
on
referr
ed to
as
isolat
ed or
predo
mina
nt
systol
ic
hyper
tensi
on
chara
cteriz
ed by
high
systol
ic
press
ures
(ofte
n
with
norm
al
diast
olic
press
ures),
whic
h are
found
prima
rily
in
elderl
y
peopl
e.
Seco
ndar
y
Hype
rtens
ion
This
pertai
ns to

the
relati
vely
small
numb
er of
cases,
about
5%
of all
hyper
tensi
on,
wher
e the
cause
of the
high
blood
press
ure
can
be
identi
fied
and
some
times
treate
d.
The
main
types
of
secon
dary
hyper
tensi
on
are
chron
ic
kidne
y
disea
se,
renal
artery
steno
sis,
exces
-sive
aldos
teron
e
secret
ion,
pheo
chro
mocy
toma,

and
sleep
apnea
.
A
simpl
e
scree
ning
appro
ach
for
identi
fying
secon
d-ary
hyper
tensi
on is
given
later.

MAK
ING
THE
DIA
GN
OSI
S
OF
HYP
ERT
ENS
ION
Bloo
d
press
ure
can
be
meas
ured
by
either
a
conv
entional
sphy
gmo
mano
meter
using
a
steth
oscop
e or
by an
auto

mate
d
electr
onic
devic
e.
The
electr
onic
devic
e, if
avail
able,
is
prefe
rred
becau
se it
provi
des
more
repro
ducib
le
result
s than
the
older
meth
od
and is
not
influe
nced
by
variat
ions
in
techn
ique
or by
the
bias
of the
obser
vers.
If the
auscu
ltator
y
meth
od is
used,
the
first
and
fifth
Korot
koff
soun
ds
(the
appea

rance
and
disap
peara
nce
of
soun
ds)
will
correspo
nd to
the
systol
ic
and
diast
olic
blood
press
ures.
Arm
cuffs
are
prefe
rred.
Cuffs
that
fit on
the
finge
r or
wrist
are
often
inacc
urate
and
shoul
d, in
gener
al,
not
be
used.
It is
impo
rtant
to
ensur
e that
the
corre
ct
size
of the
arm
cuff
is
used

(in
partic
ular,
a
wider
cuff
in
patie
nts
with
large
arms
[>32
cm
circu
mfere
nce]).
At
the
initial
evalu
ation,
blood
press
ure
shoul
d be
meas
ured
in
both
arms;
if the
readi
ngs
are
differ
ent,

ASH/IS
H
Hypert
ension
Guideli
nes |
Weber
et al.

the
arm
with
the
highe
r
readi
ng
shoul
d be
used
for
meas
urem
ents
there
after.
The
blood
press
ure
shoul
d be
taken
after
patie
nts
have
empti
ed
their
bladd
ers.
Patie
nts
shoul
d be
seate
d
with
their
backs
supp
orted
and
with
their
legs
restin
g on
the
groun
d and

in the
uncro
ssed
positi
on
for 5
minut
es.
The
patie
nts
arm
being
used
for
the
meas
urem
ent
shoul
d be
at the
same
level
as the
heart,
with
the
arm
restin
g
comf
ortabl
y on
a
table.
It is
prefe
rable
to
take
2
readi
ngs,
1 to 2
minut
es
apart,
and
use
the
avera
ge of
these
meas
urem
ents.

It is
usefu
l to
also
obtai
n
stand
ing
blood
press
ures
(usua
lly
after
1
minut
e and
again
after
3
minut
es) to
check
for
postu
ral
effect
s,
partic
ularly
in
older
peopl
e.
In
gener
al,
the
diagn
osis
of
hyper
tensi
on
shoul
d be
confi
rmed
at an
additi
onal
patie
nt
visit,
usual
ly 1
to
4
week
s

after
the
first
meas
urem
ent.
On
both
occasions,
the
systol
ic
blood
press
ure
shoul
d be
140
mm
Hg or
the
diast
olic
press
ure
90
mmH
g, or
both,
in
order
to
make
a
diagn
osis
of
hyper
tensi
on.
If the
blood
press
ure is
very
high
(for
insta
nce, a
systol
ic
blood
press
ure
180
mm
Hg),
or if
avail
able
resou

rces
are
not
adeq
uate
to
permi
ta
conv
enien
t
secon
d
visit,
the
diagn
osis
and,
if
appro
priate
,
treat
ment
can
be
starte
d
after
the
first
set of
readi
ngs
that
demo
nstrat
e
hyper
tensi
on.
For
practi
tioner
s and
their
staff
not
exper
ience
d in
meas
uring
blood
press
ures,
it is
neces
sary
to
recei

ve
appro
priate
traini
ng in
perfo
rmin
g this
impo
rtant
techn
ique.
Some
patie
nts
may
have
blood
press
ures
that
are
high
in the
clinic
or
office
but
are
norm
al
elsew
here.
This
is
often
calle
d
white
-coat
hyper
tensi
on. If
it is
suspe
cted,
consi
der
gettin
g
home
blood
press
ure
readi
ngs
(see
belo
w) to
check
this

possi
bility.
Anot
her
appro
ach is
to use
ambu
latory
blood
press
ure
monit
oring,
if it is
avail
able.
In
this
proce
dure,
the
patie
nt
wears
an
arm
cuff
conn
ected
to a
devic
e that
auto
matic
ally
measures
and
recor
ds
blood
press
ures
at
regul
ar
interv
als
usual
ly
over
a 24hour
perio
d.
It can
be
helpf
ul to
meas

ure
blood
press
ures
at
home
. If
avail
able,
the
electr
onic
devic
e is
simpl
er to
use
and is
proba
bly
more
reliab
le
than
the
sphy
gmo
manome
ter.
The
avera
ge of
blood
press
ures
meas
ured
over
5 to 7
days,
if
possi
ble in
dupli
cate
at
each
meas
urem
ent,
can
be a
usefu
l
guide
for
diagn
ostic
and
treat
ment
decisi

ons.

EVA
LUA
TIN
G
THE
PATI
ENT
Often
, high
blood
press
ure is
only
one
of
sever
al
cardi
ovasc
ular
risk
factor
s that
requi
re
attent
ion.
Befor
e
starti
ng
treat
ment
for
hyper
tensi
on, it
is
usefu
l to
evalu
ate
the
patie
nt
more
thoro
ughly
. The
three
meth
ods
are
perso
nal
histor
y,

physi
cal
exam
inatio
n.

and
select
ive
testin
g.

Official Journal of the

American Society of
Hypertension, Inc.
The Journal
of Clinical Hypertension

3
ASH/IS
H
Hypert
ension
Guideli
nes |
Weber
et al.

Histo
ry
Ask
about
previ
ous
cardi
ovasc
ular
event
s
becau
se
they
often
sugge
st an
incre
ased
proba
bility
of
futur
e
event
s that
can
influe
nce
the
choic
e of
drugs
for
treati
ng
hyper
tensi
on
and

will
also
requi
re
more
aggre
ssive
treat
ment
of all
cardi
ovasc
ular
risk
factor
s.
Also
ask
patie
nts if
they
have
previ
ously
been
told
that
they
have
hyper
tensi
on
and,
if
relev
ant,
their
respo
nses
to
any
drugs
they
might
have
been
given
.
Impo

rtant
previ
ous
event
s
inclu
de.
Strok
e or
transi
ent
ische
mic
attac
ks or
deme
ntia.
Why
is
this
infor
mati
on
impo
rtant
? For
patie
nts
with
these
previ
ous
event
s, it
may
be
neces
sary
to
inclu
de
partic
ular
drug
types
in
their
treat
ment,
for
insta
nce
angio
tensi
n
recep
tor
block
ers or
angio
tensin-

conv
erting
enzy
me
inhibi
tors,
calci
um
chan
nel
block
ers,
and
diuret
ics,
as
well
as
drugs
for
lowdensi
ty
lipop
rotein
(LDL
)
chole
sterol
(stati
ns)
and
antipl
atelet
drugs
.
Coro
nary
artery
disea
se,
inclu
ding
myoc
ardial
infarc
tions,
angin
a
pecto
ris,
and
coron
ary
revas
culariza
tions.
Why
is
this

impo
rtant
?
Certa
in
medicatio
ns
woul
d be
prefe
rred,
for
insta
nce
bblock
ers,
angio
tensi
nconv
erting
enzy
me
inhibi
tors
or
angio
tensi
n
recep
tor
block
ers,
statin
s, and
antipl
atelet
agent
s
(aspir
in).
Heart
failur
e or
symp
toms
sugge
sting
left
ventri
c-ular
dysfu
nctio
n
(short
ness
of
breat

h,
edem
a).
Why
is
this
impo
rtant
?
Certa
in
medi
catio
ns
woul
d be
prefe
rred
in
such
patie
nts,
inclu
ding
angio
tensi
n
recep
tor
block
ers or
angio
tensi
nconv
erting
enzy
me
inhibi
tors,
bblock
ers,
diuret
ics,
and
spiro
nolac
-tone.
Also,
certai
n
medi
catio
ns
shoul
d be
avoid
ed,
such
as
nondi

hydro
pyrid
ine
calci
um
chan
nel
block
ers
(vera
pamil
,
diltia
zem),
in
patie
nts
with
systol
ic
heart
failur
e.
IV.
Chro
nic
kidne
y
disea
se.
Why
is
this
impo
rtant
?
Certa
in
medi
catio
ns
woul
d be
prefe
rred,
inclu
ding
angio
tensi
nconv
erting
enzy
me
inhibi
tors
or
angio
tensi

n
recep
tor
block
ers
(altho
ugh
these
two
drug
class
es
shoul
d not
be
presc
ribed
in
comb
inatio
n
with
each
other
),
statin
s, and
diuret
ics
(loop
diuret
-ics
may
be
requi
red if
the
estim
ated
glom
erular
filtrat
ion
rate
is
belo
w 30)
and
blood
press
ure
treat
ment
target
s
might
be
lower
(130/
80
mm
Hg)
if

albu
minu
ria is
prese
nt.
Note:
In
patie
nts
with
more
adva
nced
kidne
y
disea
se,
the
use
of
some
of
these
drugs
often
requi
res
the
exper
tise
of a
nephr
ologi
st.
Perip
heral
artery
disea
se.
Why
is
this
impo
rtant
?
This
findi
ng
sugge
sts
adva
nced
arteri
al
disea
se
that
may
also
exist
in the
coron

ary or
brain
circul
ation
s,
even
in the
absen
ce of
clinic
al
histor
y. It
is
vital
that
smok
ing
be
disco
ntinu
ed. In
most
cases,
antipl
atelet
drugs
shoul
d be
used.
VI.
Diab
etes.
Why
is
this
impo
rtant
?
This
condi
tion
is
com
monl
y
assoc
iated
with
hyper
tensi
on
and
an
incre
ased
risk
of
cardi
ovasc
ular
event

s.
Certa
in
medi
catio
ns
such
as
angio
tensi
n
recep
tor
block
ers

and
angio
tensi
nconv
erting
enzy
me
inhibi
tors
shoul
d be
used,
partic
ularly
if
there
is
evide
nce
of
albu
minu
ria or
chron
ic
kidne
y
disea
se.
Good
blood
press
ure
contr
ol,
often
requi
ring
the
additi
on of
calci

um
chan
nel
block
ers
and
diuret
ics, is
also
impo
rtant
in
these
patie
nts.
VII.
Sleep
apnea
.
Why
is
this
impo
rtant
?
Speci
al
treatment
s are
often
requi
red
for
these
patie
nts
and
their
use
may
make
it
possi
ble to
impr
ove
blood
press
ure
contr
ol as
well
as
other
findi
ngs
of
this
condi
tion.

Ask
about
other
risk
factor
s.
Why
is
this
impo
rtant
?
Risk
factor
s can
affect
blood
press
ure
target
s and
treat
ment
select
ion
for
the
hyper
tensi
on.
Thus,
know
ing
about
age,
dysli
pide
mia,
micro
albu
minu
-ria,
gout,
or
famil
y
histor
y of
hyper
tensi
on
and
diabe
tes
can
be
valua
ble.
Cigar
ette
smok
ing is
a risk

factor
that
must
be
identi
fied
so
that
couns
eling
can
be
given
about
stopp
ing
this
dang
erous
habit.
Ask
about
conc
urren
t
drugs
.
Com
monl
y
used
drugs
(for
indic
ation
s
unrel
ated
to
treati
ng
hyper
tensi
on)
can
incre
ase
blood
press
ure
and
theref
ore
shoul
d be
stopp
ed if
possi
ble.
Thes
e

inclu
de
nonst
eroid
al
antiinfla
mmat
ory
drugs
used
for
arthri
tis
and
pain
relief,
some
tricyc
lic
and
other
types
of
antid
epres
sants,
older
highdose
oral
contr
acept
ives,
migra
ine
medi
catio
ns,
and
cold
reme
dies
(eg,
pseud
oeph
edrine
). In
additi
on,
some
patie
nts
may
be
takin
g
herba
l
medi
catio

ns,
folk
reme
dies,
or
recre
ation
al
drugs
(eg,
cocai
ne),
whic
h can
incre
ase
blood
press
ure.

PHY
SIC
AL
EXA
MIN
ATI
ON
At
the
first
visit
it is
impo
rtant
to
perfo
rm a
comp
lete
physi
cal
exam
inatio
n
becau
se
often
gettin
g
care
for
hyper
tensi
on is
the
only
conta
ct
that
patie

nts
have
with
a
medi
cal
practi
tioner
.
Meas
uring
blood
press
ure
(disc
ussed
earlie
r).
Docu
ment
the
patie
nts
weig
ht
and
heigh
t and
calcu
late
body
mass
index
. This
can
be
done
by
going
onlin
e to
Goog
le,
searc
hing
BMI,
and
enteri
ng
the
patie
nts
weig
ht
and
heigh
t as
instru
cted
(http:
//

www.
nhlbi.
nih.g
ov/gu
idelin
es/ob
esity/
BMI/
bmic
alc.
htm)
Why
is
this
impo
rtant
?
This
helps
to set
target
s for
weig
ht
loss
and,
as
discu
ssed
later,
know
ing
whet
her a
patie
nt is
obese
or not
obese
might
affect
the
choic
e of
hyper
tensi
on
treat
ment.
It
shoul
d be
noted
that
the
risk
of
cardi
ovasc
ular
event
s,
inclu

d-ing
strok
e,
parad
oxica
lly
may
be
highe
r in
lean
hyper
tensi
ve
patie
nts
than
in
obese
patie
nts.
Waist
circu
mfere
nce.
Why
is
this
impo
rtant
?
Independ
ent of
weig
ht,
this
helps
deter
mine
whet
her a
patie
nt has
the
meta
bolic
syndr
ome
or is
at
risk
for
type
2
diabe
tes.
Risk
is

high
when
the
meas
urem
ent
is
>102
cm in
men
or
>88
cm in
wom
en.
Signs
of
heart
failur
e.
Why
is
this
impo
rtant
?
This
diagn
osis
stron
gly
influe
nces
the
choic
e of
hyper
tension
thera
py.
Left
ventri
cular
hyper
troph
y can
be
suspe
cted
by
chest
palpa
tion,
and
heart
failur
e can

The Journal
of Clinical Hypertension
Official
Journal of the American
Society of Hypertension,
Inc.

be
indic
ated
by
diste
nded
jugul
ar
veins,
rales
on
chest
exam
inatio
n, an
enlar
ged
liver,
and
perip
heral
edem
a.
Neur
ologi
c
exam
inatio
n.
Why
is this
impo
rtant?
This
may
revea
l
signs
of
previ
ous
strok
e and
affect
treat
ment
select
ion.
Eyes:
If

possi
ble,
the
optic
fundi
shoul
d be
check
ed for
hyper
tensi
ve or
diabe
tic
chan
ges
and
the
areas
aroun
d the
eyes
for
findi
ngs
such
as
xanth
omas.
Pulse
: It is
impo
rtant
to
check
perip
heral
pulse
rates;
if
they
are
dimin
ished
or
absen
t, this
can
indic
ate
perip
heral
artery
disea
se.

TES
TS
Bloo
d
samp
le
Note:
This
prefe
rably
shoul
d be
a
fastin
g
samp
le so
that a
fastin
g
blood
gluco
se
level
and
more
accur
ate
lipid
profil
es
can
be
obtai
ned.
Elect
rolyte
s.
Why
is
this
impo
rtant
?
There
is a
speci
al
emph
asis
on
potas
sium:
high
levels
can
sugge
st
renal

disea
se,
partic
ularly
if
creati
nine
is
eleva
ted.
Low
value
s can
sugge
st
aldos
teron
e
exces
s. In
additi
on,
illnes
ses
assoc
iated
with
sever
e
diarr
hea
are
com
mon
in
some
com
munit
ies
and
can
cause
hypo
kale
mia
and
other
electr
olyte
chan
ges.
Fasti
ng
gluco
se
conce
ntrati
on.
Why
is
this
impo

rtant?
If
eleva
ted,
this
could
be
indic
ative
of
impai
red
gluco
se
tolera
nce,
or, if
suffic
iently
high,
of
diabe
tes. If
avail
able,
glyca
ted
hemo
globi
n
shoul
d be
meas
ured
to
furth
er
asses
s an
eleva
ted
gluco
se
level
and
help
in
maki
ng a
diagn
osis.
Seru
m
creati
nine
and
blood
urea
nitro
gen.
Why

are
thes
e
impo
rtant
?
Incre
ased
creati
nine
levels
are
usual
ly
indic
ative
of
kidne
y
disea
se;
creati
nine
is
also
used
in
form
ulae
for
eGF
R.
Whe
n
appro
priate
, use
form
ulae
desig
ned
for
eGF
R
calcu
lations
in
patie
nts of
Afric
an
ances
try.
IV.
Lipid
s.
Why
are
thes

e
impo
rtant
?
Eleva
ted
LDL
chole
sterol
or
low
value
s of
highdensi
ty
lipop
rotein
chole
sterol
are
assoc
iated
with
incre
ased
cardi
ovascular
risk.
High
LDL
chole
sterol
can
typic
ally
be
treate
d
with
avail
able
drugs
,
usual
ly
statin
s.
Hem
oglob
in/he
mato
crit.
Why
are
thes
e
impo
rtant?
Thes

e
meas
urem
ents
can
identi
fy
issue
s
beyo
nd
hyper
tensi
on
and
cardi
ovasc
ular
disea
se,
inclu
ding
sickle
cell
anem
ia in
vulne
rable
population
s and
anem
ia
assoc
iated
with
chron
ic
kidney
disea
se.
VI.
Liver
functi
on
tests.
Why
are
thes
e
impo
rtant
?
Certa
in
blood
press
ure
drugs
can
affect

liver
functi
on,
so it
is
usefu
l to
have
baseli
ne
value
s.
Also,
obese
peopl
e can
have
fatty
liver
disor
ders
that
shoul
d be
identi
fied
and
consi
dered
in
overa
ll
mana
geme
nt.

Urine
samp
le
Albu
minu
ria.
Why
is
this
impo
rtant
? If
prese
nt,
this
can
be
indic
ative
of
kidne
y
disea
se
and is

ASH/IS
H
Hypert
ension
Guideli
nes |
Weber
et al.

also
assoc
iated
with
an
incre
ased
risk
of
cardi
ovascu
lar
event
s.
Ideall
y, an
albu
min/c
reatin
ine
ratio
shoul
d be
obtai
ned,
but
even
dipsti
ck
evide
nce
of
albu
minu
ria
(+1
or
great
er) is
helpf
ul.
Red
and
white
cells.
Why
are
thes
e
impo
rtant
?

Positi
ve
findi
ngs
can
be
indic
ative
of
urina
ry
tract
infect
ions,
kidne
y
stone
s, or
other
poten
tially
serio
us
urina
ry
tract
condi
tions,
inclu
ding
bladd
er
tumo
rs.
Elect
rocar
diogr
aphy.
Why
is
this
impo
rtant
?
Electrocar
diogr
aphy
(ECG
) can
help
identi
fy
previ
ous
myoc
ardial
infarc
tions
or
left

atrial
and
ventri
cular
hyper
troph
y
(whic
h is
evide
nce
of
target
organ
dama
ge
and
indic
ative
of the
need
for
good
contr
ol of
blood
press
ure).
ECG
might
also
identi
fy
cardi
ac
arrhy
thmia
s
such
as
atrial
fibrill
ation
(whic
h
woul
d
dictat
e the
use
of
certai
n
drugs
) or
condi
tions
such
as
heart
block
(whic
h

woul
d
contr
aindi
cate
certai
n
drugs
, eg,
bblock
ers,
rateslowi
ng
calci
um
chan
nel
block
ers).
Echo
cardi
ograp
hy, if
avail
able,
can
also
be
helpf
ul in
diagn
osing
left
ventri
cular
hyper
troph
y and
quant
ifyin
g the
ejecti
on
fracti
on in
patie
nts
with
suspe
cted
heart
failur
e,
altho
ugh
this
test is
not
routi
ne in

hyper
tensi
ve
patie
nts.

OVE
RAL
L
GO
ALS
OF
TRE
ATM
ENT
I.
The
goal
of
treat
ment
is to
mana
ge
hyper
tensi
on
and
to
deal
with
all
the
other
identi
fied
risk
factor
s for
cardi
ovasc
ular
disea
se,
inclu
ding
lipid
disor
ders,
glucose
intole
rance
or
diabe
tes,
obesi
ty,
and
smok
ing.

For
hyper
tensi
on,
the
treat
ment
goal
for
systol
ic
blood
press
ure is
usual
ly
<140
mm
Hg
and
for
diast
olic
blood
press
ure
<90
mm
Hg.
In the
past,
guide
lines
have
reco
mme
nded
treat
ment
value
s of
<130/
80
mm
Hg
for
patie
nts
with
diabe
tes,
chron
ic
kidne
y
disea
se,
and
coron
ary
artery
disea

se.
However,
evide
nce
to
supp
ort
this
lower
target
in
patie
nts
with
these
condi
tions
is
lacki
ng,
so the
goal
of
<140/
90
mm
Hg
shoul
d
gener
ally
be
used,
altho
ugh
some
exper
ts
still
reco
mme
nd
<130/
80
mm
Hg if
albuminu
ria is
prese
nt in
patie
nts
with
chron
ic
kidne
y
disea
se.

Are
there
other
excep
tions
to
<140/
90
mm
Hg?
Most
evide
nce
linkin
g the
effect
s on
cardi
ovasc
ular
or
renal
outco
mes
to
treate
d
blood
press
ures
have
been
based
on
clinic
al
trials
in
middl
eaged
to
elderl
y
patie
nts
(typic
ally
betw
een
55
and
80
years
).
Some
recen
t
trials
sugge
st
that
in

peopl
e 80
or
older,
achie
ving
a
systol
ic
blood
press
ure of
<150
mm
Hg is
assoc
iated
with
stron
g
cardi
ovasc
ular
and
strok
e
prote
ction
and
so a
target
of
<150/
90
mm
Hg is
now
reco
mme
nded
for
patie
nts in
this
age
group
. We
have
almo
st no
clinic
al
trial
evide
nce
regar
ding
blood
press
ure
target
s in
patie

nts
youn
ger
than
50
years.
Diast
olic
blood
press
ure
may
be
impo
rtant
in
this
age
group
, so
achie
ving
a

value
<90
mm
Hg
shoul
d be
a
priori
ty. In
additi
on, it
is
also a
reaso
nable
expec
tation
that
target
s
<140/
90
mm

Official Journal of the

American Society of
Hypertension, Inc.
The Journal
of Clinical Hypertension

5
ASH/IS
H
Hypert
ension
Guideli
nes |
Weber
et al.

Hg
(eg, <
130/8
0 mm
Hg)
could
be
appro
priate
in
youn
g
adult
s and
can
be
consi
dered
.
IV.It
is
impo
rtant
to

infor
m
patie
nts
that
the
treat
ment
of
hyper
tensio
n is
usuall
y
expec
ted to
be a
lifelong
com
mitm
ent
and
that it
can
be
dange
rous
for
them
to
termi
nate
their

treat
ment
with
drugs
or
lifest
yle
chan
ges
witho
ut
first
consu
lting
their
practi
tioner
.

NO
NPH
AR
MA
COL
OGI
C
TRE
ATM
ENT
Sever
al
lifest
yle
interv
entio
ns
have
been
show
n to
reduc
e
blood
press
ure.
Apart
from
contri
butin
g to
the
treat
ment
of
hyper
tensi
on,
these
strate
gies
are

benef
icial
in
mana
ging
most
of the
other
cardi
ovasc
ular
risk
factor
s. In
patie
nts
with
hyper
tensio
n that
is no
more
sever
e
than
stage
1 and
is not
assoc
iated
with
evide
nce
of
abnor
mal
cardi
ovasc
ular
findin
gs or
other
cardi
ovascular
risks,
6 to
12
mont
hs of
lifest
yle
chang
es
can
be
attem
pted
in the
hope
that
they
may

be
suffic
iently
effect
ive to
make
it
unne
cessa
ry to
use
medi
cines.
How
ever,
it
may
be
prude
nt to
start
treat
ment
with
drugs
soone
r if it
is
clear
that
the
blood
press
ure is
not
respo
nding
to the
lifest
yle
meth
ods
or if
other
risk
factor
s
appea
r.
Also,
in
practi
ce
settin
gs
wher
e
patie
nts
have
logist
ical
diffic

ulties
in
maki
ng
regul
ar
clinic
visits,
it
might
be
most
practi
cal to
start
drug
thera
py
early.
In
gener
al,
lifest
yle
chang
es
shoul
d be
regar
ded
as a
comp
leme
nt to
drug
thera
py
rather
than
an
altern
ative.
Weig
ht
loss:
In
patie
nts
who
are
over
weig
ht or
obese
,
weig
ht
loss
is
helpf
ul in
treati

ng
hyper
tensi
on,
diabe
tes,
and
lipid
disor
ders.
Subst
itutin
g
fresh
fruits
and
veget
ables
for
more
tradit
ional
diets
may
have
benef
its
beyo
nd
weig
ht
loss.
Unfo
rtunat
ely,
these
diets
can
be
relati
vely
expe
nsive
and
incon
venie
nt for
patie
nts,
and
can
work
only
if
patie
nts
are
provi
ded
with
a
stron
g

suppo
rt
syste
m.
Even
mode
st
weig
ht
loss
can
be
helpf
ul.
Salt
reduc
tion:
Highsalt
diets
are
com
mon
in
many
com
munit
ies.
Redu
ction
of
salt
intak
e is
reco
mmend
ed
becau
se it
can
reduc
e
blood
press
ure
and
decre
ase
the
need
for
medi
catio
ns in
patie
nts
who
are
salt
sensit
ive,

whic
h
may
be a
fairly
com
mon
findi
ng in
black
com
munit
ies.
Often
,
patie
nts
are
unaw
are
that
there
is a
large
amou
nt of
salt
in
foods
such
as
bread
,
canne
d
good
s, fast
foods
,
pickl
es,
soups
, and
proce
ssed
meats
. This
intak
e can
be
diffic
ult to
chan
ge
becau
se
salty
foods
are
often
part
of the
tradit

ional
diets
found
in
many
cultur
es. A
relate
d
probl
em is
that
many
peopl
e eat
diets
that
are
low
in
potas
sium,
and
they
shoul
d be
taugh
t
about
availa
ble
sourc
es of
dietar
y
potas
sium.
Exerc
ise:
Regul
ar
aerob
ic
exerc
ise
can
help
reduc
e
blood
press
ure,
but
oppor
tuniti
es to
follo
wa
structured
exerc

ise
regim
en
are
often
limite
d.
Still,
patie
nts
shoul
d be
enco
urage
d to
walk,
use
bicyc
les,
climb
stairs,
and
pursu
e
mean
s of
integr
ating
physical
activi
ty
into
their
daily
routi
nes.
IV.Al
cohol
consu
mptio
n: Up
to 2
drink
sa
day
can
be
helpf
ul in
prote
cting
again
st
cardi
ovasc
ular
event
s,

but
great
er
amou
nts of
alcoh
ol
can
raise
blood
press
ure
and
shoul
d
theref
ore
be
disco
urage
d. In
wom
en,
alcoh
ol
shoul
d be
limite
d to 1
drink
a day.
Cigar
ette
smok
ing:
Stopp
ing
smok
ing
will
not
reduc
e
blood
press
ure,
but
since
smok
ing
by
itself
is
such
a
major
cardi
ovasc
ular
risk

factor
,
patie
nts
must
be
stron
gly
urged
to
disco
ntinu
e this
habit.
Patie
nts
shoul
d be
warn
ed
that
stopp
ing
smok
ing
may
be
assoc
iated
with
a
mode
st
incre
ase in
body
weig
ht.

DRU
G
TRE
ATM
ENT
OF
HYP
ERT
ENS
ION
Starti
ng
treat
ment:
(see
the
algori
thm
in the
Figur
e).
Treat

ment
with
drugs
shoul
d be
starte
d in
patie
nts
with
blood
press
ures
>140/
90
mm
Hg in
who
m
lifest
yle
treat
ments
have
not
been
effect
ive.
(Note
: As
discu
ssed
earlie
r in
Secti
on 12
on
Nonp
harm
acolo
gic
Treat
ment,
drug
treat
ment
can
be
delay
ed for
some
mont
hs in
patie
nts
with
stage
1
hyper
tensio
n
who
do

not
have
evide
nce
of
abnor
mal
cardi
ovasc
ular
findi
ngs
or
other
risk
factor
s. In
settin
gs
wher
e
healt
hcare
resou
rces
are
highl
y
limite
d,
clinic
ians
can
consi
der
exten
ding
the
nondr
ug
obser
vatio
n
perio
d in
unco
mplic
ated
stage
1
hyper
tensi
ve
patie
nts
provi
ded
there
is no
evidence
for an
incre

ase in
blood
press
ure or
the
appea
rance
of
cardi
ovasc
ular
or
renal
findin
gs).
In
patie
nts
with
stage
2
hyper
tensio
n
(bloo
d
press
ure
160/
100
mm
Hg),
drug
treat
ment
shoul
d be
starte
d
imme
diatel
y
after
diagn
osis,
usuall
y
with
a 2drug
comb
inatio
n,
witho
ut
waiti
ng to
see
the
effect
s of
lifest

yle
chan
ges.
Drug
treat
ment
can
also
be
starte
d
imme
diatel
y in
all
hyper
tensi
ve
patie
nts in
who
m,
for
logist
ical
or
other
practi
cal
reaso
ns,
the
practi
tioner
belie
ves it
is
neces
sary
to
achie
ve
more
rapid
contr
ol of
blood
press
ure.
The
prese
nce
of
other
cardi
ovasc
ular
risk
factor
s
shoul
d also

accel
erate
the
start
of
hyper
tensio
n
treat
ment.
For
patie
nts
older
than
80
years,
the
sugge
sted
thres
hold
for
starti
ng
treat
ment
is at
levels
150/
90
mm
Hg.
Thus,
the
target
of
treat
ment
shoul
d be
<140/
90
mm
Hg
for
most
patie
nts
but
<150/
90
mm
Hg
for
older
patie
nts
(unle
ss
these
patie
nts

have
chron
ic
kidne
y
disea
se or
diabe
tes,
when
<140/
90
mm
Hg
can
be
consi
dered
).
The
treat
ment
regim
en:
Most
patie
nts
will
requi
re
more
than
one
drug
to
achie
ve
contr
ol of
their
blood
press
ure.
In
gener
al,
incre
ase
the
dose
of
drugs
or
add
new
drugs
at
appro
ximat
ely 2to 3-

week
interv
als.
This
frequ
ency
can
be
faster
or
slowe
r
depen
d-ing
on
the
judg
ment
of the
practi
tioner
. In
gener
al,
the
initial
doses
of
drugs
chose
n
shoul
d be
at
least
half
of the
maxi
mum
dose
so
that
only
one
dose
adjust
ment
is
requir
ed
there
after.
It is
gener
ally
antici
pated
that
most
patie
nts
shoul
d

reach
an
effect
ive
treat
ment
regim
en,
whet
her 1,
2, or
3
drugs
,
withi
n 6 to
8
week
s.

If the
untre
ated
blood
press
ure is
at
least
20/
10
mm
Hg
above
the
target
blood
press
ure,

The Journal
of Clinical Hypertension
Official
Journal of the American
Society of Hypertension,
Inc.

ASH/ISH Hypertension Guidelines | Weber et al.

FIGURE. This algorithm summarizes the main recommendations of these guidelines. At any stage it is entirely appropriate to seek help from a
hypertension expert if treatment is proving difficult. In patients with stage 1 hypertension in whom there is no history of cardiovascular, stroke,
or renal events or evidence of abnormal findings and who do not have diabetes or other major risk factors, drug therapy can be delayed for
some months. In all other patients (including those with stage 2 hypertension), it is recommended that drug therapy be started when the
diagnosis of hypertension is made. CCB indicates calcium channel blocker; ACE-i, angiotensin-converting enzyme inhibitors; ARB,
angiotensin receptor blocker; thiazide, thiazide or thiazide-like diuretics. Blood pressure values are in mm Hg.

consider starting treatment immediately with 2 drugs.

IV. Choice of drugs:
This should be influenced by the age, ethnicity/ race, and
other clinical characteristics of the patient (Table I).
The choice of drugs will also be influenced by other

conditions (eg, diabetes and coronary disease)

associated with the hypertension (Table II).
Pregnancy also influences drug choice.
Long-acting drugs that need to be taken only once
daily are preferred to shorter-acting drugs that
require multiple doses because patients are more
likely to follow a simple treatment regi-men. For
the same reason, when more than one drug is
prescribed, the use of a combination product with

two appropriate medications in a single tablet can simplify

treatment for patients, although these products can
sometimes be more

availability and affordability. In many cases, it is

necessary to use whichever drugs have been
provided by government or other agencies. For this
reason, we will only make recommendations for
drug classes, not individ-ual agents, recognizing
that there may be a limited selection of drugs that
can be prescribed by a practitioner. Even among
generic drugs there can be a wide variation in cost.

expensive than individual drugs. Once-daily drugs can be

taken at any time during the day, most usually either in the
morning or in the evening before sleep. If multiple drugs
are needed, it is possible to divide them between the
morning and the evening.

Recommendations for drug selection are shown in

Table I (Part 1) for patients whose primary problem
is hypertension, and in Table I (Part 2)

The choice of drugs will further be influenced by their

Official Journal of the American Society of Hypertension, Inc.

The Journal of Clinical Hypertension

ASH/ISH Hypertension Guidelines | Weber et al.

TABLE I. Drug Selection in Hypertensive Patients With or Without Other Major Conditions
Add Second Drug If

If Third Drug is Needed

to Achieve a BP of
<140/90 mm Hg

Needed to Achieve a

Patient Type

First Drug BP <140/90 mm Hg

White and other non-black
a
CCB or thiazide diuretic
(Although ACE
b
ARB or ACE inhibitor (or
patients: 60 y and older
inhibitors or ARBs are also
usually effective)
CCB or thiazide if ACE

A. When hypertension is the only or main condition

Black patients (African
CCBa or thiazide diuretic
b
ARB or ACE inhibitor
ancestry): All ages
(If unavailable can add

inhibitor or ARB used first)

alternative first drug

Combination of CCB + ACE

inhibitor or ARB + thiazide
diuretic

choice)
White and other non-black
b
ARB or ACE inhibitor
CCBa or thiazide diuretic
Patients: Younger than 60

Combination of CCB + ACE

inhibitor or ARB + thiazide
diuretic
Combination of CCB + ACE
inhibitor or ARB + thiazide
diuretic
inhibitor

B. When hypertension is associated with other

conditions
Hypertension and diabetes
black patients,

ARB or ACE inhibitor Note: in

CCB or thiazide diuretic

coronary artery
diseased
Hypertension and
stroke
ACE
inhibitor or ARB

it is acceptable to start with a CCB or thiazide

history

Hypertension and chronic

black patients,

kidney disease

ARB or ACE inhibitor Note: in

good evidence for renal protective effects of

ACE inhibitors

Hypertension and clinical

Thiazide diuretic or CCB

The alternative second

drug (thiazide or CCB)

CCB or thiazide
diuretic Note: in
black patients, if
starting with a CCB
or thiazide, add an
ARB or ACE inhibitor
CCB or thiazide
c
diuretic

The alternative second

drug (thiazide or CCB)
The alternative second
step drug (thiazide or
CCB)
The alternative second
drug (CCB or thiazide)

b-Blocker plus ARB or ACE

Hypertension and heart

Patients with symptomatic heart failure should usually receive an ARB or ACE inhibitor + b-blocker + diuretic +
failure
spironolactone regardless of blood pressure. A dihydropyridine CCB can be added if needed for BP control.
Abbreviations: ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; BP, blood pressure; CCB, calcium
channel blocker; eGFR, estimated glomerular filtration rate.
a

CCBs are generally preferred, but thiazides may cost less.

ARBs can be considered because ACE inhibitors can cause cough and angioedema, although ACE inhibitors may cost less.

If eGFR <40 mL/min, a loop diuretic (eg, furosemide or torsemide) may be needed.

d
e

Note: If history of myocardial infarction, a b-blocker and ARB/or ACE inhibitor are indicated regardless of blood pressure.
Note: If using a diuretic, there is good evidence for indapamide (if available).

for patients who have a major comorbidity

associated with their hypertension. The Figure
1 displays an algorithm that summarizes the
use of therapy for most patients with
hypertension. The recommendations for
particular drug classes are made with the
recognition that sometimes only alternative
drug classes will be available. However, most
of the time, the use of any drugs that reduce
blood pressure is more likely to help protect
patients from strokes and other serious events
than giving patients no drug at all.

BRIEF COMMENTS ON DRUG

CLASSES
Note: There is an assumption, unless
otherwise stated, that all drugs in a class are
similar to each other. We only mention
individual agents if they have an

The Journal of Clinical Hypertension

Daily Dosage, mg

Low Dosage
Usual Dosage

Angiotensin-converting enzyme Inhibitors

These agents reduce blood pressure by
blocking the renin-angiotensin system. They
do this by preventing conversion of
angiotensin I to the blood pressure-raising
hormone angiotensin II. They also increase
availability of the vasodilator bradykinin by
blocking its breakdown.
Angiotensin-converting enzyme inhibitors are
well tolerated. Their main side effect is cough
(most common in women and in patients of
Asian and African background). Angioedema
is an uncommon but potentially serious
complication that can threa-

Official Journal of the American Society of Hypertension, Inc.

TABLE II. Dosages of Commonly Used

Antihypertensive Drugs

important property that is not shared by the

others in its class. Table II provides a list of
commonly used antihypertensive drugs and
their doses.

Amlodipine
2.5
510
Felodipine
2.5
510
Isradipine
2.5 twice
510 twice daily
daily
Nifedipine
30
3090
Nitrendipine
10
20
Drugs that target the renin-angiotensin system
Angiotensin-converting enzyme inhibitors

Calcium channel blockers

Nondihydropyridines

Diltiazem
120
240360
Verapamil
120
240480
Dihydropyridines

Benazepril
5
1040
Captopril
12.5 twice daily
50100 twice daily
Enalapril
5
1040
Fosinopril
10
1040
Lisinopril
5
1040
Perindopril
4
48

Quinapril
5
1040
Ramipril
2.5
510
Trandolapril
12
28
Angiotensin receptor blockers
Azilsartan
40
80
Candesartan
4
832
Eprosartan
400
600800
Irbesartan
150
150300
Losartan
50
50100
Olmesartan
10
2040
Telmisartan
40
4080
Valsartan
80
80320
Direct renin inhibitor

Aliskiren
75
150300
Diuretics

Thiazide and thiazide-like diuretics

Bendroflumethiazide
5
10
Chlorthalidone
12.5
12.525
Hydrochlorothiazide
12.5
12.550
Indapamide
1.25
2.5
Loop diuretics

Bumetanide
0.5
1
Furosemide
20 twice daily
40 twice daily
Torsemide
5
10
Potassium-sparing diuretics
Amiloride
5
510
Eplerenone
25
50100
Spironolactone
12.5
2550

Triamterene
100
100
b-Blockers

Acebutalol
200
200400

ASH/ISH Hypertension Guidelines | Weber et al.

0.1 twice daily

0.10.2 twice daily
Clonidine patch
TTS-1, once weekly
TTS-1, 2, or 3,

TABLE II. (Continued)

Daily Dosage, mg

Low Dosage
Usual Dosage

once weekly
Methyldopa
125 twice daily
250500 twice daily
Adrenergic depleters

Reserpine
0.1
0.10.25
All doses are given once-daily unless otherwise specified.

Atenolol
25
100
Bisoprolol
5
510
Carvedilol
3.125 twice daily
6.2525 twice daily
Labetalol
100 twice daily
100300 twice daily
Metoprolol succinate
25
50100
Metoprolol tartrate
25 twice daily
50100 twice daily
Nadolol
20
4080
Nebivolol
2.5
510
Propranolol
40 twice daily
40160 twice daily
a-Adrenergic receptor blockers
Doxazosin
1
12
Prazosin
1 twice daily
15 twice daily
Terazosin
1
12
Vasodilators, central a-agonists, and adrenergic depleters
Vasodilators

Hydralazine
10 twice daily
25100 twice daily
Minoxidil
2.5
510
Central alpha-agonists

Clonidine

Official Journal of the American Society of Hypertension, Inc.

ten airway function, and it occurs most

frequently in black patients.
These drugs can increase serum creatinine by
as much as 30%, but this is usually because
they reduce pressure within the renal
glomerulus and decrease filtration. This is a
reversible change in function and is not
harmful. An even greater increase in
creatinine sometimes occurs when
angiotensin-converting enzyme inhibitors are
combined with diuretics and produce large
blood pressure reductions. Again, this change
is reversible, although it may be necessary to
reduce doses of one or both drugs. If
creatinine levels increase substantially this
can be caused by concom-itant treatment with
nonsteroidal anti-inflammatory drugs or it
may indicate the presence of renal artery
stenosis.
The side effects associated with angiotensinconvert-ing enzyme inhibitors are generally
not dose-depen-dent, as they occur as
frequently at low doses as at high doses. Thus,
it can be perfectly acceptable when using
these agents to start at medium or even high
doses. The one exception to this rule is in
hyperkal-emia, which may occur more
frequently at higher
angiotensin-converting enzyme inhibitor
doses.
These drugs have established clinical outcome
ben-efits in patients with heart failure, post
myocardial
The Journal of Clinical Hypertension

ASH/ISH Hypertension Guidelines | Weber et al.

infarction, left ventricular systolic

dysfunction, and diabetic and nondiabetic

chronic kidney disease.
In general, angiotensin-converting enzyme
inhibitors are more effective as monotherapy
in reducing blood pressure in white patients
than in black patients, possibly because the
renin-angiotensin system is often less active
in black patients. However, these drugs are
equally effective in reducing blood pressure
in all ethnic and racial groups when combined
with
either calcium channel blockers or diuretics.
Do not combine angiotensin-converting
enzyme inhibitors with angiotensin receptor
blockers; each of these drug types is
beneficial in patients with kidney disease, but
in combination they may actually
have adverse effects on kidney function.
When starting treatment with an angiotensincon-verting enzyme inhibitor, there is a risk of
hypoten-sion in patients who are already
taking diuretics or are on very low-salt diets
or are dehydrated (eg, laborers in hot climates
and patients with diarrhea). For patients
taking a diuretic, skipping a dose before
starting the angiotensin-converting enzyme
inhibitor
helps prevent this sudden effect on blood
pressure. Angiotensin-converting enzyme
inhibitors must not be used in pregnancy,
especially in the second or third trimesters,
since they can compromise the
normal development of the fetus.
Angiotensin Receptor Blockers
Angiotensin receptor blockers, like
angiotensin-con-verting enzyme inhibitors,
antagonize the renin-angiotensin system.
They reduce blood pressure by blocking the
action of angiotensin II on its AT1 receptor
and thus prevent the vasoconstrictor effects
of this receptor.
The angiotensin receptor blockers are well
toler-ated. Because they do not cause cough
and only rarely cause angioedema, and have
effects and benefits similar to angiotensinconverting enzyme inhibitors, they are
generally preferred over angio-tensinconverting enzyme inhibitors if they are
available and affordable. Like angiotensin-

convert-ing enzyme inhibitors, angiotensin

receptor blockers can increase serum
creatinine (see comments about angiotensinconverting enzyme inhibitors), but usu-ally
this is a functional change that is reversible
and
not harmful.
These drugs do not appear to have dosedependent side effects, so it is perfectly
reasonable to start treatment
with medium or even maximum approved
doses.
These drugs have the same benefits on
cardiovascular and renal outcomes as
angiotensin-converting
enzyme inhibitors.
Like angiotensin-converting enzyme
inhibitors, they tend to work better in white
and Asian patients than in black patients, but,
when combined with either calcium channel
blockers or diuretics, they become equally
effective in all patient groups.

Do not combine angiotensin receptor blockers

with angiotensin-converting enzyme
inhibitors; each of these drug types is
beneficial in patients with kidney disease, but
in combination they may actually have
adverse effects on renal events.
When starting treatment with an angiotensin
recep-tor blocker in patients already taking
diuretics, it may be beneficial to skip a dose
of the diuretic to
prevent a sudden fall in blood pressure.
Angiotensin receptor blockers must not be
used in pregnancy, especially in the second or
third trimes-ters, since they can compromise
the normal devel-opment of the fetus.
Thiazide and Thiazide-like Diuretics
These agents work by increasing excretion of
sodium by the kidneys and additionally may
have some
vasodilator effects.

Clinical outcome benefits (reduction of

strokes and major cardiovascular events) have
been best estab-lished with chlorthalidone,
indapamide, and hydro-chlorothiazide,
although evidence for the first two of

Diuretics are most effective in reducing blood

pressure when combined with angiotensinconvert-ing enzyme inhibitors or angiotensin
receptor block-ers, although they are also
effective when combined with calcium
channel blockers.

these agents has been the strongest.

Chlorthalidone has more powerful effects on
blood pressure than hydrochlorothiazide
(when the same doses are compared) and has
a longer duration of
action.

Calcium Channel Blockers

The main side effects of these drugs are

metabolic (hypokalemia, hyperglycemia, and
hyperuricemia). The likelihood of these
problems can be reduced by using low doses
(eg, 12.5 mg or 25 mg of hydrochlorothiazide or chlorthalidone) or by
combining these diuretics with angiotensinconverting enzyme inhibitors or angiotensin
receptor blockers, which have been shown to
reduce these metabolic changes. Combining
diuretics with potassium-sparing agents
also helps prevent hypokalemia.

10

Note: Thiazides plus b-blockers are also an

effective combination for reducing blood
pressure, but since both classes can increase
blood glucose concentrations this
combination should be used with caution in
patients at risk for developing diabetes.

The Journal of Clinical Hypertension

These agents reduce blood pressure by

blocking the inward flow of calcium ions
through the L channels
of arterial smooth muscle cells.
There are two main types of calcium channel
blockers: dihydropyridines, such as
amlodipine and nifedipine, which work by
dilating arteries; and nondihydropyridines,
such as diltiazem and verapa-mil, which
dilate arteries somewhat less but also reduce
heart rate and contractility.

Official Journal of the American Society of Hypertension, Inc.

condition.
Most experience with these agents has been
with the dihydropyridines, such as amlodipine
and nifedipine, which have been shown to
have beneficial effects on cardiovascular and
stroke outcomes in hypertension

Because the nondihydropyridine drugs,

verapamil and diltiazem, can slow heart rate,
they are some-times preferred in patients with
fast heart rates and even for rate control in
patients with atrial fibrilla-

trials.

tion who cannot tolerate b-blockers.

Nondihydro-pyridine drugs can also reduce
proteinuria.

The main side effect of calcium channel

blockers is peripheral edema, which is most
prominent at high doses; this finding can
often be attenuated by combining these agents
with angiotensin-convert-ing enzyme
inhibitors or angiotensin receptor blockers.
Nondihydropyridine calcium channel
blockers are not recommended in patients
with heart failure, but amlodipine appears to
be safe when given to heart failure patients
receiving standard therapy (including
angiotensin-converting enzyme inhibitors) for
this

Calcium channel blockers have powerful

blood pressure-reducing effects, particularly
when com-bined with angiotensin-converting
enzyme inhibitors or angiotensin receptor
blockers. They are equally
effective in all racial and ethnic groups.
The dihydropyridine, but not the
nondihydropyri-dine, agents can be safely
combined with b-blockers.

b-Blockers

ASH/ISH Hypertension Guidelines | Weber et al.

b-blockers reduce cardiac output and also

decrease the release of renin from the kidney.
They have strong clinical outcome benefits in
patients with histories of myocardial
infarction and heart failure and are effective
in the management of
angina pectoris.
They are less effective in reducing blood
pressure in black patients than in patients of
other ethnicities.
b-blockers may not be as effective as the
other major drug classes in preventing stroke
or cardiovascular events in hypertensive
patients, but they are the drugs of choice in
patients with histories of myocardial infarction or heart failure.
Many of these agents have adverse effects on
glucose metabolism and therefore are not
recommended in patients at risk for diabetes,
especially in combina-tion with diuretics.
They may also be associated with
heart block in susceptible patients.
The main side effects associated with bblockers are reduced sexual function, fatigue,
and reduced exercise tolerance.
The combined a- and b-blocker, labetalol, is
widely used intravenously for hypertensive
emergencies, and is also used orally for
treating hypertension in pregnant and
breastfeeding women.

a-Blockers
a-Blockers reduce blood pressure by blocking
arte-rial a-adrenergic receptors and thus
preventing the vasoconstrictor actions of
these receptors.
These drugs are less widely used as first-step
agents than other classes because clinical
outcome benefits have not been as well
established as with other agents. However,
they can be useful in treating resistant
hypertension when used in combination
with agents such as diuretics, b-blockers, and
angio-tensin-converting enzyme inhibitors.
To be maximally effective, they should
usually be combined with a diuretic. Since ablockers can have somewhat beneficial effects
on blood glucose and lipid levels, they can
potentially neutralize some of
the adverse metabolic effects of diuretics.
The a-blockers are effective in treating
benign prostatic hypertrophy, and so can be a
valuable part of hypertension treatment
regimens in older men who have this
condition.
Centrally Acting Agents
These drugs, the most well-known of which
are clonidine and a-methyldopa, work
primarily by reducing sympathetic outflow
from the central nervous system.
They are effective in reducing blood pressure
in most patient groups.
Bothersome side effects such as drowsiness
and dry mouth have reduced their popularity.
Treatment with a clonidine skin patch causes
fewer side effects than the oral agent, but the
patch is not always
available and can be more costly than the
tablets. In certain countries, including the
United States,
a-methyldopa is widely employed for treating
hyper-tension in pregnancy.

Direct Vasodilators
Because these agents, specifically hydralazine
and minoxidil, often cause fluid retention and
tachycar-dia, they are most effective in
reducing blood
pressure when combined with diuretics and bblockers or sympatholytic agents. For this
reason, they are now usually used only as
fourth-line or later
additions to treatment regimens.
Hydralazine is the more widely used of these

Official Journal of the American Society of Hypertension, Inc.

agents. The powerful drug minoxidil is

sometimes used by specialists in patients
whose blood pressures are difficult to control.
Fluid retention and tachycardia are frequent
problems with minoxidil, as well as unwanted
hair growth (particularly in women).
Furosemide is often required to cope with the
fluid retention.
Mineralocorticoid Receptor Antagonists
The best known of these agents is
spironolactone. Although it was originally
developed for the treat-ment of high
aldosterone states, it recently has become part
of standard treatment for heart failure.

The Journal of Clinical Hypertension

ASH/ISH Hypertension Guidelines | Weber et al.

Eplerenone is a newer and better-tolerated

agent, although most experience in difficultto-control hypertension has been with
spironolactone.
In addition, these agents can be effective in
reducing blood pressure when added to
standard 3-drug regimens (angiotensinconverting enzyme inhibitor or angiotensin
receptor blocker/ calcium channel
blocker/diuretic) in treatment-resistant
patients. This may be because aldosterone
excess can contribute to

11

TREATMENT RESISTANT
HYPERTENSION
Hypertension can be controlled (blood
pressure <140/90 mm Hg in most patients) by
using either 1, 2, or 3 drugs as described
earlier (angiotensin-converting enzyme
inhibitor or angiotensin receptor blocker/
calcium channel blocker/diuretic) in full or
maximally tolerated doses. The most widely
used two-drug combination, angiotensinconverting enzyme inhibitors plus either
calcium channel block-ers or diuretics, or
angiotensin receptor blockers plus either
calcium channel blockers or diuretics, can
control blood pressure in about 80% of
patients.

resistant hypertension.
Symptomatic side effects of gynecomastia
(swelling and tenderness of breasts in both
men and women) and sexual dysfunction are
common. These can be minimized by using
spironolactone in a low dose (no more than 25
mg daily) or by using the more selective (but
more expensive) agent, eplerenone.
Hyperkalemia can also become a problem
with these agents, particularly when added to
angiotensin-converting enzyme inhibitors or
angiotensin receptor blockers in patients with
reduced renal function. These agents should
be used with caution when the eGFR is <50.
In particular, when mineralocorticoid receptor
blockers are combined with angiotensinconverting enzyme inhibitors or angiotensin
receptor blockers, potassium levels must be
monitored within
the first month of treatment and then on a
regular basis (every 36 months).

Confirm that the blood pressure is truly

uncontrolled by checking home pressures, or
if available, by using
ambulatory blood pressure monitoring.
For patients not controlled on 3 drugs, adding
a mineralocorticoid antagonist such as
spironolactone,
a b-blocker, a centrally acting agent, an ablocker, or a direct vasodilator will often be
helpful.
If blood pressure is still not controlled it is
important to make certain that patients are
actually taking their medicines. Question their
families, check their pre-scriptions, and ask
questions about side effects to
help confirm compliance with treatment.

Check whether patients are taking other

medicines that can interfere with their
hypertension treatment. For example:
nonsteroidal anti-inflammatory drugs, cold
remedies, and some antidepressants. Also, ask
about diet: blood pressures in some patients
are especially sensitive to factors such as
excessive salt intake.

association. A preliminary diagnosis can be

made by finding a history of snoring during
sleep and daytime tiredness. A definitive
diagnosis usually requires a sleep lab-oratory
study.

Consider secondary causes of hypertension if

all these more simple approaches are
unsuccessful.

FINAL COMMENT

Secondary hypertension can be suggested by

the sudden onset of hypertension, or by the
loss of blood pressure control in patients
previously
well managed or by the occurrence of a
hyper-tension emergency
Chronic kidney disease: this common
secondary cause of hypertension should
normally be revealed by the initial patient
evaluation (eg, laboratory tests of creatinine).
These patients, if possible, should be referred
to a nephrologist.
Aldosterone excess: this is suggested by
hypo-kalemia during the initial evaluation,
although this condition can occur even when
potassium levels appear normal. About 20%
of patients whose blood pressures remain high
despite taking 3 drugs have evidence of
aldosterone excess. Confirming this diagnosis
usually
requires assistance from clinical hypertension
specialists.
Sleep apnea: This is common in obese
patients. Not all patients with sleep apnea
have hyperten-sion but there is a clear
12

The Journal of Clinical Hypertension

Other secondary causes of hypertension such

as renal artery stenosis or coarctation of the
aorta usually require evaluation by a
specialist.

The authors of this statement acknowledge

that there are insufficient published data from
clinical trials in hypertension to create
recommendations that are com-pletely
evidence-based, and so inevitably some of our
recommendations reflect expert opinion and
experience.
We also should point out that because of the
major differences in resources among points
of care it is not possible to create a uniform
set of guidelines. For this reason we have
written a broad statement on the management
of hypertension and have not presumed to
anticipate the conditions or shortfalls that
might exist in particular communities. We
expect that experts who are familiar with
local circumstances will feel free to use their
own judgment in modifying our recommendations and to create practical instructions to
help guide front-line practitioners in
providing the best care possible.

A NOTE TO COLLEAGUES
The authors of this statement would welcome
comments and suggestions from colleagues.
We recognize that in this initial version of the
guidelines there will probably be omissions,
redundancies, and inaccuracies. Please feel
free to get in touch with us either by letters to
the Journal or by personal communication.

Official Journal of the American Society of Hypertension, Inc.

Acknowledgments: This statement was written under the

sponsorship of the American Society of Hypertension and
the International Society of Hyperten-sion. In addition, the
Asia Pacific Society of Hypertension has endorsed these
guidelines. The statement was prepared without any
external funding. The work and time of the authors was
provided by them entirely on a volunteer basis.
Disclosures: MAW: Research funding: Medtronics. Consulting:
Boehringer-Ingelheim, Novartis, Daichi Sankyo, Takeda, Forest.
Speaker: Daiichi Sankyo, Takeda, Forest. ELS: Research
Funding: Canadian Institutes of Health Research, Canada
Research Chairs program of CIHR/Government of Canada,

Servier France. Consultant: Servier, Novartis. Speaker: Forest

Canada, Pfizer Japan. WBW: Research Funding: National
Institutes of Health. Consulting: Safety Committees (DSMB,
CEC, Steering Committees); Ardea Biosciences, Inc.;
AstraZeneca; Dendreon, Forest Research Institute, Inc.; Roche;
St. Judes Medical, Takeda Global Research, Teva
Neuroscience. SM, LHL, JGK, BJM, DLC, JCC, RRJC, ST, AJR,
AES, RMT: No conflicts of interest. JMF: Research Funding:
Novartis, Medtronic. Consultant: Novartis, Medtron-ic, Back Beat
Hypertension. BLC: Research Funding: NIH and VA. VSR: Consultant: Medtronic, Daiichi-Sankyo, Forest. DK: Research
Funding: Medtronic. RT: Research Funding: NIH. Consultant:
Medtronic, Janssen, Merck, GSK. JC: Research Funding and
Speaker: Servier in relation to ADVANCE trial and Post-trial
study. GLB: Research Funding: Takeda. Consultant: Takeda,
AbbVie, Daiichi-Sankyo, Novartis, CVRx, Medtronic, Relypsa,
Janssen, BMS. JW: Consultant and Speaker: BoehringerIngelheim, MSD, Novartis, Omron, Pfizer, Servier, and Takeda.
JDB: Research and Consultant: CVRx. DS: Research:
Medtronic, CVRx. Consultant: Takeda, UCB, Novartis, Med-

tronic, CVRx. Speaker: Takeda. SBH: Speaker: Novartis,

Servier.

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