Ht12 - GP education seminar
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147 The number of different anti-
hypertensives in Mims
3 The number of guidelines applicable
to Hypertension with largely dissimilar recommendations
Australian GuidelinesEvidence Base
1 The number of studies it took for
the Australian guidelines to recommend a treatment pathway based on a drug which is not available in
AUSTRALIA
10
The number of promotional mail-outs received per week by GPs in 2008
Choice, August 2008
Measurement Lifestyle factors When to investigate for secondary
causes, and when not to Postural hypertension New drugs on the horizon New procedures
Targets
What to do if you don’t hit targets Should there be targets? Are the targets correct
Hypertension
Exciting new horizons and updates
Sunday 1st April 2012
Dr Alistair Begg
Consultant cardiologist Ashford Heart Centre Conflicts of interest…presentations
for various pharmaceutical companies on hypertension
HYPERTENSION IS ASSOCIATEDWITH NUMEROUS COMORBIDITIES
Comorbidity Hypertension involvement
Coronary artery disease 50% of patients with coronary artery disease have hypertension1
Left ventricular hypertrophy
15 to 20% of hypertensive adults have an increased left ventricular mass2
Ischaemic stroke 77% of patients who have a first stroke have a blood pressure >140/90 mmHg3
Chronic kidney disease8 to 15% of hypertensive adults have decreased renal function4
30 to 40% of patients with microalbuminuria have hypertension5
Diabetes 75% of added cardiovascular risk in diabetic patients is attributable to hypertension6
Peripheral artery disease 74% of patients with peripheral artery disease have hypertension7
Reference: 1.Pepine CJ. Am J Cardiol 1998;82(3A):21H-24H; 2. Diamond JA, Phillips RA. Hypertens Res 2005;28:191-202; 3.
Rosamond W, et al. Circulation 2008; Reference: 1. National Heart Foundation of Australia (National Blood Pressure and Vascular Disease Advisory Committee). Guide to management of hypertension 2008; Available at: www.heartfoundation.org.au. Accessed: January 2009.117:e25-146; 4.Segura J, et al. Curr Opin Nephrol Hypertens 2004;13:495-500; 5. Volpe M. Int J Clin Pract 2008;62:97-108; 6. El-Atat F, et al. Curr Hypertens Rep 2004;6:215-23; 7.Selvin E, Erlinger TP. Circulation. 2004;110:738-43.
National Heart Survey 2004-2005
Prevalence of hypertension (%)*
*Weighted estimates Self-reported hypertension Australian Bureau of Statistics 2006
45.0
40.0
35.0
30.0
25.0
20.0
15.0
10.0
5.0
0.0Children 0-14
yearsChildren 15-17
years18-64 years 65-75 years 75 years and
over
0.1 0.1
9.1
38.041.0
Pre
vale
nce
of H
yper
tens
ion
(%)*
Classification of BP in Australian National Heart Foundation GuidelinesDiagnostic category Systolic
(mmHg)Diastolic (mmHg)
Normal <120 <80
High-normal 120-139 80-89
Grade 1 (mild) hypertension 140-159 90-99
Grade 2 (moderate) hypertension 160-179 100-109
Grade 3 (severe) hypertension ≥ 180 ≥ 110
Isolated systolic hypertension ≥ 140 <90
Isolated systolic hypertension with widened pulse pressure
≥ 160 ≤ 70
National Heart Foundation of Australia. Guide to management of Hypertension, 2008.
Cerebrovascular disease
Cardiovascular Mortality Risk Doubles with each 20/10 mmHg Increase in Usual Systolic/Diastolic BP*
Systolic BP/Diastolic BP (mmHg)
Ris
k of
dea
th f
rom
IH
D a
nd o
ther
va
scu
lar
caus
es (
excl
udin
g st
roke
)*
8
6
4
2
0115/75 135/85 175/105
1X risk 2X risk4X risk
8X risk
155/95
*Individuals aged 40–69 years Adapted from Lewington et al. Lancet 2002;360:1903–13
TREATMENT TARGETS
National Heart Foundation Guidelines: Target BP Goals in Adults
Patient Group Target (mmHg)
People with proteinuria >1 g/day(with or without diabetes)
<125/75
People with associated condition/s or end organ damage:
coronary heart disease, diabetes, chronic kidney disease, proteinuria (> 300 mg/day), or Stroke/TIA*
< 130/80
People with none of the following:coronary heart disease, diabetes, chronic kidney disease, proteinuria (> 300 mg/day), or Stroke/TIA*
< 140/90
*TIA: transient ischaemic attack National Heart Foundation of Australia. Guide to management of Hypertension, 2008.
Consequences of doctors failing to meet hypertension targets
Title and artist 1 the downfall of man Raffaella Sazio da
Urbino 2 expulsion of adam and eve Michaelangelo di Lodoviro Buonarotti3 The wrath of God Leonardo da Vinci4 the moment of mortal Sin Peter Paul Rubens
Across the Ditch
In New Zealand, there is no numerical BP target.
They recommend you reduce the overall CV risk by a certain amount
Figure 5
Source: American Journal of Medicine, The 2010; 123:719-726 (DOI:10.1016/j.amjmed.2010.02.014 )
Copyright © 2010 Terms and Conditions
Targets The J curve is real Nadirs are probably age depndent Nadirs are very important in Ischaemic
heart disease patients Treatment should be lightenned
at110/60, and maybe at higher levels in the elderly
These nadirs hold in the diabetic,”lower the better” is not strictly true
MEASURING BLOOD PRESSUREACCURATELY IN THE CLINIC1
Practice tips• Service mercury sphygmomanometers annually
• Calibrate non-mercury sphygmomanometers every 6 months
• In new patients, measure BP on both arms
• In patients with suspected orthostatic hypotension, measure BP both sitting and standing
• Ensure patient has not had caffeine/caffeinated soft drink/coffee before having BP reading
Reference: 1. National Heart Foundation of Australia (National Blood Pressure and Vascular Disease Advisory Committee). Guide to management of hypertension 2008; Available at: www.heartfoundation.org.au. Accessed: January 2009.
Left subclavian stenosis
PTCA/stent to sublavian stenosis
BP measurement outside the clinic 15% have isolated clinic or white coat HT Similar proportion have normal clinic BP
but high ambulatory BP (often referred to as ‘masked’,or’reverse white coat’,or isolated ambulatory HT
Normal ambulatory BP values lower than clinic readings ie
Daytime less than 135>85 mm Hg Nocturnal <120/70 mm Hg Over 24 hrs <130/80
Stuff about 5 measurements here
Medications that may increase blood pressure Clozapine Corticosteroids Haemopoietic agents (darbopoetin,epoetin) Immunomodifiers (cyclosporin,tacrolimus) Leflunomide (Arava) Monoamine oxidase inhibitors : reversible
(moclobemide),irreversible (phenelzine,tranylcypromine) Oral contraceptives Oral decongestants (eg pseudoephedrine) Stimulants(dexamphetamine sulfate,methylphenidate
hcl=Ritalin) Sympathomimetic agents Venflaxine (=Efexor,dose related) Rebound hypertension may be seen after abrupt withdrawl
of Bromocriptine or clonidine
PANADOL RAISES BP
Complementary medicines and hypertension
Complementary medicines that may increase blood pressure American mistletoe Angel’s trumpet Butcher’s broom Caffeine containing products eg guarana,black
and green tea,yerba mate Ephedra (ma huang) Gentian Ginger preparations Liquorice Melatonin St John’s wart
Examination pointers
Identify all CV risk factorsDetect end organ damage eg
CCF,CAD,PVDDetect related or comorbid clinical
conditions eg CKD,neurological disease,obesity (waist <94 cm males,<80cm females,BMI<25
Identify secondary causes eg Cushingoid
Initial investigations Urinary micoalbuminuria on spot
urine,if confirmed obtain a 24 hour urine for accurate assessment
Blood analysis for Na/K/Ur/Cr/Urate,Hb,fasting BSL,Lipid profile,LFTs
ECG for conduction disease,arrhythmias,CHD,LVH (incr CV risk)
Echocardiography
Further investigations Renin:aldosterone ratio if treatment
resistant,moderate to severe,or hypokalemia (morning sample)
24 hr urine catecholamines,cortisol Renal artery stenosis assessment eg
renal US,CTA,nuclear scan if suspect renal artery stenosis
Renal artery stenosis assessment
Renal CTCA most precise anatomical test but lacks functionality
Nuclear scan-functional test,limitations
Renal ultrasound-low sensitivity MRI
Renal artery stenosis
Renal artery stenting
Sleep apnoea testing
NHF: When to Initiate Treatment of Hypertension
Are any of the following present?• Grade 3 hypertension (SBP ≥ 180 mmHg and/or DBP ≥ 110 mmHg)• Isolated systolic hypertension with widened pulse pressure
(SBP ≥ 160 mmHg and DBP ≤ 70 mmHg)• Associated conditions or target-organ damage (Table 3)
Start drug treatment immediately (See Figure 3: Initiating drug treatment)• Lifestyle modification• Manage associated conditions†
• Confirmed hypertension grades 1–2 (SBP 140–179 mmHg or DBP 90–109 mmHg)
• All other adultsAssess 5-year absolute cardiovascular risk (Figure 1)*
SBP < 140 mmHgDBP < 90 mmHgContinue monitoring‡
Start drug treatment immediately(See Figure 3: Initiating drug treatment)• Lifestyle modification• Manage associated conditions†
• Lifestyle modification• Monitor BP
Reassess 5-year absolute cardiovascular risk in 3–6 months
• Lifestyle modification• Monitor BP
Reassess 5-year absolute cardiovascular risk in 6–12 months
Start drug treatment immediately(See Figure 3: Initiating drug treatment)• Lifestyle modification• Manage associated conditions†
SBP 140–150 mmHgDBP < 90 mmHgContinue monitoring‡
SBP ≥ 140 mmHgDBP ≥ 90 mmHg
SBP ≥ 150 mmHgDBP ≥ 90 mmHg
NoYes
High (>15%) Low (<10%)Moderate (10–15%)
Moderate (10–15%)
Low (<10%)
National Heart Foundation of Australia. Guide to Management of Hypertension, 2008.
Lifestyle modification Advise patients to aim for healthy targets: • At least 30 minutes of moderate-intensity physical activity on most, if not all, days of the week (daily total can be accumulated e.g. three 10-minute sessions). Advise patients of all ages to become more active.
• Smoking cessation. Refer patients to Quitline. Consider recommending nicotine replacement
therapy and/or prescribing oral therapy (bupropion or varenicline) in patients who smoke more than 10 cigarettes per day and have no contraindications.
• Waist measurement < 94 cm for men and < 80 cm for women, body mass index (BMI) < 25 kg/m2. When recommending weight loss, advise patients on reducing kilojoule intake as well as increasing physical activity.
• Dietary salt restriction: ≤ 4 g/day (65 mmol/day sodium). Recommend low-salt and reducedsalt
foods as part of a healthy eating pattern.
• Limited alcohol intake: ≤ two standard drinks per day for men or ≤ one standard drink per day for women.
Benefits of lifestyle modification
Smoking cessation….may not reduce BP but 2-6 fold increase risk MI and 3 fold increase risk of CVA
Regular physical activity…regular aerobic exercise 4/2.5 mm Hg…..30/60 a day
Salt restriction .avge reduction 4.5/2mm Hg while increased dietary potassium can reduce BP by 6 mm in HT and 2 mm Hg in normotensives (unless renal impairment)
SALT RESTRICTION
How many patients have you had that have a good therapeutic response to a low salt diet
0 1 2-4 >5
DASH DIET
DASH DIET A few guidelines of the DASH diet menu: the diet includes a minimum of 4-5 servings of fruits and
vegetables a day three servings of low-fat dairy product 7-8 servings of grains 2 servings of non-vegetarian food fat/oils should be around 2-3 servings on a weekly basis one needs to consume 4-5 serves of
nuts, seeds and legumes the sweet consumption should not exceed 5 serves a
week (foods with little or no sugar as best, although sugar from fruits is considered natural and benefiting)
avoid or at least use moderation on alcohol consumption
DASH PYRAMID
Additional lifestyle factors
Weight reduction…every 1% reduction in body weight lowers SBP by average of 1%
Alchohol limited to max 2 standard drinks for males and one for females,advise at least 2 alchohol free days a week
Treatment decision making
National Heart Foundation of Australia. Guide to Management of Hypertension, 2008.
If target BP not reached
ACE inhibitor or angiotensin II receptor antagonist + calcium channel blocker
OR
ACE inhibitor or angiotensin II receptor antagonist + low-dose thiazide diuretic
If target BP not reachedACE inhibitor or angiotensin II receptor antagonist
+ calcium channel blocker + low-dose thiazide diuretic
If target BP not reachedConsider seeking specialist advice
NHF: Initiating Antihypertensive Therapy
First ChoiceACE inhibitor or angiotensin II receptor antagonist
ORCalcium channel blocker
ORLow-dose thiazide diuretic (consider for people aged ≥65 years only)
Factors determining drug choices
Patient age Presence of associated conditions
or end organ damage Potential interactions with other
drugs Adherence implications cost
Summary of Recommendations for Multiple-mechanism Therapy: What the NHF Hypertension Management Guidelines Say
Start with lowest recommended dose of selected first line agent; If not well tolerated, change to a drug of a different class
If BP target is not reached or there is no significant BP reduction with initial monotherapy, add another agent from a different drug class at low dose, rather than increasing dose of the first agent
If BP still above target and both agents well tolerated, increase dose of one of the agents (other than thiazide diuretic) incrementally to maximal recommended dose before increasing the dose of the other agent
Once a combination is established as long-term therapy, it may be more convenient for the patient to use a combined preparation
National Heart Foundation of Australia. Guide to management of Hypertension, 2008.
*Lower doses generally used in fixed-dose combinations+ = potential advantage*Lower doses generally used in fixed-dose combinations+ = potential advantage
Advantages of Fixed Dose versus Free Dose Combinations of Two Antihypertensive Drugs
Fixed Free
Simplicity of treatment + –
Persistence + –
Efficacy + +
Tolerability +* –
Price + –
Flexibility – +
Burnier M. Am J Hypertens 2006;19:1190–6.
Inadequacy of Agents with a Single Mechanism of Action (MoA)
Materson et al. observed that antihypertensive agents with a single MoA were inadequate to achieve a diastolic BP <95 mmHg in 4158%of hypertensive patients1
In patients with hypertension and diabetes, more than 65% will require two or more antihypertensive agents to achieve a BP of 130/80 mmHg2
Because hypertension is a multifactorial disease, in most cases at least two antihypertensive agents are needed for patients to achieve BP goal3
1. Materson et al. N Engl J Med 1993;328:914212. Bakris et al. Am J Kidney Dis 2000;36:646613. Milani. Am J Manag Care 2005;11:S2207
Advantages of Multiple-mechanism Therapy: Efficacy
Components with a different mechanism of action interact on complementary pathways of BP control1
Each component can potentially neutralise counter-regulatory mechanisms, e.g. Diuretics reduce plasma volume, which in turn
stimulates the renin angiotensin system (RAS) and thus increases BP; addition of a RAS blocker attenuates this effect1,2
Multiple-mechanism therapy may result in BP reductions thatare additive2
Multiple-mechanism therapy results in a greater BP reduction than seen with its single-mechanism components alone1,2
1. Sica. Drugs 2002;62:443622. Quan et al. Am J Cardiovasc Drugs 2006;6:10313
Multiple Antihypertensive Agents are Needed to Reach BP Goal
Bakris et al. Am J Med 2004;116(5A):30S–8 Dahlöf et al. Lancet 2005;366:895–906; Jamerson et al. Blood Press 2007;16:80–6
Average no. of antihypertensive medications*Interim 6-month data
ACCOMPLISH* (132 mmHg)Initial 2-drug combination
therapy1 2 3 4
ASCOT-BPLA (136.9 mmHg)
ALLHAT (138 mmHg)
IDNT (138 mmHg)
RENAAL (141 mmHg)
UKPDS (144 mmHg)
ABCD (132 mmHg)
MDRD (132 mmHg)
HOT (138 mmHg)
AASK (128 mmHg)
Trial (SBP achieved)
Dynamic duos
1. Pitt et al. Circulation 2000;102:1503–10; 2. Nissen et al. JAMA 2004;292:2217–26; 3. Dahlof et al. Lancet 2005;366:895–906; 4. Williams et al. Circulation 2006;113:1213–25; 5. Leenen et al. Hypertension 2006;48:374–84
Amlodipine: Wealth of CV Outcomes Data
PREVENT1
825 CAD patients (≥30%): Multicentre, randomised, placebo controlled
Primary outcome: No difference in mean 3 yr coronary angiographic changes vs. placebo
35% hospitalisation for heart failure + angina43% coronary revascularisation procedures
CAMELOT2
1,991 CAD patients (>20% stenosis by coronary angiography): Double-blind, randomised study vs. placebo and enalapril 20 mg
Primary outcome: 31% in CV events vs. placebo (P = 0.003)
42% hospitalisation for angina (P = 0.002)27% coronary revascularisation (P = 0.03)
ASCOT-BPLA/CAFE3,4
19,257 HTN patients: Multicentre, randomised, prospective study vs. atenolol
Primary outcome: 10% in non-fatal MI & fatal CHD (NS*)
16% total CV events and procedures (P< 0·0001)30% new-onset diabetes (P< 0·0001)23% fatal & non-fatal stroke (P= 0·0003)11% all-cause mortality (P= 0·0247)
central aortic systolic blood pressure by 4.3 mmHg (P< 0.0001)
ALLHAT5
18,102 HTN patients: Randomized, prospective study vs. lisinopril
Primary outcome: No difference in composite of fatal CHD+ non-fatal MI vs. lisinopril6% combined CVD (P = 0.047)23% stroke (P = 0.003)
*NS: NOT SIGNIFICANT
Accomplish is the name of the trial which saw the australian guidelines recommend
Therapy when the drug used in the trial is not available in Australia
ARB use with CCB, when no ARBs where used in the trial
All of the above other
Combination therapies….50-75% will need 2+ agents for control ACE/ARB + CCB……..diabetes/lipid abnormalities
ACE/ARB + diuretic…..congestive cardiac failure/cerebrovascular disease
ACE/ARB + betablocker…post myocardial infarction/congestive cardiac failure
Betablocker + dihydropyridine CCB…coronary heart disease
Thiazide plus dihydropyridine CCB…..isolated systolic hypertension
Side effects
Side effects
Specific side effect patterns Constipation…….CCB especially Verapamil
Cough……….ACE inhibitors
Dyspnoea……Betablockers
Hyperglycaemia..thiazides
Hyperkalemia…..ACE inhibitor/ARB
Erectile dysfunction…thiazides/beta blockers
Oedema……..CCB
Postural hypotension..all except b.blockers
Pregnancy and hypertension
Hypertension in preganacy Women planning pregnancy. Consider using
either betablockers in particular labetalol/oxprenolol, or methyldopa,or clonidine
Hydrallazine second line agent
ACE/ARB/diuretics contraindicated
CCB contraindicated in first half pregnancy
Managing other CV risk factors Consider antiplatelet therapy with aspirin if
stable Evidence for lipid lowering in HT shown to
reduce CV events and stroke
Nonresponsive hypertension
If BP remains elevated despite maximal doses of at least two appropriate agents, reassess for:
• non-adherence • undiagnosed secondary hypertension • hypertensive effects of other drugs • treatment resistance due to sleep apnoea • undisclosed use of alcohol or recreational drugs • unrecognised high salt intake (particularly in patients taking
ACE inhibitors or angiotensin II receptor antagonists) • ‘white coat’ hypertension • technical factors affecting measurement • volume overload, especially with chronic kidney disease
(CKD).
Renal denervation
SYMPLICITY TRIAL Renal sympathetic denervation in patients with treatment-resistant hypertension (The Symplicity
HTN-2 Trial): a randomised controlled trial Symplicity HTN-2 Investigators‡ Summary Background Activation of renal sympathetic nerves is key to pathogenesis of essential hypertension. We aimed to assess
effectiveness and safety of catheter-based renal denervation for reduction of blood pressure in patients with treatment-resistant hypertension.
Methods In this multicentre, prospective, randomised trial, patients who had a baseline systolic blood pressure of 160
mm Hg or more (≥150 mm Hg for patients with type 2 diabetes), despite taking three or more antihypertensive drugs, were randomly allocated in a one-to-one ratio to undergo renal denervation with previous treatment or to maintain previous treatment alone (control group) at 24 participating centres. Randomisation was done with sealed envelopes. Data analysers were not masked to treatment assignment. The primary effectiveness endpoint was change in seated office-based measurement of systolic blood pressure at 6 months. Primary analysis included all patients remaining in follow-up at 6 months. This trial is registered with ClinicalTrials.gov, number NCT00888433.
Findings 106 (56%) of 190 patients screened for eligibility were randomly allocated to renal denervation (n=52) or control
(n=54) groups between June 9, 2009, and Jan 15, 2010. 49 (94%) of 52 patients who underwent renal denervation and 51 (94%) of 54 controls were assessed for the primary endpoint at 6 months. Office-based blood pressure measurements in the renal denervation group reduced by 32/12 mm Hg (SD 23/11, baseline of 178/96 mm Hg, p<0·0001), whereas they did not differ from baseline in the control group (change of 1/0 mm Hg [21/10], baseline of 178/97 mm Hg, p=0·77 systolic and p=0·83 diastolic). Between-group differences in blood pressure at 6 months were 33/11 mm Hg (p<0·0001). At 6 months, 41 (84%) of 49 patients who underwent renal denervation had a reduction in systolic blood pressure of 10 mm Hg or more, compared with 18 (35%) of 51 controls (p<0·0001). We noted no serious procedure-related or device-related complications and occurrence of adverse events did not differ between groups; one patient who had renal denervation had possible progression of an underlying atherosclerotic lesion, but required no treatment.
Interpretation Catheter-based renal denervation can safely be used to substantially reduce blood pressure in treatment-
resistant hypertensive patients.Lancet Published Online: 17 November 2010
CAROTID BARORECEPTOR STIMULATION
BARORECEPTOR STIMULATION
You be the judge!