The World Health Organization's goal to reduce mortality due to chronic non-communicable diseases (NCDs) by 2% per year demands a huge effort from member countries.1–4 This challenge for health professionals requires global political action on implementation of social measures, with cost-effective population interventions to reduce NCDs and their risk factors. Health professionals need their governments to implement acceptable cost measures, such as counseling for smoking cessation, guidance on healthy diets, encouragement of regular physical exercise, control of systemic arterial hypertension, and teaching and training programs aimed at these issues. These measures would contribute around 70% to the goal of a 2% per year reduction in NCDs.2,5 Dyslipidemia, hypertension and obesity are highly prevalent multifactorial diseases in Portuguese-speaking countries.5,6 Systemic hypertension is a major risk factor for complications such as stroke, myocardial infarction and chronic kidney disease, rivaling dyslipidemia and obesity in importance for the development of atherosclerotic disease.5,6 In addition to their significant epidemiological impact, non-pharmacological treatments of cardiovascular risk factors have a significant effect on the expenditure of ministries of health, social security and finance, because these conditions are major causes, directly or indirectly, of workplace absenteeism. There is evidence that preventive actions are more promising in the primary health care setting.

The number of adults with hypertension increased from 594 million in 1975 to 1.13 billion in 2015, of whom 597 million were men and 529 million women. This increase is due to both population growth and aging.6 Analysis of trends in blood pressure (BP) levels of 19.1 million adults from several population studies in the past four decades (1975-2015) shows that the highest BP levels have shifted from high-income to low- and middle-income countries of South Asia and sub-Saharan Africa. However, BP levels remain high in Eastern and Central Europe and Latin America.6

Several trends have been identified in changes in proportional mortality due to hypertensive disease and its outcomes, ischemic heart disease (IHD) and stroke, in Portuguese-speaking countries from 1990 to 2015 (Table 1). The highest proportional mortality rates due to hypertensive disease were observed in Brazil, Mozambique and Angola. Portugal had the highest human development index in 2015 and the highest mortality due to stroke.7–9 Limited access (around 50-65%) to essential pharmacological treatment in low- and low-middle income countries may have contributed to these results. In addition, in 40% of these countries there is less than one physician per 1000 population, and few hospital beds for the care of outcomes related to uncontrolled hypertension.7 Thus, joint actions to implement primary prevention measures can reduce outcomes related to hypertensive disease, especially IHD and stroke. It is essential to ensure the implementation of guidelines for the management of hypertension via a continuous process involving educational actions, lifestyle changes and guaranteed access to pharmacological treatment.

The risk associated with high BP increases with age, and every 2-mmHg rise is associated with a 7% and 10% increase in the risk of death due to IHD and stroke, respectively.2

Hypertension is defined as systolic BP (SBP) ≥140 mmHg and/or diastolic BP (DBP) ≥90 mmHg at least on two occasions. BP can be assessed in the physician's office by either automated or auscultatory methods. The classification of BP according to office BP values for individuals aged over 18 years is shown in Table 2. Twenty-four-hour ambulatory BP monitoring (ABPM) or home BP monitoring (HBPM) can help in the diagnosis of white-coat hypertension (WCH) and masked hypertension (MH). In WCH, BP measured at the office is high and that measured with ABPM or HBPM is normal, while in MH, the opposite is the case (Figure 1). In both WCH and MH, ABPM is mandatory. Figure 1 shows a flowchart for the diagnosis of hypertension.

Figure 1.

Flowchart for the diagnosis of arterial hypertension. ABPM: ambulatory blood pressure monitoring; BP: blood pressure; DBP: diastolic blood pressure; ED: emergency department; HBPM: home BP monitoring; SBP: systolic BP.

(0.29MB).

ABPM enables identification of circadian BP changes, especially those related to sleep. In ABPM, BP is considered elevated when 24-hour BP is ≥130/80 mmHg, ranging from ≥135/85 mmHg when awake to ≥120/70 mmHg when sleeping. For HBPM, BP is considered elevated when ≥135/85 mmHg.1

Patients should be previously informed about the procedure, and the steps in Table 3 should be followed.3,10,11 Blood pressure should be measured by all health professionals on every clinical assessment and at least once a year.

Complementary assessment is aimed at detecting target organ damage (TOD), aiding cardiovascular risk stratification and identifying signs of secondary hypertension.

TOD should be investigated with the recommended complementary tests (routine and for specific populations) shown in Table 4, in addition to screening for the following conditions:

• •

  Left ventricular hypertrophy, assessed on electrocardiogram: Sokolow-Lyon index (S in V1+R in V5 or V6 [whichever is larger]) >35 mm and Ra in VL >1.1 mV; Cornell index (S in V3+R in aVL >28 mm in men and >20 mm in women); or on echocardiogram: left ventricular mass index ≥116 g/m2 (men) and ≥96 g/m2 (women);

• •

  Atherosclerotic disease in other sites and chronic kidney disease stage ≥3 (estimated glomerular filtration rate <60 ml/min/1.73 m2) (Table 5).

  Table 5.

  Stratification based on risk factors, target organ damage and cardiovascular or kidney disease.

  

  CKD: chronic kidney disease; CVD: cardiovascular disease; DBP: diastolic blood pressure; HTN: hypertension; SBP: systolic blood pressure; TOD: target organ damage.

  Adapted with permission from Malachias et al.1

Risk stratification should consider classical risk factors, relating them to BP levels as shown in Table 5.

The following are considered risk factors:

• •

  male gender and age (men >55 years and women >65 years);

• •

  smoking,

• •

  dyslipidemia (triglycerides >150 mg/dl, low density lipoprotein cholesterol >100 mg/dl, high-density lipoprotein cholesterol <40 mg/dl),

• •

  obesity (body mass index ≥30 kg/m2),

• •

  abdominal obesity (waist circumference >102 cm for men and >88 cm for women),

• •

  diabetes, abnormal oral glucose tolerance test or fasting blood glucose 102-125 mg/dl,

• •

  family history of premature cardiovascular disease (men <55 years and women <65 years).

Blood pressure reduction is associated with a significant reduction in cardiovascular risk that is higher in individuals at high cardiovascular risk, with a smaller risk reduction in other individuals.2,11 Non-pharmacological therapy with lifestyle changes should be initially implemented for all stages of hypertension and for individuals with BP 135-139/85-89 mmHg (Table 6). For stage 1 hypertensives at low or intermediate cardiovascular risk, management can start with lifestyle changes for 3-6 months before deciding whether to start pharmacological treatment. For other stages, antihypertensive therapy should be initiated as soon as the diagnosis is established.

A target BP of less than 130/80 mmHg is recommended for individuals at high cardiovascular risk, including those with diabetes, and less than 140/90 mmHg for stage 3 hypertensives. For patients with coronary artery disease, BP should not be lower than 120/70 mmHg because of the risk of coronary hypoperfusion, myocardial damage and cardiovascular events. For hypertensives aged ≥80 years, BP should be less than 145/85 mmHg. Figure 2 shows the pharmacological approach to hypertension.

Figure 2.

Flowchart for the treatment of arterial hypertension.12–14 ACEI: angiotensin-converting enzyme inhibitor; ARB: angiotensin receptor blocker; BP: blood pressure; CCB: calcium channel blocker; CV: cardiovascular; K: potassium. a High doses of chlorthalidone should be used instead of another thiazide unless it has been used previously.

Adapted with permission from Malachias et al.1

(0.14MB).

When angiotensin-converting enzyme inhibitors (ACEIs) are not tolerated, they should be replaced with low-cost angiotensin receptor blockers (ARBs). Beta-blockers should be considered for young individuals intolerant of ACEIs and ARBs, breastfeeding women, individuals with increased adrenergic tone, and those with IHD or heart failure (HF). In cases of intolerance to calcium channel blockers (CCBs) because of edema, or HF or suspected HF, thiazide diuretics can be used (chlorthalidone 12.5-25 mg once daily or indapamide 1.5-2.5 mg once daily). Individuals with dark skin should be prescribed ARBs rather than ACEIs in pharmacological combinations.2,11–14

Approximately two-thirds of patients will need combinations of at least two drugs to control BP. The advantage of such associations is the synergy of different mechanisms of action that enables lower doses and thus fewer adverse effects, in addition to better therapeutic adherence.

No specific drug class is indicated to treat a hypertensive patient with previous stroke, but target BP should be less than 130/80 mmHg.

Table 7 depicts the clinical situations with indication for or contraindication to specific drugs. For chronic kidney disease, ACEIs and ARBs reduce albuminuria, and thiazide diuretics are used for stages 1 to 3, while loop diuretics are used for stages 4 and 5.2,11–14

Pregnant women with uncomplicated chronic hypertension should have BP levels lower than 150/100 mmHg, but DBP should not be <80 mmHg.1,2,11–14 ACEIs and ARBs are contraindicated during pregnancy, and atenolol and prazosin should be avoided. Methyldopa, beta-blockers (except atenolol), hydralazine and CCBs (nifedipine, amlodipine and verapamil) can be safely used.2,11–14

In chronic gestational hypertension with TOD, BP levels should be maintained under 140/90 mmHg, and the pregnant woman should be referred to a specialist for appropriate care during delivery and to avoid teratogenicity. Delivery should not be induced if BP <160/110 mmHg (with or without antihypertensive drugs) up to the 37th week. Fetal growth and amniotic fluid volume should be monitored by ultrasound between the 28th and 30th weeks and between the 32nd and 34th weeks, and by umbilical artery Doppler. During delivery, BP levels should be monitored continuously.1,2,12–14 During the puerperium period, BP levels should be maintained under 140/90 mmHg, preferably with drugs that are safe to use during breastfeeding: hydrochlorothiazide, spironolactone, alpha-methyldopa, propranolol, hydralazine, minoxidil, verapamil, nifedipine, nimodipine, nitrendipine, benazepril, captopril and enalapril.1,2,12–15

Pre-eclampsia is defined as hypertension after the 20th gestational week associated with significant proteinuria and may also be characterized by headache, blurred vision, abdominal pain, low platelet count (<100000/mm3), elevated liver enzymes (twice baseline level), renal dysfunction (creatinine >1.1 mg/dl or twice baseline level), pulmonary edema, cerebral disorders or visual disturbances. Eclampsia is defined as tonic-clonic seizures occurring in a woman with pre-eclampsia. Magnesium sulfate is recommended to prevent and treat eclampsia, at a loading dose of 4-6 g intravenously (IV) for 10-20 min, followed by infusion of 1-3 g/h, usually for 24 h after the seizure. In the event of relapse, 2-4 g IV can be administered. Corticosteroids, IV antihypertensives (hydralazine, labetalol) and blood volume expansion are recommended. Patients should be admitted to the intensive care unit.1,2,11–15

Table 8 lists reasons for failure to control BP. It is important to rule out pseudoresistance due to WCH.

The prevalence of secondary hypertension in the hypertensive population is around 3-5%. The most common cause (responsible for 2-5% of hypertension cases) is renal parenchymal disease. Adrenal causes and pheochromocytoma are found in fewer than 1% of cases of hypertension. However, 80% of patients with Cushing's syndrome have hypertension. Physicians should maintain a high level of clinical suspicion when managing hypertension that is difficult to control. Table 9 lists the clinical findings of the major etiologies of secondary hypertension, associating them with the complementary tests that should be used to establish the diagnosis.

As in NCDs, lifelong adherence to hypertension treatment is poor; 40% of patients quit regular treatment in the first year, and thus do not benefit from reductions in TOD and cardiovascular events such as myocardial infarction and stroke. The main factors affecting non-adherence to treatment are adverse effects, number of daily doses and drug tolerance. Fixed drug combinations make adherence to treatment easier, reducing the likelihood of irregularities in daily doses. The involvement of patients and families, as well as a multidisciplinary approach, enhance adherence to treatment. The use of interactive apps that increase patients’ participation in BP control can encourage them to persist in taking their medication regularly.16

None.