Hypertension Physiology, Pathophysiology and Clinical Managements Jun  Tao
Stroke and Ischemic Heart Disease (IHD) Mortality Rate in Each Decade of Age, Versus Usual Systolic BP at the Start of that Decade Mortality* Usual SBP (mmHg) 50–59 y 60–69 y 70–79 y 80–89 y Stroke Age at risk 256 128 64 32 16 8 4 2 1 0 120 140 160 180 IHD Usual SBP (mmHg ) 50–59 y 60–69 y 70–79 y 80–89 y Age at risk 40–49 y 256 128 64 32 16 8 4 2 1 0 120 140 160 180 *Floating absolute risk and 95% CI Reproduced from The Lancet, 360, Lewington et al. pp. 1903–13 Copyright  © 2002, with permission from Elsevier
Introduction Primary hypertension is a clinical syndrome characterized by the increase in systemic arterial pressure.
95% 0f the patients with hypertension are primary hypertension with unknown causes and 5% secondary hypertension with definitive causes.
Hypertension affects approximately 1 billion individual worldwide. In China the incidence of hypertension is about 180 million individuals.
Primary hypertension
Etiology and pathogenesis The   pathogenesis of primary hypertension is still unclear. There are many factors associate with it.
Genetic factors Sodium intake Renin agiotensin systems Sympathetic nervous system Endothelial dysfunction Insulin resistance Other factors
Genetic factors The offsprings of the hypertensive parents are prone to suffering from essential hypertension compared with that without hypertensive family.
Sodium intake  The mechanisms leading to hypertension are due to increased blood volume and the content of the sodium in the smooth muscle cells enhance following subsequent calcium increase.
RAAS system Renin -> Angiotensinogen  ->  Angiotensin I ->   Angiothesin II  ->  Increase   systemic arterial pressure
Sympathetic nervous activation The activation of Sympathetic nervous can augment periphery resistant which increase systemic   arterial   pressure.
Endothelial dysfunction Endothelium-derived vasodilating factors: NO; PGI2; EDHF. Endothelial-derived vasoconstricting  factors:ET; AGII; Superoxide anion.
Insulin resistance Increased absorbability to sodium Increased sympathetic nervous activation Increased cellular contents in sodium and  calcium Caused vascular wall hypertrophy
Other factors Obesity Smoking Intake alcohol OSAS Low calcium , magnesium and potassium.
Pathology Systemic atherosclerosis develops with increased intimal-medium thickness leading to ischemic alterations in target organs such as heart, brain, kidney and peripheral artery.
Blood vessel change Aorta and large arteries recurrent pulsatile stress produces uncoiling, disruption and calcification of elasstic fibres. At the same time, relatively inelastic collagen is increased.
This is a result of ageing as well as hypertension : both processes therefore cause loss of the normal elastic reservoir funtion of the aorta and large arteries.
 
This explains one curious feature of elderly hypertensive patients. Diastolic blood pressure in patients with isolated systolic hypertension is inversely related to prognosis.
Medium-sized arteries The predominant pathological change is wall thickening caused by increased deposition of collagenous material.
Resistance vessel The characteristic structural change in smaller arteries and arterioles responsible for peripheral vascular resistance is an increase in wall:lumen ratio.
In recent years it has become clear that what was thought to be a trophic response is largely if not entirely due to rearrangement of smooth muscle cells around a smaller lumen.
Specific organ changes in hypertension The heart Angina and myocardial infarction in the hypertensive patient are usually due to coronary atheroma.
Left ventricular hypertrophy is demonstrable in about 50 per cent of untreated hypertensive patients when echocardiography is used, and in 5 to 10 per cent with electrocardiography using conventional criteria.
Hpertrophy of left ventricle
 
Central nervous system Cerebral infarction in a hypertensive patient is usually attributable to atheroma of one of the larger cerebral arteries (usually the middle cerebral artery) and accounts for about 80 percent of the strokes which these patients suffer.
Intracerebral haemorrhage accounts for 10 to 15 percent,  usually the result of rupture of a small intracerebral degenerative microaneurysm.
 
 
The kidney The long-term renal damage produced by glomerular hypertension probably accountd for progressive glomerulosclerosis in essential hypertension.
Atheromatous renal vascular disease much more commonly causes renal impairment in elderly hypertensive subjects than younger patients with treated mild to moderate hypertension.
肾动脉硬化 肾动脉硬化 致密的肾盂 X 线影象
Malignant hypertension:  Fibrinoid necrosis of damaged arteriole of kidney
Retinopathy Keith-Wagener classification Stage I: constriction of retinal arterioles only. Stage II: constriction and sclerosis of retinal arterioles. Stage III: hemorrhages and exudates in addition to vascular changes. Stages IV: papilledema.
 
Symptoms Headache the classic hypertensive headache is present on walking in the morning, situated  in the occipital region of the head, radiating to the frontal area, throbbing in quality, and wears off during the course of the day.
Most headaches in hypertensive patients are tension headaches not directly related to blood pressure. Nevertheless, effective treatment of hypertension reduces the incidence of headache.
Epistaxis Whilst epistaxis is not associated with mild hypertension, it is much more common in moderate to severe hypertension.
Nocturia  this is one of the most frequent clinically apparent consequences of blood pressure elevation resulting from reduction in urine-concentrating capacity.
Others  dizziness;  flushed face;  fatigue; palpitation.
Symptoms associated with target organ damage Cardiovascular system Effort dyspnoea and orthopnoea suggest cardiac failure. Increased left ventricular mass is associated with decreased compliance and impaired cardiac output response to exercise.
Central nervous system Extensive disease of the perforating arteries may give rise to a lacunar state characterized by progressive pseudobulbar plasy and dementia.
Renal system Haematuria suggest the malignant phase of hypertension in the absence of any other cause.
Retinopathy Scotomas suggest fundal haemorrhages or exudates, whilst blurring of vision is associated with papilloedema.
Complications  Hypertensive emergencies Hypertensive encephalopathy Cerebrovascular disease Heart failure Chronic kidney disease   Dissection of aorta
physical examination  SBP>=140 mmHg or DBP>=90 mmHg. Loud aortic second sound Other physical signs indicate target organ damage
Diagnosis  Diagnosis of primary hypertension depends on repeatedly demonstrating higher –than-normal systolic and /or diastolic BP and excluding secondary hypertension.
 
CVD Risk Factors Hypertension* Cigarette smoking Obesity* (BMI  > 30 kg/m 2 ) Physical inactivity Dyslipidemia* Diabetes mellitus* Microalbuminuria or estimated GFR <60 ml/min Age (older than 55 for men, 65 for women) Family history of premature CVD  (men under age 55 or women under age 65) *Components of the metabolic syndrome.
Cardiovascular risk category of hypertension   Blood pressure ( mmHg )   Grade 1(SBP 140 ~ 159 or DBP 90 ~ 99)  Grade 2(SBP 160 ~ 179 or DBP 100 ~ 109) Grade 3(SBP ≥180 or DBP ≥110) No other risk factors Low-risk   Medium-risk High-risk   1 ~ 2  risk factors Moderate-risk   Medium-risk Very High-risk 3 or more  risk factors   , or diabetes , or target organ damage High-risk   High-risk   Very High-risk complications Very High-risk Very High-risk Very High-risk
Laboratory examinations Serum potassium, creatine, blood glucose, blood lipids, complete blood count, uric acid, ECG, cardiac and chest x-ray exam and funduscopic exam for retinopathy. ABPM Double peaks and one hollow
Goals of Therapy Reduce CVD and renal morbidity and mortality.  Treat to BP <140/90 mmHg or BP <130/80 mmHg in patients with diabetes or chronic kidney disease.  Achieve SBP goal especially in persons  > 50 years of age .
Blood Pressure Reduction of 2 mmHg Decreases the Risk of Cardiovascular Events by 7–10% Meta-analysis of 61 prospective, observational studies 1 million adults 12.7 million person-years 2 mmHg decrease in mean SBP 10% reduction in risk of stroke mortality 7% reduction in risk of ischaemic heart disease mortality Lewington et al. Lancet 2002;360:1903–13
Lifestyle Modification Weight reduction: the trial of hypertension prevention produced an average weight loss of 3.8 kg at 18 months, reduction of SBP and DBP by 2.9 and 2.3 mm Hg.
Exercise: Following increased physical activity, BP falls up 6-7 mm Hg for both SBP and DBP.
Sodium restriction Alcohol reduction and smoking cessation Stress reduction/relaxing training Dietary changes: low salt intake; potassium, magnesium and calcium supplementation; others.
Algorithm for Treatment of Hypertension Not at Goal Blood Pressure (<140/90 mmHg)  (<130/80 mmHg for those with diabetes or chronic kidney disease) Initial Drug Choices Lifestyle Modifications Drug(s) for the compelling indications  Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB)  as needed.  With Compelling  Indications Stage 2 Hypertension   (SBP  > 160 or DBP  > 100 mmHg)  2-drug combination for most (usually thiazide-type diuretic and  ACEI, or ARB, or BB, or CCB) Stage 1 Hypertension (SBP 140–159 or DBP 90–99 mmHg)  Thiazide-type diuretics for most.  May consider ACEI, ARB, BB, CCB,  or combination. Without Compelling  Indications Not at Goal  Blood Pressure Optimize dosages or add additional drugs  until goal blood pressure is achieved. Consider consultation with hypertension specialist.
Drug treatment  Diuretics ß -Blockers Calcium channel blockers ACE inhibitors Angiotensin II receptor blockers α-Adrenergic blockers
Diuretics  Indications : cardiac failure elderly patients systolic hypertension in elderly
ß –Blockers Indications :angina after myocardial infarction tachyarrhythmias cardiac failure (with care) Contraindications :asthma and chronic  obstructive airway disease peripheral vascular disease
Calcium antagonists: Indications :systolic hypertension in the elderly Contraindications:heart block (verapamil and diltiazem)
ACEI Indications: cardiac failure left ventricular dysfunction after myocardiac infarction (higher-  risk patients) diabetic nephropathy and other proteinuric renal disease Contraindications: pregnancy renovascular disease sodium and fluid depletion hyperkalaemia
ARB Indications: as for ACEI in presence of ACEI induced cough or intolerance Contraindications: as for ACEI
α-Adrenergic blockers Indications: prostatism Contraindications: urinary incontience ,
 
 
Classification and Management  of BP for adults *Treatment determined by highest BP category. † Initial combined therapy should be used cautiously in those at risk for orthostatic hypotension. ‡ Treat patients with chronic kidney disease or diabetes to BP goal of <130/80 mmHg.  BP classification   SBP* mmHg   DBP* mmHg  Lifestyle modification   Initial drug therapy   Without compelling indication  With compelling indications Normal  <120  and <80  Encourage  Prehypertension  120–139  or 80–89  Yes  No antihypertensive drug indicated.  Drug(s) for compelling indications.  ‡   Stage 1 Hypertension  140–159  or 90–99  Yes  Thiazide-type diuretics for most.  May consider ACEI, ARB, BB, CCB, or combination.  Drug(s) for the compelling indications. ‡ Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed.  Stage 2 Hypertension  > 160  or  > 100  Yes  Two-drug combination for most †  (usually thiazide-type diuretic and ACEI or ARB or BB or CCB).
 
 
Other medications for hypertensive patients Primary prevention ( 1 ) Aspirin: use 75mg daily if patient is aged   50 years with blood pressure controlled to <150/90 mm Hg and either; target organ damage, diabetes mellitus, or 10 year risk of cardiovascular disease of   20% (measured by using the new Joint British Societies’ cardiovascular disease risk chart) ( 2 ) Statin: use sufficient doses to reach targets if patient is aged up to at least 80 years, with a 10 year risk of cardiovascular disease of   20% (measured by using the new Joint British Societies’ cardiovascular disease risk chart) and with total cholesterol concentration   3.5mmol/l ( 3 ) Vitamins—no benefit shown, do not prescribe
Secondary prevention  (including patients with type 2 diabetes) Aspirin: use for all patients unless contraindicated ( 2 ) Statin: use sufficient doses to reach targets if patient is aged up to at least 80 years with a total cholesterol concentration   3.5 mmol/l (3) Vitamins— no benefit shown, do not prescribe Other medications for hypertensive patients
Targets for lipid lowering Ideal - TC<4.0mmol/l or LDL <2.0mmol/l or 25%    in TC or 30%    in LDL-C whichever is the greater ‘ Audit’ - TC <5.0mmol/l or LDL <3.0mmol/l or 25%    in TC or 30%    in LDL-C whichever is the greater Lipid targets
Some key points of the 2007 ESH and ESC guidelines
CVD Risk Factors There are some new risk factors : fasting blood glucose  5.6 ~ 6.9mmol/L ; pulse pressure (in the elderly)
Target organ damage ECG shows Left ventricular hypertrophy; PWV>12 m/s ; ABI<0.9;  GFR<50ml/ ( min·1.75m 2 )  creatinine clearance rate <60ml/min
ESH - ESC Guidelines, J Hypertens 2008 -BP < 140/90 mmHg in all hypertensive patients < 130/80 mmHg in hypertensive patients  with diabetes or renal disease -Control of all cardiovascular risk factors Goals of treatment
About drug treatment Diuretics, ß –Blockers, Calcium channel blockers, ACE inhibitors and Angiotensin II receptor blockers can be used in onset and maintenane therapy. Diuretics combined with ß –Blockers is not suitable for metabolic syndrome or high-risk diabetes patients. Low-dose combination therapy as first line treatment of mild-to-moderate hypertension
Screening and treatment of secondary forms of hypertension Renal parenchymal disease Renovascular hypertension Phaeochromocytoma Primary aldosteronism Cushing’syndrome Obstructive sleep apnoea Coarctation of aorta Drug-induced hypertension
谢谢!

10 hypertension

  • 1.
    Hypertension Physiology, Pathophysiologyand Clinical Managements Jun Tao
  • 2.
    Stroke and IschemicHeart Disease (IHD) Mortality Rate in Each Decade of Age, Versus Usual Systolic BP at the Start of that Decade Mortality* Usual SBP (mmHg) 50–59 y 60–69 y 70–79 y 80–89 y Stroke Age at risk 256 128 64 32 16 8 4 2 1 0 120 140 160 180 IHD Usual SBP (mmHg ) 50–59 y 60–69 y 70–79 y 80–89 y Age at risk 40–49 y 256 128 64 32 16 8 4 2 1 0 120 140 160 180 *Floating absolute risk and 95% CI Reproduced from The Lancet, 360, Lewington et al. pp. 1903–13 Copyright © 2002, with permission from Elsevier
  • 3.
    Introduction Primary hypertensionis a clinical syndrome characterized by the increase in systemic arterial pressure.
  • 4.
    95% 0f thepatients with hypertension are primary hypertension with unknown causes and 5% secondary hypertension with definitive causes.
  • 5.
    Hypertension affects approximately1 billion individual worldwide. In China the incidence of hypertension is about 180 million individuals.
  • 6.
  • 7.
    Etiology and pathogenesisThe pathogenesis of primary hypertension is still unclear. There are many factors associate with it.
  • 8.
    Genetic factors Sodiumintake Renin agiotensin systems Sympathetic nervous system Endothelial dysfunction Insulin resistance Other factors
  • 9.
    Genetic factors Theoffsprings of the hypertensive parents are prone to suffering from essential hypertension compared with that without hypertensive family.
  • 10.
    Sodium intake The mechanisms leading to hypertension are due to increased blood volume and the content of the sodium in the smooth muscle cells enhance following subsequent calcium increase.
  • 11.
    RAAS system Renin-> Angiotensinogen -> Angiotensin I -> Angiothesin II -> Increase systemic arterial pressure
  • 12.
    Sympathetic nervous activationThe activation of Sympathetic nervous can augment periphery resistant which increase systemic arterial pressure.
  • 13.
    Endothelial dysfunction Endothelium-derivedvasodilating factors: NO; PGI2; EDHF. Endothelial-derived vasoconstricting factors:ET; AGII; Superoxide anion.
  • 14.
    Insulin resistance Increasedabsorbability to sodium Increased sympathetic nervous activation Increased cellular contents in sodium and calcium Caused vascular wall hypertrophy
  • 15.
    Other factors ObesitySmoking Intake alcohol OSAS Low calcium , magnesium and potassium.
  • 16.
    Pathology Systemic atherosclerosisdevelops with increased intimal-medium thickness leading to ischemic alterations in target organs such as heart, brain, kidney and peripheral artery.
  • 17.
    Blood vessel changeAorta and large arteries recurrent pulsatile stress produces uncoiling, disruption and calcification of elasstic fibres. At the same time, relatively inelastic collagen is increased.
  • 18.
    This is aresult of ageing as well as hypertension : both processes therefore cause loss of the normal elastic reservoir funtion of the aorta and large arteries.
  • 19.
  • 20.
    This explains onecurious feature of elderly hypertensive patients. Diastolic blood pressure in patients with isolated systolic hypertension is inversely related to prognosis.
  • 21.
    Medium-sized arteries Thepredominant pathological change is wall thickening caused by increased deposition of collagenous material.
  • 22.
    Resistance vessel Thecharacteristic structural change in smaller arteries and arterioles responsible for peripheral vascular resistance is an increase in wall:lumen ratio.
  • 23.
    In recent yearsit has become clear that what was thought to be a trophic response is largely if not entirely due to rearrangement of smooth muscle cells around a smaller lumen.
  • 24.
    Specific organ changesin hypertension The heart Angina and myocardial infarction in the hypertensive patient are usually due to coronary atheroma.
  • 25.
    Left ventricular hypertrophyis demonstrable in about 50 per cent of untreated hypertensive patients when echocardiography is used, and in 5 to 10 per cent with electrocardiography using conventional criteria.
  • 26.
  • 27.
  • 28.
    Central nervous systemCerebral infarction in a hypertensive patient is usually attributable to atheroma of one of the larger cerebral arteries (usually the middle cerebral artery) and accounts for about 80 percent of the strokes which these patients suffer.
  • 29.
    Intracerebral haemorrhage accountsfor 10 to 15 percent, usually the result of rupture of a small intracerebral degenerative microaneurysm.
  • 30.
  • 31.
  • 32.
    The kidney Thelong-term renal damage produced by glomerular hypertension probably accountd for progressive glomerulosclerosis in essential hypertension.
  • 33.
    Atheromatous renal vasculardisease much more commonly causes renal impairment in elderly hypertensive subjects than younger patients with treated mild to moderate hypertension.
  • 34.
  • 35.
    Malignant hypertension: Fibrinoid necrosis of damaged arteriole of kidney
  • 36.
    Retinopathy Keith-Wagener classificationStage I: constriction of retinal arterioles only. Stage II: constriction and sclerosis of retinal arterioles. Stage III: hemorrhages and exudates in addition to vascular changes. Stages IV: papilledema.
  • 37.
  • 38.
    Symptoms Headache theclassic hypertensive headache is present on walking in the morning, situated in the occipital region of the head, radiating to the frontal area, throbbing in quality, and wears off during the course of the day.
  • 39.
    Most headaches inhypertensive patients are tension headaches not directly related to blood pressure. Nevertheless, effective treatment of hypertension reduces the incidence of headache.
  • 40.
    Epistaxis Whilst epistaxisis not associated with mild hypertension, it is much more common in moderate to severe hypertension.
  • 41.
    Nocturia thisis one of the most frequent clinically apparent consequences of blood pressure elevation resulting from reduction in urine-concentrating capacity.
  • 42.
    Others dizziness; flushed face; fatigue; palpitation.
  • 43.
    Symptoms associated withtarget organ damage Cardiovascular system Effort dyspnoea and orthopnoea suggest cardiac failure. Increased left ventricular mass is associated with decreased compliance and impaired cardiac output response to exercise.
  • 44.
    Central nervous systemExtensive disease of the perforating arteries may give rise to a lacunar state characterized by progressive pseudobulbar plasy and dementia.
  • 45.
    Renal system Haematuriasuggest the malignant phase of hypertension in the absence of any other cause.
  • 46.
    Retinopathy Scotomas suggestfundal haemorrhages or exudates, whilst blurring of vision is associated with papilloedema.
  • 47.
    Complications Hypertensiveemergencies Hypertensive encephalopathy Cerebrovascular disease Heart failure Chronic kidney disease Dissection of aorta
  • 48.
    physical examination SBP>=140 mmHg or DBP>=90 mmHg. Loud aortic second sound Other physical signs indicate target organ damage
  • 49.
    Diagnosis Diagnosisof primary hypertension depends on repeatedly demonstrating higher –than-normal systolic and /or diastolic BP and excluding secondary hypertension.
  • 50.
  • 51.
    CVD Risk FactorsHypertension* Cigarette smoking Obesity* (BMI > 30 kg/m 2 ) Physical inactivity Dyslipidemia* Diabetes mellitus* Microalbuminuria or estimated GFR <60 ml/min Age (older than 55 for men, 65 for women) Family history of premature CVD (men under age 55 or women under age 65) *Components of the metabolic syndrome.
  • 52.
    Cardiovascular risk categoryof hypertension   Blood pressure ( mmHg ) Grade 1(SBP 140 ~ 159 or DBP 90 ~ 99) Grade 2(SBP 160 ~ 179 or DBP 100 ~ 109) Grade 3(SBP ≥180 or DBP ≥110) No other risk factors Low-risk Medium-risk High-risk 1 ~ 2 risk factors Moderate-risk Medium-risk Very High-risk 3 or more risk factors , or diabetes , or target organ damage High-risk High-risk Very High-risk complications Very High-risk Very High-risk Very High-risk
  • 53.
    Laboratory examinations Serumpotassium, creatine, blood glucose, blood lipids, complete blood count, uric acid, ECG, cardiac and chest x-ray exam and funduscopic exam for retinopathy. ABPM Double peaks and one hollow
  • 54.
    Goals of TherapyReduce CVD and renal morbidity and mortality. Treat to BP <140/90 mmHg or BP <130/80 mmHg in patients with diabetes or chronic kidney disease. Achieve SBP goal especially in persons > 50 years of age .
  • 55.
    Blood Pressure Reductionof 2 mmHg Decreases the Risk of Cardiovascular Events by 7–10% Meta-analysis of 61 prospective, observational studies 1 million adults 12.7 million person-years 2 mmHg decrease in mean SBP 10% reduction in risk of stroke mortality 7% reduction in risk of ischaemic heart disease mortality Lewington et al. Lancet 2002;360:1903–13
  • 56.
    Lifestyle Modification Weightreduction: the trial of hypertension prevention produced an average weight loss of 3.8 kg at 18 months, reduction of SBP and DBP by 2.9 and 2.3 mm Hg.
  • 57.
    Exercise: Following increasedphysical activity, BP falls up 6-7 mm Hg for both SBP and DBP.
  • 58.
    Sodium restriction Alcoholreduction and smoking cessation Stress reduction/relaxing training Dietary changes: low salt intake; potassium, magnesium and calcium supplementation; others.
  • 59.
    Algorithm for Treatmentof Hypertension Not at Goal Blood Pressure (<140/90 mmHg) (<130/80 mmHg for those with diabetes or chronic kidney disease) Initial Drug Choices Lifestyle Modifications Drug(s) for the compelling indications Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed. With Compelling Indications Stage 2 Hypertension (SBP > 160 or DBP > 100 mmHg) 2-drug combination for most (usually thiazide-type diuretic and ACEI, or ARB, or BB, or CCB) Stage 1 Hypertension (SBP 140–159 or DBP 90–99 mmHg) Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination. Without Compelling Indications Not at Goal Blood Pressure Optimize dosages or add additional drugs until goal blood pressure is achieved. Consider consultation with hypertension specialist.
  • 60.
    Drug treatment Diuretics ß -Blockers Calcium channel blockers ACE inhibitors Angiotensin II receptor blockers α-Adrenergic blockers
  • 61.
    Diuretics Indications: cardiac failure elderly patients systolic hypertension in elderly
  • 62.
    ß –Blockers Indications:angina after myocardial infarction tachyarrhythmias cardiac failure (with care) Contraindications :asthma and chronic obstructive airway disease peripheral vascular disease
  • 63.
    Calcium antagonists: Indications:systolic hypertension in the elderly Contraindications:heart block (verapamil and diltiazem)
  • 64.
    ACEI Indications: cardiacfailure left ventricular dysfunction after myocardiac infarction (higher- risk patients) diabetic nephropathy and other proteinuric renal disease Contraindications: pregnancy renovascular disease sodium and fluid depletion hyperkalaemia
  • 65.
    ARB Indications: asfor ACEI in presence of ACEI induced cough or intolerance Contraindications: as for ACEI
  • 66.
    α-Adrenergic blockers Indications:prostatism Contraindications: urinary incontience ,
  • 67.
  • 68.
  • 69.
    Classification and Management of BP for adults *Treatment determined by highest BP category. † Initial combined therapy should be used cautiously in those at risk for orthostatic hypotension. ‡ Treat patients with chronic kidney disease or diabetes to BP goal of <130/80 mmHg. BP classification SBP* mmHg DBP* mmHg Lifestyle modification Initial drug therapy Without compelling indication With compelling indications Normal <120 and <80 Encourage Prehypertension 120–139 or 80–89 Yes No antihypertensive drug indicated. Drug(s) for compelling indications. ‡ Stage 1 Hypertension 140–159 or 90–99 Yes Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination. Drug(s) for the compelling indications. ‡ Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed. Stage 2 Hypertension > 160 or > 100 Yes Two-drug combination for most † (usually thiazide-type diuretic and ACEI or ARB or BB or CCB).
  • 70.
  • 71.
  • 72.
    Other medications forhypertensive patients Primary prevention ( 1 ) Aspirin: use 75mg daily if patient is aged  50 years with blood pressure controlled to <150/90 mm Hg and either; target organ damage, diabetes mellitus, or 10 year risk of cardiovascular disease of  20% (measured by using the new Joint British Societies’ cardiovascular disease risk chart) ( 2 ) Statin: use sufficient doses to reach targets if patient is aged up to at least 80 years, with a 10 year risk of cardiovascular disease of  20% (measured by using the new Joint British Societies’ cardiovascular disease risk chart) and with total cholesterol concentration  3.5mmol/l ( 3 ) Vitamins—no benefit shown, do not prescribe
  • 73.
    Secondary prevention (including patients with type 2 diabetes) Aspirin: use for all patients unless contraindicated ( 2 ) Statin: use sufficient doses to reach targets if patient is aged up to at least 80 years with a total cholesterol concentration  3.5 mmol/l (3) Vitamins— no benefit shown, do not prescribe Other medications for hypertensive patients
  • 74.
    Targets for lipidlowering Ideal - TC<4.0mmol/l or LDL <2.0mmol/l or 25%  in TC or 30%  in LDL-C whichever is the greater ‘ Audit’ - TC <5.0mmol/l or LDL <3.0mmol/l or 25%  in TC or 30%  in LDL-C whichever is the greater Lipid targets
  • 75.
    Some key pointsof the 2007 ESH and ESC guidelines
  • 76.
    CVD Risk FactorsThere are some new risk factors : fasting blood glucose 5.6 ~ 6.9mmol/L ; pulse pressure (in the elderly)
  • 77.
    Target organ damageECG shows Left ventricular hypertrophy; PWV>12 m/s ; ABI<0.9; GFR<50ml/ ( min·1.75m 2 ) creatinine clearance rate <60ml/min
  • 78.
    ESH - ESCGuidelines, J Hypertens 2008 -BP < 140/90 mmHg in all hypertensive patients < 130/80 mmHg in hypertensive patients with diabetes or renal disease -Control of all cardiovascular risk factors Goals of treatment
  • 79.
    About drug treatmentDiuretics, ß –Blockers, Calcium channel blockers, ACE inhibitors and Angiotensin II receptor blockers can be used in onset and maintenane therapy. Diuretics combined with ß –Blockers is not suitable for metabolic syndrome or high-risk diabetes patients. Low-dose combination therapy as first line treatment of mild-to-moderate hypertension
  • 80.
    Screening and treatmentof secondary forms of hypertension Renal parenchymal disease Renovascular hypertension Phaeochromocytoma Primary aldosteronism Cushing’syndrome Obstructive sleep apnoea Coarctation of aorta Drug-induced hypertension
  • 81.

Editor's Notes

  • #3 These data are taken from a meta-analysis of 61 prospective observational studies on deaths from vascular disease among subjects without vascular disease at baseline. The results demonstrated that the relationship of stroke mortality (left panel) and ischemic heart disease (IHD) mortality (right panel) to usual BP is strong and direct at all ages. As highlighted on the following slide, each difference of 20 mmHg in usual systolic BP is associated with a two-fold difference in the risk of stroke mortality and IHD mortality (between ages 40–69 years). The annual absolute difference in risk is greater in old age. Reference Lewington S, et al. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet 2002;360:1903–13.
  • #56 Trials have shown that BP lowering can produce rapid reductions in cardiovascular disease risk. In fact, even a 2 mmHg decrease in systolic BP would result in approximately 7% lower mortality risk from ischemic heart disease and a 10% lower mortality risk from stroke. Reference Lewington S, et al. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet 2002;360:1903–13.
  • #68 bhs guidelines 2004.boeh-ingel
  • #69 bhs guidelines 2004.boeh-ingel
  • #73 bhs guidelines 2004.boeh-ingel
  • #74 bhs guidelines 2004.boeh-ingel
  • #75 bhs guidelines 2004.boeh-ingel