List of abbreviations

ABI — ankle-brachial index

ABPM — ambulatory blood pressure monitoring

ACEI — angiotensin-converting enzyme inhibitor

ACR — albumin-creatinine ratio

AF — atrial fibrillation

ARB — angiotensin II receptor AT1 blocker

ARNI — angiotensin receptor-neprilysin inhibitor

ASA — acetylsalicylic acid

BARKH — brain, arteries, retina, kidneys, heart

BB — beta-blocker

BMI — body mass index

BP — blood pressure

CAC — calcium score

CCB — calcium channel blocker

CKD — chronic kidney disease

COVID-19 — coronavirus disease 2019

COX-2 — cyclooxygenase 2

CPAP — continuous positive airway pressure

CT — computed tomography

CV — cardiovascular

DBP — diastolic blood pressure

ECG — electrocardiogram

eGFR — estimated glomerular filtration rate

ESC — European Society of Cardiology

ESH — European Society of Hypertension

FMD — fibromuscular dysplasia

GLP-1 — glucagon-like peptide 1

HbA1c — glycated hemoglobin

HELLP — haemolysis, elevated liver enzymes, low platelets

HF — heart failure

HFpEF — heart failure with preserved ejection fraction

HFrEF — heart failure with reduced ejection fraction

HMOD — hypertension-mediated organ damage

HR — heart rate

HRT — hormone replacement therapy

HT — hypertension

ISH — isolated systolic hypertension

KCCQ-CCS — Kansas City Cardiomyopathy Questionnaire — The Clinical Summary Score

LEAD — lower extremity arterial disease

LVH — left ventricular hypertrophy

MAP — mean arterial hypertension

MMM — May Measurement Month

MRA — mineralocorticoid receptor antagonist

MS — metabolic syndrome

NSAID — non-steroidal anti-inflammatory drug

NT-proBNP — N-terminal pro-B-type natriuretic peptide

op-BP — opportunistic blood pressure measurements

OC — oral contraceptive

OGTT — oral glucose tolerance test

OSA — obstructive sleep apnoea

PA — primary hyperaldosteronism

PAD — peripheral arterial disease

PCOS — polycystic ovary syndrome

PCSK9 — proprotein convertase subtilisin/kexin 9

PE — pre-eclampsia

PRES — posterior reversible encephalopathy syndrome

PTD — Polish Diabetes Association

PTK — Polish Cardiac Society

PTNT — Polish Society of Hypertension

PUFA — polyunsaturated fatty acid

PWV — brachial-ankle PWV

RRI — renal resistive index

SBP — systolic blood pressure

SCD — sudden cardiac death

SPC — single-pill combination

TIA — transient ischemic attack

TLD/TD — thiazide-like diuretic/thiazide diuretic

TSH — thyrotropin-stimulating hormone

UACR — urine albumin-creatinine ratio

USG — ultrasonography

X-ray — radiological examination

1. Introduction

For years, hypertension (HT) has remained one of the most common risk factors leading to cardiovascular disease (CVD) and death both in Poland and worldwide [1–5]. Therefore, its effective treatment has become a priority for hypertensiologists, cardiologists, general practitioners (GPs) and physicians from other specialities. In the past, the ESH and ESC cooperated on publishing the joint version of the HT treatment guidelines; however, the two societies created the most recent publications separately [3–5, 7, 8]. To increase the effectiveness of HT therapy, the activities of all specialists should be coordinated and based on common guidelines. Therefore, the Board of the Polish Society of Hypertension (PTNT) and the Board of the Polish Cardiac Society (PTK) agreed to develop a joint document Guidelines for the management of hypertension in Poland 2024 — the position of PTNT/PTK Experts. The text was first assessed by reviewers and then submitted to the Committee of 30 Polish HT Experts for opinion. Each controversial statement had to be supported by at least 23 of the 30 Committee members to be included in the final document.

Based on the analysis of the National Health Fund (NFZ) data from 2018–2022, the number of HT patients in Poland remains stable and it is approximately 11 million people (Fig. 1.1). The disease affects 34–35% of adults [9]. Additionally, global data show that HT affects a total of approximately 5% of the population aged 0–18 [10]. The disease is rarely diagnosed in the first years of life, but during puberty, the incidence of HT increases significantly, especially in boys. Polish data indicate that in adolescents aged 18 years, HT affects 9% of the population and it is almost 16% in boys, which corresponds to the prevalence of HT in young adults [11].

Figure 1.1. The prevelance of hypertension (HT) in Poland. Developed based on [9, 12, 14, 15, 17, 22]

The 2019–2021 analysis, excluding patients with heart failure (HF), found that 9.5–10.3 million people are taking antihypertensive medication [12]. In Poland, the incidence of HT is among the highest in Europe, in both women and men [13]. Monotherapy still remains the most common treatment (54% of patients in 2021). Beta-blockers (BBs) remain the most commonly used group of drugs. The popularity of single-pill combinations (SPCs) increased in the period from 2019 to 2021. In 2021, 30% of patients taking antihypertensive drugs used SPCs combining two drugs and 3% used SPCs combining three drugs. Among patients undergoing combination treatment (2 drugs or more), 46% used SPCs combining two drugs. Among patients treated with three or more antihypertensive drugs, the share of patients using SPCs combining three drugs was 20%. There is no current data on the effectiveness of HT treatment in Poland. The 2013–2014 WOBASZ study showed that effective HT therapy was achieved in 23% of the participants [14]. In contrast, the 2018–2019 POLSENIOR2 study revealed that HT affected three out of four people aged 60 and older. HT control was achieved in one-third of the population — 33%, including 39% receiving antihypertensive medication [15]. A slightly higher share of patients aged 65 and older who achieved blood pressure (BP) control was confirmed in the 2017–2018 NOMED-AF study [16]. In 2021, during the May Measurement Month (MMM) campaign, BP was measured/assesed in 1,699 persons. The control was achieved by 31% of HT patients, including 60% undergoing treatment [17]. The BP control may have been negatively affected by the coronavirus disease 2019 (COVID-19) [18–21].

In this document, the degree of recommendation is not provided. Instead, the assessed recommendations and degrees of recommendation were taken from the ESH and ESC guidelines and presented in the figures. The purpose of this approach is to make it easier to understand what should definitely be done and what is worth considering. The graphical representation of the recommendations seems more useful in practice.

2. BP measurements

BP measurements (Fig. 2.1) should be taken using validated devices. This means that their accuracy was assessed in a clinical trial in accordance with accepted protocols and the results were published in a peer-reviewed scientific journal. A list of such devices can be found at: www.dobrzemierze.pl and www.stridebp.org [3, 5].

BP measurements at the docto

Figure 2.1. Selection of blood pressure (BP) measurement method

r’s office are considered crucial in diagnosing and evaluating the effectiveness of HT treatment [4, 5]. However, studies indicate that out-of-office measurements have greater prognostic value [23, 24]. More than 90% of HT patients in Poland take home BP measurements [22], which, together with access to ambulatory blood pressure measurements (ABPM) through the National Cardiac Network and Coordinated Care, allows to consider out-of-office methods as the main means of BP monitoring [25]. Office BP measurements play an additional and verifying role.

2.1. BP classification

The correlation between BP values and cardiovascular risk in persons without blood lowering therapy is linear, starting from values as low as 100–110 mm Hg for systolic BP [26–28]. For this reason, describing BP values as “normal” may be misleading in terms of their association with cardiovascular risk. In the presented document, three BP categories (systolic and diastolic BP values for office measurements) are introduced:

The purpose of the new BP classification is not only to simplify BP categories used so far, but also to promote preventive measures against HT development and to reduce CV disease risk in people with elevated BP. In the ESC guidelines, the lowest BP category is referred to as “non-elevated” BP [5]. This may imply that BP values in this category are incorrect; moreover, such a term is not motivating to pursue healthy lifestyle. Therefore, it is proposed to refer to the BP values below 120 and below 70 mm Hg as “optimal”.

Detailed cut-off values for each category for the different BP measurement methods are presented in Figure 2.2. As the white coat effect becomes gradually less evident along with lower BP values, the criteria for “optimal BP” are the same for office and out-of-office BP [5]. Table 2.1 shows the present and new classification of BP categories.

Figure 2.2. Blood pressure (BP) cut-off values and initiation of hypertension (HT) treatment. Based on [2, 4, 5, 29]

2.2. Office BP

BP measurements taken in healthcare facilities or by medical staff are referred to as office BP. For decades, office BP constituted basic method of BP assessment. However, the wide availability of out-of-office BP measurement methods that better illustrate CV disease risk is gradually reducing role of office BP. Office measurements can be performed with an aneroid sphygmomanometer or using a validated automatic device. The cuff should be adjusted according to arm circumference and at least two, preferably three, measurements should be taken on the same arm, one minute apart. The result is presented as the average of the last two measurements [2, 4, 5, 29].

Unattended automatic office BP measurements, due to the lack of clearly defined BP thresholds for this method and the fact that they do not increase the accuracy of the cardiovascular risk assessment compared to office measurements, are not currently recommended [30, 31].

2.3. Home BP

Home BP measurements are self-measurements taken by the patient or another person. In Poland, almost all patients with HT have an access to personal BP measurement devices. Home BP monitoring over several consecutive days provides more comprehensive insight into HT control than a single 24-hour recording. Reliable home measurements help to identify patients with elevated BP. Additionally, self BP monitoring engage patients which translates to better adherence to therapy. Automatic validated devices with an appropriately selected arm cuff are recommended. Validated wrist BP measuring devices are also available, including those for overnight measurements [2, 4, 5, 29]. Interpretation of the results is shown in Figures 2.2 and 2.3.

What is the optimal regimen for home BP measurements?

Figure 2.3. Interpretation of blood pressure (BP) values and profile in out-of-office measurements. Based on [35–40]

2.4. Ambulatory blood pressure monitoring

Ambulatory blood pressure monitoring (ABPM) is a method of monitoring the BP 24 hours a day using a device worn by the patient under everyday conditions. It is a key method for verifying BP values obtained during office and out-of-office BP measurements (Fig. 2.1). It also allows the verification of BP values at night. Validated devices with an appropriately sized cuff should be used for that purpose. The measurements should be taken every 15–20 minutes during the day and every 30 minutes at night. Day and night are determined after registration is completed based on the rest time reported by the patient. For the registration to be considered valid, at least 70% of the measurements must provide reliable results. The results are interpreted according to Figures 2.2 and 2.3.

2.5. Situational hypotension

Conditions which may evoke hypotension and further confer CV events and premature death risks include the following:

Confirmation of situational hypotension as listed above usually require individualised antihypertensive therapy.

As part of the initial assessment of patients, it is recommended to perform an orthostatic test by measuring BP 1 and 3 minutes after changing the position from sitting/lying to standing (the patient should stay in a sitting/lying position for ≥ 5 minutes). Orthostatic hypotension is diagnosed when there is a decrease in systolic BP of ≥ 20 mm Hg or diastolic BP of ≥ 10 mm Hg. It is recommended to repeat the orthostatic test when suggestive symptoms of orthostatic hypotension occur [5].

2.6. Opportunistic BP measurements and BP measurements in pharmacies

BP measurements that do not meet the criteria of the categories described above are referred to as opportunistic (op-BP) measurements. Examples of op-BP are BP measurements carried out during health awareness events (e.g. White Saturdays, the international MMM campaign, the World Heart Day, etc.) [17]. The non-standard course of the op-BP measurements makes the BP readings difficult to clearly interpret, but this type of activities engage participants in preventive actions. It is recommended that the op-BP measurement organisers consider the following:

Systematic incorporation of op-BP into non-medical services, such as hairdressing services, have additional potential. Regular visits to barbershops during which clients measure their BP and receive feedback on HT have been shown to increase the effectiveness of blood-lowering treatment, especially in high CV risk populations [32].

How to assess BP values at night?

A special category of op-BP measurements are those performed in pharmacies; the procedure which was not regulated in Poland until 2023. Currently, pharmacists are authorised to measure BP according to the office measurement standard. The aim of that service, together with drug review as part of the pharmaceutical care is to improve therapeutic safety and adherence to blood lowering therapy [33, 34].

2.7. Night-time BP

Lack of BP fall during sleep, or the so-called non-dipping, is a condition in which BP does not fall at night by a physiological 10–20% compared to daytime values. Such a condition, as well as elevated BP at night, excessive night-time fall or morning surge, is associated with a higher risk of cardiovascular diseases such as HT, HF, stroke or myocardial infarction. The most favourable BP profile that is associated with the lowest CV events risk is characterised by a moderate reduction in BP during sleep and no excessive surge in the morning [35–40].

3. HT diagnosis

BP tends to rise with age. The initial BP rise is mainly driven by genetic factors, whereas the environmental factors play a pivotal role later in life. The cut-off values that define HT are set arbitrary. It is BP value beyond which its’ reduction results in longer predicted life span and better quality of life. In recent years, a large body of evidence has emerged showing the benefits of lower target BP values (< 130/80 mm Hg). However, the European guidelines uphold the cut-off for the diagnosis of HT at 140/90 mm Hg [4, 5].

The authors of this document confirm 140/90 mm Hg in office BP to be diagnostic for HTN (and corresponding values in out-of-office measurements; Fig. 2.2). However, it is emphasised that BP in the range of 120–139/70–89 mm Hg, referred to as “elevated BP”, require intensive lifestyle changes and, in some clinical settings, also pharmacotherapy [5].

Hypertension is diagnosed based on:

Figure 3.1. Principles of hypertension (HT) diagnosis

Figure 2.2 presents the BP cut-off values for the diagnosis of HT depending on the method of measurement. BP defined as elevated is also associated with a higher cardiovascular risk. Figure 3.1 presents the principles for the HT diagnosis.

The white coat effect occurs when BP in office measurements is within the range of values consistent with HT, but remains within the range of elevated BP or optimal BP values during home measurements or ABPM. Patients with that condition may be at increased cardiovascular risk and should be monitored regularly, i.e. every 6–12 months. In specific cases, especially in patients with organ complications or diagnosed CV disease, the initiation of antihypertensive treatment should be considered.

Masked HT is defined by office BP readings lower than 140/90 mm Hg which coincide with elevated home or 24-h ambulatory values. Such a condition should be treated as HT and requires appropriate treatment (Fig. 3.1).

4. Clinical assessment, diagnostic tests and assessment of target organ damage

4.1. Clinical assessment of the HT patient

Clinical assessment of a patient with HT includes patient’s medical history, physical examination, as well as routine and extended tests/evaluation. The purpose is to detect the increased risk of CV diseases and to identify specific comorbidities and potential causes of secondary HT. Additionally, the aim of the assessment is to identify HT-mediated organ damage (HMOD). The key information on HT to be obtained from the anamnesis and physical examination is summarised in Tables 4.1 and 4.2.

4.2. Routine and addtional evaluation

Routine evaluation

Routine medical assessment and additional tests to be performed at the diagnosis and monitored as indicated are summarized in Figure 4.1 and Table 4.3.

Figure 4.1. Basic and extended medical examinations in a patient with hypertension (HT)

Additional medical examination

Additional medical examination is to be considered at the initial assessment of a patient with HT, whenever the results may influence further treatment (Fig. 4.1). The aim of the examination is primarily to optimise cardiovascular disease risk assessment and to assess HMOD and secondary HT risk [41]. Plasma lipoprotein(a) concentration should be assessed in every adult once in their life [42]. Tests such as non-contrast-enhanced computed tomography (CT) scans to assess calcification index, coronary artery CT scans, ankle-brachial index (ABI), carotid artery ultrasound and echocardiography may document HMOD and confirm the presence of atherosclerotic cardiovascular disease. These test results are important in the risk re-classification (to high or very high risk category) which further justifies the redefinition of therapeutic goals. Based on the results of additional evaluation, the initiation of pharmacotherapy in elevated BP category may be justified.

4.3. Electrocardiographic assessment in a patient with HT

The 12-lead ECG is a key tool in the routine evaluation of patients with HT (Fig. 4.2). The development of left ventricular hypertrophy (LVH), a significant HMOD, which becomes more probable along with the duration and severity of HT. ECG recording not only helps to predict cardiovascular risk but also provides valuable information for the clinical assessment of the patient i.e.: detection of atrial fibrillation (AF), history of coronary events. However, the sensitivity of ECG in the diagnosis of LVH is substantially lower as compared to echocardiography.

Figure 4.2. Interpretation of an electrocardiographic examination in a patient with hypertension (HT). The criteria for diagnosing left ventricular hypertrophy (LVH) presented in the figure authorise the diagnosis of LVH, i.e. organ damage due to HT, which affects the patient’s assessment and prognosis

The Sokolow–Lyon and Cornell indices are key ECG-derived criteria for the diagnosis of LVH. Based on Sokolow–Lyon index criteria, LVH is more commonly diagnosed in people with higher BP, older persons, and males vs. females. In contrast, with reference to the Cornell index criteria, LVH is more common in people with lower BP, younger people, women and obese people. Abnormal ST-segment, and T-wave documented in the lateral precordial leads are the most pronounced signs of LVH.. Left ventricular hypertrophy on ECG is a strong indicator of the risk of arrhythmia, including sudden cardiac death (SCD), AF, heart failure and stroke [4].

In addition to the LVH assessment, the ECG provides information on heart rate (HR), type of rhythm, atrioventricular conduction and repolarisation phase disturbances. These data can help to choose an appropriate antihypertensive therapy [4].

4.4. Echocardiographic evaluation of hypertensive patient

Studies show that LVH documented in the echocardiographic examination is an independent risk factor for cardiovascular events, while its regression is associated with a risk reduction {43].

The echocardiographic examination should be considered in all patients with HT. It allows to detect subclinical changes such as LVH, left ventricular remodeling, assessment of systolic and diastolic function, as well as the morphology and function of valves and increased aorta diameter (Fig. 4.3). In hypertensive patients with heart murmurs, heart failure symptoms, chest pain, syncope or palpitations, the echocardiographic examination becomes a key diagnostic tool. Occasionally, echocardiography bears the potential to detect secondary forms of HT, such as coarctation of the aorta.

Figure 4.3. Interpretation of an echocardiographic examination in a patient with hypertension (HT) [4, 5, 45]. Abnormal parameters allow for the diagnosis of left ventricular hypertrophy (LVH) (point 2), diastolic dysfunction (point 3) or systolic dysfunction (point 4), i.e. organ damage due to HT, which affects the patient’s assessment and prognosis

Parameters of left ventricular structure and function considered as subclinical changes in the course of HT (Fig. 4.3) are the same as those assessed in patients with heart failure with preserved ejection fraction (HFpEF). This highlights the continuity of cardiovascular risk and the role of HT in the development of clinically overt disease. The basis of diagnosis in such cases is the echocardiographic examination [44].

4.5. Renal function assessment in a patient with HT

Hypertension constitutes the second most common cause of chronic kidney disease (CKD) after diabetes. Inversely, hypertension may also result from primary kidney disease. Deterioration of renal function can be detected by routine laboratory tests using estimated glomelural filtration rate (eGFR) based on either serum creatinine or cystatin C (if available) [46]. Serum creatinine poorly illustrates impaired kidney function, as significant deterioration of renal function can occur with creatinine concentrations remaining within the broad laboratory normal range. Chronic kidney disease is classified based on eGFR, using 2009 CKD-Epidemiology Collaboration formula, and the presence and severity of albuminuria [47, 48]. The albumin–creatinine ratio (ACR) is assessed in a urine sample (preferably in the morning) and is the preferred method for measuring urinary albumin excretion [49]. A single negative strip test result as well as a single normal ACR result do not rule out moderately increased albuminuria [50]. To confirm the diagnosis of moderately or severely increased albuminuria, two results within this range taken three months apart are required [48]. Serum creatinine, eGFR and ACR should be monitored in all patients with HT (Fig. 4.4). The tests should be repeated at least once a year.

Figure 4.4. Renal function assessment in a patient with hypertension (HT)

Renal ultrasound

Owing to relatively low cost and wide availability renal ultrasound is often utilized to assess kidneys morphology [51, 52]. It is a valuable method for diagnosing CKD and detecting renal artery stenosis [53]. Doppler imaging can be used to assess hemodynamic alterations in the renal artery and the kidney. Doppler spectral ultrasound allows for the measurement of the renal resistive index (RRI), which is a non-invasive and repeatable way to assess the compliance or resistance of the kidneys and systemic arteries [54]. In healthy adults, the RRI ranges from 0.58 to 0.64. A value below 0.7 is considered normal [4, 55]. In relation to age, high RRI values may indicate renal parenchymal disease (e.g. diabetic or hypertensive nephropathy). A difference in RRI between the kidneys may indicate renal artery stenosis [56, 57].

4.6. Other diagnostic tests in a patient with HT

In different settings, hypertensive patients’ evaluation may be extended with tests that aim at the HMOD assessment and risk reclassification (HMOD criteria are given in brackets) [2, 5, 58–59]:

In specific settings, the evaluation of hypertensive patients may be extended to include:

4.7. Assessment for secondary forms of HT

Symptoms that may indicate the presence of secondary HT and the screening tests are shown in Figure 4.5. Heart morphology and functional abnormalities specific for secondary forms of HT are also presented.

How often to assess BP values to detect HT?

Since BP increases throughout life and the rate of increase depends on many factors, BP measurement (office or at home) should be performed at least once a year in every adult.

People with elevated BP who are not on antihypertensive treatment should have their BP measured every three months. In the last case, it is also worth considering annual 7-day home measurements to get a more accurate picture of BP changes.

Figure 4.5. Symptoms that may indicate the presence of secondary hypertension (HT) and the screening tests. Based on [4, 5, 60, 61]

5. Cardiovascular risk assessment in a patient with HT

In most patients, HT coexists with other diseases and risk factors that affect cardiovascular health [62, 63]. In daily practice, priority should be given to patients at high and very high cardiovascular risk. A tool which allows to identify patients at high and very high cardiovascular risk are risk scorecards such as SCORE2, SCORE2-OP, SCORE2-Diabetes, as well as a scale based on “10 for Heart” being developed for the Polish population. We recommend that patients at high and very high cardiovascular risk are identified according to the scorecards, as well as using a range of risk factors and comorbid conditions, as illustrated in Figure 5.1. In patients at high and very high cardiovascular risk, it is essential to take immediate action to substantially reduce the risk, which includes blood lowering pharmacotherapy if BP ranges between 130–139 for systolic BP, and/or 80–89 mm Hg for diastolic BP [4, 25, 41, 42, 64].

Figure 5.1. Distinction of hypertension (HT) patients at high and very high cardiovascular risk. Developed based on [4, 25, 41, 42, 64]

In addition to the risk factors shown in Figure 5.1, other risk factors and clinical conditions affecting cardiovascular risk should be considered [4, 65], such as:

6. Hypertension as a component of the metabolic syndrome

Hypertension is one of the most common risk factors for cardiovascular diseases in Poland. In most cases, patients with HT have additional cardiovascular risk factors such as obesity, dyslipidaemia or glucose metabolism disorders. In response to that, in 2022, Polish experts proposed a new definition of metabolic syndrome (MS) [64].

The primary criterion for the diagnosis of MS is obesity as determined by waist circumference and/or BMI. Additional criteria are HT or elevated BP, atherogenic dyslipidaemia and pre-diabetes or diabetes. Obesity and two of the three additional criteria allow the diagnosis of MS (Fig. 6.1). Waist circumference cut-off values for the diagnosis of abdominal obesity are debated; in young people, a waist circumference > 80 cm in women and > 94 cm in men may already indicate abdominal obesity [64].

Figure 6.1. Criteria for the diagnosis of metabolic syndrome and its complications. Based on [64]

The WOBASZ II study shows that 32% of the adult Polish population meets the criteria for the diagnosis of MS [66]. Its most common component is BP ≥130/85 mm Hg or the use of antihypertensive treatment (94% of WOBASZ II participants). Atherogenic dyslipidaemia was found in 91% and prediabetes or diabetes in 61% of subjects. The increasing prevalence of obesity may lead to more frequent cases of MS.

Every patient with HT should be assessed for the remaining components of MS. Effective non-pharmacological and pharmacological treatment of each of the four components of MS can substantially reduce cardiovascular risk. Attention should also be paid to complications associated with MS, such as moderately increased albuminuria, hepatic steatosis, obstructive sleep apnoea (OSA) or HFpEF, the presence of which further confer cardiovascular risk (Fig. 5.1); prevention and treatment of MS reduces the risk of development of abovementioned complications of MS [64].

7. Initiation of treatment and target values

7.1. Initiation of HT treatment

Lowering BP is a key action that significantly reduces cardiovascular risk in patients with HT. Therefore, it is important not to delay the initiation of antihypertensive treatment in patients with a confirmed BP above 140/90 mm Hg [67]. Regardless of baseline BP values, all patients with elevated BP or HT should initiate non-pharmacological measures (sec. 8) aimed at lowering BP. At the same time, antihypertensive pharmacotherapy should be introduced in all patients with HT and considered in patients with BP within 130–139/80–89 mm Hg who are at high or very high cardiovascular risk after 3 months of non-pharmacological management (Fig. 2.2).

7.2. Antihypertensive treatment in patients with elevated BP

The basis of the inclusion of antihypertensive pharmacotherapy in patients with a systolic BP in the range 130–139/80–89 mm Hg is the results of studies showing that such treatment is effective in reducing the risk of developing HT [68–70]. Studies indicate that long-term exposure to elevated BP and other major factors contributing to cardiovascular diseases significantly increases the overall cardiovascular and death risk [71]. It is therefore reasonable to subject patients with elevated BP who are at high or very high cardiovascular risk (criteria in Fig. 5.1) to antihypertensive intervention if changes in their lifestyle do not result in BP lowering, despite the lack of hard end-point studies in that group. A decision to introduce pharmacotherapy should be made after 3 months of ineffective non-pharmacological treatment. It is then recommended to start with monotherapy while continuing with the implementation of lifestyle changes (Fig. 7.1).

Figure 7.1. Management of patients with elevated blood pressure (BP)

7.3. BP target values

Data from both observational and randomised studies support the recommendation to reduce BP below 130/80 mm Hg, but not lower than 120/70 mm Hg (Fig. 7.2) [4, 5, 72, 73]. In this document, the decision-making patterns are simplified, the previous proposals are abandoned in favour of a single, clearer algorithm — it should be assumed that the patient is to be treated considering that goal unless “exceptions” presented later in the section is met. The previous guidelines were revised, the importance of age in determining BP targets was reduced [2]. The basic strategy of pharmacologically lowering systolic BP to 120–129 mm Hg is now recommended for most patients. There are several reasons for that:

Figure 7.2. Blood pressure (BP) target values

Before starting HT pharmacotherapy, it is important to make a clinical decision as to whether the standard target of lowering BP to 120–129/70–79 mm Hg is appropriate for the patient [77]. It is sometimes necessary to set individual, more liberal targets, for example a systolic BP in the range 130–139 mm Hg, in some clinical settings:

When it comes to office BP measurements, it is worth follwoing the “trust but verify” principle. This means that, where possible, it is advisable to take BP measurements outside the office before starting therapy and while monitoring its effectiveness [5].

7.4. Dimensions of antihypertensive effectiveness

Achieving target BP is only part of effective HT control. In addition to achieving BP targets (“quantitative” control), the effect of antihypertensive treatment on BP variability (“qualitative” control) — achieving stable HT control — is also important. A growing body of data indicates that increased BP variability in ABPM, home measurements and office measurements (between visits) is associated not only with a higher risk of HMOD and cardiovascular events but also with a higher risk of cognitive impairment (Fig. 7.3). Assessing the effect of the treatment used on BP variability is, therefore, an additional exponent of the quality of HT control. Studies show that the use of long-acting antihypertensive drugs may have a beneficial effect on BP variability [78–81].

Figure 7.3. Dimensions of antihypertensive effectiveness

8. Non-pharmacological management in patients with HT

Non-pharmacological management in patients with HT is a key component of therapy. It is the basis for preventing the development of HT in people with elevated BP. It helps to reduce cardiovascular risk and improves prognosis and quality of life. Lifestyle changes result in lower BP, slow the progression of atherosclerosis and may delay the onset of HMOD and clinical signs of atherosclerosis. Non-pharmacological recommendations (lifestyle measures) with documented efficacy in the treatment of HT are shown in Figure 8.1.

Figure 8.1. Non-pharmacological (changing lifestyle) recommendations with documented efficacy in the treatment of hypertension (HT). Developed based on [4, 5, 41]

A common belief regarding non-pharmacological management is that coffee consumption should be reduced in patients with HT. Coffee consumption does not increase the risk of HT in the general population. In fact, higher coffee consumption may even lower this risk [82]. Therefore, limiting coffee consumption in HT patients is not necessary. In addition, higher consumption of coffee or tea may reduce the risk of type 2 diabetes [83]. The relationship is different with unfiltered, Turkish-brewed or boiled coffee. It contains higher concentrations of caffestol and kahweol, which may slightly increase serum LDL cholesterol concentrations. However, increased cardiovascular risk was observed in cases of consumption of nine or more such drinks per day [84, 85].

In contrast, the consumption of two or more servings of sugar-sweetened beverages per day is associated with a 35% higher risk of coronary heart disease in women [86]. Consumption of such drinks also increases the risk of all-cause mortality. In children and adolescents, sugar-sweetened beverages raise systolic BP and increase the risk of developing HT [87, 88]. From an early age, sugar-sweetened beverages should not account for more than 10% of daily energy intake.

Excessive alcohol consumption is one of the main causes of premature mortality. Increased alcohol consumption is linearly associated with a higher risk of cancer, liver disease, AF, stroke and HF. Although many scientific societies recommend limiting alcohol consumption and set limits, there is no proven safe amount of alcohol for the general population. Findings show a strong linear correlation between alcohol consumption and higher BP, while also suggesting that low consumption may be associated with a lower cardiovascular risk than total abstinence. However, potential cardioprotective benefits may arise from the overall healthier lifestyle of moderate alcohol drinkers. The risk of HT increases in both sexes when daily consumption is one to two drinks, or 10–20 g of alcohol. Reducing alcohol consumption close to abstinence can lower systolic and diastolic BP by 3.3 and 2.0 mm Hg. Binge drinking is particularly dangerous and, together with uncontrolled HT, it increases the risk of haemorrhagic stroke. Reducing or stopping alcohol consumption, especially in Poland, is recommended for better BP control and overall health [89, 90].

9. Basic algorithm for the treatment of HT

Most antihypertensive drugs used in monotherapy lower BP by less than 20/10 mm Hg and only in approximately half of patients. For that reason, most people with HT require combination therapy. Due to the limited efficacy of monotherapy, it is recommended to start HT therapy with combination therapy, preferably in the form of SPCs. Exceptions are patients in poor general condition, with at least mild frailty (Fig. 11.9) or with no HT but with elevated BP, in whom the treatment decision is made on an individual basis, generally starting with monotherapy (Fig. 9.1). One to two months after starting two-drug therapy its effectiveness should be assessed and, if target BP values are not achieved, intensification should be considered by adding a third drug to achieve target BP values within three months [2–6, 58, 91]. In recent years, data has been published indicating the effectiveness and safety of starting therapy with a combination of three or four antihypertensive drugs, including the use of SPCs, at low or very low doses. However, this regimen cannot currently be recommended as a routine in daily practice [92].

The use of appropriately selected combinations of two or three drugs, especially in the form of SPCs, can control BP in most patients. The treatment algorithm based on SPCs is effective and better tolerated, promotes patient cooperation and ensures rapid achievement of BP targets. This reduces cardiovascular risk, which is a key goal of HT therapy [2–6, 58, 91, 93].

Groups of antihypertensive drugs that effectively reduce the incidence of cardiovascular events are angiotensin-converting enzyme inhibitors (ACEIs)/angiotensin II receptor AT1 blockers (ARBs, also known as sartans), calcium channel blockers1 (CCBs), thiazide-like diuretics/thiazide diuretics (TLDs/TDs) and beta-blockers (BBs). The first three groups (the so-called “basic three”) are recommended as first-line solutions for the initiation of HT therapy due to their superior efficacy in reducing cardiovascular risk [2–6, 58, 91]. It should be noted that in Poland, among patients using two or three antihypertensive drugs, only 34% use a regimen based on the recommended combinations [12].

The basic treatment strategy should include (Fig. 9.1) [2–6, 58, 91]:

Figure 9.1. Basic strategy for the treatment of hypertension (HT) (A) and exceptions to this strategy (B)

Beta-blockers should be used in selected clinical situations in combination with other drugs or independently of the use of the “basic three” (sec. 10). When choosing drugs, one should take into account their ability to significantly lower BP, reduce its variability and reduce the risk of developing or worsening HMOD and cardiovascular diseases, as well as their tolerability profile [2–6, 58, 91]. Exceptions to the use of the „basic three” are shown in Figure 9.1.

9.1. Dosage of antihypertensive drugs versus intensification of therapy

As part of the basic algorithm of HT therapy, two approaches to the selection and intensification of doses of antihypertensive drugs are proposed. The first involves starting with lower doses of a two-drug combination, increasing them to maximum doses and then adding a third drug. The second involves starting therapy with low doses of two drugs and moving on to three drugs in low doses. Based on a practical approach in daily practice, it is recommended:

When to use antihypertensive drugs: in the morning or evening?

10. The place of beta-blockers in HT therapy

In previous guidelines, BBs were mainly recommended for exceptional indications [2, 6]. Despite this, BBs are the most commonly used group of antihypertensive drugs in Poland [12]. Numerous studies have shown that BBs significantly reduce the risk of HF and serious cardiovascular events in HT patients compared with placebo. BBs are also comparatively effective in preventing serious CV events, as are other classes of antihypertensive drugs. The exception is stroke prevention, where they are less effective. This difference may be due to small differences in the BP achieved, including central systolic BP, which has a particular impact on cerebrovascular events [115–119].

Beta-blockers are a diverse group of drugs. Of particular interest are their beta1 selectivity and vasodilatory properties. Studies on nebivolol (additional vasodilatory effect) and bisoprolol, which have higher beta-1 selectivity, showed that these drugs have a more favourable side-effect profile, including a lower incidence of erectile dysfunction [120–122]. Studies using carvedilol, bisoprolol, metoprolol succinate and nebivolol have confirmed their beneficial effects on prognosis in patients with HFrEF [123]. Beta-blockers such as metoprolol and bisoprolol are also effective in treating cardiac arrhythmias. In addition, metoprolol and propranolol are used for non-cardiac conditions such as essential tremor, prevention of migraine attacks or psychosomatic disorders [4, 116, 124].

A resting HR above 80 beats per minute is common in HT and indicates increased sympathetic nervous system activity [125]. An increase in resting HR is directly associated with a higher risk of AF, HF and increased mortality, both in the general population and in patients with HT. Although the evidence for the benefit of lowering HR in HT is mainly based on post hoc analyses, some data suggest that patients with HT and elevated HR may particularly benefit from BB therapy [124, 126–128]. The use of BBs in HT therapy is illustrated in Figure 10.1 by introducing a three-category division: (1) BBs should or (2) can be considered in specific clinical situations, independent of other drugs, and (3) BBs can be considered after the basic three antihypertensive drugs (ACEIs/ARBs, CCBs and TLDs/TDs) have been used as primary therapy [4, 58].

Figure 10.1. Use of beta-blockers (BBs) in hypertension (HT) treatment

11. Differences in hypertension management

11.1. Hypertension in women

Hypertension in women is associated with a higher risk of myocardial infarction than in men at comparable BP values. Women are more likely to develop concentric LVH and HFpEF and have a higher risk of developing renal failure [129, 130]. Women are also more likely to report adverse effects of antihypertensive drugs, such as oedema, cough, hyponatraemia and hypokalaemia. Although they are more likely to start treatment, it is less likely to be effective. Treatment regimens for HT in women vary according to the patient’s age, reproductive plans and metabolic and haemodynamic profile (Fig. 11.1).

Figure 11.1. Hypertension (HT) management in women by age

Hypertension in women of childbearing age

When taking a medical history, attention should be paid to female-specific risk factors such as early menarche, menstrual disorders, polycystic ovary syndrome (PCOS) features, history of pregnancy and use of oral contraceptives (OCs). The clinical assessment should also consider the secondary causes of HT, like fibromuscular dysplasia (FMD) or primary hyperaldosteronism (PA), as well as the quantive assessment of proteinuria [131].

The drug choice in this patients group includes CCBs, BBs and TLDs/TDs. It is recommended to start treatment with a two-drug combination therapy using SPCs (Fig. 9.1).

The use of ACEIs, ARBs and MRAs in uncomplicated HT is not recommended due to their teratogenicity. The prescription of these drugs should be limited to female patients with diabetic kidney disease, hypertensive nephropathy, or heart failure, with the provision of effective contraception methods. Patients should be informed about the risks and give their informed consent.

If a woman with HT is planning a pregnancy, her treatment may be continued or changed to drugs dedicated to hypertension treatment during pregnancy, such as labetalol, metoprolol, methyldopa or extended-release nifedipine (possibly amlodipine). This is particularly recommended for women planning to use assisted reproduction technologies, as in vitro fertilisation may increase the risk of developing pre-eclampsia (PE) and gestational HT [132].

Oral contraceptives may slightly elevate BP by an average of 5 mm Hg, which applies to systolic and diastolic BP. It is estimated that 2% of women using OCs for four years may develop HT. Their use is also associated with a higher thromboembolic risk and a slight increase in the risk of arterial thrombosis. The described relationship depends on other risk factors present in the patient [133].

Menopause

After menopause, BP in women increases more rapidly than in men of the same age. Vasomotor symptoms may indicate future cardiovascular risk [135]. Activation of the sympathetic nervous system plays a role in the pathogenesis of HT and vasomotor symptoms. Patients may benefit from combining ACEIs/ARBs with BBs.

Postmenopausal treatment of HT in women is similar to that used in men and based on the individual characteristics of the patient, such as metabolic and haemodynamic profile and concomitant diseases.

HRT may be used to relieve the menopausal symptoms in women with HT, but it is not recomended for primary prevention of cardiovascular diseases. It does not affect BP but may improve lipid profile and endothelial function. HRT is contraindicated in women after cardiovascular events and at high thrombotic risk.

What contraceptive can be used in a patient with chronic HT?

Progestogen-only pills are safe for women with well-controlled HT as they do not affect BP [134].

Combined oral contraceptive pills can be used if more suitable methods are not available or acceptable. The risk of cardiovascular diseases depends on the dose of oestrogen and risk factors such as obesity, smoking and lipid disorders. They should not be used by women over 35 who smoke, patients with diagnosed cardiovascular diseases, uncontrolled HT or those at very high risk of cardiovascular diseases [45].

Intrauterine devices (with copper or levonorgestrel) are an effective and safe option for women with HT.

Progestogen-only subdermal implants (e.g. etonogestrel), effective for three years, are also a good alternative.

A patient using oral contraceptives develops HT: how to manage her?

It is recommended to discontinue oral contraceptives, as it usually lowers BP, and to consider other contraceptives. If BP does not return to normal within three to six months, a comprehensive diagnostic evaluation for HT is required. The initiation of treatment depends on the patient’s overall cardiovascular risk.

11.2. The “metabolic” patient with hypertension on a continuum of obesity  MS  diabetes  HFpEF

Obesity is a significant gateway to the development of cardiovascular diseases. One of its first consequences is the development of HT, prediabetes, diabetes and atherogenic dyslipidaemia [64]. These early complications of obesity, which are the main risk factors for cardiovascular disease, make up MS. This leads to further sequelae of obesity, such as LVH, moderately increased albuminuria, hepatic steatosis and OSA. Left ventricular diastolic dysfunction also occurs, which can result in AF and HFpEF.

This sequence of adverse events can be referred to as the obesity cardiovascular continuum, in which treatment of obesity is crucial (Fig. 11.2). The processes along the chain of obesity  MS  diabetes  HFpEF may progress at different rates. Therefore, these patients require an individualised approach to treating HT, taking into account the different severity of obesity complications.

Figure 11.2. Therapy goals of hypertension (HT) and comorbid conditions on the continuum of obesity  metabolic syndrome  diabetes  HFpEF

Heart failure with preserved ejection fraction can be considered one of the sequelae of obesity-induced MS [64]. Metabolic syndrome is a significant risk factor for HFpEF. Hypertension leads to concentric LVH (with reduced compliance), and obesity and metabolic disorders, through inflammation and microcirculatory dysfunction, exacerbate left ventricular diastolic dysfunction [64].

Heart failure with preserved ejection fraction is not a homogeneous condition. One can differentiate between its phenotypes associated with obesity and MS and those associated with older age, arterial stiffness or CKD. The co-occurrence of obesity and HFpEF increases the risk of hospitalisation for HF exacerbations [136].

The treatment of obesity improves HT and diabetes control, which is evidence of the importance of the sequence of events outlined above. Reducing the BMI by 10 kg/m², for example, through bariatric surgery, allows some patients with HT to achieve normal BP without antihypertensive medication [137, 138]. Recent studies indicate that bariatric surgery reduces the incidence of AF episodes, and pharmacological treatment of obesity improves exercise tolerance in patients with HFpEF and reduces the severity of OSA [139–141].

Management of the patient in the continuum of obesity  MS  diabetes  HFpEF is based on intensive implementation of lifestyle modification principles and measures to achieve treatment goals in four dimensions: (1) weight reduction, (2) glycaemic control, (3) BP reduction and (4) control of serum LDL and non-HDL cholesterol levels (Fig. 11.2) [64, 142–145].

Obesity treatment

Treatment of prediabetes/diabetes

Hypertension treatment

Table 11.1 shows the characteristics of HT patients with relation to a continuum of obesity  MS  diabetes  HFpEF. The principles of HT treatment on a continuum of obesity  MS  diabetes  HFpEF are described below (Fig. 11.3) [64, 142–145]:

Figure 11.3. Treatment of hypertension (HT) and comorbid conditions on the continuum of obesity  metabolic syndrome  diabetes  HFpEF

Treatment of lipid disorders

Pharmacotherapy of lipid disorders in patients on a continuum of obesity  MS  diabetes  HFpEF is based on the following principles [64, 167, 168]:

Additional drugs in the continuum of obesity  MS  diabetes  HFpEF with cardio- and nephroprotective effects

As shown in Figure 11.3, the use of SGLT2 inhibitors, GLP-1 receptor agonists, and MRAs plays an important role in the obesity  MS  diabetes  HFpEF continuum.

The use of SGLT2 inhibitors carries important cardioprotective benefits. In addition, they are well-established in the treatment of HFpEF, where they lower the risk of hospitalisation for HF. These benefits include reduction of left atrial volume and left ventricular mass, improved left ventricular diastolic function, reduced AF risk, a significant decrease in NT-proBNP levels and reduced risk of major ventricular arrhythmias, cardiac arrest and sudden death in patients with HT [169–176].

In patients with CKD, SGLT2 inhibitors further reduce the risk of a composite endpoint, including a 50% or greater reduction in eGFR, development of end-stage renal failure and death from renal causes [177, 178]. In addition, they reduce albuminuria, regardless of glycaemic status, eGFR level or baseline severity of albuminuria [179].

There is also increasing evidence supporting the cardioprotective and nephroprotective benefits of GLP-1 receptor agonists [180]. In studies involving patients with HFpEF and obesity, semaglutide significantly reduced the severity of HFpEF symptoms according to the Kansas City Cardiomyopathy Questionnaire — The Clinical Summary Score (KCCQ-CCS), increased the distance in the 6-minute walk test and had a beneficial effect on echocardiographic parameters, including a reduction in left atrial volume [140, 141, 181].

Mineralocorticoid receptor antagonists are also an important component of therapy in the obesity  metabolic syndrome  diabetes  HFpEF continuum. In the FINEARTS-HF trial, finerenone demonstrated the ability to reduce the risk of hospitalisation for HF in patients with HFpEF and a composite endpoint including deaths and hospitalisations. Previous studies indicate that MRAs reduce albuminuria and inhibit the progression of CKD in patients with diabetes and CKD (finerenone), reduce the frequency of AF attacks, reduce left ventricular hypertrophy and inhibit myocardial fibrosis [161, 180, 182–186].

11.3. The “cardiac” patient with HT and a continuum of atherosclerotic cardiovascular disease

The change in approach to coronary artery disease through the concept of chronic coronary syndromes (CCS) allows a holistic view of atherosclerosis-induced cardiovascular disease. This process starts with atherosclerosis risk factors, leads to subclinical coronary atherosclerosis, CCS with angina, acute coronary syndrome (ACS) and ends with heart failure with reduced ejection fraction (HFrEF) (Fig. 11.4) [5, 148, 188].

Figure 11.4. Treatment of hypertension (HT) in the continuum of atherosclerotic cardiovascular disease

Management of HT in patients on the continuum of cardiovascular disease secondary to atherosclerosis

Other drugs reducing cardiovascular risk in patients with CCS

11.4. Hypertension in patients with a history of stroke

Hypertension is a key and modifiable risk factor for vascular damage to the central nervous system. The association of HT with stroke risk is stronger than for other complications such as ischaemic heart disease [191, 192]. Observational studies have shown an almost linear relationship between BP values and its variability and the risk of ischaemic stroke, intracerebral haemorrhage and vascular dementia [191–194]. HT is estimated to cause at least 45% of ischaemic strokes and 74% of primary intracerebral haemorrhages [191, 192]. Diabetes and HT sequelae such as AF and heart failure (HFpEF and HFrEF) further increase the risk of stroke in patients with HT [195, 196].

In the context of long-term stroke prevention, several placebo-controlled studies have shown that HT pharmacotherapy is effective in reducing the risk of first and subsequent acute cerebrovascular events, regardless of the drugs used [58, 197–200]. Fewer data are available for dementia risk reduction [201, 202].

Patients who benefit more from antihypertensive therapy in terms of stroke risk are those who:

Principles of hypertension therapy

11.5. Hypertension in patients with peripheral artery disease

Antihypertensive therapy in patients with peripheral artery disease (PAD) should holistically consider other cardiovascular diseases, treating HT as a concomitant disease. It is crucial to minimise the use of symptomatically acting drugs that do not affect the patient’s life expectancy and overall morbidity. A patient with PAD should have BP measured in both arms at each visit. In patients with lower extremity arterial disease (LEAD), it is also important to determine the AHI. Because of the risk of atherosclerotic changes in the small vessels, including the retinal microcirculation, patients with LEAD should have an ABPM performed once a year to assess the degree of BP control and diurnal profile. This is especially important in those with glaucoma (risk of excessive night-time BP drops).

Treatment of HT with coexisting PAD raises concerns of worsening ischaemia and increasing the risk of stroke or amputation. However, therapy strives to balance the benefits of BP control and not exacerbate ischaemia (Fig. 11.5). Effective antihypertensive therapy significantly reduces the long-term risk of cardiovascular events [224–226]. With good tolerance, lowering BP to 120–129/70–79 mm Hg is recommended in most patients [225]. The principles of pharmacotherapy are similar to those used in uncomplicated HT [4].

Figure 11.5. Blood pressure (BP) and the risk of worsening limb perfusion and increasing cardiovascular risk. Based on [224, 225]

Myths about the risk of deterioration of limb blood supply by BBs need to be dispelled [227]. Meta-analyses indicate that these drugs do not worsen the symptoms of intermittent claudication or increase the risk of ischaemia. On the contrary, BBs may improve prognosis, especially in patients with HFrEF. BBs can be safely used for HT coexisting with LEAD and specific indications. The guideline emphasises that especially those with vasodilatory effects may prolong the distance in the intermittent claudication and improve the clinical condition of the patient [228, 229].

11.6. Hypertension in patients with chronic kidney disease

Hypertension is a key risk factor for the development and progression of CKD. Effective treatment of HT and achievement of target BP slow the progression of CKD and reduce cardiovascular risk. HT and nephroprotective treatment in patients with CKD should start immediately after diagnosis. SGLT2 inhibitors have a strong nephroprotective effect, especially in patients with moderately/significantly increased albuminuria. They also have, as described above, a weak antihypertensive effect [230, 231].

Nephroprotective treatment should be implemented in CKD patients with elevated BP (Fig. 11.6) [230, 231]. If BP remains elevated, additional antihypertensive drugs should be considered in addition to the ACEIs/ARBs used, especially with an ACR ≥ 30 mg/g [4, 5, 48].

Figure 11.6. Management of patients with hypertension (HT) and chronic kidney disease. Developed based on [4, 5, 48]

Target BP in patients with CKD is controversial and varies in guidelines [4, 5, 48]. Generally, it should be 120–129/70–79 mm Hg with regular control of serum creatinine, avoiding too-low BP [4, 5]. SPRINT and ESPRIT trials, for instance, have shown that intensive BP control was associated with increased rates of acute kidney injury (SPRINT) and renal events (ESPRIT) but reduced the risk of death and cardiovascular events [75, 76].

When to discontinue ACEIs/ARBs in patients with CKD?

ACEI/ARB discontinuation increases cardiovascular and renal risk and should be avoided [234]. Inclusion of these drugs can lower the eGFR by 10–15%. If the decrease exceeds 30%, then withdrawal should be considered, and renal artery stenosis or other causes should be ruled out [4]. For hyperkalaemia in patients with an eGFR < 45 mL/min/1.73 m2, potassium-binding drugs such as patiromer, available in Poland, may be considered, preventing the need to discontinue ACEIs/ARBs [235]. Regardless of the eGFR, one should try to reduce dietary potassium supply, use or increase doses of TLDs/TDs or loop diuretics, and consider including SGLT2 inhibitors as indicated.

Principles of HT therapy (Fig. 11.6)

11.7. Hypertension in patients with atrial fibrillation

Patients with HT are almost twice as likely to develop AF as those with normal BP [236, 237]. Regular screening for AF in patients with HT is therefore recommended [238]. In patients with paroxysmal AF and HT, optimal pressure control is crucial, reducing the risk of recurrent AF and cardiovascular events [238–240]. Studies indicate that patients with AF whose BP is adequately controlled are less likely to experience strokes [241, 242]. Target BP in patients with HT and AF is 120–129/70–80 mm Hg [243, 244].

Appropriate pharmacological treatment of HT and HF can prevent AF. It works by limiting atrial stretch, and drugs that inhibit the renin–angiotensin system may further protect against electrical and structural remodelling of the heart. As an outcome and marker of atrial remodelling, AF is closely associated with atrial cardiomyopathy. Drugs affecting atrial remodelling may prevent new episodes of AF and act as unconventional antiarrhythmics [238].

ACEIs or ARBs are preferred in the treatment of patients with AF and HT, but MRAs should also be considered. Effective combinations of ACEIs/ARBs with CCBs or TLDs/TDs are recommended for optimal BP control. Beta-blockers are recommended to control HR [238]. In patients with HT and AF, anticoagulant treatment is necessary for the prevention of ischaemic stroke. HT increases both the risk of stroke and the risk of haemorrhagic complications. HT is not a contraindication to anticoagulant treatment, whereas poor BP control increases the risk of haemorrhages.

Antihypertensive drugs and the prevention of AF

11.8. Gestational hypertension

Hypertensive disorders of pregnancy include [4, 131]:

If women with pre-existing HT after the 20th week of gestation experience an exacerbation of HT and develop symptoms typical of pre-eclampsia, such as proteinuria or significant organ dysfunction, a diagnosis of HT with superimposed pre-eclampsia is made [4, 131].

The cut-offs values for diagnosing HT in pregnant women are the same as in the general population: ≥ 140/90 mm Hg, confirmed by out-of-office measurements within seven days in the first trimester and up to three days in the second and third trimesters [4, 131].

Gestational hypertension

Management of gestational HT includes [4, 131, 248, 249]:

Figure 11.7. Treatment of gestational hypertension (HT). Based on [131]

Pre-eclampsia

Pre-eclampsia develops after the 20th week of gestation in women with previously normal BP or exacerbates pre-existing HT; it is accompanied by proteinuria and/or a risk to fetal or maternal well-being. It rarely develops in the puerperium. It is caused by increased vascular resistance, platelet propensity to aggregate, activation of the coagulation system, impaired endothelial function, and placental abnormalities. Risk factors are shown in Table 11.2 [4, 131, 248].

In women at high risk of PE, ASA at 150 mg daily, started by the 16th week of gestation, and moderate physical activity are recommended as prophylaxis. Women with a history of gestational HT or PE have an increased risk of HT, HF, cardiovascular events and premature death. They should be regularly assessed for risk factors, and intensive treatment should be instituted if they develop [4, 131, 248].

11.9. Hypertension in young adults

Diagnosis of HT at a young age increases the risk of death and accelerates the occurrence of HMOD. High BP in young adults often persists also in later years of life, which is known as “tracking”. This phenomenon is associated with an unfavourable prognosis in both short and medium-term follow-up and increases the risk of cardiovascular events [250].

Selected patients should be referred to specialist centres for detailed assessment for secondary causes of HT. In young adults, it is worth considering early introduction of pharmacological treatment alongside lifestyle modifications. Patient education and close collaboration between GPs, hypertensiologists, cardiologists and the patients are crucial. This integration of efforts increases the effectiveness of HT diagnosis and therapy in young adults.

Recent studies indicate that ISH is most common in older adolescents and young adults with primary HT. This type is diagnosed in 66% of patients, mainly among boys and men. Systolic-diastolic HT was found in 30% of patients and isolated diastolic HT in 4% [251]. Among young adults aged 18 to 40 (mean 25 years), ISH predominates in men. Women are more commonly affected by systolic-diastolic HT or isolated diastolic HT [252].

Isolated systolic HT in young people is a complex phenomenon. In some, particularly tall and physically active men, it may result from pulse pressure amplification. Despite a normal central BP in the aorta, it may reflect an extreme physiology, called pseudohypertension. This type of HT is also sometimes the result of increased cardiac output with not yet increased peripheral resistance (hyperkinetic circulation).

The management of young people with ISH follows the following principles:

11.10. Hypertension in cancer patients

Hypertension is the most common comorbidity in cancer patients. Unhealthy diet, obesity, physical inactivity, smoking and alcohol consumption are common risk factors that contribute to the prevalence of HT in this group. In cancer patients, HT, like other cardiovascular risk factors and recognised cardiovascular disease, increases the risk of cardiotoxicity of anticancer treatment (Fig. 11.8).

Figure 11.8. Management of hypertension (HT) in cancer patients

Hypertension may develop or worsen due to malignancy (stress, pain) or treatment such as vascular endothelial growth factor receptor (VEGF) inhibitors, second- and third-generation BCR-ABL tyrosine kinase inhibitors (TKIs), brigatinib, ibrutinib, fluoropyrimidines, cisplatin, abiraterone, bicalutamide, enzalutamide and non-cancer therapies such as corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDs) [253].

Increases in BP during the use of VEGF pathway inhibitors

The management of HT in cancer patients should follow standard principles for other patient groups. It is important to optimise BP control before starting cancer treatment and to monitor it closely. The choice of treatment should take into account the type of cancer treatment and the risk of drug interactions.

Drugs from the ACEI/ARB and CCB groups are preferred. In contrast, TLDs/TDs, which are the mainstay of treatment in the general HT patient population, should be used with caution in this group. In patients with bone metastases, TLDs/TDs may increase the risk of hypercalcaemia, and in patients with gastrointestinal symptoms (vomiting, diarrhoea) during cancer treatment, TLDs/TDs may exacerbate electrolyte disturbances. In patients treated with androgen synthesis inhibitors or androgen receptor antagonists, MRAs may be effective [253, 254].

Diltiazem and verapamil are not recommended during anticancer treatment as their metabolism is via the cytochrome P450 3A4 system, which may lead to interactions with chemotherapeutics and increase drug concentrations in the blood [253].

The inclusion of ACEIs or ARBs and BBs — recommended in HF — should be considered for primary prevention in high-risk patients, especially when targeted drugs are used that may induce heart failure [253].

A distinctive form of HT is observed during treatment with angiogenesis inhibitors, whose main target is the VEGF receptor. When using VEGF inhibitors, close monitoring of BP during the first cycle of treatment is recommended — daily home measurements are preferred. An increase in BP during therapy with these drugs is observed in the majority of patients; antihypertensive treatment often needs to be intensified during cancer treatment and then reduced after the end of the cycle. The aims of monitoring BP values and optimising treatment are to reduce cardiovascular risk and to allow continuation of cancer treatment. The threshold values for withholding cancer treatment are a rise in BP ≥ 180/110 mm Hg [253].

11.11. Hypertension in elderly patients with frailty and/or multimorbidity

The changing age structure in Western societies, better health and longer life expectancy of the elderly lead to a discussion on the arbitrariness of the definition of old age. As a result, this position paper refrains from setting specific boundaries for old age [5, 15, 41]. Instead, priority is given to assessing the fitness of patients, regardless of age, in the diagnostic and therapeutic process of HT.

In light of the unequivocal intervention studies that have shown benefits of antihypertensive treatment even after the age of 80, elderly HT patients should be treated similarly to younger patients in decision-making algorithms [206]. This means using the same diagnostic criteria and decision-making BP values for pharmacotherapy. However, in the case of elderly patients, specific conditions that are more common in this age group should be taken into account, such as:

Each of these situations requires an individual approach to therapy, which makes it difficult to formulate uniform recommendations. It should also be borne in mind that problems such as frailty or multimorbidity are not just a matter of age and may also be present in people under 60 years of age.

Management in elderly patients

Figure 11.9. Management of hypertension (HT) in elderly patients

12. Management of emergencies

Emergencies — are characterised by severe HT (≥ 180/≥ 110–120 mm Hg) accompanied by acute signs of organ damage (Tab. 12.1). Such cases are life-threatening and in most patients require immediate intervention (intravenous pharmacotherapy). The key in such circumstances is a rapid lowering of BP with intravenous pharmacotherapy (Fig. 12.1) [2, 4, 263].

Figure 12.1. Clinical conditions with elevated blood pressure (BP) values in office measurements. Based on [263]

Typical emergencies:

The term “urgent cases” — currently proposed as asymptomatic significantly elevated BP — refers to HT with significantly elevated BP values that are not associated with acute organ damage at the time of the patient’s assessment (Fig. 12.1).

Malignant HT is a distinct form of emergency in HT characterised by a very poor prognosis when left untreated. It is defined as the coexistence of very high BP and thrombotic microangiopathy and acute renal failure. It is an emergency in which there is fibrinoid necrosis of small arteries and arterioles in the kidneys, retina and brain. Lesions of the fundus, microangiopathy, disseminated intravascular coagulation, encephalopathy or acute heart failure are also possible. Symptoms depend on the organs involved. They may include headaches, visual disturbances, dizziness and other neurological deficits, as well as chest pain and dyspnoea. Patients with hypertensive encephalopathy may experience drowsiness, lethargy, tonic-clonic seizures and cortical disorders; blindness may precede loss of consciousness [4, 264]. The management of malignant HT is discussed in detail in a recently published paper [264].

12.1. Management of asymptomatic significantly elevated BP [4, 263]

12.2. Management of emergencies [4, 263]

13. Perioperative treatment of HT

13.1. Qualification for surgery and preoperative management

The basic recommendations for preoperative management [4, 266] are as follows:

Changes in BP values may occur during perioperative management. Increases in BP may be induced by induction of anaesthesia, intubation, pain associated with surgery and vasopressors, and decreases — by continued anaesthesia, volume loss and blood loss.

13.2. Intraoperative management

During surgery, both low and high BP values may increase the risk of complications due to impaired autoregulation of blood flow, especially in older patients. There are no clear guidelines as to the specific BP values that should be maintained during surgery. It is important to try to keep them within a safe range, avoiding large fluctuations, especially episodes of hypotension, and aim for haemodynamic stability [4, 266].

13.3. Postoperative period

In the initial two hours after surgery, it is common to see an elevation in BP values, which usually resolves when antihypertensive treatment is reintroduced. Oral BBs should be restarted as soon as possible. Oral diuretics and ACEIs/ARBs should be restarted within 48 hours, after a thorough assessment of BP and the hydration status of the patient, taking into account the type of surgery performed, i.e. whether it was cardiac or non-cardiac surgery [4, 266].

14. Uncontrolled hypertension

14.1. Definition, characteristics and causes of uncontrolled and resistant HT

Hypertension is considered resistant when, despite the use of three drugs, including a diuretic, in appropriate combinations (ACEIs/ARBs and TLDs/TDs and CCBs) and at maximum tolerated doses, BP values in office measurements remain ≥ 140/90 mm Hg. Resistant HT defined in this way affects 10–20% of patients. However, after taking into account ABPM to exclude the white coat effect and adherence to therapeutic recommendations (taking at least 80% of medication doses), the incidence of truly resistant HT is lower at around 5% [2, 4, 5, 268].

The reduction of target BP values to below 130/80 mm Hg means that many patients, although not meeting the definition of resistant HT, have uncontrolled HT. This is an increasingly common clinical problem. Patients with uncontrolled HT, especially those with resistant HT, have a higher incidence of HMOD and a higher cardiovascular risk. This risk also depends on the number of antihypertensive drugs used.

The pathophysiology of resistant HT includes overexpression of vasoconstrictive neurohormonal factors, renal dysfunction with fluid overload and, in the elderly, aortic and large artery stiffness. Common clinical conditions associated with resistant HT include obesity, alcohol abuse, salt-rich diet, CKD and diseases causing secondary HT [2, 4, 268, 269].

14.2. Diagnostic and therapeutic management of patients with suspected resistant HT

Figure 14.1 shows the algorithm for the diagnostic and therapeutic management of patients with suspected resistant HT.

Figure 14.1. Algorithm for the management of patients with suspected resistant hypertension (HT)

The first step is to verify the appropriate choice of HT pharmacotherapy. The best option is to replace the current treatment with a single pill triple drug combination containing ACEIs/ARBs, TLDs/TDs and CCBs at maximum tolerated doses. This improves BP control in many patients [2, 4, 5, 268].

The second step is to check whether BP is indeed inadequately controlled, by taking home measurements (correctly taken) or ABPM. This helps to rule out the white coat effect, which is the second most common cause of pseudo-resistant HT [270].

The third step: in conversation with the patient, it is also worth verifying compliance with therapeutic recommendations (non-adherence is the most common cause of pseudo-resistant HT), including regular medication and lifestyle changes. Weight reduction, regular physical activity, reduction of salt and alcohol intake are important. A significant antihypertensive effect of intensive implementation of lifestyle modification recommendations has been shown in patients with resistant HT [271, 272]. Common reasons for non-adherence to therapeutic recommendations are: forgetting to take medication, poor motivation due to lack of awareness of the effects of HT, side effects of medication (including so-called multiple drug intolerance), poor tolerance of lower BP values and lack of symptoms at the onset of HT, too many medications used [273, 274]. Improvements in adherence can be achieved by using SPCs [2, 4, 5, 268, 269].

The fourth step: it is important to review the medications and substances taken by the patient, including those taken ad hoc, which may increase BP. These include drugs such as NSAIDs, corticosteroids, pseudoephedrine and combined contraceptives, theophylline, as well as substances such as liquorice and cocaine and other stimulants and dietary supplements.

The fifth step: often carried out already in reference centres, is screening for secondary causes of HT, which often lead to resistant HT. If a secondary form of HT is diagnosed, the key is to treat the underlying disease (Fig. 4.5, sec. 4.7) [2, 4, 5, 268]. This diagnostic step is carried out in parallel with intensification of antihypertensive therapy for resistant HT.

14.3. Antihypertensive therapy of truly resistant HT

For truly resistant HT, a fourth antihypertensive drug should be added. According to current recommendations, aldosterone-inhibiting drugs and BBs are recommended (Fig. 14.2). The treatment of choice is the use of MRAs, especially spironolactone, even at low doses (25–50 mg/day). In the PATHWAY-2 study, spironolactone was shown to have a stronger antihypertensive effect than bisoprolol or doxazosin [275]. Its effect can be attributed to the inhibition of aldosterone, the concentration of which is often elevated in resistant HT (increased secretion after an initial reduction due to renin-angiotensin system blockade or undiagnosed primary hyperaldosteronism). In patients with an eGFR below 45 mL/min/1.73 m² or a potassium concentration of more than 4.5 mmol/L, spironolactone should be used with caution due to the risk of hyperkalaemia. If spironolactone is not tolerated, eplerenone may be an alternative, although it is not currently registered for the treatment of HT and its efficacy is significantly lower [2, 4, 276]. Approval of the selective aldosterone synthesis inhibitor, baxdrostat, which has shown efficacy in the BrighHTN trial in patients with resistant HT can be expected soon [277]. Due to the high incidence of cardiac complications in resistant HT, BBs, especially bisoprolol, are also a recommended fourth drug [275, 278]. In clinical practice, patients with indications for BBs receive them earlier. It has been shown to be effective in intensifying ineffective therapy based on three essential drugs with an SPC containing four antihypertensive drugs using bisoprolol — ACEIs, TLDs/TDs, CCBs and BBs [279]. A vasodilating BB such as nebivolol (10 mg dose) may also be considered for selection.

Figure 14.2. Algorithm for the treatment of resistant hypertension (HT)

In subsequent treatment steps, an increase in the number of drugs to five-seven may be considered, including:

In patients with resistant HT, drugs often need to be administered twice daily. In the case of refractory HT, which cannot be controlled despite treatment with five to seven drugs, and in the case of suspected secondary forms of HT, patients should be referred to a specialist HT centre [282]. In Poland, the diagnosis of resistant HT allows the patient to access priority hospital treatment within the National Cardiac Network.

15. Interventional treatment of HT

Renal artery denervation stands out among interventional treatments for HT in terms of the greatest evidence of antihypertensive efficacy from clinical trials, including those in which sham surgery was performed. However, there is a lack of data on its long-term efficacy, especially in terms of cardiovascular risk reduction [283–288]. Also worth noting are domestic studies on the efficacy of cardioneuromodulation in BP lowering. The cardioneuromodulation is the alghorithm available on a pacemaker that affects the autonomic system through changes in the PQ interval. This method requires further research [289].

Currently, only in centres with suitably experienced staff renal artery denervation can be considered as a therapeutic option, in patients with HT uncontrolled with at least three drugs in full doses, including TDLs/TDs. The decision to perform the procedure is made by a team of specialists, consisting of a hypertensiologist and an interventional cardiologist, after a detailed discussion with the patient about the potential benefits and risks. The procedure is not recommended in patients with an eGFR below 40 mL/min/1.73 m² [4, 5].

Although patients with an eGFR below 40 mL/min/1.73 m² were not eligible for randomised trials with the sham procedure, the results of observational studies demonstrate the safety and nephroprotecitive effect of the procedure in patients with CKD.

In patients who do not adhere to therapeutic recommendations or who cannot tolerate many antihypertensive drugs, especially the three essential ones, are at least at high cardiovascular risk and have not achieved target BP values, renal denervation may also be considered. The prerequisite is that patients are willing to undergo this procedure following a shared decision-making process. This process requires that patients are fully informed of the benefits, limitations and risks of renal denervation [5].

The issue of renal artery denervation will be discussed in detail in a forthcoming position paper of PTK and PTNT experts.

16. Importance of patient co-operation in long-term BP control

Non-adherence to therapeutic recommendations, including both lifestyle modifications and pharmacotherapy, is increasingly recognised as a major cause of failure to achieve therapeutic goals. This leads to increased morbidity and mortality from cardiovascular causes and increases healthcare costs, i.a. avoidable hospitalisations. This problem particularly concerns HT [290].

Two groups of patients are particularly vulnerable: the young and middle-aged, who, according to research, show the least persistence with therapy, and those who are just starting therapy with cardiovascular risk reducing drugs, including antihypertensive drugs. Early discontinuation of such treatment, for example with antihypertensive drugs and statins, is associated with a higher risk of morbidity and death from cardiovascular causes [291–293].

To increase adherence to treatment in cardiovascular diseases, there are several key areas to focus on. Improving communication skills and building a partnership between patient and clinician are a key. This allows for a fully informed decision by the patient and acceptance of the actions taken. Patient education, dispelling myths and misinformation from the internet, and the use of electronic reminder methods such as SMS can help. Eliminating economic barriers and monitoring treatment progress are also important. Simplifying treatment regimens through SPCs also promotes better adherence [294–296].

Multidirectional interventions to improve adherence, including building physician–patient partnerships so that all therapeutic decisions are autonomously made by the patient, can significantly increase treatment persistence and reduce morbidity and mortality from cardiovascular causes in society.

17. Editorial Committee, Opinion Committee and Reviewers

Editorial Committee

Aleksander Prejbisz, Piotr Dobrowolski, Adrian Doroszko, Agnieszka Olszanecka, Agnieszka Tycińska, Andrzej Tykarski, Robert Gil, Jacek Wolf.

Opinion Committee

Marcin Adamczak, Beata Begier-Krasińska, Marzena Chrostowska, Grzegorz Dzida, Krzysztof J. Filipiak, Zbigniew Gaciong, Marek Gierlotka, Marcin Grabowski, Tomasz Grodzicki, Piotr Jankowski, Karol Kamiński, Agnieszka Kapłon-Cieślicka, Aneta Klotzka, Przemysław Leszek, Jacek Lewandowski, Mieczysław Litwin, Łukasz Obrycki, Artur Mamcarz, Przemysław Mitkowski, Beata Naumnik, Marek Rajzer, Janina Stępińska, Katarzyna Stolarz-Skrzypek, Anna Szyndler, Anna Tomaszuk-Kazberuk, Izabella Uchmanowicz, Marcin Wełnicki, Barbara Wizner, Beata Wożakowska-Kapłon, Tomasz Zdrojewski

Additional opinions

Dariusz Kozłowski, Dariusz Gąsecki

Reviewers

Waldemar Banasiak, Andrzej Januszewicz, Agnieszka Mastalerz-Migas, Krzysztof Narkiewicz, Andrzej Więcek, Adam Witkowski