RECENT GUIDELINES FOR THE MANAGEMENT OF ARTERIAL HYPERTENSION Apostolos I. Hatzitolios Associate...

RECENT GUIDELINES FOR THE MANAGEMENT OF ARTERIAL HYPERTENSION

Apostolos I. Hatzitolios Associate Professor of Internal Medicine1st Propedeutic Department of Internal MedicineDepartment of Vascular Diseases and HypertensionAristotle University of Thessaloniki, AHEPA HospitalThessaloniki, Central Macedonia, HELLAS

Diagnosis, regulation and treatment of hypertension in USA

NHANES III (Phase 2) 1991-1994

NHANES III (Phase 1) 1988-1991

51%

73%68%

31%

55% 54%

10%

29% 27%

Diagnosis

NHANES II 1976-1980

Treatment

Regulation

NHANES 1999-2000

70%

59%

34%

Hypert

en

sive

%

Guidelines 2007

European Society of Hypertension European Society of Cardiology

Journal of Hypertension 2007;25:1105-1187

Definitions and Classification of BP Levels (mmHg)

Category Systolic Diastolic

Optimal <120 and <80

Normal 120-129 and/or 80-84

High Normal 130-139 and/or 85-89

Grade 1 Hypertension

140-159 and/or 90-99

Grade 2Hypertension

160-179 and/or 100-109

Grade 3 Hypertension

≥ 180 and/or ≥ 110

Isolated Systolic Hypertension

≥ 140 and < 90

Stratification of CV risk in four categoriesBlood pressure (mmHg)

Other risk factors, TOD or disease

Normal SBP 120-129 or DBP 80-84

High normal SBP 130-139 or DBP 85-89

Grade 1 HTSBP 140-159 or DBP 90-99


Grade 3 HT SBP ≥180 or DBP ≥110

No other risk factors

Average risk

Average risk

Low added risk

Moderate added risk

High added risk

1-2 risk factors

Low added risk

Low added risk

Moderate added risk

Moderate added risk

Very high added risk

3 or more risk factors, TOD, DM or MS

Moderate added risk

High added risk

High added risk

High added risk


Established CV or renal disease






High/Very High Risk Subjects

BP ≥ 180 mmHg systolic and/or ≥ 110 mmHg diastolic High systolic BP > 160 mmHg with low diastolic BP (< 70

mmHg) ≥ 3 cardiovascular risk factors Diabetes mellitus or Metabolic syndrome Hypertension Target Organ Damage or Established CV or

renal disease

High/Very High Risk Subjects

One or more subclinical organ damages: Electrocardiographic (particularly with strain) or echocardiographic (particularly

concentric) LVH Ultrasound evidence of carotid artery wall thickening or plaque Increased arterial stiffness Slight increase in serum creatinine Reduced estimated glomerular filtration rate or creatinine clearance Microalbuminuria or proteinuria

Established cardiovascular disease • Heart • Cerebrovascular • Renal • Peripheral artery • Ophthalmic disease

Appropriate BP measurement

Allow the patients to relax for several minutes in a quiet place Take at least two measurements spaced by 1-2 min and additional measurements if

the first two are quite different [use phase I and V (disappearance) Korotkoff sounds to identify SBP and DBP]

Use a standard bladder but have a larger for fat arms and a smaller one for thin arms and children

Have the cuff at the heart level

Measure BP in both arms at first visit to detect possible differences due to peripheral vascular disease. In this instance, take the higher value as the reference one

Measure BP 1 and 5 min after assumption of the standing position in elderly subjects, diabetic patients and in other conditions in which postural hypotension may be frequent or suspected (e.g. heart, renal failure, SNS dysfunction, use of vasodilative agents)

Measure heart rate (at least 30 sec) after the second measurement in the sitting position

Home BP measurements

Self-measurement of BP at home is of clinical value, its prognostic significance is now demonstrated and these measurements should be encouraged in order to: provide more information on the BP lowering effect of

treatment at through and thus on the therapeutic coverage throughout the dose-to-dose time interval

improve patient’s adherence to treatment regimens

On the contrary, Self-measurement of BP should be discouraged when: it causes anxiety to the patient it induces self-modification of the treatment regimen

Ambulatory BP measurements

Although office BP should be used as reference, 24-h ambulatory BP monitoring may improve prediction of CV risk

Ambulatory BP should be considered, in particular, when: considerable variability of office BP is found over the same or

different visits high office BP is measured in subjects otherwise at low CV risk there is a marked discrepancy between BP values measured in the

office and at home there is a resistance to drug treatment hypotensive episodes are suspected, particularly in elderly and

diabetic patients office BP is elevated in pregnant women and pre-eclampsia is

suspected

BP thresholds (mmHg) for definition of Hypertension with different types of measurement

SBP DBP

Office or clinic 140 90

Home 130-135 85

24-hour 125-130 80

Day 130-135 85

Night 120 70

Particular conditions

Isolated office hypertension (White coat hypertension)

Office BP persistently ≥ 140/90 mmHg Normal daytime ambulatory or home BP < 130-135/85 Due to stress and SNS stimulation. CV risk is less than by raised office and ambulatory or home

BP but may be slightly greater than by normotension

Isolated ambulatory hypertension (Masked hypertension)

Office BP persistently normal (< 140/90 mmHg) Elevated ambulatory (≥ 125-130/80 mmHg) or home BP (≥ 130-135/85 mmHg)

CV risk is close to that of hypertension. Due to «normal» variation of circadian rhythm, autonomic

nervous system dysfunction, physical or psychological stress, night consumption of alcohol, smoking

and sleep apnea.

Guidelines for family and clinical history

1. Duration and previous level of high BP

2. Indications of secondary hypertension: family history of renal disease (polycystic kidneys)

renal disease, urinary tract infection, haematuria, analgesic abuse (parenchymal renal disease)

drug/substance intake, such as: oral contraceptives, liquorice, carbenoxolone, nasal drops, amphetamines, steroids, non-steroidal anti-inflammatory drugs, erythropoietin, cyclosporine, cocaine (drug induced hypertension)

episodes of sweating, headache, anxiety, palpitation (phaeochromocytoma)

episodes of muscle weakness and tetany (aldosteronism)


3. Risk factors:

family and personal history of hypertension and CV disease

family and personal history of dyslipidaemia

family and personal history of diabetes mellitus

smoking habits

dietary habits ; lack of physical exercise

obesity

snoring; sleep apnea (information also from partner)

Personality type; stress due to personal, family and environmental factors


4. Symptoms of organ damage: brain and eyes: headache, vertigo, transient ischemic

attacks, sensory or motor deficit , impaired vision heart: palpitation, chest pain, shortness of breath, swollen

ankles kidneys: thirst, polyuria, nocturia, haematuria peripheral arteries: cold extremities, intermittent

claudication

5. Previous antihypertensive therapy: Drug(s) used, efficacy and adverse effects

Physical examination for secondary hypertension, organ damage and visceral obesity

Signs suggesting secondary hypertension

Features of Cushing syndrome

Skin stigmata of neurofibromatosis (phaeochromocytoma)

Palpation of enlarged kidneys (polycystic kidneys)

Auscultation of abdominal murmurs

(renovascular hypertension)

Auscultation of precordial or chest murmurs; Diminished and delayed femoral pulses femoral BP

(aortic coarctation or aortic disease)

Physical examination for secondary hypertension, organ damage and visceral obesity

Signs of organ damage

Brain: murmurs over neck arteries, motor or sensory defects

Retina: fundoscopic adnormalities

Heart: location and characteristics of apical impulse, abnormal cardiac rhythms, ventricular gallop, pulmonary rates, peripheral oedema

Peripheral arteries: absence, reduction or asymmetry of pulses, cold extremities, ischemic skin lesions

Carotid arteries: systolic murmurs

Physical examination for secondary hypertension organ damage and visceral obesity

Evidence of visceral obesity

Body weight

Increased body mass index

[body weight (Kg)/height (m2)]

overweight ≥ 25 Kg/m2; obesity ≥ 30 Kg/m2

Increased waist circumference

(standing position) ♂ > 102 cm; ♀ > 88 cm

Laboratory investigations

Routine tests:

Hemoglobin and hematocrit Fasting plasma glucose Fasting serum triglycerides Serum total cholesterol, LDL-cholesterol, HDL-cholesterol Serum creatinine, potassium, uric acid

Urinalysis (complemented by microalbuminuria dipstick test and microscopic examination)

Estimated creatinine clearance (Cockroft-Gault formula) or glomerular filtration rate (MDRD formula)

Electrocardiogram (ECG) Thorax X-ray


Recommended tests

Echocardiogram

Carotid ultrasound

Quantitative proteinuria (if dipstick test positive)

Ankle-brachial BP index

Fundoscopy

Glucose tolerance test (if fasting plasma glucose > 5,6 mmol/l (102 mg/dL)

Home and 24h ambulatory BP monitoring

Pulse wave velocity measurement (where available)


Extended evaluation (domain of the specialist)

Further search for cerebral, cardiac, renal and vascular disease, mandatory in complicated hypertension

Search for suspected secondary hypertension suggested by history, physical examination or routine tests: measurement of renin, aldosterone,

corticosteroids,

catecholamines in plasma and/or urine;

renal and adrenal ultrasound;

computer-assisted tomography (CT);

magnetic resonance imaging (MRI);

arteriographies

Searching for subclinical organ damage Importance of subclinical organ damage as an intermediate stage

in the continuum of vascular disease and as a determinant of total CV risk.

Heart

Electrocardiography should be part of all routine assessment of hypertensives in order to detect LVH, LV strain, ischemic condition and arrhythmias

Echocardiography is recommended whenever a more sensitive detection of LVH is considered useful. Concentric remodeling and hypertrophy carries the worst prognosis, while LV diastolic dysfunction, consists an early ECHO sign, which can be evaluated by Doppler measurement of transmittal velocities.

Searching for subclinical organ damage

Blood vessels

Ultrasound scanning of extracranial carotid arteries is recommended in symptomatic carotid stenosis (previous TIA), but also in asymptomatic atherosclerosis suspected by carotid murmurs and reveals vascular hypertrophy, increased IMT, thickening of carotid bifurcation and presence of plaques.

Peripheral large artery stiffening (an important vascular alteration leading to isolated systolic hypertension in the elderly), can be measured by pulse wave velocity. This method might be more widely recommended if its availability were greater.

A low ankle-brachial BP index (<0,9) signals advanced peripheral artery disease


Kidney

Diagnosis of hypertension-related renal damage is based on a reduced renal function or detection of hyperalbuminuria

Measurement of serum creatinine as well as estimation of glomerular filtration rate by specific formulas, should be part of routine procedures, allowing classification of renal dysfunction and respective stratification of CV risk

Presence of urinary protein should be sought in all hypertensives by dipstick. In dipstick negative patients, low grade albuminuria, namely microalbuminuria, should also be determined in spot urine and as ratio to creatinine excretion


Fundoscopy

Examination of eye grounds is recommended only in hypertensive with severe hypertension, since mild retinal changes (grade 1: arteriolar narrowing; grade 2: arteriovenous nipping) appear to be largely non-specific alterations except in young patients

In contrast, grade 3 (hemorrhages and exudates) and 4 (papilloedema) retinal changes, present only in severe hypertension and are associated with an increased CV risk


Brain Silent brain infarcts, lacunar infarction (small / deep vessel

disease), microbleeds and white matter lesions are not infrequent among hypertensives, especially elderly and can be detected by MRI or CT (MRI being generally superior to CT)

Availability and costs do not allow use of these techniques in asymptomatic patients

In elderly hypertensives, cognitive tests (e.g. Mini-mental scale) may also help to detect initial brain deterioration

Treatment of hypertension

1. Non pharmacological

2. Pharmacological

Goals of treatment

Primary goal of treatment is to achieve the maximum reduction in the long-term total risk of CV disease

This requires not only the treatment of raised BP per se, but also of all associated reversible CV risk factors

BP should be reduced at least below 140/90 mmHg and even to lower values, if tolerated, in all hypertensive patients

Goals of treatment

Target BP should be at least < 130/80 mmHg in diabetics and in high or very high risk patients, such as those with associated clinical conditions, mainly stroke, myocardial infarction, renal dysfunction. Especially in proteinuria (<125/75 mmHg when >1gr/24h)

Despite the use of combination treatment, reducing SBP to <140 mmHg may be difficult and more so if the target is a reduction to <130 mmHg, moreover while a DBP reduction < 70 mmHg could be not beneficial.

Additional difficulties should be expected in elderly, obese and diabetic patients and in general, in patients with CV damage. In order to more easily achieve goal BP, antihypertensive treatment should be initiated before significant CV damage develops

Lifestyle changes

Lifestyle measures should be instituted whenever appropriate, in all patients, including those who require drug treatment, in order to lower BP, to control other risk factors and to reduce the number of doses of antihypertensive drugs to be subsequently administered

Lifestyle measures are also advisable in subjects with high normal BP (130-139 / 85-89) and additional risk factors to reduce the risk of developing hypertension

Lifestyle recommendations should not be given as lip service but instituted with adequate behavioral and expert support and reinforced periodically

Lifestyle changes

Lifestyle measures widely recognized to lower BP or CVrisk are:

smoking cessation weight reduction (and stabilization) physical exercise reduction of salt intake reduction of excessive alcohol intake increase in fruit and vegetable intake and decrease in

saturated and total fat intake (Mediterranean diet)

Lifestyle changes

Lifestyle changes Possible reduction in SBP(mmHg; mean= 38 mmHg)

Weight loss 5-20 mmHg/10Kg

Adoption of DASH diet 8-14 mmHg

Reduction of salt intake 2-8 mmHg

Physical exercise 4-9 mmHg

Reduction of excessive alcohol intake

2-4 mmHg

As long-term compliance with lifestyle measures is low and the BP response highly variable, patients under non pharmacological treatment should be followed-up closely to start drug therapy when needed and timely

Initiation of antihypertensive treatmentOther risk factors, Target Organ Damage or disease

Normal SBP 120-129 or DBP 80-84

High normal SBP 130-139 or DBP 85-89



Grade 3 HT SBP ≥180 or DBP ≥110

No other risk factors

No BP intervention No BP intervention

Lifestyle changes for several months then drug treatment if BP uncontrolled

Lifestyle changes for several weeks then drug treatment if BP uncontrolled

Lifestyle changes + immediate drug treatment

1-2 risk factors

Lifestyle changes Lifestyle changes




>3 risk factors, MS or TOD Lifestyle changes

Lifestyle changes and consider drug treatment Lifestyle changes +

drug treatmentLifestyle changes + drug treatment


Diabetes Lifestyle changesLifestyle changes + drug treatment

Established CV or renal disease






RECENT GUIDELINES FOR THE MANAGEMENT OF ARTERIAL HYPERTENSION Apostolos I. Hatzitolios Associate...

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