Current trends and controversies in the diagnosis and

Current trends and controversies in the diagnosis and treatment of hypertension Focus on the Renin Angiotensin Aldosterone System and Direct Renin Inhibition Tom Smiley BSc. Phm, Pharm. D CCCEP File 853 -0109 L 1 FT

Disclosure n 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 -0109 L 1 FT) Supported by an educational grant from Novartis Canada Inc. 2

Learning Objectives After successful completion of this workshop pharmacists will be better able to: n n n 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 BSc. Phm, Pharm. D

What percent of Canadians have hypertension? 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

Age Adjusted ave Annual Incidence /1000 Risk of Cardiovascular Event (aged 75 -94) SBP DBP Blood Pressure Kannel, Am J Hypertens 2000; 13: 3 S-10 S. 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 mm. Hg systolic or 10 mm. Hg diastolic Bakris GL et al. Special Report on DM and HTN above target 10 Am J Kidney Dis 2000; 36: 646 -661

The Renin Angiotensin Aldosterone System (RAAS)

Classic understanding of RAAS Angiotensinogen Ang I Renin ACE Ang II Aldosterone AT 1 Receptor Na+/H 2 O 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 AT 1 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 Adapted from Dzau V, Braunwald E. Am Heart J. 1991; 121: 1244 -1263. 14

Angiotensin II in atherosclerosis 15

Physiologic effects of RAAS activation Exerts significant effects on cardiovascular and renal function n Many aspects of cardiovascular disease progression can be directly linked to the RAAS system n Vascular inflammation, generation of reactive oxygen species and endothelial dysfunction play a role in atherosclerosis n Activation of the RAAS system is central to these multiple pathways n 16

Physiologic effects of RAAS inhibition n n 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 n Dilates the efferent more than the afferent arterioles n Intraglomerular pressure drops 17

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19 9 1

Benefits of RAAS Inhibition beyond BP lowering n n n End-organ protection: Kidney Vascular protection: Vessel wall and vascular endothelium n 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 n Several mechanisms have been hypothesized for this including hemodynamic effects and non-hemodynamic 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 n n 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) n n n 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 AT 1 receptors n 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 n ARB benefits beyond BP-lowering effects n n 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) n n n 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 FEEDBACK LOOP ACE PRA ACEIs Ang II ARBs AT 1 Receptor BIOLOGICAL EFFECTS Ang I ACEI ARB Aliskiren Azizi M et al. 2006 Ang II Renin PRA ↑ ↑ ↓ ↓ ↑ ↑ ↑ ↓ 26

Introduction to Direct Renin Inhibitors (DRIs) n Newest class of RAAS-active antihypertensives n n n 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 Placebo (n=53) Aliskiren 150 (n=52) Aliskiren 300 (n=56) Aliskiren 600 (n=55) Mean ambulatory BP (mm. Hg) Systolic 160 T/P ratio – 0. 64 0. 98 0. 86 150 140 130 120 110 100 Early morning surge Diastolic 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 n The efficacy of aliskiren has been extensively studied in monotherapy compared to: Placebo 1, 2 n Active Control: n n ARB (irbesartan)2 n ACE (ramipril)3 n 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): 371 A 1014 -173 4. Schmieder RE, et al: J Clin Hypertens 2007; 9(Suppl A)(5): A 182. 30 30

Efficacy in DRI Hypertension Trials: Monotherapy Trial & primary outcome Oh et al (2007) Change in ms. BP vs. placebo from BL to wk 8 Gradman et al (2005) Change in trough ms. BP 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 ms. BP 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 ms. SBP 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 ms. BP 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 n The efficacy of aliskiren was extensively studied in combination with other antihypertensive agents: ACE inhibitor (ramipril)1 n Diuretic (HCTZ)2 n ARB (valsartan)3 n CCB (amlodipine)4 n 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 Valsartan 320 58 184 180 HCTZ 25 175 187 173 Amlodipine 5 177 188 − 5. 0 + aliskiren 150 + aliskiren 300 + aliskiren 150 − 20 60 + aliskiren 300 − 10 60 + aliskiren 150 − 5 − 15 58 + aliskiren 300 0 n = 275 274 HCTZ 12. 5 − 11. 0 − 12. 0 − 13. 9 − 16. 6 † − 15. 5 − 16. 6 † − 14. 3 − 17. 6 − 16. 5 − 18. 0 − 25 Change from baseline in ms. SBP (mm. Hg) * − 19. 8 * − 19. 5 * − 21. 2 * *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 n The efficacy of aliskiren has been extensively studied in the following populations: n Young and elderly 1 n Obesity 2 n Diabetes 3 n Metabolic syndrome 4, 5 n Impaired renal function 6 1. Dahlöf B, et al: J Clin Hypertens 2007; 9(Suppl. A): A 157 [abstract P-376]. 2. Prescott MF, et al: Int J Obes 2007; 31(Suppl. 1): S 99 [abstract T 2: PO. 88]. 3. Taylor AA, et al: . Diabetes 2007; 56(Suppl. 1): A 129 [abstract 483 -P]. 4. White WB, et al: Eur Heart J 2007; 28(Suppl 1): 868 [abstract P 4845]. 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 BP-lowering in Patients with Impaired Renal Function: Pooled Analysis DBP 0 SBP e. GFR <60 e. GFR ≥ 60 n=26 n=740 n=25 n=736 e. GFR <60 n=26 n=25 e. GFR ≥ 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 (mm. Hg) Aliskiren 150 mg Aliskiren 300 mg e. GFR: estimated glomerular filtration rate (assessed in m. L/min/1. 73 m 2) 38 38 Weir MR, et al. 2007 (Pooled analysis)

Tolerability of Aliskiren 39 39

Aliskiren monotherapy: Tolerability Placebo n = 781 Aliskiren 75 mg 150 mg n = 478 Any SAE, n (%) Any AE, n (%) Discontinuations due to AE, n (%) Aliskiren 300 mg n = 774 n = 768 All Aliskiren+ n = 2316 5 (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) Any AE 33. 8 32. 3 30. 0 Serious AEs 2. 2 2. 8 1. 4 Discontinuation due to AEs 4. 0 3. 9 2. 2 Treatment-related AEs 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 Most frequent AEs (³ 2% 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. Rasilez® Product Monograph, March 13, 2008 41

HCTZ plus Aliskiren or Amlodipine: Incidence of Edema in Patients with Obesity and Hypertension Aliskiren/ HCTZ Irbesartan/ HCTZ Amlodipine/ 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) 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 n Aliskiren 150– 300 mg: n provides dose-dependent reductions in DBP and SBP as monotherapy n n 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 n 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 n The combination of aliskiren with other antihypertensive agents, such as ACE inhibitors, ARBs, dihydropyridine CCBs, or thiazide diuretics, is well tolerated n When combined with ramipril, aliskiren appears to reduce the incidence of cough n Long-term combination therapy with aliskiren and valsartan is well tolerated n The combination of aliskiren and amlodipine results in a lower incidence of edema compared with increasing the amlodipine dose n 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 Continue to follow-up Diagnosis of HTN Hypertension visit 4 -5 >140 SBP or >90 DBP Diagnosis of HTN < 140 / 90 >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 n Prescription Drugs: n n n n n 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: n n n 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 n n n 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 n n n 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 mm. Hg should be considered elevated. 2008 CHEP Recommendations 52

Home BP Measurement: CHEP Recommendations n Encourage hypertensive patients to use an approved blood pressure measuring device and use proper technique to assess blood pressure at home n 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 mm. Hg 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: n INDIVIDUALIZING THERAPY n n 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 n n 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: n n TREATING TO TARGET BP n treat aggressively using combinations of drugs and lifestyle modification to achieve individualized target PROMOTING ADHERENCE n a multi-faceted approach should be used to improve adherence with both non pharmacological and pharmacological strategies 2008 CHEP Recommendations 62