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Epidemiology and treatment of hypertension

Epidemiology and treatment of hypertension. Note the first part of this presentation on risk-based assessment of BP treatment has been provided by Professor Rod Jackson, Head of Division of Community Health Faculty of Medical & Health Sciences University of Auckland. Part 1.

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Epidemiology and treatment of hypertension

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  1. Epidemiology and treatment of hypertension Note the first part of this presentation on risk-based assessment of BP treatment has been provided by Professor Rod Jackson, Head of Division of Community Health Faculty of Medical & Health Sciences University of Auckland

  2. Part 1 • Defining ‘hypertension’ and making decisions based on cardiovascular risk

  3. Argument 1. There is no clinically relevant entity that can be defined by a mildly raised blood pressure. 2. A mildly raised blood pressure level is not a major determinant of which patients benefit from blood pressure lowering

  4. what is mild hypertension?

  5. Systolic blood pressure distribution: Framingham Study participants 35-64 years top x%?? 74-119 120-139 140-159 160-179 180-300 SBP (mmHg)

  6. ??

  7. ?? 32 30 28 26 18 17 16 16 11 10

  8. Definitions of mild hypertension & prevalence

  9. Definitions of mild hypertension & prevalence ?? ≥130/80

  10. what is mild hypertension? • it’s the wrong question

  11. who benefits from blood pressure lowering?

  12. Meta-analysis of RCTs of BP lowering drugs: 15,559 patients, SBP diff 17 mmHg, DBPdiff 9 mmHg, follow-up 4.1 years (≥ 60 years) • Endpoint Odds ratio (Relative risk red.) • Stroke mortality 36 % • Stroke morbidity 35 % • CHD mortality 25 % • CHD morbidity 15 % 0 0.5 1.0 1.5 Insua et al Ann Intern Med 1994;121:355-62

  13. Stroke and blood pressure lowering:subgroup analysis from 17 RCTs Trial % Events Relative risk red. group control treatment All entry 2.2 % 1.3 % 39% DBP < 110 Some ≥ 110, 6.5 % 4.6 % 32 % all ≤ 115 Some or all 8.2 % 4.7 % 45 % ≥ 115 0 0.5 1.0 1.5 MacMahon & Rogers J Vasc Med Biol 1993;4:265-71

  14. Stroke and blood pressure lowering:subgroup analysis from 17 RCTs Trial % Events Odds ratio (Relative risk red.) group control treatment Younger 2.3 % 1.3 % 43 % patients Older 7.0 % 4.6 % 34 % patients 1º prev. 3.2 % 2.0 % 38 % 2º prev. 27.3 % 18.8 % 38 % 0 0.5 1.0 1.5 MacMahon & Rogers J Vasc Med Biol 1993;4:265-71

  15. Stroke and blood pressure lowering:subgroup analysis from 17 RCTs Trial % Events Odds ratio (Relative risk red.) group control treatment Younger 2.3 % 1.3 % 43 % patients 1% Older 7.0 % 4.6 % 34 % patients 2.4% 1º prev. 3.2 % 2.0 % 38 % 1.2% 2º prev. 27.3 % 18.8 % 38 % 8.5% 0 0.5 1.0 1.5 MacMahon & Rogers J Vasc Med Biol 1993;4:265-71

  16. which patients should be treated? • “individual treatment can only be justified if there is individual benefit” • “only absolute benefits are relevant to patients”

  17. (45 prospective studies: 450,000 people 13,000 events) PSC Lancet 1995;346:1647-53

  18. PSC Lancet 1995;346:1647-53

  19. Absolute risk of CVD risk in 40 year old men by SBP and other risk factors, Framingham, USA 700 CVD risk per 1000 in 8 years 459 326 210 46 SBP 105 ----189 105 ----189 105 ----189 105 ----189 105 ----189 high chol. - + + + + gluc intol. - - + + + cigarettes - - - + + LVH - - - - +

  20. WOMEN Nonsmoker Smoker Nonsmoker Smoker 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 180/105 180/105 160/95 160/95 140/85 140/85 120/75 120/75 180/105 180/105 160/95 160/95 140/85 140/85 120/75 120/75 180/105 180/105 160/95 160/95 140/85 140/85 120/75 120/75 180/105 180/105 160/95 160/95 140/85 140/85 120/75 120/75 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 No D iabet es Diabet es Ratio of Total Cholesterol:HDL Ratio of Total Cholesterol:HDL AGE 70 AGE 60 AGE 50 AGE 40 Ratio of Total Cholesterol:HDL Ratio of Total Cholesterol:HDL

  21. Nonsmoker Smoker Nonsmoker Smoker 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 4 5 6 7 8 180/105 180/105 160/95 160/95 140/85 140/85 120/75 120/75 No Diabetes Diabetes Ratio of Total Cholesterol:HDL Ratio of Total Cholesterol:HDL AGE 70

  22. CVD risk & NNTs 5yr CVD risk 5 yr NNT* > 30% < 10 . 5-10% 40 2.5-5% 85 < 2.5% >120 * assumes 33% RRR

  23. is BP lowering therapy indicated ? 60 yr old man BP 148/ 88 mmHg smoker TC 240 mg/dl HDLC 38 mg/dl BMI 25 no Hx CVD 50 yr old woman BP 160/95 mmHg non smoker TC 240 mg/dl HDLC 62 mg/dl BMI 25 no Hx CVD

  24. is BP lowering therapy indicated ? 60 yr old man BP 148/ 88 mmHg smoker TC 240 mg/dl HDLC 38 mg/dl 50 yr old woman BP 160/95 mmHg non smoker TC 240 mg/dl HDLC 62 mg/dl 5 yr absolute CVD risk: 24% 5 yr NNT: 12 5 yr absolute CVD risk: 4% 5 yr NNT: 72

  25. 50/60 yr old woman non smoker TC 240 mmol/L HDLC 60 mmol/L No diabetes SBP mmHg: 150 160 170 5 yr NNT: 90 / 50 70 / 42 60 / 37

  26. To treat or not to treat “mild hypertension” “treat risk not blood pressure” “only absolute risks and benefits are relevant to patients” “the payer should choose the threshold”

  27. Part 2Pharmacological considerations in hypertension management Sue Hill and David Henry Discipline of Clinical Pharmacology

  28. Factors that influence blood pressure • sympathetic nervous system • total peripheral resistance • mainly arterioles • intravascular volume (renin-angiotensin) • renal excretion • atheroma, thrombosis

  29. things that alter vascular resistance • vascular smooth muscle • mediators from sympathetic nerves and vascular endothelium • calcium dependent • contraction due to  intracellular calcium • relaxation due to  calcium entry or cGMP, cAMP • depends on intact endothelium • complex, interdependent biochemical reactions

  30. drugs that will reduce vascular resistance • nitric oxide, nitrates • - antagonists • - antagonists • Calcium channel blockers • angiotensin II antagonsists • (lots more)

  31. other mechanisms to remember • central control - • methyldopa, ganglion blocking drugs • renal excretion of sodium and water • diuretics, spironolactone

  32. drugs we use for hypertension • - blockers • thiazide diuretics • Calcium channel blockers • angiotensin converting enzyme inhibitors • ( others - alphamethyldopa, reserpine, hydralazine, prazosin )

  33. thiazide diuretics • ACTION: increase sodium and water excretion by decreasing reabsorption of sodium and chloride in the distal tubule (later effect on vessels) • EFFECT lowers blood pressure- over several days decreases complications, morbidity and mortality ( good clinical trials) • Side effects: • metabolic effects: diabetes, gout, low Na, K, impotence

  34. - adrenoceptor antagonists • ACTION: • effects on heart (1) and smooth muscle (2 ) via noradrenaline • lowers BP: • reduces cardiac output • reduces renin release • reduces central sympathetic activity • effect on pre-synaptic noradrenaline release • nonselective antagonist = propranolol • relatively selective 1 = metoprolol, atenolol • mixed agonist/antagonist - oxprenolol

  35. - adrenoceptor antagonists • EFFECT lowers blood pressure - over several days decreases complications, mortality and morbidity (good clinical trials) • SIDE EEFECTS • bronchospasm, fatigue, bad dreams, cold extremities • worsening cardiac failure, heart block • hypoglyacaemia

  36. ACE-inhibitors • ACTION • inhibits conversion of angiotensin I to angiotensin II - effects on vasculature in kidney , brain, heart • vasodilator • eg: captopril, enalapril, lisinopril, ramipril • EFFECTS • lower blood pressure- relatively rapidly • effect on mortality, morbidity and complications?? • Reduces mortality in cardiac failure, post-AMI; good clinical trials

  37. ACE-inhibitors • SIDE EFFECTS: • cough, rash, taste disturbances • renal failure, neutropenia, proteinuria • COST • relatively expensive

  38. Angiotensin II antagonists • losarten, ibersarten, candesarten • actions similar to ACE inhibitors • effects • lower blood pressure- relatively rapidly • effects on clinical outcomes? • Side effects: • rash, cough • cost: expensive

  39. calcium antagonists • ACTION: • three classes: verapamil, dihydropyridines, benzothiazepines • block calcium entry into cells by preventing opening of voltage gated calcium channels • act on heart and smooth muscle, depending on type • vasodilator effect (mainly dihydropyridines) • two forms - immediate and slow release • EFFECTS • lower blood pressure - can be rapid • mortality, morbidity, complications??

  40. Calcium antagonists • SIDE EFFECTS • flushing, headache, ankle swelling, constipation • heart block, worsening cardiac failure

  41. BENEFITS short-term long term RISKS side-effects lack of beneficial effect ( unnecessary medication) choices

  42. issues • Preventive versus curative treatment • need for joint decision making • use of drugs with clinical effects versus elegant pharmacologically active molecules • benefits versus risks!!

  43. terms • agonist, partial agonist • receptor • antagonist, competitive antagonist • ligand • affinity • mediators • tolerance

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