Hypertension lecture prof zak (1)
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Power point presentation on management of hypertension based on current evidence
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Hypertension lecture prof zak (1)
- 1. UPDATE ON HYPERTENSION Prof. Dr. M Zak Khalil, MD, FACP, FACC, FESC, MRCP (UK)
- 2. Case 1 40 y.o. white male was found to have Bp (158/92) on pre-employment physical exam. A) ARB B) ACE I C) B blocker D) Diuretic E) Calcium Ch blocker F) None of the above
- 4. Prevalence of hypertension in China, Egypt, and USA
- 5. Prevalence of hypertension in USA JAMA 2003; 190:199
- 6. Female Male 23.9 28.7 0 5 10 15 20 25 30 %prevalence Saudis Hypertension Al Nozha et al, S Med J, 2007.
- 7. 22.4 27.9 0 5 10 15 20 25 30 RuralUrban Residence Hypertension in Saudi Arabia Al Nozha et al, S Med J, 2007.
- 8. Al Nozha et al, S Med J, 2007. Hypertension is a silent killer Uawareness = 58%
- 9. JNC 7
- 10. ESC & ESH Guidelines 2007 Category Systolic Diastolic Optimal <120 <80 Normal 120-129 80-84 High normal 130-139 85-89 Grade 1 140-159 90-99 Grade 2 160-179 100-109 Grade 3 ≥180 ≥110 Isolated sys ≥140 <90 European Heart Journal (2007) 28, 1462-1536
- 11. ESC/ESH 2007 Bp (mmHg) with different measurement SBP DBP Office or clinic 140 90 24-hour 125 -130 80 Day 130 – 135 85 Night 120 70 Home 130-135 85 European Heart Journal 2007
- 12. Consequences of Hypertension Hypertension Brain Heart Kidney End-stage renal disease MI, heart failure, sudden death Stroke, dementia
- 15. Framingham Heart Study - Risk of Cardiovascular Events by Hypertensive Status in Patients Aged 35-64 Years; 36-Year Follow-Up 9.5 3.3 2.4 5 2 3.5 2.1 45.4 21.3 12.4 6.2 9.9 7.3 13.9 6.3 22.7 0 10 20 30 40 50 Men Women Men Women Men Women Men Women Normotensive Hypertensive Risk Ratio 2.0 2.2 3.8 2.6 2.0 3.7 4.0 3.0 Excess Risk 22.7 11.8 9.1 3.8 4.9 5.3 10.4 4.2 Coronary Disease Stroke Peripheral Artery Disease Cardiac Failure BiennialAge-AdjustedRate per1000 Kannel WB JAMA 1996;275(24):1571-1576.
- 16. HealthStatus/QOL Time, years Normotensive Elevated Blood Pressure Left Ventricular Dysfunction Heart Failure LowerHigher Death Renal Impairment Decline in Glomerular Filtration Rate Kidney Failure Vascular Hypertrophy Stroke Consequences of Hypertension Am Heart J. 1991;121:1244–1263.
- 17. 0 5 10 15 20 0 100 200 300 5YearRisk(%) Stroke Myocardial Infarction Systolic Blood Pressure (mmHg) Differing influence of hypertension on absolute and relative risk of stroke and MI Brown, M.J. Lancet 2000; 355: 659 - 660 20 40 60 80 120 140 160 180 220 240 260 280 Normotensives Hypertensives
- 18. MI and Stroke in Hypertension Trials N Engl J Med 2003 0 1 2 3 4 5 6 7 8 Percentageofpatientswithevent Stroke Myocardial Infarction
- 19. The circadian pattern of BP Weber M.A. et al., Rev Cardiovasc Med 2004 24-hour BP levels
- 20. The circadian pattern of BP Weber M.A. et al., Rev Cardiovasc Med 2004 Correlation with CV events (ISAM study) SCD
- 22. Proteinuria: predicting cardiovascular events and survival in diabetes A: U-Prot <150 mg/L B: U-Prot 150–300 mg/L C: U-Prot >300 mg/L Incidence (%) Survival Months A B C Overall p<0.001 1.0 0.9 0.8 0.7 0.6 0.5 0 0 10 30 50 70 90 Stroke Coronary Events 0 10 20 30 40 Overall p<0.001 Overall p<0.001 U-Prot=concentration of urinary protein Miettinen et al. Stroke 1996; 27: 2033–9
- 23. What level of blood pressure should be achieved? BHS 2004 <140/85 mm Hg (<130/80 for diabetics)1 ESH/ESC 2003 + 2007 <140/80 mm Hg (<130/80 for diabetics)2 JNC 7: 2003 <140/90 mm Hg (<130/80 for diabetics)3 1. Williams et al. J Hum Hypertens 2004;18:139–85 2. Guidelines committee. J Hypertens 2003;21:1011–53 3. Chobanian et al. Hypertension 2003;42:1206–52
- 24. AASK MAP <92 Target BP (mm Hg) Multiple antihypertensive agents are needed to achieve target BP No. of antihypertensive agents 1 UKPDS DBP <85 ABCD DBP <75 MDRD MAP <92 HOT DBP <80 Trial 2 3 4 DBP, diastolic blood pressure; MAP, mean arterial pressure; SBP, systolic blood pressure. Bakris GL et al. Am J Kidney Dis. 2000;36:646-661. Lewis EJ et al. N Engl J Med. 2001;345:851-860. Cushman WC et al. J Clin Hypertens. 2002;4:393-404. IDNT SBP <135/DBP <85 ALLHAT SBP <140/DBP <90
- 25. Value of excellent vs. good blood pressure control in NIDDM (144/82 vs. 154/87mmHg) 0 10 20 30 40 0 1 2 3 4 5 6 7 8 9 PatientsWithEvents(%) Less tight control Tight control Years From Randomisation UKPDS, BMJ 1998;317:703-713. Reduction in risk with tight control 32% (95% CI 6% to 51%) (P=0.019)
- 26. LIFE Trial: Blood-Pressure Reductions 0 6 12 18 24 30 36 42 48 54 Study Month 40 50 60 70 80 90 100 110 120 130 140 150 160 170 180 Systolic Diastolic Mean Arterial mmHg Atenolol 145.4 mmHg Losartan 144.1 mmHg Atenolol 80.9 mmHg Losartan 81.3 mmHg Dahlöf B et al Lancet 2002;359:995-1003. Atenolol 102.4 mmHg Losartan 102.2 mmHg
- 27. SBP Control in Trials * Mancia and Grassi, J Hypert 2002 FACET Micro HOPE CAPPP INSIGHT HOT VALUE STOP-2 UKPDS LIFE RENAAL IDNT IRMA ABCD 130 140 150 160 170 180 190 200 mmHg 120 Diabetic s B T ALLHAT 1 HOPE PROGRESS CAPPP INSIGHT NORDIL HOT STONE STOP-2 LIFE ALLHAT 2 ANBP2 INVEST SCOPE ASCOT VALUE All patients 130 140 150 160 170 180 190 200 mmHg B T * Most patients under ≥ 2 drugs
- 28. USA 27 Canada 13 England 6 France 24 Adapted from G. Mancia / L.Adapted from G. Mancia / L. RuilopeRuilope < 140/90 mmHg MarquesMarques--Vidal P et al. JVidal P et al. J Hum HypertensHum Hypertens 19971997 Percentages of Patients whose Hypertension is Controlled Percentages of Patients whosePercentages of Patients whose Hypertension is ControlledHypertension is Controlled Finland Spain 20 Germany Scotland < 160/95 mmHg Australia 19 India 9 20.5 17.522.5 > 65 years USA:USA: JNC VI.JNC VI. Arch Intern MedArch Intern Med 19971997 Canada:Canada: JoffresJoffres et al.et al. AmAm JJ HypertensHypertens 20012001 England:England: Colhoun et al. J Hypertens 1998Colhoun et al. J Hypertens 1998 France:France: Chamontin etChamontin et al.al. AmAm JJ HypertensHypertens 19981998
- 32. Limitations of Clinical Trials • Mostly high risk / elderly patients: i.e. younger / low risk patients are not represented • Short durations (4 – 5 years): i.e. the extra 20 – 30 years are not studied • Multiple combined primary end points: i.e. single end point as a beneficial effect, can not be concluded • Limitations of meta-analysis: i.e.: by definition, they are post-hoc analysis
- 33. Facts that we now know: • Antihypertensive Rx = Less CV morbidity & mortality • The benefits extend to isolated systolic hypertension • The beneficial effect is present across men & women in various ethnic groups • 30 -40% risk reduction in stroke • 20% risk reduction in coronary events • Large reduction in heart failure
- 35. 25 Biochemical Results – Fasting Glucose – mg/dL 100.5 (19.5)*103.1 (27.7)104.4 (28.5)4 Years Diabetes Incidence (follow-up fasting glucose 126 mg/dL) Among baseline nondiabetics with baseline <126 mg/dL Total 4 Years Baseline 4 Years Baseline 8.1%*9.8%*11.6% 93.3 (11.8)93.0 (11.4)93.1 (11.7) 121.5 (51.3)*123.7 (52.0)126.3 (55.6) 122.9 (56.1)123.1 (57.0)123.5 (58.3) LisinoprilAmlodipineChlorthalidone *p<.05 compared to chlorthalidone ALLHAT
- 36. Intention-to-Treat LIFE: New Onset Diabetes Losartan Atenolol EndpointRate Study Day 0 180 360 540 720 900 1080 1260 1440 1620 1800 1980 0.00 0.01 0.02 0.03 0.04 0.05 0.06 0.07 0.08 0.09 0.10 Adjusted Risk Reduction 25%, p<0.001 Unadjusted Risk Reduction 25%, p<0.001 7 B Dahlof et al. Lancet 2002;359:995-1003
- 37. CAPPP ACEI vs Conv STOP-2 ACEI vs Conv ALLHAT ACEI vs D HOPE ACEI vs PL STOP-2 CA vs Conv INSIGHT CA vs D ALLHAT CA vs D STOP-2 ACEI vs CA LIFE ARB vs BB SCOPE ARB vs Conv CHARM ARB vs PL INVEST CA vs Conv SOLVDT ACEI vs PL ASCOT CA vs Conv VALUE ARB vs CA -14 -4 -40 -34 -74 -2 -16 -23 -25 -2 -33 -25 -20 -21 -23 -80 -70 -60 -50 -40 -30 -20 -10 0 -30* -16** *=2 yrs, **=4 yrs New DM in antihypertensive drug trials%
- 41. Choosing drugs for patients newly diagnosed with hypertension < 55 years > 55 years or black patients at any age A* C or D A* + C or A* + D A* + C + D Consider 4th line drug: Further diuretic therapy or Alpha blocker or Beta blocker A = ACE inhibitor (* consider ARB if ACE intolerant) C = calcium channel blocker D = thiazide type diuretic
- 42. Conclusions • Hypertension is the commonest cause of major morbidity, but less than a quarter of patients are adequately treated. • A reduction in cardiovascular disease mortality and morbidity can be achieved through improved treatment and control of hypertension. • A greater choice of drugs are available for hypertension than for other chronic diseases • Rational choice of single and combination drugs facilitated by understanding their effects on the renin system, but systematic trial and error may still be necessary
Notes de l'éditeur
- It is well known that untreated hypertension can cause a progressive decline to cardiac failure or kidney failure.
- 3
- Circadian rhythms - the body’s 24-hour pattern of cyclical activity - have attracted attention for many years, most frequently with respect to the human sleep-wake cycle. A number of studies have assessed the impact of circadian variations on blood pressure (BP). BP levels follow a typical pattern: they are highest in the early morning and then decline to a trough value after midnight, to rise again at awakening (“morning surge”). Weber M.A. et al.; Rev Cardiovasc Med 5 (3): 148-155; 2004
- Several large-scale epidemiological studies have shown that adverse cardiovascular events occur unevenly during the circadian cycle, peaking in the early hours after awakening. An analysis of the data from the ISAM study, for example, demonstrated a circadian pattern in the incidence of MI: researchers timed the occurrence of MI on the basis of the onset of clinical symptoms, and found a significantly higher incidence between 6 a.m. and noon than in the other periods of the day. There is also evidence showing a circadian variation in the occurrence of sudden cardiac death, which was more prevalent between 7 and 11 a.m. Weber M.A. et al.; Rev Cardiovasc Med 5 (3): 148-155; 2004
- Proteinuria: predicting cardiovascular events and survival in diabetes Increased urinary albumin and protein excretion is associated with cardiovascular disease mortality independent of other cardiovascular risk factors in patients with type 2 diabetes. In a 7-year follow up of non-diabetic and type 2 diabetic patients, survival in type II diabetics was also shown to be related to the severity of proteinuria experienced by the patients (no proteinuria, borderline proteinuria and overt proteinuria). Furthermore, as well as overall survival, the incidence of cardiovascular events such as stroke, non-fatal myocardial infarction and coronary events also increase with severity of proteinuria. These findings are compatible with the hypothesis that increased urinary protein excretion is not merely an indicator of renal damage, but may be indicative of more widespread vascular damage.