2020 International Society of Hypertension global hypertension practice guidelines : Journal of Hypertension

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2020 International Society of Hypertension global hypertension practice guidelines

Unger, Thomasa; Borghi, Claudiob; Charchar, Fadic,d,e; Khan, Nadia A.f,g; Poulter, Neil R.h; Prabhakaran, Dorairaji,j,k; Ramirez, Agustinl; Schlaich, Markusm,n; Stergiou, George S.o; Tomaszewski, Maciejp,q; Wainford, Richard D.r,s,t; Williams, Bryanu; Schutte, Aletta E.v,w

Author Information
Journal of Hypertension 38(6):p 982-1004, June 2020. | DOI: 10.1097/HJH.0000000000002453
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Document reviewers: 

Hind Beheiry (Sudan), Irina Chazova (Russia), Albertino Damasceno (Mozambique), Anna Dominiczak (UK), Anastase Dzudie (Cameroon), Stephen Harrap (Australia), Hiroshi Itoh (Japan), Tazeen Jafar (Singapore), Marc Jaffe (USA), Patricio Jaramillo-Lopez (Colombia), Kazuomi Kario (Japan), Giuseppe Mancia (Italy), Ana Mocumbi (Mozambique), Sanjeevi N.Narasingan (India), Elijah Ogola (Kenya), Srinath Reddy (India), Ernesto Schiffrin (Canada), Ann Soenarta (Indonesia), Rhian Touyz (UK), Yudah Turana (Indonesia), Michael Weber (USA), Paul Whelton (USA), Xin Hua Zhang, (Australia), Yuqing Zhang (China).

Table of Contents









    8.1     Lifestyle modification 989

    8.2     Pharmacological treatment 989

    8.3     Adherence to antihypertensive treatment 989



    10.1     Resistant hypertension 994

    10.2     Secondary hypertension 994

    10.3     Hypertension in pregnancy 994

    10.4     Hypertensive emergencies 996

    10.5     Ethnicity, race and hypertension 997






Context and purpose of this guideline

Statement of remit: To align with its mission to reduce the global burden of raised blood pressure (BP), the International Society of Hypertension (ISH) has developed worldwide practice guidelines for the management of hypertension in adults, aged 18 years and older. The ISH Guidelines Committee extracted evidence-based content presented in recently published extensively reviewed guidelines and tailored ESSENTIAL and OPTIMAL standards of care in a practical format that is easy-to-use particularly not only in low-resource settings but also in high-resource settings- by clinicians, but also nurses and community health workers, as appropriate. Although distinction between low-resource and high-resource settings often refers to high (HIC) and low-income and middle-income countries (LMIC), it is well established that in HIC, there are areas with low-resource settings, and vice versa.

Herein optimal care refers to evidence-based standard-of-care articulated in recent guidelines [1,2] and summarized here, whereas essential standards recognize that optimal standards would not always be possible. Hence, essential standards refer to minimum standards of care. To allow specification of essential standards of care for low-resource settings, the Committee was often confronted with the limitation or absence in clinical evidence, and thus applied expert opinion.

In the Guidelines, differentiation between optimal and essential standards were not always possible, and were made in sections where it was most practical and sensible. The Guidelines Committee is also aware that some recommended essential standards may not be feasible in low-resource settings, for example, out-of-office BP measurements, the requirement of multiple visits for the diagnosis of hypertension, or advising the use of single pill combination therapy. Although challenging to implement, these guidelines may aid in local initiatives to motivate policy changes and serve as an instrument to drive local improvements in standards of care. Every effort should be made to achieve essential standards of care to reduce hypertension-induced cardiovascular morbidity and mortality.

Motivation: Raised BP remains the leading cause of death globally, accounting for 10.4 million deaths per year [3]. When reviewing global figures, an estimated 1.39 billion people had hypertension in 2010 [4]. However, BP trends show a clear shift of the highest BPs from high-income to low-income regions [5], with an estimated 349 million with hypertension in HIC and 1.04 billion in LMICs [4].

The large disparities in the regional burden of hypertension are accompanied by low levels of awareness, treatment, and control rates in LMIC, when compared with HIC. In response to poor global awareness for hypertension (estimated 67% in HIC and 38% in LMIC) [4], the ISH launched a global campaign to increase awareness of raised BP, namely the May Measurement Month initiative [6,7].

Despite several initiatives, the prevalence of raised BP and adverse impact on cardiovascular morbidity and mortality are increasing globally, irrespective of income [4,5]. It is, therefore, critical that population-based initiatives are applied to reduce the global burden of raised BP, such as salt-reduction activities and improving the availability of fresh fruit and vegetables. To improve the management of hypertension, the ISH has published in 2014 with the American Society of Hypertension, Clinical Practice Guidelines for the Management of Hypertension in the Community (see Section 11: Resources). Recently, we have observed a recent flurry of updated evidence-based guidelines arising mainly from high-income regions and countries, including the United States of America [2], Europe [1], United Kingdom [8], Canada [9], and Japan [10]. New developments include redefining hypertension [2], initiating treatment with a single pill combination therapy [1], advising wider out-of-office BP measurement [2,10], and lower BP targets [1,2,8,11,12].

Low-income and middle-income regions often follow the release of guidelines from high-income regions closely, as their resources and health systems to develop and implement local guidelines remain challenging. In Africa, only 25% of countries have hypertension guidelines [13], and in many instances, these guidelines are adopted from those of high-income regions. However, the adoption of guidelines from high-income regions are sometimes impractical as low-resource settings are confronted with a substantial number of obstacles including severe lack of trained healthcare professionals, unreliable electricity in rural clinics, low access to basic office BP devices and limited ability to conduct basic recommended diagnostic procedures and poor access to affordable high-quality medications. In both low-income and high-income regions, the ambiguities of latest guidelines are often met with confusion among health care providers, anxiety among patients [14], and they resulted in a call for global harmonization [15]. Guidelines from high-income regions may thus not fit global purpose [16].

Guideline development process: The 2020 ISH Global Hypertension Practice Guidelines were developed by the ISH Hypertension Guidelines Committee based on evidence criteria, (a) to be used globally; (b) to be fit for application in low-resource and high-resource settings by advising on essential and optimal standards; and (c) to be concise, simplified, and easy to use. They were critically reviewed and evaluated by numerous external hypertension experts from HIC and LMIC with expertise in the optimal management of hypertension and management in resource-constraint settings. These guidelines were developed without any support from industry or other sources.

Composition of the International Society of Hypertension Hypertension Guidelines Committee and Selection of External Reviewers: The ISH Hypertension Guidelines Committee was composed of members of the ISH Council; they were included on the basis of the following: specific expertise in different areas of hypertension; previous experience with the generation of hypertension guidelines, as well as representation of different regions of the world. A similar strategy was followed concerning the selection of external reviewers with particular consideration of representatives from LMICs.


  • In accordance with most major guidelines, it is recommended that hypertension be diagnosed when a person's SBP in the office or clinic is ≥140 mmHg and/or their DBP is ≥90 mmHg following repeated examination (see below, Section 3). Table 1 provides a classification of BP based on office BP measurement, Table 2 provides ambulatory and home BP values used to define hypertension; these definitions apply to all adults (>18 years old). These BP categories are designed to align therapeutic approaches with BP levels.
  • High-normal BP is intended to identify individuals who could benefit from lifestyle interventions and who would receive pharmacological treatment if compelling indications are present (see Section 9).
  • Isolated systolic hypertension defined as elevated SBP (≥140 mmHg) and low DBP (<90 mmHg) is common in young and in elderly people. In young individuals, including children, adolescents and young adults, isolated systolic hypertension is the most common form of essential hypertension. However, it is also particularly common in the elderly, in whom it reflects stiffening of the large arteries with an increase in pulse pressure (difference between SBP and DBP).
  • Individuals identified with confirmed hypertension (Grade 1 and Grade 2) should receive appropriate pharmacological treatment.
  • Details of home BP, office BP, and ambulatory BP measurement techniques are addressed in Section 3.
Classification of hypertension based on office blood pressure measurement
Criteria for hypertension based on office blood pressure, ambulatory blood pressure, and home blood pressure measurement



Hypertension diagnosis: office blood pressure measurement

  • The measurement of BP in the office or clinic is most commonly the basis for hypertension diagnosis and follow-up. Office BP should be measured according to recommendations in Table 3 and Fig. 1[1,2,17,18].
  • Whenever possible, the diagnosis should not be made on a single office visit. Usually two to three office visits at 1--4-week intervals (depending on the BP level) are required to confirm the diagnosis of hypertension. The diagnosis might be made on a single visit, if BP is ≥180/110 mmHg and there is evidence of cardiovascular disease (CVD) [1,2,17,18].
  • The recommended patient management according to office BP levels is presented in Table 4.
  • If possible and available, the diagnosis of hypertension should be confirmed by out-of-office BP measurement (see below) [1,2,19–21].
Recommendations for office blood pressure measurement
How to measure blood pressure.
Blood pressure measurement plan according to office blood pressure levels


Hypertension diagnosis: office blood pressure measurement

  • Initial evaluation: measure BP in both arms, preferably simultaneously. If there is a consistent difference between arms >10 mmHg in repeated measurements, use the arm with the higher BP. If the difference is >20 mmHg consider further investigation.
  • Standing blood pressure: measure in treated hypertensive patients after 1 min and again after 3 min when there are symptoms suggesting postural hypotension and at the first visit in the elderly and people with diabetes.
  • Unattended office blood pressure: multiple automated BP measurements taken while the patient remains alone in the office provide more standardized evaluation but also lower BP levels than usual office measurements with uncertain threshold for hypertension diagnosis [17,18,23,24]. Confirmation with out-of-office BP is again needed for most treatment decisions.

Hypertension diagnosis: out-of-office blood pressure measurement

  • Out-of-office BP measurements [by patients at home or with 24-h ambulatory blood pressure monitoring (ABPM)] are more reproducible than office measurements, more closely associated with hypertension-induced organ damage and the risk of cardiovascular events and identify the white-coat and masked hypertension phenomena (see below).
  • Out-of-office BP measurement is often necessary for the accurate diagnosis of hypertension and for treatment decisions. In untreated or treated subjects with office BP classified as high-normal BP or grade 1 hypertension (systolic 130–159 mmHg and/or diastolic 85–99 mmHg), the BP level needs to be confirmed using home or ambulatory BP monitoring (Table 5) [1,2,17–21].
  • Recommendations for performing home and ambulatory BP measurement are presented in Table 5.
Clinical use of home and ambulatory blood pressure monitoring

White-coat and masked hypertension

  • The use of office and out-of-office (home or ambulatory) BP measurements identifies individuals with white-coat hypertension, who have elevated BP only in the office (nonelevated ambulatory or home BP), and those with masked hypertension, who have nonelevated BP in the office but elevated BP out of the office (ambulatory or home) [1,2,17–21,25–27]. These conditions are common among both untreated subjects and those treated for hypertension. About 10–30% of subjects attending clinics because of high BP have white-coat hypertension and 10–15% have masked hypertension.
  • White-coat hypertension: these subjects are at intermediate cardiovascular risk between normotensives and sustained hypertensive patients. The diagnosis needs confirmation with repeated office and out-of-office BP measurements. If their total cardiovascular risk is low and there is no hypertension-mediated organ damage (HMOD), drug treatment may not be prescribed. However, they should be followed with lifestyle modification, as they may develop sustained hypertension requiring drug treatment [1,2,17–21,25–27].
  • Masked hypertension: these patients are at similar risk of cardiovascular events as sustained hypertensive patients. The diagnosis needs confirmation with repeated office and out-of-office measurements. Masked hypertension may require drug treatment aiming to normalize out-of-office BP [1,2,17–21,25–27].



Medical history

Patients with hypertension are often asymptomatic; however, specific symptoms can suggest secondary hypertension or hypertensive complications that require further investigation. A complete medical and family history is recommended and should include [1]:

  • Blood pressure: new onset hypertension, duration, previous BP levels, current and previous antihypertensive medication, other medications/over-the counter medicines that can influence BP, history of intolerance (side-effects) of antihypertensive medications, adherence to antihypertensive treatment, previous hypertension with oral contraceptives or pregnancy.
  • Risk factors: personal history of CVD [myocardial infarction, heart failure, stroke, transient ischemic attacks (TIA)], diabetes, dyslipidemia, chronic kidney disease (CKD), smoking status, diet, alcohol intake, physical activity, psychosocial aspects, history of depression. Family history of hypertension, premature CVD, (familial) hypercholesterolemia, diabetes.
  • Assessment of overall cardiovascular risk: in line with local guidelines/recommendations (see risk scores in Section 11 at the end of the document).
  • Symptoms/signs of hypertension/co-existent illnesses: chest pain, shortness of breath, palpitations, claudication, peripheral edema, headaches, blurred vision, nocturia, haematuria, dizziness.
  • Symptoms suggestive of secondary hypertension: muscle weakness/tetany, cramps, arrhythmias (hypokalemia/ primary aldosteronism), flash pulmonary edema (renal artery stenosis), sweating, palpitations, frequent headaches (pheochromocytoma), snoring, daytime sleepiness (obstructive sleep apnea), symptoms suggestive of thyroid disease (see Section 10 for full list of symptoms).

Physical examination

A thorough physical examination can assist with confirming the diagnosis of hypertension and the identification of HMOD and/or secondary hypertension and should include:

  • Circulation and heart: pulse rate/rhythm/character, jugular venous pulse/pressure, apex beat, extra heart sounds, basal crackles, peripheral edema, bruits (carotid, abdominal, femoral), radiofemoral delay.
  • Other organs/systems: enlarged kidneys, neck circumference >40 cm (obstructive sleep apnea), enlarged thyroid, increased BMI/waist circumference, fatty deposits, and coloured striae (Cushing's disease/syndrome).

Laboratory investigations and ECG

  • Blood tests: sodium, potassium, serum creatinine, and estimated glomerular filtration rate (eGFR). If available, lipid profile and fasting glucose.
  • Urine test: dipstick urine test.
  • 12-lead ECG: detection of atrial fibrillation, left ventricular hypertrophy (LVH), ischemic heart disease.


Additional diagnostic tests

Additional investigations whenever indicated can be undertaken to assess and confirm suspicion of HMOD, co-existent diseases, or/and secondary hypertension.

Imaging techniques

  • Echocardiography: LVH, systolic/diastolic dysfunction, atrial dilation, aortic coarctation.
  • Carotid ultrasound: plaques (atherosclerosis), stenosis.
  • Kidneys/renal artery and adrenal imaging: ultrasound/renal artery Duplex; CT-angiography/MR-angiography: renal parenchymal disease, renal artery stenosis, adrenal lesions, other abdominal pathology.
  • Fundoscopy: retinal changes, hemorrhages, papilledema, tortuosity, nipping.
  • Brain CT/MRI: ischemic or hemorrhagic brain injury because of hypertension.

Functional tests and additional laboratory investigations

  • Ankle--brachial index: peripheral (lower extremity) artery disease.
  • Further testing for secondary hypertension if suspected: aldosterone--renin ratio, plasma free metanephrines, late-night salivatory cortisol or other screening tests for cortisol excess.
  • Urinary albumin/creatinine ratio
  • Serum-Uric Acid (s-UA) levels
  • Liver function tests


Diagnostic approach

  • More than 50% of hypertensive patients have additional cardiovascular risk factors [28,29].
  • The most common additional risk factors are diabetes (15–20%), lipid disorders [elevated low density lipoprotein-cholesterol (LDL-C) and triglycerides (30%)], overweight-obesity (40%), hyperuricemia (25%) and metabolic syndrome (40%), as well as unhealthy lifestyle habits (e.g. smoking, high alcohol intake, sedentary lifestyle) [28–30].
  • The presence of one or more additional cardiovascular risk factors proportionally increases the risk of coronary, cerebrovascular, and renal diseases in hypertensive patients [1].

  • An evaluation of additional risk factors should be part of the diagnostic workup in hypertensive patients particularly in the presence of a family history of CVD.
  • Cardiovascular risk should be assessed in all hypertensive patients by easy-to-use scores based on BP levels and additional risk factors according to a simplified version of the approach proposed by ESC-ESH Guidelines (Table 6) [1].
  • A reliable estimate of cardiovascular risk can be obtained in daily practice by including:
  • Other risk factors: age (>65 years), sex (men > women), heart rate (>80 beats/min), increased body weight, diabetes, high LDL-C/TG, family history of CVD, family history of hypertension, early onset menopause, smoking habits, psychosocial or socio-economic factors. HMOD: LVH (LVH with ECG), moderate--severe CKD (CKD; eGFR <60 ml/ min/1.73 m2), any other available measure of organ damage. Disease: previous coronary heart disease (CHD), HF, stroke, peripheral vascular disease, atrial fibrillation, CDK stage 3+.
Simplified classification of hypertension risk according to additional risk factors, hypertension-mediated organ damage, and previous diseasea

  • The therapeutic strategy must include lifestyle changes, BP control to target, and the effective treatment of the other risk factors to reduce the residual cardiovascular risk.
  • The combined treatment of hypertension and additional cardiovascular risk factors reduces the rate of CVD beyond BP control.

Other additional risk factors

  • Elevated serum uric acid (s-UA) is common in patients with hypertension and should be treated with diet, urate-influencing drugs (losartan, fibrates, atorvastatin) or urate-lowering drugs in symptomatic patients [gout with s-UA >6 mg/dl (0.357 mmol/l)].
  • An increase in cardiovascular risk must be considered in patients with hypertension and chronic inflammatory diseases, chronic obstructive pulmonary disease (COPD), psychiatric disorders, psycho-social stressors where an effective BP control is warranted [1].


Definition and role of hypertension-mediated organ damage in hypertension management

Hypertension-mediated organ damage (HMOD) is defined as the structural or functional alteration of the arterial vasculature and/or the organs it supplies that is caused by elevated BP. End organs include the brain, the heart, the kidneys, central and peripheral arteries, and the eyes.

While assessment of overall cardiovascular risk is important for the management of hypertension, additional detection of HMOD is unlikely to change the management of those patients already identified as high risk (i.e. those with established CVD, stroke, diabetes, CKD, or familial hypercholesterolemia). However, it can provide important therapeutic guidance on 1) management for hypertensive patients with low or moderate overall risk through re-classification because of presence of HMOD, and 2) preferential selection of drug treatment based on the specific impact on HMOD [1].

Specific aspects of hypertension-mediated organ damage and assessment

  • Brain: TIA or strokes are common manifestations of elevated BP. Early subclinical changes can be detected most sensitively by MRI and include white matter lesions, silent microinfarcts, microbleeds, and brain atrophy. Due to costs and limited availability, brain MRI is not recommended for routine practice but should be considered in patients with neurologic disturbances, cognitive decline, and memory loss.
  • Heart: a 12-lead ECG is recommended for routine workup of patients with hypertension and simple criteria (Sokolow--Lyon index: SV1+RV5 ≥35 mm, Cornell index: SV3+RaVL >28 mm for men or >20 mm for women and Cornell voltage duration product: >2440 mm·ms) are available to detect presence of LVH. Sensitivity of ECG-LVH is very limited and a two-dimensional transthoracic echocardiogram (TTE) is the method of choice to accurately assess LVH [left ventricular mass index (LVMI): men >115 g/m2; women >95 g/m2] and relevant parameters including LV geometry, left atrial volume, LV systolic and diastolic function, and others.
  • Kidneys: kidney damage can be a cause and consequence of hypertension and is best assessed routinely by simple renal function parameters (serum creatinine and eGFR) together with investigation for albuminuria [dipstick or urinary albumin creatinine ratio (UACR) in early morning spot urine].
  • Arteries: three vascular beds are commonly assessed to detect arterial HMOD: 1) the carotid arteries through carotid ultrasound to detect atherosclerotic plaque burden/stenosis and intima--media thickness (IMT); 2) the aorta by carotid---femoral pulse wave velocity (PWV) assessment to detect large artery stiffening; and the lower extremity arteries by assessment of the ankle--brachial index (ABI). Although there is evidence to indicate that all three provide added value beyond traditional risk factors, their routine use is currently not recommended unless clinically indicated, that is, in patients with neurologic symptoms, isolated systolic hypertension, or suspected peripheral artery disease, respectively.
  • Eyes: fundoscopy is a simple clinical bedside test to screen for hypertensive retinopathy although interobserver and intraobserver reproducibility is limited. Fundoscopy is particularly important in hypertensive urgencies and emergencies to detect retinal haemorrhage, microaneurysms, and papilledema in patients with accelerated or malignant hypertension. Fundoscopy should be performed in patients with grade 2 hypertension, ideally by experienced examiners or alternative techniques to visualize the fundus (digital fundus cameras) where available.


The following assessments to detect HMOD should be performed routinely in all patients with hypertension:

  • serum creatinine and eGFR
  • dipstick urine test
  • 12-lead ECG

All other techniques mentioned above can add value to optimize management of hypertension in affected individuals and should be considered wherever clinically indicated and available. Serial assessment of HMOD (LVH and albuminuria) to monitor regression with antihypertensive treatment may be helpful to determine the efficacy of treatment in individual patients but this has not been sufficiently validated for most measures of HMOD.



Several medications and substances may increase BP or antagonize the BP-lowering effects of antihypertensive therapy in individuals (Table 7). It is important to note that the individual effect of these substances on BP can be highly variable with greater increases noted in the elderly, those with higher baseline BP, using antihypertensive therapy or with kidney disease.

  • Screen all patients (with hypertension and those at risk for hypertension) for substances that may increase BP or interfere with the BP-lowering effect of antihypertensive medications.
  • Where appropriate, consider reducing or eliminating substances that raise BP. If these substances are required or preferred, then treat BP to target regardless. (see resource [31] on possible antihypertensive therapies that target mechanisms underlying the raised BP induced by these substances).
Drug/substance exacerbators and inducers of hypertension


8.1. Lifestyle modifications

Healthy lifestyle choices can prevent or delay the onset of high BP and can reduce cardiovascular risk [46]. Lifestyle modification is also the first line of antihypertensive treatment. Modifications in lifestyle can also enhance the effects of antihypertensive treatment. Lifestyle modifications should include the following (Table 8) [47–64].

Lifestyle modifications
Ideal characteristics of drug treatment

Seasonal blood pressure variation [65]

BP exhibits seasonal variation with lower levels at higher temperatures and higher at lower temperatures. Similar changes occur in people travelling from places with cold to hot temperature, or the reverse. A meta-analysis showed average BP decline in summer of 5/3 mmHg (systolic/diastolic). BP changes are larger in treated hypertensive patients and should be considered when symptoms suggesting over-treatment appear with temperature rise, or BP is increased during cold weather. BP below the recommended goal should be considered for possible down-titration, particularly if there are symptoms suggesting overtreatment.

8.2. Pharmacological treatment

Contemporary data from over 100 countries [66,67] suggest that on average, <50% of adults with hypertension receive BP-lowering medication, with few countries performing better than this and many worse. This is despite the fact that a difference in BP of 20/10 mmHg is associated with a 50% difference in cardiovascular risk [68].

The pharmacological treatment strategies recommended here (Figs. 2–4) are largely compatible with those made in the most recent United States [2] and European guidelines [1,8].

Pharmacological treatment of hypertension: general scheme. See Table 2 (Section 2) for equivalent BP levels based on ambulatory or home BP recordings.
Office blood pressure targets for treated hypertension.
ISH core drug-treatment strategy. Data from [69–73]. Ideal characteristics of drug treatment (see Table 9).

8.3. Adherence to antihypertensive treatment


Adherence is defined as to the extent to which a person's behaviours, such as taking a medication, following a diet or executing lifestyle changes corresponds with agreed recommendations from a healthcare provider [74]. Nonadherence to antihypertensive treatment affects 10–80% of hypertensive patients and is one of the key drivers of suboptimal BP control [75–77]. Poor adherence to antihypertensive treatment correlates with the magnitude of BP elevation and is an indicator of poor prognosis in hypertensive patients [78–81]. The etiology of nonadherence to antihypertensive treatment is multifactorial and includes causes associated with the healthcare system, pharmacological therapy, the disease, patients, and their socioeconomic status [74].

Recommendations: adherence to antihypertensive therapy


  • Objective indirect (i.e. review of pharmacy records, pill counting, electronic monitoring devices) and direct (i.e. witnessed intake of medications, biochemical detection of medications in urine or blood) are generally preferred over subjective methods to diagnose nonadherence to antihypertensive treatment [80,85].
  • The most effective methods for management of nonadherence require complex interventions that combine counselling, self-monitoring, reinforcements, and supervision.



  • Hypertensive patients have several common and other comorbidities that can affect cardiovascular risk and treatment strategies.
  • The number of comorbidities increases with age, with the prevalence of hypertension and other diseases.
  • Common comorbidities include coronary artery disease (CAD), stroke, CKD, heart failure, and COPD.
  • Uncommon comorbidities include rheumatic diseases and psychiatric diseases.
  • Uncommon comorbidities are largely underestimated by guidelines and frequently treated with drugs often self-prescribed and possibly interfering with BP control.
  • Common and uncommon comorbidities should be identified and managed according to available evidence.

Common comorbidities and complications

Hypertension and coronary artery disease (CAD)

  • A strong epidemiological interaction exists between CAD and hypertension that accounts for 25–30% of acute myocardial infarctions [88].
  • Lifestyle changes are recommended (smoking cessation, diet, and exercise).
  • BP should be lowered if ≥140/90 mmHg and treated to a target <130/80 mmHg (<140/80 in elderly patients).
  • RAS-blockers, beta-blockers irrespective of BP levels calcium-channel blockers (CCBs) are first-line drugs in hypertensive patients [1].
  • Lipid-lowering treatment with an LDL-C target <55 mg/dl (1.4 mmol/l) [89].
  • Antiplatelet treatment with acetyl salicylic acid is routinely recommended [1].

Hypertension and previous stroke

  • Hypertension is the most important risk factor for ischemic or hemorrhagic stroke [90].
  • Stroke can be largely prevented by BP control.
  • BP should be lowered if ≥140/90 mmHg and treated to a target <130/80 mmHg (<140/80 in elderly patients) [1].
  • RAAS blockers, CCBs, and diuretics are first-line drugs [1].
  • Lipid-lowering treatment is mandatory with a LDL-C target <70 mg/dl (1.8 mmol/l) in ischemic stroke [1].
  • Antiplatelet treatment is routinely recommended for ischemic but not hemorrhagic stroke and should be carefully considered in patients with hemorrhagic stroke only in the presence of a strong indication [1].

Hypertension and heart failure (HF)

  • Hypertension is a risk factor for the development of heart failure with reduced ejection fraction (HFrEF), and with preserved ejection fraction (HFpEF). Clinical outcome is worse and mortality is increased in the hypertensive patients with HF [2].
  • Lifestyle changes are recommended (diet and exercise).
  • Treating hypertension has a major impact on reducing the risk of incident heart failure and heart failure hospitalization. BP should be lowered if ≥140/90 mmHg and treated to a target <130/80 mmHg but >120/70 mmHg.
  • RAS blockers, beta-blockers, and mineralocorticoid receptor antagonists are all effective in improving clinical outcome in patients with established HFrEF, whereas for diuretics, evidence is limited to symptomatic improvement [1]. CCBs are indicated on in case of poor BP control.
  • Angiotensin receptor-neprilysin inhibitor (ARNI; Sacubitril-Valsartan) is indicated for the treatment of HFrEF as an alternative to ACE inhibitors or ARBs also in hypertensive populations. The same treatment strategy can be applied to patients with HFpEF even if the optimal treatment strategy is not known [91].

Hypertension and chronic kidney disease (CKD)

  • Hypertension is a major risk factor for the development and progression of albuminuria and any form of CKD [92].
  • A lower eGFR is associated with resistant hypertension, masked hypertension, and elevated night-time BP values [92].
  • The effects of BP-lowering on renal function (and albuminuria) are dissociated from cardiovascular benefit [1].
  • BP should be lowered if ≥140/90 mmHg and treated to a target <130/80 mmHg (<140/80 in elderly patients) [1].
  • RAS blockers are first-line drugs because they reduce albuminuria in addition to BP control. CCBs and diuretics (loop-diuretics if eGFR <30 ml/min/1.73 m2) can be added [1].
  • eGFR, microalbuminuria, and blood electrolytes should be monitored [1].

Hypertension and chronic obstructive pulmonary disease (COPD)

  • Hypertension is the most frequent comorbidity in patients with COPD.
  • BP should be lowered if ≥140/90 mmHg and treated to a target <130/80 mmHg (<140/80 in elderly patients).
  • Lifestyle changes (smoking cessation) are mandatory [93].
  • Environmental (air) pollution should be considered and avoided if possible [93].
  • The treatment strategy should include an Angiotensin AT1-Receptor Blocker (ARB) and CCB and/or diuretic, whereas beta blockers (β1-receptor selective) may be used in selected patients (e.g. CAD, HF).
  • Additional cardovascular risk factors should be managed according to cardiovascular risk profile.


  • People living with HIV are at increased cardiovascular risk [40].
  • There may be a drug interaction with CCB under most of the antiretroviral therapies.
  • Hypertension management should be similar to the general hypertensive populations.

Management of comorbidities:



  • BP should be lowered if ≥140/90 mmHg and treated to a target <130/80 mmHg (<140/80 in elderly patients) [96].
  • The treatment strategy should include a renin--angiotensin system (RAS) inhibitor [and a calcium channel blocker (CCB) and/or thiazide-like diuretic].
  • The treatment should include a statin in primary prevention if LDL-C >70 mg/dl (1.8 mmol/l) (diabetes with target organ damage) or >100 mg/dl (2.6 mmol/l) (uncomplicated diabetes).
  • The treatment should include glucose and lipid lowering as per current guidelines (see Resources, Section 11).

Lipid disorders

  • BP should be lowered as done in the general population, preferentially with RAS-inhibitors (ARB, ACE-I) and CCBs [97].
  • Statins are the lipid-lowering treatment of choice with or without ezetimibe and/or PCSK9 inhibitor (in the optimal setting) [98].
  • Serum triglyceride lowering should be considered if >200 mg/dl (2.3 mmol/l) particularly in patients with hypertension and diabetes mellitus. Possible additional benefits using fenofibrate in low HDL/high triglyceride subgroup.

Metabolic syndrome (MS)

  • Patients with hypertension and MS have a high-risk profile.
  • The diagnosis of MS should be made by separate evaluation of single components.
  • The treatment of MS is based on changes in lifestyle (diet and exercise).
  • The treatment of hypertension and MS should include BP control as in the general population and treatment of additional risk factors based on level and overall cardiovascular risk (SCORE and/or ASCVD calculator).

Other comorbidities

(see Table 10)

Outline of evidence-based management of other comorbidities and hypertension

Hypertension and inflammatory rheumatic diseases (IRD)

  • IRD (rheumatoid arthritis, psoriasis--arthritis, etc.) are associated with an increased prevalence of hypertension under diagnosed and poorly controlled [99,100].
  • IRD show an increase in cardiovascular risk only partially related to cardiovascular risk factors [99].
  • Rheumatoid arthritis is predominant among IRD.
  • The presence of IRD should increase one step of cardiovascular risk [99].
  • BP should be lowered as in the general population, preferentially with RAS-inhibitors (evidence of an overactive RAAS system [100]) and CCBs.
  • Underlying diseases should be effectively treated by reducing inflammation and by avoiding high doses of NSAIDs.
  • Lipid-lowering drugs should be used according to cardiovascular risk profile (SCORE/ASCVD calculator) also considering the effects of biologic drugs [100].

Hypertension and psychiatric diseases

  • The prevalence of hypertension is increased in patients with psychiatric disorders and in particular depression [101,102].
  • According to guidelines, psychosocial stress and major psychiatric disorders increase the cardiovascular risk.
  • Depression has been associated with cardiovascular morbidity and mortality, suggesting the importance of BP control [101].
  • BP should be lowered as in the general population, preferentially with RAS-inhibitors and diuretics with a lesser rate of pharmacological interactions under antidepressants. CCBs and alpha1-blockers should be used with care in patients with orthostatic hypotension [e.g. serotonin reuptake inhibitors (SRI's)].
  • The risk of pharmacologic interactions, ECG abnormalities and postural BP changes must be considered.
  • Beta-blockers (not metoprolol) should be used in presence of drug-induced tachycardia (antidepressant drugs, antipsychotic drugs) [103].
  • Additional risk factors should be managed according to cardiovascular risk profile (SCORE/ASCVD calculator, see Section 11, Resources).


10.1. Resistant hypertension


Resistant hypertension is defined as seated office BP >140/90 mmHg in a patient treated with three or more antihypertensive medications at optimal (or maximally tolerated) doses including a diuretic and after excluding pseudo-resistance (poor BP measurement technique, white-coat effect, nonadherence, and suboptimal choices in antihypertensive therapy) [104,105] as well as the substance/drug-induced hypertension and secondary hypertension [79]. Resistant hypertension affects around 10% of hypertensive individuals, has a negative impact on well-being [106] and increases the risk of coronary artery disease, chronic heart failure, stroke, end-stage renal disease, and all-cause mortality [107]. Approximately 50% of patients diagnosed with resistant hypertension have pseudoresistance rather than true resistant hypertension [104,105,108].


  • If seated office BP >140/90 mmHg in patients managed with three or more antihypertensive medications at optimal (or maximally tolerated) doses including a diuretic, first exclude causes of pseudoresistance (poor BP measurement technique, white-coat effect, nonadherence, and suboptimal choices in antihypertensive therapy), and substance-induced increases in BP.
  • Consider screening patients for secondary causes as appropriate (refer to Section 10.2).
  • Optimize the current treatment regimen including health behaviour change and diuretic-based treatment (maximally tolerated doses of diuretics, and optimal choice of diuretic: use of thiazide-like rather than thiazide diuretics, and initiation of loop diuretics for eGFR <30 ml/min/1.73 m2 or clinical volume overload) [109].
  • Add a low dose of spironolactone as the fourth line agent in those whose serum potassium is <4.5 mmol/l and whose eGFR is >45 ml/min/1.73 m2 to achieve BP targets [8,71,110]. If spironolactone is contraindicated or not tolerated, amiloride, doxazosin, eplerenone, clonidine, and beta-blockers are alternatives, or any available antihypertensive class not already in use [1,111–114].
  • Resistant hypertension should be managed in specialist centres with sufficient expertise, and resources necessary to diagnose and treat this condition [115].

10.2. Secondary hypertension [116–121]


A specific cause of secondary hypertension can be identified in 5–10% of hypertensive patients (Table 11). Early diagnosis of secondary hypertension and the institution of appropriate targeted treatment have the potential to cure hypertension in some patients or improve BP control/reduce the number of prescribed antihypertensive medications in others. The most common types of secondary hypertension in adults are renal parenchymal disease, renovascular hypertension, primary aldosteronism, chronic sleep apnea, and substance/drug-induced.

Features of secondary hypertension


  • Consider screening for secondary hypertension in 1) patients with early-onset hypertension (<30 years of age) in particular in the absence of hypertension risk factors (obesity, metabolic syndrome, familial history, etc.), 2) those with resistant hypertension, 3) individuals with sudden deterioration in BP control, 4) hypertensive urgency and emergency, 5) those presenting with high probability of secondary hypertension based on strong clinical clues.
  • In patients with resistant hypertension, investigations for secondary hypertension should generally be preceded by exclusion of pseudoresistant hypertension and drug/substance-induced hypertension.
  • Basic screening for secondary hypertension should include a thorough assessment of history, physical examination (see clinical clues), basic blood biochemistry (including serum sodium, potassium, eGFR, TSH) and dipstick urine analysis.
  • Further investigations for secondary hypertension (additional biochemistry/imaging/others) should be carefully chosen based on information from history, physical examination, and basic clinical investigations.
  • Consider referring for further investigation and management of suspected secondary hypertension to a specialist centre with access to appropriate expertise and resources.

10.3. Hypertension in pregnancy [122–126]

Hypertension in pregnancy is a condition affecting 5–10% of pregnancies worldwide. Maternal risks include placental abruption, stroke, multiple organ failure (liver, kidney), disseminated vascular coagulation. Fetal risks include intrauterine growth retardation, preterm birth, intrauterine death. Hypertension in pregnancy includes the following conditions:

  • Pre-existing hypertension: starts before pregnancy or <20 weeks of gestation, and lasts >6 weeks postpartum combined with proteinuria.
  • Gestational hypertension: starts >20 weeks of gestation, and lasts <6 weeks postpartum.
  • Pre-existing hypertension with superimposed gestational hypertension with proteinuria.
  • Pre-eclampsia: hypertension with proteinuria [>300 mg/24 h or ACR >30 mg/mmol (265 mg/g)]. Predisposing factors are pre-existing hypertension, hypertensive disease during previous pregnancy, diabetes, renal disease, first or multiple pregnancy, autoimmune disease (SLE). Risks are fetal growth restriction, pre-term birth.
  • Eclampsia: hypertension in pregnancy with seizures, severe headaches, visual disturbance, abdominal pain, nausea and vomiting, low urinary output: immediate treatment and delivery required.
  • HELLP Syndrome: Hemolysis, Elevated Liver enzymes, Low Platelets: Immediate treatment and delivery required.

Blood pressure measurement in pregnancy

ESSENTIAL Office BP measurement following general guidelines. Take office BP measurement using a manual auscultatory device, or an automated upper-arm cuff device which has been validated specifically in pregnancy and pre-eclampsia (list of validated devices at www.stridebp.org).

OPTIMAL ABPM or home BP monitoring using devices validated specifically in pregnancy and pre-eclampsia to evaluate white coat hypertension, diabetes mellitus, nephropathy.

Investigation of hypertension in pregnancy


Urine analysis, full blood count, liver enzymes, hematocrit, serum creatinine, and s-UA. Test for proteinuria in early pregnancy (pre-existing renal disease) and second half of pregnancy (pre-eclampsia). A dipstick test >1+ should be followed up with UACR in a single spot urine; UACR <30 mg/mmol excludes proteinuria.


Ultrasound of kidneys and adrenals, free plasma metanephrines (if clinical features of pheochromocytoma); Doppler ultrasound of uterine arteries (after 20 weeks of gestation is useful to detect those at higher risk of gestational hypertension, pre-eclampsia, and intrauterine growth retardation).

Prevention of pre-eclampsia:

Women at high risk (hypertension in previous pregnancy, CKD, autoimmune disease, diabetes, chronic hypertension), or moderate risk (first pregnancy in a woman >40, pregnancy interval >10 years, BMI >35 kg/m2, family history of pre-eclampsia, multiple pregnancies): 75–162 mg aspirin at weeks 12–36. Oral calcium supplementation of 1.5–2 g/day is recommended in women with low dietary intake (<600 mg/day).

Management of hypertension in pregnancy

Mild hypertension: drug treatment at persistent BP >150/95 mmHg in all women.

Drug treatment at persistent BP >140/90 mmHg in gestational hypertension, pre-existing hypertension with superimposed gestational hypertension; hypertension with subclinical HMOD at any time during pregnancy. First choices: Methyldopa, beta-blockers (labetalol), and dihydropyridine-calcium channel blockers (DHP-CCBs) [nifedipine (not capsular), nicardipine). Contraindicated: RAS Blockers (ACE-I, ARB, direct renin inhibitors (DRI)] because of adverse fetal and neonatal outcomes.

Severe hypertension: At BP >170 mmHg systolic and/or >110 mmHg diastolic: immediate hospitalization is indicated (emergency). Treatment with intravenous labetalol (alternative intravenous nicardipine, esmolol, hydralazine, urapidil), oral methyldopa or DHP-CCBs [nifedipine (not capsular) nicardipine]. Add magnesium (hypertensive crisis to prevent eclampsia). In pulmonary edema: Nitroglycerin intravenous infusion. Sodium-nitroprusside should be avoided because of the danger of fetal cyanide poisoning with prolonged treatment.

Delivery in gestational hypertension or pre-eclampsia: at week 37 in asymptomatic women. Expedite delivery in women with visual disturbances, haemostatic disorders.

Blood pressure postpartum: if hypertension persists, any of recommended drugs except methyldopa (postpartum depression).

Breastfeeding: all antihypertensives excreted into breast milk at low concentrations. Avoid atenolol, propranolol, nifedipine (high concentration in milk). Prefer long-acting CCBs. Refer to prescribing information.

Long-term consequences of gestational hypertension: increased risk of hypertension and CVD (stroke, ischemic heart disease) in later life.

ESSENTIAL Lifestyle adjustment

OPTIMAL Lifestyle adjustment and annual checkups (BP, metabolic factors)

10.4. Hypertensive emergencies

Definition of hypertensive emergencies and their clinical presentation

A hypertensive emergency is the association of substantially elevated BP with acute HMOD. Target organs include the retina, brain, heart, large arteries, and the kidneys [127]. This situation requires rapid diagnostic workup and immediate BP reduction to avoid progressive organ failure. Intravenous therapy is usually required. The choice of antihypertensive treatment is predominantly determined by the type of organ damage. Specific clinical presentations of hypertensive emergencies include:

Malignant hypertension: severe BP elevation (commonly >200/120 mmHg) associated with advanced bilateral retinopathy (hemorrhages, cotton wool spots, papilledema).

Hypertensive encephalopathy: severe BP elevation associated with lethargy, seizures, cortical blindness, and coma in the absence of other explanations.

Hypertensive thrombotic microangiopathy: severe BP elevation associated with haemolysis and thrombocytopenia in the absence of other causes and improvement with BP lowering therapy.

Other presentations of hypertensive emergencies include: severe BP elevation associated with cerebral hemorrhage, acute stroke, acute coronary syndrome, cardiogenic pulmonary edema, aortic aneurysm/dissection, and severe pre-eclampsia and eclampsia.

Patients with substantially elevated BP who lack acute HMOD are not considered a hypertensive emergency and can typically be treated with oral antihypertensive therapy [128].

Clinical presentation and diagnostic workup

The clinical presentation of a hypertensive emergency can vary and is mainly determined by the organ (s) acutely affected. There is no specific BP threshold to define a hypertensive emergency.

Symptoms include: headaches, visual disturbances, chest pain, dyspnoea, neurologic symptoms, dizziness and more unspecific presentations.

Medical history: pre-existing hypertension, onset and duration of symptoms, potential causes [nonadherence with prescribed antihypertensive drugs, lifestyle changes, concomitant use of BP-elevating drugs (NSAIDS, steroids, immune-suppressants, sympathomimetics, cocaine, anti-angiogenic therapy)].

ESSENTIALThorough physical examination: cardiovascular and neurologic assessment. Laboratory analysis: haemoglobin, platelets, creatinine, sodium, potassium, lactate dehydrogenase (LDH), haptoglobin, urinalysis for protein, urine sediment. Examinations: fundoscopy, ECG.

OPTIMAL Additional investigations may be required and indicated depending on presentation and clinical findings and may be essential in the context: Troponins (chest pain), chest X-ray (congestion/fluid overload), transthoracic echocardiogram (cardiac structure and function), CT/MRI brain (cerebral hemorrhage/stroke), CT-angiography thorax/abdomen (acute aortic disease). Secondary causes can be found in 20–40% of patients presenting with malignant hypertension [118] and appropriate diagnostic workup to confirm or exclude secondary forms is indicated.

Diagnostic tests and acute therapeutic management

The overall therapeutic goal in patients presenting with hypertensive emergencies is a controlled BP reduction to safer levels to prevent or limit further hypertensive damage while avoiding hypotension and related complications. There is a lack of randomized controlled trial data to provide clear cut guidance on BP targets and times within which these should be achieved. Most recommendations are based on expert consensus. The type of acute HMOD is the main determinant of the preferred treatment choice. The timeline and magnitude of BP reduction is strongly dependent on the clinical context. For example, acute pulmonary edema and aortic dissection require rapid BP reduction, whereas BP levels not exceeding 220/120 mmHg are generally tolerated in acute ischemic stroke for certain periods. Table 12 provides a general overview of timelines and BP targets as well as preferred antihypertensive drug choices with most common clinical presentations. Availability of drugs and local experience with individual drugs are likely to influence the choice of drugs. Labetalol and nicardipine are generally safe to use in all hypertensive emergencies and should be available wherever hypertensive emergencies are being managed. Nitroglycerine and nitroprusside are specifically useful in hypertensive emergencies including the heart and the aorta.

Hypertensive Emergencies Requiring Immediate blood pressure lowering

Specific situations

Sympathetic hyperreactivity: If intoxication with amphetamines, sympathomimetics or cocain is suspected as cause of presentation with a hypertensive emergency, use of benzodiazepines should be considered prior to specific antihypertensive treatment. Phentolamine, a competitive alpha-receptor blocking agent and clonidine, a centrally sympatholytic agent with additional sedative properties are useful if additional BP-lowering therapy is required. Nicardipine and nitroprusside are suitable alternatives.

Pheochromocytoma: the adrenergic drive associated with pheochromocytoma responds well to phentolamine. Beta-blockers should only be used once alpha-blockers have been introduced to avoid acceleration of hypertension. Urapidil and nitroprusside are additional suitable options.

Pre-eclampsia/eclampsia: see section 10.3 ‘Hypertension in pregnancy’.


Patients who experienced a hypertensive emergency are at increased risk of cardiovascular and renal disease [129,130]. Thorough investigation of potential underlying causes and assessment of HMOD is mandatory to avoid recurrent presentations with hypertensive emergencies. Similarly, adjustment and simplification of antihypertensive therapy paired with advice for lifestyle modification will assist to improve adherence and long-term BP control. Regular and frequent follow-up (monthly) is recommended until target BP and ideally regression of HMOD has been achieved.

10.5. Ethnicity, race, and hypertension

Hypertension prevalence, treatment, and control rates vary significantly according to ethnicity. Such differences are mainly attributed to genetic differences, but lifestyle and socioeconomic status possibly filters through into health behaviours, such as diet – which appear to be major contributors.

Populations from African descent

  • Black populations, whether residing in Africa, the Caribbean, USA or Europe, develop hypertension and associated organ damage at younger ages, have a higher frequency of resistant and night-time hypertension, and a higher risk of kidney disease [131], stroke, heart failure, and mortality [132], than other ethnic groups.
  • This increased cardiovascular risk may be because of physiological differences including a suppressed RAAS [133,134], altered renal sodium handling [135], increased cardiovascular reactivity [136], and early vascular aging (large artery stiffness) [137].
  • Management of hypertension:
    • - Wherever possible, annual screening for hypertension is advised for adults 18 years and older.
    • - Lifestyle modification should place additional focus on salt restriction, increased intake of vegetables and fruits (potassium intake), weight management, and reducing alcohol intake.
    • - First-line pharmacological therapy is recommended as a single pill combination including a thiazide-like diuretic with CCB or CCB with ARB (see Sections 8 and 12) [71,138].
    • - Among RAS-inhibitors, ARBs may be preferred as angioedema is about three times more likely to occur with ACE inhibitors among black patients [139].

Populations from Asia

  • Ethnic-specific characteristics are recognized for East Asian populations. Hypertensive patients have a greater likelihood of salt-sensitivity accompanied with mild obesity. When compared with Western populations, East Asian people present a higher prevalence of stroke (particularly hemorrhagic stroke), and nonischemic heart failure [1].
  • Morning hypertension and night-time hypertension [140] are also more common in Asia, compared with European populations.
  • South Asian populations originating from the Indian subcontinent have a particularly high risk for cardiovascular and metabolic diseases, including CAD and type 2 DM. With large hypertensive populations residing in India and China, clinical trials in these populations are required to advise whether current treatment approaches are ideal [141,142].
  • Management of hypertension:
    • a. South East Asia: standard treatment as indicated in these guidelines is advised, until more evidence becomes available [138].


  • 2018 European Society of Cardiology/European Society of Hypertension Guidelines (Williams B, Mancia G, Spiering W, et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension: The Task Force for the management of arterial hypertension of the European Society of Cardiology and the European Society of Hypertension: The Task Force for the management of arterial hypertension of the European Society of Cardiology and the European Society of Hypertension. J Hypertens 2018; 36: 1953–2041). These comprehensive and evidence-based guidelines form a complete detailed resource.
  • 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/AphA/ASH/ASPC/NMA/PCNA Guidelines (Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High blood pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension 2017; 71:e13--e115]. The Guidelines from the United States of America, which attracted much comment on redefining hypertension, is very comprehensive and evidence-based, and largely in agreement with the 2018 European guidelines.
  • Weber MA, Poulter NR, Schutte AE, et al. Is it time to reappraise blood pressure thresholds and targets? Statement from the International Society of Hypertension – a global perspective. Hypertension 2016; 68:266--268.
  • Clinical Practice Guidelines for the Management of Hypertension in the Community: A Statement by the American Society of Hypertension and the International Society of Hypertension. [Weber MA, Schiffrin EL, White WB et al. The Journal of Clinical Hypertension 2014; 16:14–26].
  • NICE Guideline: Hypertension in adults: diagnosis and management. Published: 28 August 2019. Available at: www.nice.org.uk/guidance/ng136
  • The Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2019).Hypertens Res 2019; 42:1235–1481. Available at: https://doi.org/10.1038/s41440-019-0284-9
  • 2018 Chinese Guidelines for Prevention and Treatment of Hypertension – A report of the Revision Committee of Chinese Guidelines for Prevention and Treatment of Hypertension. Liu LS, Wu ZS, Wang JG, Wang W. J Geriatr Cardiol 2019;16: 182--241.
  • Guidelines on the management of arterial hypertension and related comorbidities in Latin America Task Force of the Latin American Society of Hypertension. J Hypertens 2017; 35:1529–1545.
  • 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Mach F, Baigent C, Catapano AL et al. Eur Heart J 2020; 41:111–188 doi:10.1093/eurheartj/ehz455.
  • 2019 ESC Guidelines on diabetes, pre-diabetes, and cardiovascular diseases developed in collaboration with the EASD: The Task Force for diabetes, pre-diabetes, and cardiovascular diseases of the European Society of Cardiology (ESC) and the European Association for the Study of Diabetes (EASD). Cosentino F, Peter J, Grant PJ, Aboyans V, et al. Eur Heart J 2020;41:255–323. Available at: https://doi.org/10.1093/eurheartj/ehz486
  • The HOPE Asia Network contributes largely to evidence for this region: Kario K et al. HOPE Asia (Hypertension Cardiovascular Outcome Prevention and Evidence in Asia) Network. The HOPE Asia Network for “zero” cardiovascular events in Asia. J Clin Hypertens 2018; 20:212--214.
  • World Health Organization, HEARTS Technical Package: [https://www.who.int/cardiovascular_diseases/hearts/en/]: The HEARTS package contains free modules (in English, French, Spanish and Russian) on e.g. Healthy-lifestyle counselling; Risk based charts, but particularly for Team-based care which is particularly relevant in low resource settings where task-sharing is highly relevant. Available at: https://apps.who.int/iris/bitstream/handle/10665/260424/WHO- NMH-NVI-18.4-eng.pdf;jsessionid=7AC6EC215FEB390CBD93898B69C4705C?sequence=1
  • Cardiovascular Risk Scores: Several scoring systems are available. Some are based only on European populations, for example, SCORE.
  • World Heart Federation Roadmap to the Management and Control of Raised blood pressure provides guidance on achieving the target of a relative reduction of the prevalence of raised blood pressure by 25% by 2025: https://www.world-heart-federation.org/cvd-roadmaps/whf-global-roadmaps/hypertension/.
  • On the basis of this Roadmap, an Africa-specific roadmap was also developed: [Dzudie A, Rayner B, Ojji D, Schutte AE, et al. Roadmap to achieve 25% hypertension control in Africa by 2025. Global Heart 2018; 13:45--59]

Listings of validated electronic blood pressure devices that were independently assessed for accuracy:

Blood pressure management in pediatric populations:

  • Flynn JT, Kaelber DC, Baker-Smith CM, et al. Clinical practice guideline for screening and management of high blood pressure in children and adolescents. Pediatrics 2017; 140: e20171904.
  • Lurbe E, Agabiti-Rosei E, Cruickshank JK, et al. 2016 European Society of Hypertension guidelines for the management of high blood pressure in children and adolescents. J Hypertens 2016; 34:1887--1920.
  • Xi B, Zong X, Kelishadi R, Hong YM, et al. Establishing international blood pressure references among non-overweight children and adolescents aged 6 to 17 years. Circulation 2016; 133:398--408.
  • Dong Y, Ma J, Song Y, Dong B, et al. National blood pressure reference for Chinese Han children and adolescents aged 7 to 17 years. Hypertension 2017; 70:897--890.


International Society of Hypertension 2020: ESSENTIAL recommendations (minimum standards of care).
International Society of Hypertension 2020: OPTIMAL recommendations (evidence-based standards of care).


The authors are grateful to Elena Kaschina and Michél Strauss-Kruger for their help in preparing and editing this manuscript.

Conflicts of interest

The authors have no conflict of interest to declare, but declare lecture honoraria or consulting fees as follows: T.U., Bayer, Boehringer Ingelheim, Hexal, Vifor Pharma; C.B., Servier, Menarini, Merck Pharma, Novartis, Egis, Daichy Sankyo, Gilead; N.R.P., Servier, Pfizer, Sanofi, Eva Pharma; D.P., Torrent Pharmaceuticals; M.S., Medtronic, Abbott, Novartis, Servier, Pfizer, Boehringer-Ingelheim; G.S.S., AstraZeneca, Menarini, Pfizer, Servier; B.W., Vascular Dynamics USA Inc, Relypsa Inc. USA; Daiichi Sankyo, Pfizer, Servier, Novartis, Menarini, Omron; A.E.S., Omron, Novartis, Takeda, Servier, Abbott.


1. Williams B, Mancia G, Spiering W, Agabiti Rosei E, Azizi M, Burnier M, et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension: The Task Force for the management of arterial hypertension of the European Society of Cardiology and the European Society of Hypertension. J Hypertens 2018; 36:1953–2041.
2. Whelton PK, Carey RM, Aronow WS, Casey DE Jr, Collins KJ, Dennison Himmelfarb C, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension 2018; 71:1269–1324.
3. Global Burden of Disease Risk Factor CollaboratorsGlobal, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet 2018; 392:1923–1994.
4. Mills KT, Bundy JD, Kelly TN, Reed JE, Kearney PM, Reynolds K, et al. Global disparities of hypertension prevalence and control: a systematic analysis of population-based studies from 90 countries. Circulation 2016; 134:441–450.
5. Non-communicable Disease Risk Factor CollaborationWorldwide trends in blood pressure from 1975 to 2015: a pooled analysis of 1479 population-based measurement studies with 19.1 million participants. Lancet 2017; 389:37–55.
6. Beaney T, Burrell LM, Castillo RR, Charchar FJ, Cro S, Damasceno A, et al. MMM InvestigatorsMay Measurement Month 2018: a pragmatic global screening campaign to raise awareness of blood pressure by the International Society of Hypertension. Eur Heart J 2019; 40:2006–2017.
7. Beaney T, Schutte AE, Tomaszewski M, Ariti C, Burrell LM, Castillo RR, et al. May measurement month 2017: an analysis of blood pressure screening results worldwide. Lancet Glob Health 2018; 6:e736–e743.
8. Hypertension in adults: Diagnosis and management. NICE guideline [NG136]. August 2019. Available at: https://www.nice.org.uk/guidance/ng136.
9. Nerenberg KA, Zarnke KB, Leung AA, Dasgupta K, Butalia S, McBrien K, et al. Hypertension CanadaHypertension Canada's 2018 guidelines for diagnosis, risk assessment, prevention, and treatment of hypertension in adults and children. Can J Cardiol 2018; 34:506–525.
10. Umemura S, Arima H, Arima S, Asayama K, Dohi Y, Hirooka Y, et al. The Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2019). Hypertens Res 2019; 42:1235–1481.
11. Nakagawa N, Hasebe N. Impact of the 2017 American College of Cardiology/American Heart Association Blood Pressure Guidelines on the next blood pressure guidelines in Asia. Curr Hypertens Rep 2019; 21:2.
12. Kario K, Wang JG. Could 130/80 mm Hg be adopted as the diagnostic threshold and management goal of hypertension in consideration of the characteristics of Asian populations? Hypertension 2018; 71:979–984.
13. Dzudie A, Rayner B, Ojji D, Schutte AE, Twagirumukiza M, Damasceno A, et al. PASCAR Task Force on HypertensionRoadmap to achieve 25% hypertension control in Africa by 2025. Glob Heart 2018; 13:45–59.
14. Messerli FH, Bangalore S. The blood pressure landscape: Schism among guidelines, confusion among physicians, and anxiety among patients. J Am Coll Cardiol 2018; 72:1313–1316.
15. Rehan HS, Grover A, Hungin AP. Ambiguities in the guidelines for the management of arterial hypertension: Indian perspective with a call for global harmonization. Curr Hypertens Rep 2017; 19:17.
16. Poulter NR, Castillo R, Charchar FJ, Schlaich MP, Schutte AE, Tomaszewski M, et al. Are the American Heart Association/American College of Cardiology high blood pressure guidelines fit for global purpose?: thoughts from the International Society of Hypertension. Hypertension 2018; 72:260–262.
17. Stergiou GS, Palatini P, Asmar R, Bilo G, de la Sierra A, Head G, et al. Blood pressure monitoring: theory and practice. European Society of Hypertension Working Group on Blood Pressure Monitoring and Cardiovascular Variability Teaching Course Proceedings. Blood Press Monit 2018; 23:1–8.
18. Muntner P, Einhorn PT, Cushman WC, Whelton PK, Bello NA, Drawz PE, et al. Blood pressure assessment in adults in clinical practice and clinic-based research: JACC Scientific Expert Panel. J Am Coll Cardiol 2019; 73:317–335.
19. O’Brien E, Parati G, Stergiou G, Asmar R, Beilin L, Bilo G, et al. European Society of Hypertension Working Group on Blood Pressure MonitoringEuropean Society of Hypertension position paper on ambulatory blood pressure monitoring. J Hypertens 2013; 31:1731–1768.
20. Parati G, Stergiou GS, Asmar R, Bilo G, de Leeuw P, Imai Y, et al. ESH Working Group on Blood Pressure MonitoringEuropean Society of Hypertension guidelines for blood pressure monitoring at home: a summary report of the Second International Consensus Conference on Home Blood Pressure Monitoring. J Hypertens 2008; 26:1505–1526.
21. Kario K, Shin J, Chen CH, Buranakitjaroen P, Chia YC, Divinagracia R, et al. Expert panel consensus recommendations for ambulatory blood pressure monitoring in Asia: the HOPE Asia Network. J Clin Hypertens (Greenwich) 2019; 21:1250–1283.
22. Stergiou GS, O’Brien E, Myers M, Palatini P, Parati G. STRIDE BP Scientific Advisory BoardSTRIDE BP: an international initiative for accurate blood pressure measurement. J Hypertens 2019; 38:395–399.
23. Stergiou GS, Kyriakoulis KG, Kollias A. Office blood pressure measurement types: different methodology-different clinical conclusions. J Clin Hypertens 2018; 20:1683–1685.
24. Myers MG, Asmar R, Staessen JA. Office blood pressure measurement in the 21st century. J Clin Hypertens (Greenwich) 2018; 20:1104–1107.
25. Mancia G, Facchetti R, Bombelli M, Grassi G, Sega R. Long-term risk of mortality associated with selective and combined elevation in office, home, and ambulatory blood pressure. Hypertension 2006; 47:846–853.
26. Stergiou GS, Asayama K, Thijs L, Kollias A, Niiranen TJ, Hozawa A, et al. International Database on HOme blood pressure in relation to Cardiovascular Outcome (IDHOCO) InvestigatorsPrognosis of white-coat and masked hypertension: International Database of HOme blood pressure in relation to Cardiovascular Outcome. Hypertension 2014; 63:675–682.
27. Asayama K, Thijs L, Li Y, Gu YM, Hara A, Liu YP, et al. International Database on Ambulatory Blood Pressure in Relation to Cardiovascular Outcomes (IDACO) Investigators. Setting thresholds to varying blood pressure monitoring intervals differentially affects risk estimates associated with white-coat and masked hypertension in the population. Hypertension 2014; 64:935–942.
28. Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CJ. Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data. Lancet 2006; 367:1747–1757.
29. Tunstall-Pedoel H, Chen R, Kramarz P. Prevalence of individuals with both raised blood pressure and raised cholesterol in WHO MONICA project population surveys 1989–1997. Eur Heart J 2004; 25: (Suppl 1): 234.
30. Neaton JD, Wentworth D. Serum cholesterol, blood pressure, cigarette smoking, and death from coronary heart disease. Overall findings and differences by age for 316,099 white men. Multiple Risk Factor Intervention Trial Research Group. Arch Intern Med 1992; 152:56–64.
31. Rossi GP, Seccia TM, Maniero C, Pessina AC. Drug-related hypertension and resistance to antihypertensive treatment: a call for action. J Hypertens 2011; 29:2295–2309.
32. Aw T-J, Haas SJ, Liew D, Krum H. Meta-analysis of cyclooxygenase-2 inhibitors and their effects on blood pressure. Arch Intern Med 2005; 165:490–496.
33. Chasan-Taber L, Willett WC, Manson JE, Spiegelman D, Hunter DJ, Curhan G, et al. Prospective study of oral contraceptives and hypertension among women in the United States. Circulation 1996; 94:483–489.
34. Grossman E, Messerli FH. Drug-induced hypertension: an unappreciated cause of secondary hypertension. Am J Med 2012; 125:14–22.
35. Robert N, Wong GW, Wright JM. Effect of cyclosporine on blood pressure. Cochrane Database Syst Rev 2010; 1:CD007893.
36. Salerno SM, Jackson JL, Berbano EP. Effect of oral pseudoephedrine on blood pressure and heart rate: a meta-analysis. Arch Intern Med 2005; 165:1686–1694.
37. Licht CM, de Geus EJ, Seldenrijk A, van Hout HP, Zitman FG, van Dyck R, et al. Depression is associated with decreased blood pressure, but antidepressant use increases the risk for hypertension. Hypertension 2009; 53:631–638.
38. Zhong Z, Wang L, Wen X, Liu Y, Fan Y, Liu Z. A meta-analysis of effects of selective serotonin reuptake inhibitors on blood pressure in depression treatment: outcomes from placebo and serotonin and noradrenaline reuptake inhibitor controlled trials. Neuropsychiatr Dis Treat 2017; 13:2781–2796.
39. Plummer C, Michael A, Shaikh G, Stewart M, Buckley L, Miles T, et al. Expert recommendations on the management of hypertension in patients with ovarian and cervical cancer receiving bevacizumab in the UK. Br J Cancer 2019; 121:109–116.
40. Nduka CU, Stranges S, Sarki AM, Kimani PK, Uthman OA. Evidence of increased blood pressure and hypertension risk among people living with HIV on antiretroviral therapy: a systematic review with meta-analysis. J Hum Hypertens 2016; 30:355–362.
41. Krapf R, Hulter HN. Arterial hypertension induced by erythropoietin and erythropoiesis-stimulating agents (ESA). Clin J Am Soc Nephrol 2009; 4:470–480.
42. Vanmolkot FH, de Hoon JN. Acute effects of sumatriptan on aortic blood pressure, stiffness, and pressure waveform. Clin Pharmacol Ther 2006; 80:85–94.
43. Forman JP, Stampfer MJ, Curhan GC. Non-narcotic analgesic dose and risk of incident hypertension in US women. Hypertension 2005; 46:500–507.
44. Haller CA, Benowitz NL. Adverse cardiovascular and central nervous system events associated with dietary supplements containing ephedra alkaloids. N Engl J Med 2000; 343:1833–1838.
45. Penninkilampi R, Eslick EM, Eslick GD. The association between consistent licorice ingestion, hypertension and hypokalaemia: a systematic review and meta-analysis. J Hum Hypertens 2017; 31:699–707.
46. Piepoli MF, Hoes AW, Agewall S, Albus C, Brotons C, Catapano AL, ESC Scientific Document Group, et al. Authors/Task Force Members2016 European Guidelines on cardiovascular disease prevention in clinical practice: The Sixth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of 10 societies and by invited experts) Developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR). Eur Heart J 2016; 37:2315–2381.
47. He FJ, Li J, Macgregor GA. Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials. BMJ 2013; 346:f1325.
48. Gay HC, Rao SG, Vaccarino V, Ali MK. Effects of different dietary interventions on blood pressure: systematic review and meta-analysis of randomized controlled trials. Hypertension 2016; 67:733–739.
49. Cicero AFG, Grassi D, Tocci G, Galletti F, Borghi C, Ferri C. Nutrients and nutraceuticals for the management of high normal blood pressure: an evidence-based consensus document. High Blood Press Cardiovasc Prev 2019; 26:9–25.
50. Xie C, Cui L, Zhu J, Wang K, Sun N, Sun C. Coffee consumption and risk of hypertension: a systematic review and dose-response meta-analysis of cohort studies. J Hum Hypertens 2018; 32:83–93.
51. Roerecke M, Kaczorowski J, Tobe SW, Gmel G, Hasan OSM, Rehm J. The effect of a reduction in alcohol consumption on blood pressure: a systematic review and meta-analysis. Lancet Public Health 2017; 2:e108–e120.
52. Alberti G, Zimmet P, Shaw J, Grundy SM. The IDF consensus worldwide definition of the metabolic syndrome. Brussels: International Diabetes Federation. 2006. Available at: https://www.idf.org/e-library/consensus-statements/60-idfconsensus-worldwide-definitionof-the-metabolic-syndrome.html.
53. Ashwell M, Gunn P, Gibson S. Waist-to-height ratio is a better screening tool than waist circumference and BMI for adult cardiometabolic risk factors: systematic review and meta-analysis. Obes Rev 2012; 13:275–286.
54. Browning LM, Hsieh SD, Ashwell M. A systematic review of waist-to-height ratio as a screening tool for the prediction of cardiovascular disease and diabetes: 0.5 could be a suitable global boundary value. Nutr Res Rev 2010; 23:247–269.
55. Global Burden of Disease Risk Factor CollaboratorsGlobal, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet 2017; 390:1345–1422.
56. Casonatto J, Goessler KF, Cornelissen VA, Cardoso JR, Polito MD. The blood pressure-lowering effect of a single bout of resistance exercise: a systematic review and meta-analysis of randomised controlled trials. Eur J Prev Cardiol 2016; 23:1700–1714.
57. Costa EC, Hay JL, Kehler DS, Boreskie KF, Arora RC, Umpierre D, et al. Effects of high-intensity interval training versus moderate-intensity continuous training on blood pressure in adults with pre-to established hypertension: a systematic review and meta-analysis of randomized trials. Sports Med 2018; 48:2127–2142.
58. Cornelissen VA, Smart NA. Exercise training for blood pressure: a systematic review and meta-analysis. J Am Heart Assoc 2013; 2:e004473.
59. Matthews KA, Katholi CR, McCreath H, Whooley MA, Williams DR, Zhu S, et al. Blood pressure reactivity to psychological stress predicts hypertension in the CARDIA study. Circulation 2004; 110:74–78.
60. Solano Lopez AL. Effectiveness of the mindfulness-based stress reduction program on blood pressure: A systematic review of literature. Worldviews Evid Based Nurs 2018; 15:344–352.
61. Wang J, Xiong X. Evidence-based chinese medicine for hypertension. Evid Based Complement Alternat Med 2013; 2013:978398.
62. Liwa AC, Smart LR, Frumkin A, Epstein HA, Fitzgerald DW, Peck RN. Traditional herbal medicine use among hypertensive patients in sub-Saharan Africa: a systematic review. Curr Hypertens Rep 2014; 16:437.
63. Giorgini P, Di Giosia P, Grassi D, Rubenfire M, Brook RD, Ferri C. Air pollution exposure and blood pressure: an updated review of the literature. Curr Pharm Des 2016; 22:28–51.
64. Fedak KM, Good N, Walker ES, Balmes J, Brook RD, Clark ML, et al. Acute effects on blood pressure following controlled exposure to cookstove air pollution in the STOVES Study. J Am Heart Assoc 2019; 8:e012246.
65. Stergiou GS, Palatini P, Modesti PA, Asayama K, Asmar R, Bilo G, et al. Seasonal variation in blood pressure: evidence, consensus and recommendations for clinical practice. Consensus statement by the European Society of Hypertension Working Group on Blood Pressure Monitoring and Cardiovascular Variability. J Hypertens 2020; [Epub ahead of print].
66. Geldsetzer P, Manne-Goehler J, Marcus ME, Ebert C, Zhumadilov Z, Wesseh CS, et al. The state of hypertension care in 44 low-income and middle-income countries: a cross-sectional study of nationally representative individual-level data from 1.1 million adults. Lancet 2019; 394:652–662.
67. Non-communicable Disease Risk Factor CollaborationLong-term and recent trends in hypertension awareness, treatment, and control in 12 high-income countries: an analysis of 123 nationally representative surveys. Lancet 2019; 394:639–651.
68. Lewington S, Clarke R, Qizilbash N, Peto R, Collins R. Prospective Studies CollaborationAge-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; 360:1903–1913.
69. Dahlof B, Sever PS, Poulter NR, Wedel H, Beevers DG, Caulfield M, et al. ASCOT InvestigatorsPrevention of cardiovascular events with an antihypertensive regimen of amlodipine adding perindopril as required versus atenolol adding bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm (ASCOT-BPLA): a multicentre randomised controlled trial. Lancet 2005; 366:895–906.
70. Jamerson K, Weber MA, Bakris GL, Dahlof B, Pitt B, Shi V, et al. Benazepril plus amlodipine or hydrochlorothiazide for hypertension in high-risk patients. N Engl J Med 2008; 359:2417–2428.
71. Williams B, MacDonald TM, Morant S, Webb DJ, Sever P, McInnes G, et al. British Hypertension Society's PATHWAY Studies GroupSpironolactone versus placebo, bisoprolol, and doxazosin to determine the optimal treatment for drug-resistant hypertension (PATHWAY-2): a randomised, double-blind, crossover trial. Lancet 2015; 386:2059–2068.
72. Chapman N, Chang CL, Dahlof B, Sever PS, Wedel H, Poulter NR. ASCOT InvestigatorsEffect of doxazosin gastrointestinal therapeutic system as third-line antihypertensive therapy on blood pressure and lipids in the Anglo-Scandinavian Cardiac Outcomes Trial. Circulation 2008; 118:42–48.
73. Ojji DB, Mayosi B, Francis V, Badri M, Cornelius V, Smythe W, et al. CREOLE Study InvestigatorsComparison of dual therapies for lowering blood pressure in black Africans. N Engl J Med 2019; 380:2429–2439.
74. Sabaté E. Adherence to long-term therapies: evidence for action. Geneva:World Health Organization; 2003.
75. Tomaszewski M, White C, Patel P, Masca N, Damani R, Hepworth J, et al. High rates of non-adherence to antihypertensive treatment revealed by high-performance liquid chromatography-tandem mass spectrometry (HP LC-MS/MS) urine analysis. Heart 2014; 100:855–861.
76. Mazzaglia G, Ambrosioni E, Alacqua M, Filippi A, Sessa E, Immordino V, et al. Adherence to antihypertensive medications and cardiovascular morbidity among newly diagnosed hypertensive patients. Circulation 2009; 120:1598–1605.
77. Corrao G, Parodi A, Nicotra F, Zambon A, Merlino L, Cesana G, et al. Better compliance to antihypertensive medications reduces cardiovascular risk. J Hypertens 2011; 29:610–618.
78. Gupta P, Patel P, Strauch B, Lai FY, Akbarov A, Maresova V, et al. Risk factors for nonadherence to antihypertensive treatment. Hypertension 2017; 69:1113–1120.
79. Wei FF, Zhang ZY, Huang QF, Staessen JA. Diagnosis and management of resistant hypertension: state of the art. Nat Rev Nephrol 2018; 14:428–441.
80. Gupta P, Patel P, Horne R, Buchanan H, Williams B, Tomaszewski M. How to screen for non-adherence to antihypertensive therapy. Curr Hypertens Rep 2016; 18:89.
81. Abegaz TM, Shehab A, Gebreyohannes EA, Bhagavathula AS, Elnour AA. Nonadherence to antihypertensive drugs: a systematic review and meta-analysis. Medicine (Baltimore) 2017; 96:e5641.
82. Conn VS, Ruppar TM. Medication adherence outcomes of 771 intervention trials: Systematic review and meta-analysis. Prev Med 2017; 99:269–276.
83. Conn VS, Ruppar TM, Chase JA, Enriquez M, Cooper PS. Interventions to improve medication adherence in hypertensive patients: Systematic review and meta-analysis. Curr Hypertens Rep 2015; 17:94.
84. Verma AA, Khuu W, Tadrous M, Gomes T, Mamdani MM. Fixed-dose combination antihypertensive medications, adherence, and clinical outcomes: a population-based retrospective cohort study. PLoS Med 2018; 15:e1002584.
85. Gupta P, Patel P, Strauch B, Lai FY, Akbarov A, Gulsin GS, et al. Biochemical screening for nonadherence is associated with blood pressure reduction and improvement in adherence. Hypertension 2017; 70:1042–1048.
86. Ruppar TM, Dunbar-Jacob JM, Mehr DR, Lewis L, Conn VS. Medication adherence interventions among hypertensive black adults: a systematic review and meta-analysis. J Hypertens 2017; 35:1145–1154.
87. Costa E, Giardini A, Savin M, Menditto E, Lehane E, Laosa O, et al. Interventional tools to improve medication adherence: review of literature. Patient Prefer Adherence 2015; 9:1303–1314.
88. Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, et al. INTERHEART Study InvestigatorsEffect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 2004; 364:937–952.
89. Mach F, Baigent C, Catapano AL, Koskinas KC, Casula M, Badimon L, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J 2020; 41:111–188.
90. O’Donnell MJ, Xavier D, Liu L, Zhang H, Chin SL, Rao-Melacini P, et al. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): a case-control study. Lancet 2010; 376:112–123.
91. Bohm M, Young R, Jhund PS, Solomon SD, Gong J, Lefkowitz MP, et al. Systolic blood pressure, cardiovascular outcomes and efficacy and safety of sacubitril/valsartan (LCZ696) in patients with chronic heart failure and reduced ejection fraction: results from PARADIGM-HF. Eur Heart J 2017; 38:1132–1143.
92. Drawz PE, Alper AB, Anderson AH, Brecklin CS, Charleston J, Chen J, et al. Masked hypertension and elevated nighttime blood pressure in CKD: prevalence and association with target organ damage. Clin J Am Soc Nephrol 2016; 11:642–652.
93. Farsang C, Kiss I, Tykarski A, Narkiewicz K. Treatment of hypertension in patients with chronic obstructive pulmonary disease (COPD). European Society of Hypertension Scientific Newsletter 2016; 17:62.
94. Borghi C, Rosei EA, Bardin T, Dawson J, Dominiczak A, Kielstein JT, et al. Serum uric acid and the risk of cardiovascular and renal disease. J Hypertens 2015; 33:1729–1741.
95. Arnett DK, Blumenthal RS, Albert MA, Buroker AB, Goldberger ZD, Hahn EJ, et al. 2019 ACC/AHA Guideline on the primary prevention of cardiovascular disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol 2019; 74:1376–1414.
96. American Diabetes AssociationStandards of medical care in diabetes 2017. Diabetes Care 2017; 40: (Suppl 1): S1–S135.
97. Sever PS, Dahlof B, Poulter NR, Wedel H, Beevers G, Caulfield M, et al. ASCOT InvestigatorsPrevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial--Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet 2003; 361:1149–1158.
98. Nordestgaard BG. Triglyceride-rich lipoproteins and atherosclerotic cardiovascular disease: new insights from epidemiology, genetics, and biology. Circ Res 2016; 118:547–563.
99. Agca R, Heslinga SC, Rollefstad S, Heslinga M, McInnes IB, Peters MJ, et al. EULAR recommendations for cardiovascular disease risk management in patients with rheumatoid arthritis and other forms of inflammatory joint disorders: 2015/2016 update. Ann Rheum Dis 2017; 76:17–28.
100. Ikdahl E, Wibetoe G, Rollefstad S, Salberg A, Bergsmark K, Kvien TK, et al. Guideline recommended treatment to targets of cardiovascular risk is inadequate in patients with inflammatory joint diseases. Int J Cardiol 2019; 274:311–318.
101. Musselman DL, Evans DL, Nemeroff CB. The relationship of depression to cardiovascular disease: epidemiology, biology, and treatment. Arch Gen Psychiatry 1998; 55:580–592.
102. Patten SB, Williams JV, Lavorato DH, Campbell NR, Eliasziw M, Campbell TS. Major depression as a risk factor for high blood pressure: epidemiologic evidence from a national longitudinal study. Psychosom Med 2009; 71:273–279.
103. Siwek M, Woroń J, Gorostowicz A, Wordliczek J. Adverse effects of interactions between antipsychotics and medications used in the treatment of cardiovascular disorders. Pharmacol Rep 2020; doi: 10.1007/s43440-020-00058-6. [Epub ahead of print].
104. Bhatt H, Siddiqui M, Judd E, Oparil S, Calhoun D. Prevalence of pseudoresistant hypertension due to inaccurate blood pressure measurement. J Am Soc Hypertens 2016; 10:493–499.
105. de Jager RL, van Maarseveen EM, Bots ML, Blankestijn PJ. SYMPATHY investigatorsMedication adherence in patients with apparent resistant hypertension: Findings from the SYMPATHY trial. Br J Clin Pharmacol 2018; 84:18–24.
106. Vongpatanasin W. Resistant hypertension: a review of diagnosis and management. JAMA 2014; 311:2216–2224.
107. Ayala DE, Hermida RC, Mojon A, Fernandez JR. Cardiovascular risk of resistant hypertension: dependence on treatment-time regimen of blood pressure-lowering medications. Chronobiol Int 2013; 30:340–352.
108. Nazarzadeh M, Pinho-Gomes AC, Rahimi K. Resistant hypertension in times of changing definitions and treatment recommendations. Heart 2019; 105:96–97.
109. Rossignol P, Massy ZA, Azizi M, Bakris G, Ritz E, Covic A, et al. ERA-EDTA EURECA-m working groupThe double challenge of resistant hypertension and chronic kidney disease. Lancet 2015; 386:1588–1598.
110. Williams B, MacDonald TM, Morant SV, Webb DJ, Sever P, McInnes GT, et al. Endocrine and haemodynamic changes in resistant hypertension, and blood pressure responses to spironolactone or amiloride: the PATHWAY-2 mechanisms substudies. Lancet Diabetes Endocrinol 2018; 6:464–475.
111. Sinnott SJ, Tomlinson LA, Root AA, Mathur R, Mansfield KE, Smeeth L, Douglas IJ. Comparative effectiveness of fourth-line anti-hypertensive agents in resistant hypertension: a systematic review and meta-analysis. Eur J Prev Cardiol 2017; 24:228–238.
112. Krieger EM, Drager LF, Giorgi DMA, Pereira AC, Barreto-Filho JAS, Nogueira AR, et al. ReHOT InvestigatorsSpironolactone versus clonidine as a fourth-drug therapy for resistant hypertension: the ReHOT Randomized Study (Resistant Hypertension Optimal Treatment). Hypertension 2018; 71:681–690.
113. Brown MJ, Williams B, Morant SV, Webb DJ, Caulfield MJ, Cruickshank JK, et al. Effect of amiloride, or amiloride plus hydrochlorothiazide, versus hydrochlorothiazide on glucose tolerance and blood pressure (PATHWAY-3): a parallel-group, double-blind randomised phase 4 trial. Lancet Diabetes Endocrinol 2016; 4:136–147.
114. Manolis AA, Manolis TA, Melita H, Manolis AS. Eplerenone versus spironolactone in resistant hypertension: an efficacy and/or cost or just a men's issue? Curr Hypertens Rep 2019; 21:22.
115. Denker MG, Haddad DB, Townsend RR, Cohen DL. Blood pressure control 1 year after referral to a hypertension specialist. J Clin Hypertens 2013; 15:624–629.
116. Funder JW, Carey RM, Mantero F, Murad MH, Reincke M, Shibata H, et al. The management of primary aldosteronism: case detection, diagnosis, and treatment. An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2016; 101:1889–1916.
117. Gornik HL, Persu A, Adlam D, Aparicio LS, Azizi M, Boulanger M, et al. First international consensus on the diagnosis and management of fibromuscular dysplasia. J Hypertens 2019; 37:229–252.
118. Nieman LK, Biller BM, Findling JW, Newell-Price J, Savage MO, Stewart PM, Montori VM. The diagnosis of Cushing's syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2008; 93:1526–1540.
119. Rimoldi SF, Scherrer U, Messerli FH. Secondary arterial hypertension: when, who, and how to screen? Eur Heart J 2014; 35:1245–1254.
120. Viera AJ, Neutze DM. Diagnosis of secondary hypertension: an age-based approach. Am Fam Physician 2010; 82:1471–1478.
121. Borgel J, Springer S, Ghafoor J, Arndt D, Duchna HW, Barthel A, et al. Unrecognized secondary causes of hypertension in patients with hypertensive urgency/emergency: prevalence and co-prevalence. Clin Res Cardiol 2010; 99:499–506.
122. Regitz-Zagrosek V, Roos-Hesselink JW, Bauersachs J, Blomström-Lundqvist C, Cífková R, De Bonis M, et al. 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy: the Task Force for the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC). Eur Heart J 2018; 39:3165–3241.
123. American College of Obstetricians and GynecologistsHypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists’ Task Force on Hypertension in Pregnancy. Obstet Gynecol 2013; 122:1122–1131.
124. Lowe SA, Bowyer L, Lust K, McMahon LP, Morton MR, North RA, et al. Society of Obstetric Medicine of Australia and New ZealandThe SOMANZ guidelines for the management of hypertensive disorders of pregnancy 2014. Aust N Z J Obstet Gynaecol 2015; 55:11–16.
125. Rolnik DL, Wright D, Poon LC, O’Gorman N, Syngelaki A, de Paco Matallana C, et al. Aspirin versus placebo in pregnancies at high risk for preterm preeclampsia. N Engl J Med 2017; 377:613–622.
126. Abalos E, Duley L, Steyn DW. Antihypertensive drug therapy for mild to moderate hypertension during pregnancy. Cochrane Database Syst Rev 2014; 2:CD002252.
127. van den Born BH, Lip GYH, Brguljan-Hitij J, Cremer A, Segura J, Morales E, et al. ESC Council on hypertension position document on the management of hypertensive emergencies. Eur Heart J Cardiovasc Pharmacother 2019; 5:37–46.
128. van den Born BJ, Koopmans RP, Groeneveld JO, van Montfrans GA. Ethnic disparities in the incidence, presentation and complications of malignant hypertension. J Hypertens 2006; 24:2299–2304.
129. Amraoui F, Van Der Hoeven NV, Van Valkengoed IG, Vogt L, Van Den Born BJ. Mortality and cardiovascular risk in patients with a history of malignant hypertension: a case-control study. J Clin Hypertens (Greenwich) 2014; 16:122–126.
130. Gonzalez R, Morales E, Segura J, Ruilope LM, Praga M. Long-term renal survival in malignant hypertension. Nephrol Dial Transplant 2010; 25:3266–3272.
131. Tarver-Carr ME, Powe NR, Eberhardt MS, LaVeist TA, Kington RS, Coresh J, et al. Excess risk of chronic kidney disease among African-American versus white subjects in the United States: a population-based study of potential explanatory factors. J Am Soc Nephrol 2002; 13:2363–2370.
132. Benjamin EJ, Muntner P, Alonso A, Bittencourt MS, Callaway CW, Carson AP, et al. Heart disease and stroke statistics-2019 update: a report from the American Heart Association. Circulation 2019; 139:e56–e528.
133. van Rooyen JM, Poglitsch M, Huisman HW, Mels C, Kruger R, Malan L, et al. Quantification of systemic renin-angiotensin system peptides of hypertensive black and white African men established from the RAS-Fingerprint(R). J Renin Angiotensin Aldosterone Syst 2016; 17: pii: 1470320316669880.
134. Opie LH, Seedat YK. Hypertension in Sub-Saharan African populations. Circulation 2005; 112:3562–3568.
135. Bochud M, Staessen JA, Maillard M, Mazeko MJ, Kuznetsova T, Woodiwiss A, et al. Ethnic differences in proximal and distal tubular sodium reabsorption are heritable in black and white populations. J Hypertens 2009; 27:606–612.
136. Huisman HW, Schutte AE, Schutte R, van Rooyen JM, Fourie CM, Mels CM, et al. Exploring the link between cardiovascular reactivity and end-organ damage in African and Caucasian men: the SABPA study. Am J Hypertens 2013; 26:68–75.
137. Mokwatsi GG, Schutte AE, Kruger R. Ethnic differences regarding arterial stiffness of 6-8-year-old black and white boys. J Hypertens 2017; 35:960–967.
138. Brewster LM, van Montfrans GA, Oehlers GP, Seedat YK. Systematic review: antihypertensive drug therapy in patients of African and South Asian ethnicity. Intern Emerg Med 2016; 11:355–374.
139. Kostis JB, Kim HJ, Rusnak J, Casale T, Kaplan A, Corren J, Levy E. Incidence and characteristics of angigra associated with enalapril. Arch Intern Med 2005; 165:1637–1642.
140. Hoshide S, Kario K, de la Sierra A, Bilo G, Schillaci G, Banegas JR, et al. Ethnic differences in the degree of morning blood pressure surge and in its determinants between Japanese and European hypertensive subjects: data from the ARTEMIS study. Hypertension 2015; 66:750–756.
141. Anchala R, Kannuri NK, Pant H, Khan H, Franco OH, Di Angelantonio E, Prabhakaran D. Hypertension in India: a systematic review and meta-analysis of prevalence, awareness, and control of hypertension. J Hypertens 2014; 32:1170–1177.
142. Wang Z, Chen Z, Zhang L, Wang X, Hao G, Zhang Z, et al. China Hypertension Survey InvestigatorsStatus of hypertension in China: results from the China hypertension survey, 2012–2015. Circulation 2018; 137:2344–2356.

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