Transcript Aliskiren

Current trends and controversies in the diagnosis
and treatment of hypertension
Focus on the Renin Angiotensin Aldosterone
System and Direct Renin Inhibition
Tom Smiley BScPhm, PharmD
CCCEP File 853-0109L1FT
Disclosure

Tom Smiley has previously prepared and
delivered pharmacist education sponsored
by Novartis Inc.
The Canadian Council on Continuing Education in Pharmacy has
accredited this program for 2 CEUs (CCCEP File # 853-0109L1FT)
Supported by an educational grant from Novartis Canada Inc.
2
Learning Objectives
After successful completion of this workshop
pharmacists will be better able to:






Discuss care gaps in current treatment of hypertension
Discuss pathophysiology of RAAS and mechanisms of RAAS
inhibition
Discuss efficacy and tolerability of direct renin inhibition on
hypertension
Assess and recommend appropriate blood pressure monitoring and
hypertension management according to CHEP Guidelines
Discuss the renal outcome evidence for the benefit of RAAS
blockade in patients with type 2 diabetes
Discuss alternatives to ACE-I + ARB combination
3
Current trends and
controversies in the diagnosis
and treatment of hypertension
Part 1: A Pharmacist’s
Perspective
Tom Smiley BScPhm, PharmD
What percent of Canadians have
hypertension?
% of Canadians
60
50
40
30
20
10
0
18-24
25-34
44-55
35-44
56-65
65-74
age
CCHS CMAJ 1992
5
Changes in Management of
Hypertension in Canada
Large Treatment Gap Still Exists in
Diabetes
(DM 9)
BUT ONLY 37% Control in
Pts with Diabetes
Joffres, et al. Am J Hyper 2001; 14: 1099-1105
6
Effect of SBP and DBP on
Age-Adjusted CAD Mortality: MRFIT
Domanski M et al. JAMA 2002;287:2677-2683
7
Risk of Cardiovascular Event (aged 75-94)
Age Adjusted ave Annual Incidence /1000
140
140
120
120
SBP
100
Men
Women
DBP
100
80
80
60
60
40
40
20
20
0
0
74-119
120-139
140-159
160-179
180-300
20-74
75-84
85-94
95-104
105-160
Blood Pressure
Kannel, Am J Hypertens 2000;13:3S-10S.
8
Lowering BP Reduces Cardiovascular
Risk
Small SBP reductions yield significant benefit
Meta-analysis of 61 prospective, observational studies
One million adults, 12.7 million person-years
7% reduction in risk of
ischemic heart-disease
(IHD) mortality
2 mm Hg
decrease in mean
SBP
10% reduction in risk
of stroke mortality
Lewington S, et al. Lancet 2002;360:1903
9
Average Number of BP Medications to Achieve Goals
**UKPDS (<85 mm Hg – Diastolic*)
**ABCD (<75 mm Hg – Diastolic*)
MDRD (<92 mm Hg MAP*)
**HOT (<80 mm Hg Diastolic*)
AASK (<92 mm Hg MAP*)
* Individual Study BP Targets
** Diabetic Patients
1
2
Number of BP Meds
3
4
CHEP 2008: Consider initiating therapy with a combination of
first line drugs if BP is 20 mmHg systolic or 10 mmHg diastolic
Bakris GL et al. Special Report on DM and HTN
above target
Am J Kidney Dis 2000;36:646-661
10
The Renin Angiotensin
Aldosterone System
(RAAS)
Classic understanding of RAAS
Angiotensinogen
Ang I
Renin
ACE
Ang II
Aldosterone
AT1 Receptor
Na+/H2O
retention
Vasoconstriction
Hypertension
Adapted from: Laragh JH. 1989
12
ACEIs and ARBs cause compensatory rises in
Plasma Renin Activity (PRA)
Consequences in RAS Activation
Non ACE
pathways
Angiotensinogen
Ang I
Renin
KIDNEY
 Glomerular
vasoconstriction
 Inflammation
 Fibrosis
HEART
FEEDBACK LOOP
 Hypertrophy
 Fibrosis
 Vasoconstriction
PRA
ACEIs
VESSELS
Ang II
AT1 Receptor
BIOLOGICAL EFFECTS
ARBs
 Hyperplasia
hypertrophy
 Inflammation
 Oxidation
 Fibrosis
BRAIN
 Vasoconstriction
Adapted from: Müller DN & Luft FC. 2006
13
New understandings in the
cardiovascular continuum:
The central role of angiotensin II
Remodeling
Myocardial
infarction &
stroke
Congestive heart
failure/secondary
stroke
Microalbuminuria
Atherosclerosis
and LVH
Ventricular dilation/
cognitive
dysfunction
Macroproteinuria
Nephrotic
proteinuria
Endothelial
dysfunction
Hypertension risk factors
Diabetes, obesity, elderly
End-stage heart
disease, brain
damage and dementia
End-stage
renal disease
Angiotensin II
Cardio/
cerebrovascular
death
Adapted from Dzau V, Braunwald E. Am Heart J. 1991;121:1244-1263.
14
Angiotensin II in
atherosclerosis
Autostimulation
Tissue
remodeling
Proliferation
fibrosis
Oxidative stress
Thrombosis
Endothelial
dysfunction
Inflammation
Angiotensin II
15
Physiologic effects of RAAS
activation




Exerts significant effects on cardiovascular
and renal function
Many aspects of cardiovascular disease
progression can be directly linked to the
RAAS system
Vascular inflammation, generation of
reactive oxygen species and endothelial
dysfunction play a role in atherosclerosis
Activation of the RAAS system is central to
these multiple pathways
16
Physiologic effects of RAAS
inhibition




Reduces systemic vascular resistance
Lowers blood pressure
Vasodilatation occurs, preferentially in the
vital organs leading to a redistribution of blood flow
In the kidneys RAAS inhibition increases effective renal
blood flow and alters intrarenal hemodynamics
 Dilates the efferent more than the afferent arterioles
 Intraglomerular pressure drops
17
18
19
19
Benefits of RAAS Inhibition
beyond BP lowering





End-organ protection: Kidney
Vascular protection: Vessel wall and vascular
endothelium
 RAAS inhibitors improve carotid intima-media
thickness (IMT) (Lonn 2001), vascular remodeling,
endothelial function (Schiffrin 2000), and arterial
compliance (Asmar 1988)
Regression of left ventricular hypertrophy
Prevention of de novo diabetes mellitus
 Several mechanisms have been hypothesized for this
including hemodynamic effects and nonhemodynamic effects
(Jandeleit-Dahm 2005)
Reduction in risk of stroke, coronary artery disease and
heart failure
20
Risk Reduction for stroke, CAD and HF
associated with RAAS Inhibition





Prevention of morbidity and mortality from cardiovascular
events is a major treatment goal
ACE inhibitors are known to be vasculo-protective
Outcome trials (HOPE, EUROPA) demonstrated the
beneficial role of ACE inhibition
HOPE showed effectiveness of ramipril in preventing
major CV events in high-risk patients with and without
hypertension
EUROPA showed perindopril reduces CV events in
patients with coronary heart disease without apparent
heart failure
21
Angiotensin II receptor blockers (ARBs)



Clinical trials (e.g., LIFE, REGAAL, CATCH)
show that ARBs induce LVH regression
ARBs achieve LVH regression through
efficient BP-lowering effects and inhibition of
angiotensin II
ARBs inhibit all of the actions of angiotensin II
mediated through AT1 receptors

Unlike ACE-Is, which allow some production of
angiotensin II via non-ACE pathways
Carson PE. Am Heart J 2000;140:361
Dahlöf B, et al. Lancet 2002;359:995
22
LIFE results

ARB benefits beyond BP-lowering effects


Patients with ECG signs of LVH (13% with diabetes)
The risk of death, MI, or stroke was reduced by 13%
with the ARB compared with the β-blocker (P = .02)



This occurred despite similar BP reduction
The difference in risk is primarily explained by a
significant (25%) reduction in risk of fatal/non-fatal
stroke
The difference was even more significant in diabetic
patients
Dahlöf B, et al. Lancet 2002;359:995
23
The Newest Class Of Anti-Hypertensive Agents
DIRECT RENIN
INHIBITORS
24
Aliskiren binds to active site of
renin
Renin
Aliskiren
Angiotensinogen
Ang I
Aliskiren binds to a
pocket in the renin
molecule, blocking
cleavage of
angiotensinogen to
angiotensin I
Adapted from Rahuel J et al. J Struct Biol. 1991;107:227-236.
25
Aliskiren reduces Ang I, Ang II and PRA
Direct renin inhibitor
Angiotensinogen
Non ACE pathways
Ang I
Renin
ACE
PRA
FEEDBACK LOOP
ACEIs
Ang II
ARBs
AT1 Receptor
BIOLOGICAL EFFECTS
ACEI
ARB
Aliskiren
Azizi M et al. 2006
Ang I
Ang II
Renin
PRA
↑
↑
↓
↓
↑
↓
↑
↑
↑
↑
↑
↓
26
Introduction to Direct Renin
Inhibitors (DRIs)

Newest class of RAAS-active antihypertensives





Aliskiren is the agent with the most comprehensive evidence to
date
Inhibit the ability of renin to cleave angiotensinogen to
form angiotensin I
Reduce angiotensin II levels
Associated with rise in plasma renin concentration, but
no rise in plasma renin activity (PRA)
May also partially inhibit the binding of prorenin to its
receptor (Clinical effects unknown)
Danser AH: J Cardiovasc Pharmacol 2007; 50(2):105-11.
27
27
Direct Renin Inhibitors
HYPERTENSION
STUDIES
28
Sustained 24-hour BP Control
with the DRI Aliskiren
T/P ratio
Placebo (n=53)
Aliskiren 150 (n=52)
Aliskiren 300 (n=56)
Aliskiren 600 (n=55)
Mean ambulatory BP (mmHg)
Systolic
160
–
0.64
0.98
0.86
150
140
130
120
110
Early
morning
surge
Diastolic
100
90
80
70
60
08:00
12:00
16:00
20:00
Time (hours)
T/P: trough/peak
Adapted from Ruilope LM, et al. Abstract and poster presented at ESC 2007.
00:00
04:00
08:00
29
29
Efficacy with DRI Hypertension
Trials: Monotherapy

The efficacy of aliskiren has been
extensively studied in monotherapy
compared to:
Placebo1,2
 Active Control:

ARB (irbesartan)2
 ACE (ramipril)3
 Diuretics (HCTZ)4

1. Oh B-H, et al: JACC 2007;49(11):1157-63.
2. Gradman AH, et al: Circulation. 2005;111:1012–1018.
3. Andersen K, et al: J Am Coll Cardiol 2007;49(Suppl A):371A 1014-173
4. Schmieder RE, et al: J Clin Hypertens 2007; 9(Suppl A)(5):A182.
30
30
Efficacy in DRI Hypertension Trials:
Monotherapy
Trial & primary
outcome
Oh et al (2007)
Change in msBP vs.
placebo from BL to wk 8
Gradman et al (2005)
Change in trough msBP
from BL to wk 8
Regimens
4 groups:
- Aliskiren 75, 150, 300 mg o.d.
- Placebo
5 groups:
- Aliskiren 150, 300, 600 mg o.d.
- Irbesartan 150 mg o.d.
- Placebo
Duration
(n)
Conclusions
8 weeks
(n = 672)
Aliskiren provides significant
antihypertensive efficacy,, with no
rebound effects on BP after
treatment withdrawal.
8 weeks
(n = 652)
Aliskiren lowers BP effectively;
aliskiren 150 mg is as effective as
irbesartan 150 mg.
Safety and tolerability of aliskiren
were comparable to irbesartan and
placebo.
Andersen K et al (2007)
Change in msBP from
BL to wk 6
2 groups:
- Aliskiren 150 mg o.d. (option to titrate to 300
mg)
- Ramipril 5 mg o.d. (option to titrate to 10 mg)
12 weeks
(n = 842)
Aliskiren 150 mg provided
significantly greater reductions in
msSBP compared with ramipril 5
mg.
Reductions in MSDBP were similar
with aliskiren 150 mg and ramipril
5 mg at Week 6.
Schmieder et al (2007)
Change in msBP from
BL to wk 26
3 groups:
- Aliskiren 150 mg o.d. (forced titration to 300
mg, then option to add amlodipine)
- HCTZ 12.5 mg o.d (forced titration to 25 mg,
then option to add amlodipine)
- Placebo (randomized to one of the above
groups at week 6)
52 weeks
(n =
1124)
Aliskiren-based therapy provides
greater long-term BP-lowering than
HCTZ-based therapy over up to 12
months of treatment.
31
31
Direct Renin Inhibitors
DUAL RAAS
BLOCKADE
32
Rationale for ARB/ACEI + DRI combinations
Ang II
production
Further
lowering of
BP and
potential endorgan
protection
Complementary
Mechanism
PRA
Peripheral
vasoconstriction
& hypertension
Compensatory
response mechanism
blocked with DRI
ARBs /
ACEIs
BP
Stimulation
of RAS
& SNS
DRI
33
Combination Therapy with DRIs:
Efficacy

The efficacy of aliskiren was extensively
studied in combination with other
antihypertensive agents:
ACE inhibitor (ramipril)1
 Diuretic (HCTZ)2
 ARB (valsartan)3
 CCB (amlodipine)4

1. Uresin Y, et al: J Renin Angiotensin Aldosterone Syst 2007; 8(4):190-8.
2. Villamil A, et al: J Hypertens 2007; 25:217-226.
3. Oparil S, et al: Lancet 2007; 370(9583):221-9.
4. Drummond W, et al: J Clin Hypertens (Greenwich) 2007; 9(10):742-50.
34
34
Efficacy in DRI Hypertension Trials:
Combination Therapy
Trial & primary
outcome
Regimens
Villamil et al
(2007)
Change in
MSBP from BL
to wk 8
15 groups:
- 3 HCTZ mono: 6.25, 12.5, 25 mg
- 3 Aliskiren mono: 75, 150, 300 mg
- 8 different HCTZ/aliskiren combinations
- 1 Placebo
Drummond et
al (2007)
Change in BP
from BL to wk 6
3 groups:
- Amlodipine 5 mg
- Amlodipine 10 mg
- Amlodipine 5 mg + aliskiren 150 mg
Uresin et al
(2007)
Change in BP
from BL to wk 8
3 groups:
- Aliskiren 150 mg → 300 mg
- Ramipril 5 mg → 10 mg
- Aliskiren 150 mg / ramipril 5 mg → 300
/ 10 mg
Oparil et al
(2007)
Change in BP
from BL to wk 8
4 groups:
- Valsartan 160 mg → 320 mg
- Aliskiren 150 mg → 300 mg
- Valsartan 160 mg + aliskiren 150 mg →
320 / 300 mg
- Placebo
Duration
(n)
8 weeks
(n = 2776)
Conclusions
Aliskiren monotherapy
demonstrated significant BP
lowering; effect considerably
greater combined with HCTZ.
6 weeks
(n = 545)
Aliskiren 150 mg + amlodipine 5
mg showed BP-lowering efficacy
similar to amlodipine 10 mg and
was better tolerated.
8 weeks
(n = 837)
Combining aliskiren with ramipril
provided a greater reduction in BP
than either drug alone in diabetic
patients.
8 weeks
(n = 1797)
The combination of aliskiren and
valsartan at maximum
recommended doses provides
significantly greater reductions in
BP than either agent alone.
35
35
Aliskiren Provides Additional
BP Lowering When Added to
Other Antihypertensive Agents
Treatment dose (mg)
Ramipril 10 Valsartan 160
HCTZ 25
175 187 173
Amlodipine 5
+ aliskiren
300
+ aliskiren
150
177 188
−5.0
+
aliskiren150
188 184 180
+ aliskiren 300
58
+ aliskiren 150
−20
60
HCTZ 12.5
+ aliskiren 300
−10
60
+ aliskiren
150
−5
−15
58
+ aliskiren 300
0
n = 275 274
Valsartan 320
−11.0
−12.0
−13.9
−16.6
†
−15.5
−16.6
†
−14.3
−17.6
−16.5
−18.0
−25
*
−19.8
*
−19.5
*
−21.2
*
Change from baseline in msSBP (mmHg)
*p < 0.05; †p < 0.0001 vs respective monotherapies
Adapted from Weir MR, et al: J Am Soc Hypertens 2007; 1(4):264–77.
36
36
Efficacy with DRI Therapy
in Hypertension Trials:
Different Populations

The efficacy of aliskiren has been extensively
studied in the following populations:
 Young and elderly1
 Obesity2
 Diabetes3
 Metabolic syndrome4,5
 Impaired renal function6
1. Dahlöf B, et al: J Clin Hypertens 2007; 9(Suppl. A):A157 [abstract P-376].
2. Prescott MF, et al: Int J Obes 2007; 31(Suppl. 1):S99 [abstract T2:PO.88].
3. Taylor AA, et al:. Diabetes 2007; 56(Suppl. 1):A129 [abstract 483-P].
4. White WB, et al: Eur Heart J 2007; 28(Suppl 1):868 [abstract P4845].
5. Krone W, et al: Presented at AHA 2008; Abstract #4433.
6. Weir MR, et al: J Am Soc Hypertens 2007; 1(4):264-277.
37
37
Aliskiren Provides Effective BPlowering in Patients with Impaired
Renal Function: Pooled Analysis
DBP
0
SBP
eGFR <60
eGFR ≥60
n=26
n=740
n=25
n=736
eGFR <60
n=26
n=25
eGFR ≥60
n=740
n=736
5
10
–10.4
–9.4
–11.4
–10.1
–11.2
–11.5
15
–14.7
–14.9
Mean change from baseline in mean sitting BP after 8 weeks (mmHg)
Aliskiren 150 mg
Aliskiren 300 mg
eGFR: estimated glomerular filtration rate (assessed in mL/min/1.73 m2)
38
38
Weir MR, et al. 2007 (Pooled analysis)
Tolerability of
Aliskiren
39
39
Aliskiren monotherapy: Tolerability
Any SAE, n (%)
Any AE, n (%)
Discontinuations
due to AE, n (%)
Placebo
Aliskiren
Aliskiren
Aliskiren
n = 781
75 mg
150 mg
300 mg
n = 478
n = 774
n = 768
All
Aliskiren+
n = 2316
5 (0.6)
3 (0.6)
3 (0.4)
4 (0.5)
11 (0.5)
314 (40.2)
193 (40.4)
290 (37.5)
309 (40.2)
922 (39.8)
27 (3.5)
8 (1.7)
12 (1.6)
20 (2.6)
45 (1.9)
Adverse events, reported by ≥2% of patients for aliskiren monotherapy overall, n (%)
Headache
Nasopharyngitis
Diarrhoea
68 (8.7)
31 (6.5)
42 (5.4)*
44 (5.7)*
132 (5.7)**
45 (5.8)
34 (7.1)
33 (4.3)
29 (3.8)
101 (4.4)
9 (1.2)
6 (1.3)
9 (1.2)
18 (2.3)
61 (2.6)*
AE, adverse event; SAE, serious adverse event. *p<0.05; **p<0.01
+ = Include data from patients taking 600 mg (n=296)
Weir M, et al. WCC 2006 (Pooled analysis)
40
Aliskiren/ramipril Combination
Ramipril
monotherapy*
(n=278)
Aliskiren
monotherapy*
(n=282)
Aliskiren
/ramipril
combination
therapy* (n=277)
33.8
32.3
30.0
Serious AEs
2.2
2.8
1.4
Discontinuation due to AEs
4.0
3.9
2.2
11.9
7.4
6.1
Headache
6.1
3.2
2.9
Cough
4.7
2.1
1.8
Nasopharyngitis
1.8
3.2
1.1
Diarrhoea
2.5
1.1
1.1
Any AE
Treatment-related AEs
Most frequent AEs (³2% in any group)
*Patients received aliskiren 150 mg, ramipril 5 mg, or aliskiren/ramipril 150/5 mg od. After 4 weeks, patients were titrated
to aliskiren 300 mg, ramipril 10 mg or aliskiren/ramipril 300/10 mg for an additional 4 weeks
When aliskiren was combined with an ACE inhibitor in patients with diabetes and hypertension, increases in serum
1.Uresin Y, et al. 2007 (Study 2307)
potassium (> 5.5 mmol/L) occurred in 5.5% of the patients 2.
2. Rasilez® Product Monograph, March 13, 2008
41
HCTZ plus Aliskiren or Amlodipine: Incidence of
Edema in Patients with Obesity and Hypertension
Aliskiren/
Irbesartan/
Amlodipine/
HCTZ
HCTZ
HCTZ
HCTZ
alone
n = 122
n = 119
n = 126
n = 122
48 (39.3)
43 (36.1)
57 (45.2)
47 (38.5)
Discontinuations
due to AE, n (%)
2 (1.6)
4 (3.4)
7 (5.6)
4 (3.3)
SAEs, n (%)
2 (1.6)
3 (2.5)
4 (3.2)
4 (3.3)
Any AE, n (%)
AEs, reported by ≥2% of patients in any treatment group, n (%)
Nasopharyngitis
10 (8.2)
6 (5.0)
7 (5.6)
5 (4.1)
Headache
5 (4.1)
3 (2.5)
9 (7.1)
4 (3.3)
Dizziness
4 (3.3)
3 (2.5)
1 (0.8)
2 (1.6)
Peripheral oedema
1 (0.8)
1 (0.8)
14 (11.1)
2 (1.6)
Back pain
1 (0.8)
2 (1.7)
5 (4.0)
5 (4.1)
AE, adverse event; SAE, serious adverse event
Jordan J, et al. 2007 (Study 2309)
42
Aliskiren In Hypertension
Clinical Summary

Aliskiren 150–300 mg:
 provides dose-dependent reductions in DBP and SBP
as monotherapy




BP reductions from baseline greater than HCTZ and ramipril and
similar to irbesartan
provides additional BP lowering when combined with
other antihypertensives (see next slide)
provides sustained 24-hour BP control with prolonged
effect after discontinuation
Rates of adverse effects are similar to placebo

Increases in serum potassium are infrequent in patients
with hypertension treated with aliskiren alone. When used
in combination with another RAS agent, increases in serum
potassium may be more frequent
43
43
Aliskiren In Hypertension
Clinical Summary

The combination of aliskiren with other antihypertensive
agents, such as ACE inhibitors, ARBs, dihydropyridine
CCBs, or thiazide diuretics, is well tolerated
 When combined with ramipril, aliskiren appears to
reduce the incidence of cough
 Long-term combination therapy with aliskiren and
valsartan is well tolerated
 The combination of aliskiren and amlodipine results in
a lower incidence of edema compared with increasing
the amlodipine dose
 In obese patients who fail to respond adequately to
diuretic monotherapy, adding aliskiren results in fewer
incidences of peripheral oedema than adding
amlodipine
44
44
Supporting Appropriate
Assessment and Monitoring
of Blood Pressure
45
Criteria for the diagnosis of hypertension and
recommendations for follow-up
BP: 140-179 / 90-109
Clinic BP
ABPM (If available)
Home BPM (If available)
Hypertension visit 3
>160 SBP or
>100 DBP
<160 / 100
Diagnosis
of HTN
or
ABPM or HBPM if
available
Awake BP
<135/85
and
24-hour
<130/80
Awake BP
>135 SBP or
< 135/85
>85 DBP or
or
Continue to
follow-up
Diagnosis
of HTN
Hypertension visit 4-5
>140 SBP or
>90 DBP
Diagnosis
of HTN
< 140 / 90
Continue to
follow-up
>135/85
24-hour
>130 SBP or
>80 DBP
Continue to
follow-up
Diagnosis
of HTN
Patients with high normal blood pressure (clinic SBP 130-139 and/or DBP 85-89) should be followed
annually.
2008 CHEP Recommendations
46
Criteria for the diagnosis of hypertension and
recommendations for follow-up
Diagnosis of hypertension
Non Pharmacological treatment
With or without Pharmacological treatment
Are BP readings below target during 2 consecutive visits?
Yes
Follow-up at 3-6
month intervals *
No
Symptoms, Severe
hypertension, Intolerance to
anti-hypertensive treatment
or Target Organ Damage
Yes
More frequent
visits *
No
Visits every 1 to 2
months*
* Consider Home measurement in hypertension management, to screen for masked
hypertension or white coat effect and to enhance adherence.
2008 CHEP Recommendations
47
Assessment of the overall cardiovascular risk
Search for exogenous potentially modifiable factors that
can induce/aggravate hypertension

Prescription Drugs:









NSAIDs, including Coxibs
Corticosteroids and anabolic steroids
Oral contraceptive and sex hormones
Vasoconstricting/sympathomimetic decongestants
Calcineurin inhibitors (cyclosporin, tacrolimus)
Erythropoietin and analogues
Monoamine oxidase inhibitors (MAOIs)
Midodrine
Other:





Licorice root
Stimulants including cocaine
Salt
Excessive alcohol use
Sleep apnea
2008 CHEP Recommendations
48
Home measurement of blood pressure
Home BP measurement should be encouraged to increase
patient involvement in care
Which patients?
•
•
•
•
•
•
Uncomplicated hypertension
Diabetes mellitus
Chronic kidney disease
Suspected non adherence
Office-induced blood pressure elevation (white coat effect)
Masked hypertension
Average BP equal to or over 135/85 mm Hg should be considered elevated
2008 CHEP Recommendations
49
Potential advantages of home blood
pressure measurement






More rapid confirmation of the diagnosis of
hypertension
Improved ability to predict cardiovascular
prognosis
Improved blood pressure control
Can screen for white coat hypertension (WCH)
and masked hypertension
Reduced medication use in some (WCH)
Improved adherence to drug therapy in the non
adherent
2008 CHEP Recommendations
50
Not all patients are suited to home
measurement





Undue anxiety in response to high blood
pressure readings
Physical or mental impairment prevents
accurate technique or recording
Arm not suited to blood pressure cuff (e.g.
conical shaped arm)
Irregular pulse or arrhythmias prevent
accurate readings
Lack of interest
The vast majority of patients can be trained to measure
blood pressure
2008 CHEP Recommendations
51
Suggested Protocol for Home Measurement
of Blood Pressure for the diagnosis of
hypertension
Home blood pressure values should be based
on:
- duplicate measures,
- morning and evening,
- for an initial 7-day period.
Singular and first day home BP values should
not be considered.
Daytime average BP equal to or over 135/85
mmHg should be considered elevated.
2008 CHEP Recommendations
52
Home BP Measurement:
CHEP Recommendations

Encourage hypertensive patients to use an
approved blood pressure measuring
device and use proper technique to
assess blood pressure at home

Measuring blood pressure at home has a
stronger association with cardiovascular
prognosis than office-based readings
2008 CHEP Recommendations
53
Blood Pressure Assessment:
Patient preparation and posture
Standardized technique:
Patient
1. No caffeine in the preceding hour.
2. No smoking or nicotine in the preceding 15-30
minutes.
3. No use of substances containing adrenergic
stimulants such as phenylephrine or
pseudoephedrine (may be present in nasal
decongestants or ophthalmic drops).
4. Bladder and bowel comfortable.
5. Quiet environment. Comfortable room
temperature for 5 minutes.
6. No tight clothing on arm or forearm.
7. No acute anxiety, stress or pain.
8. Patient should stay silent prior and during the
procedure.
2008 CHEP Recommendations
54
Blood Pressure
Assessment:
Patient position
2008 CHEP Recommendations
55
CHEP-recommended Electronic BP
Monitors for Home BP Measurement
Monitors that have been validated as accurate and available
in Canada are listed at www.hypertension.ca/chs.
They are also marked with
.
“Recommended by the Canadian Hypertension Society”
See speaker notes for recommended model numbers
Adapted from Approved Home BP Devices. www.hypertension.ca
2008 CHEP Recommendations
56
Use an appropriate size cuff
Arm circumference (cm)
Size of Cuff (cm)
From 18 to 26
9 x 18 (child)
From 26 to 33
12 x 23 (standard adult
model)
From 33 to 41
15 x 33 (large, obese)
More than 41
18 x 36 (extra large,
obese)
For automated devices, follow the manufacturer’s directions.
For manual readings using a stethoscope and sphygmomanometer, use the table as a guide .
2008 CHEP Recommendations
57
Home Measurement of BP:
Patient Education
How to?
Use devices:
• appropriate for the individual
• appropriate cuff size
• have met the criteria of the AAMI
and or the BHS and or IP
Adequate patient training in:
• measuring their BP
• interpreting these readings
Values over
135 / 85 mm Hg
should be
considered elevated
Home measurement can help
to improve patient adherence
Regular verifications
• accuracy of the device
• measuring techniques
AAMI=Association for the Advancement of Medical Instrumentation;
BHS=British Hypertension Society; IP: International Protocol.
2008 CHEP Recommendations
58
Home Measurement of BP: Patient Education
Assist patients select a model with the
correct size of cuff
Measure and record the patients mid arm circumference
so they can match it to cuff size
Recommend devices listed at
www.hypertension.ca or marked with this
symbol
Ask patients to carefully follow the
instructions with device and to record
only those blood pressure where they
have followed recommended procedure
Check the device accuracy on the patient
after purchase and periodically thereafter
(e.g. annually)
Advise patients that average readings equal
to or over 135/85 mmHg are high
Values equal to or over
135 / 85 mm Hg
should be
considered elevated for
those without diabetes
or chronic kidney
disease
Home measurement can
help to improve patient
adherence
a lower threshold is appropriate for those with diabetes
or chronic kidney disease
2008 CHEP Recommendations
59
Summary I
Regarding the treatment of hypertension, the recommendations
endorse:
• ASSESSMENT OF BLOOD PRESSURE AT ALL
APPROPRIATE VISITS
• Most Canadians will develop hypertension during their
lives. Routine assessment of blood pressure is required
for early detection and risk management
• ENCOURAGE APPROPRIATE PATIENTS TO MONITOR
BLOOD PRESSURE AT HOME
• Most can assess blood pressure at home. Home
measurement can confirm a diagnosis of hypertension,
improve adherence to drug treatment, improve control
rates and screen for those with white coat hypertension
and masked hypertension.
2008 CHEP Recommendations
60
Summary II
Regarding the treatment of hypertension, the
recommendations endorse:

INDIVIDUALIZING THERAPY


consider concomitant risk factors and/or concurrent
diseases, other patient characteristics and preferences
(e.g. age, diabetes, CVD) and other considerations e.g.
costs
LIFESTYLE MODIFICATION


To prevent hypertension
In those with hypertension alone if effective to reach the
goal value or in combination with pharmacological
treatment
2008 CHEP Recommendations
61
Summary III
Regarding the treatment of hypertension, the
recommendations endorse:


TREATING TO TARGET BP
 treat aggressively using combinations of drugs
and lifestyle modification to achieve
individualized target
PROMOTING ADHERENCE
 a multi-faceted approach should be used to
improve adherence with both non
pharmacological and pharmacological
strategies
2008 CHEP Recommendations
62