Essential Hypertension

Etiology and PathogenesisTop

Essential (or primary) hypertension is caused by a variety of genetic and environmental factors that interfere with the functioning of one or more of the systems involved in the regulation of blood pressure (BP) and thus lead to increased BP. The following factors play an important role in the development of hypertension: the renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system, natriuretic peptides, and substances produced by the vascular endothelium (prostacyclin, nitric oxide, endothelins). Family history increases one’s risk of developing essential hypertension; it is likely that genetic contributions to hypertension risk are mediated through many or all of the factors enumerated above. The lifetime risk of developing hypertension approaches 80% in those aged 80 years or older.Evidence 1 High Quality of Evidence (high confidence that we know true effects of the intervention). Robitaille C, Dai S, Waters C, et al. Diagnosed hypertension in Canada: incidence, prevalence and associated mortality. CMAJ. 2012 Jan 10;184(1):E49-56. doi: 10.1503/cmaj.101863. Epub 2011 Nov 21. PubMed PMID: 22105752; PubMed Central PMCID: PMC3255225. Dannenberg AL, Garrison RJ, Kannel WB. Incidence of hypertension in the Framingham Study. Am J Public Health. 1988 Jun;78(6):676-9. PubMed PMID: 3259405; PubMed Central PMCID: PMC1350281. The risk and/or severity of hypertension are increased by excessive sodium intake, physical inactivity, obesity (especially abdominal), and stress (increased sympathetic activation).

Clinical Features and Natural HistoryTop

Hypertension is usually asymptomatic. Headache, sleep disturbances, and easy fatigability may occur. Other signs and symptoms appear with the development of target organ complications of hypertension. In the majority of patients with uncomplicated essential hypertension, physical examination reveals no significant abnormalities aside from an increase in BP. Over time, ranging from months to decades, hypertension may lead to pathophysiologic changes, including the accelerated development of atherosclerosis, arterial stiffness, and left ventricular (LV) hypertrophy. The clinical manifestations of these changes lead to an increased risk of:

1) Coronary artery disease, including myocardial infarction and angina.

2) Stroke (ischemic and hemorrhagic).

3) Congestive heart failure.

4) Peripheral vascular disease.

5) Premature death from cardiovascular causes.

6) Persistent kidney injury (a urinary albumin-creatinine ratio [ACR] elevation ≥3 mg/mmol [30 mg/g] and/or decline in estimated glomerular filtration rate [eGFR] usually develops slowly; in mild to moderate hypertension the development of end-stage renal disease is rare and usually appears after many years of hypertension).

7) Aortic dissection.

8) Visual impairment.

DiagnosisTop

Diagnostic workup includes:

1) Confirmation of the diagnosis of hypertension.

2) If appropriate, search for causes of secondary hypertension.

3) Assessment of cardiovascular risk factors, target organ complications, and comorbidities.

Diagnostic Tests

1. BP measurements: To determine the BP, perform traditional measurements (office measurements using either the manual auscultatory method or automated oscillometer; the latter allows a sufficient rest period with the health-care provider out of the room, renders results that are typically 5-10 mm Hg [or more] lower, and is preferred), and make use of the self-measurements performed by the patient (see below) as well as, in some cases, also of the results of ambulatory BP monitoring (ABPM). If the value is elevated, out-of-office measurement is essential to exclude the white coat effect (see Differential Diagnosis, below). This can be done through home BP series (2 measurements each morning and evening for 7 days, with the second values of both measurements being averaged) or by using 24-hour ambulatory BP monitor.

2. Laboratory tests that are suggested include:

1) Serum levels of sodium, potassium, glucose (fasting) and/or serum glycated hemoglobin (HbA1c), creatinine (with eGFR calculation using the CKD-EPI formula; see Chronic Kidney Disease), total cholesterol, high-density (HDL-C) and low-density (LDL-C) lipoprotein cholesterols, and triglycerides.

2) Urinalysis: Urine dipstick test for blood and protein.

3. 12-lead electrocardiography (ECG) is suggested in all patients.

4. Additional studies are suggested as guided by the clinical assessment and routine laboratory tests:

1) Quantitative assessment of urinary albumin and urine microscopy (in patients with positive results of the dipstick test).

2) Measurements of daily urinary sodium excretion to evaluate sodium intake.

3) ABPM or home BP measurements (or both).

4) Echocardiography with the assessment of LV hypertrophy and cardiovascular risk in selected patients or in those with suspected LV dysfunction.

5) Screening for obstructive sleep apnea if clinically suspected (consider using the Epworth Sleepiness Scale [see Obstructive Sleep Apnea] or the STOP-Bang questionnaire [stopbang.ca]).

5. Suggested studies based on suspected etiology of secondary hypertension (frequently performed in referred/specialized care):

1) Renal parenchymal etiology if suggested by history (urinary tract infection or obstruction, hematuria, analgesic abuse; family history of polycystic kidney disease [PKD]), laboratory tests (protein and red blood cells in urine, decreased eGFR), or physical examination showing renal masses (PKD): Consider renal ultrasonography as a first-line additional test. If needed, follow with referral and more specialized tests (see Chronic Kidney Disease).

2) Renal vascular etiology if suggested by history (difficult to control hypertension, especially with early onset [fibromuscular dysplasia] or rapid onset [atherosclerosis]), physical examination (abdominal bruit) or tests (difference in kidney size on ultrasonography, rapid worsening of eGFR either spontaneously or after exposure to RAAS inhibitors (angiotensin-converting enzyme inhibitors [ACEIs] or angiotensin receptor blockers [ARBs]): Investigations: see Renovascular Hypertension.

3) Primary hyperaldosteronism if suggested by history (early onset, cardiovascular events at an age <40 years), physical examination (arrhythmia secondary to low potassium), or laboratory tests (hypokalemia, either spontaneous or diuretic-induced): Investigations: see Primary Aldosteronism.

4) Cushing syndrome if suggested by history (rapid weight gain, polyuria and polydipsia), physical examination showing typical body habitus, and laboratory tests showing hyperglycemia: Investigations: see Cushing Syndrome.

5) Pheochromocytoma may be suggested by history (paroxysmal hypertension or crisis in the course of sustained hypertension; headache, sweating, palpitations, and pallor; family history of pheochromocytoma), physical examination (cutaneous neurofibromatosis (café au lait spots or neurofibromas), and laboratory tests (adrenal mass), with further investigations for the presence of excessive urinary catecholamines or their metabolites (metanephrines).

Diagnostic Criteria

Diagnosis varies according to regional guidelines and depends on the method of BP measurement (see Hypertension) and presence of diabetes mellitus and target organ damage. In general, the thresholds range from 130/80 mm Hg (averaged over 3 visits and measured through clinician auscultation) for probable hypertension in patients with diabetes to 140/90 mm Hg in patients with no risk factors and no target organ damage. Details can be found in Hypertension Canada guidelines and highlights.

Essential hypertension (common) is considered probable if the history and/or initial testing do not suggest underlying secondary hypertension (rare).

Perform screening BP measurement in all adults periodically (frequency is based on underlying risk factors, including age and previous BP patterns).

Differential Diagnosis

1. Secondary hypertension: Clinical indications and diagnostics of secondary hypertension: see above.

2. White coat hypertension: Increase in BP in some patients during measurement performed by a physician or nurse; in such patients use ABPM. If the office BP levels are consistent with hypertension while the results of repeated home measurements or ABPM are normal, the diagnosis of white coat hypertension is made.

3. Masked hypertension: Conversely, if the patient has normal office BP levels and elevated results of home and ABPM measurements, the diagnosis of masked hypertension is established. This may be due to smoking, exercise-induced hypertension, anxiety, job stress, or other factors and is not only difficult to detect but also associated with an increased cardiovascular risk.

4. Pseudohypertension: In the elderly the results of BP measurements using auscultation may be significantly elevated due to increased arterial stiffness (sclerosis), which causes the early appearance and disappearance of pulse. This may be observed if the pulse remains palpable even after filling the cuff above the systolic blood pressure (SBP) level (the stiffened artery cannot be sufficiently compressed by the cuff). Another feature suggestive of pseudohypertension is the absence of target organ damage caused by hypertension. In patients with suspected pseudohypertension, measure the BP using oscillometric devices and not auscultation.

TreatmentTop

Acute and Urgent Treatment

The management procedure is determined by the BP values, type of target organ complications, patient’s age, and some comorbidities (Table 1). In emergencies, such as pulmonary edema, hypertensive encephalopathy, or aortic dissection, immediately lower the BP using parenteral antihypertensive drugs (Table 2), preferably in a continuous IV infusion. We suggest that in such cases the mean arterial pressure should be reduced by <25% of BP reduction during the first hours and cautiously thereafter. In the case of acute stroke, BP should be reduced more gradually, if at all.

Long-Term Treatment

General Considerations

Comprehensive lifestyle optimization strategies have been shown to lower SBP and diastolic blood pressure (DBP) among patients with hypertension by 14.2 mm Hg and 7.4 mm Hg on average, respectively.Evidence 2 Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to imprecision and lack of a no-intervention group. Appel LJ, Champagne CM, Harsha DW, et al; Writing Group of the PREMIER Collaborative Research Group. Effects of comprehensive lifestyle modification on blood pressure control: main results of the PREMIER clinical trial. JAMA. 2003 Apr 23-30;289(16):2083-93. PubMed PMID: 12709466. The evidence to date indicates that although some patients may not have hypertension as currently defined, they may nevertheless benefit from BP-lowering therapy, particularly if they have a higher baseline cardiovascular risk. One must therefore consider the current BP (and not just whether the patient has hypertension), the BP target based on the patient’s characteristics as outlined below, past tolerability of treatment, and personal preferences. With increasing evidence that targets vary among different patient groups, the utility of grading hypertension may ultimately be limited to guiding the rapidity at which to initiate pharmacologic therapy, the number of pharmacologic agents that will likely be required, and consideration of secondary causes. We have recommended a target BP in each case as a range of 10 mm Hg and suggested that treatment be initiated when the measured BP is persistently at or above the upper limit of that range.

1. Long-term treatment of hypertension includes:

1) Lifestyle optimization.

2) Treatment with antihypertensive drugs.

3) Optimization of other cardiovascular risk factors.

2. Decisions on the choice of treatment modalities depend on the patient’s BP levels and overall cardiovascular risk:

1) In patients with SBP ≥160 mm Hg and/or DBP ≥100 mm Hg, promptly start pharmacotherapy combined with lifestyle optimization regardless of the cardiovascular risk.

2) In patients with SBP ≥140 mm Hg and/or DBP ≥90 mm Hg, antihypertensive therapy should be strongly considered. Start treatment simultaneously with lifestyle modifications, especially in those with >2 cardiovascular risk factors or any one of the following: target organ damage, diabetes, cardiovascular disease, or chronic kidney disease. In patients not fulfilling these criteria it may be acceptable to delay treatment for a few weeks to observe the effects of lifestyle modifications.

3. Target BP levels: Note that these targets are guides and that in many cases the achieved BP will be higher due to treatment and patient factors, including undue adverse effects. The BP target may be 5 to 10 mm Hg higher if measured using methods different than automated oscillometric BP (AOBP) measurements, as described above. It is also worth noticing that different expert bodies, using similar data, have reached different conclusions regarding exact targetsEvidence 3High Quality of Evidence (high confidence that we know true effects of the intervention). Antza C, Doundoulakis I, Stabouli S, Kotsis V. Comparison Among Recommendations for the Management of Arterial Hypertension Issued by Last US, Canadian, British and European Guidelines. High Blood Press Cardiovasc Prev. 2018 Mar;25(1):9-16. doi: 10.1007/s40292-017-0236-x. Epub 2017 Nov 1. PubMed PMID: 29094260.:

1) SBP <140 mm Hg in all patients with hypertension, with the following exceptions:

a) In noninstitutionalized patients without dementia, diabetes, symptomatic heart failure, or prior stroke and (i) who are aged >50 years and have either clinically evident cardiovascular disease, an eGFR <60 mL/min/1.73m2, or a 10-year risk score >15% (which corresponds to ≥13 points for men and ≥16 points for women; see Table 1 in Prevention of Cardiovascular Diseases); or (ii) who are aged ≥75 years, the target SBP is <120 mm Hg (if measured using automated oscillometric BP measurement). Patients with ≥1 of these indications should participate in discussion about benefits and risks of more intensive therapy and give their consent.Evidence 4 Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to some heterogeneity in other populations. SPRINT Research Group, Wright JT Jr, Williamson JD, Whelton PK, et al. A Randomized Trial of Intensive versus Standard Blood-Pressure Control. N Engl J Med. 2015 Nov 26;373(22):2103-16. doi: 10.1056/NEJMoa1511939. Epub 2015 Nov 9. Erratum in: N Engl J Med. 2017 Dec 21;377(25):2506. PubMed PMID: 26551272; PubMed Central PMCID: PMC4689591. Lonn EM, Bosch J, López-Jaramillo P, et al; HOPE-3 Investigators. Blood-Pressure Lowering in Intermediate-Risk Persons without Cardiovascular Disease. N Engl J Med. 2016 May 26;374(21):2009-20. doi: 10.1056/NEJMoa1600175. Epub 2016 Apr 2. PubMed PMID: 27041480. Yusuf S, Bosch J, Dagenais G, et al; HOPE-3 Investigators. Cholesterol Lowering in Intermediate-Risk Persons without Cardiovascular Disease. N Engl J Med. 2016 May 26;374(21):2021-31. doi: 10.1056/NEJMoa1600176. Epub 2016 Apr 2. PubMed PMID: 27040132. Yusuf S, Lonn E, Pais P, et al; HOPE-3 Investigators. Blood-Pressure and Cholesterol Lowering in Persons without Cardiovascular Disease. N Engl J Med. 2016 May 26;374(21):2032-43. doi: 10.1056/NEJMoa1600177. Epub 2016 Apr 2. PubMed PMID: 27039945. ACCORD Study Group, Cushman WC, Evans GW, Byington RP, et al. Effects of intensive blood-pressure control in type 2 diabetes mellitus. N Engl J Med. 2010 Apr 29;362(17):1575-85. doi: 10.1056/NEJMoa1001286. Epub 2010 Mar 14. PubMed PMID: 20228401; PubMed Central PMCID: PMC4123215. Brunström M, Carlberg B. Effect of antihypertensive treatment at different blood pressure levels in patients with diabetes mellitus: systematic review and meta-analyses. BMJ. 2016 Feb 24;352:i717. doi: 10.1136/bmj.i717. Review. PubMed PMID: 26920333; PubMed Central PMCID: PMC4770818. Examples of risk calculators: Framingham Coronary Heart Disease Risk Score at mdcalc.com; ACC/AHA 2013 Cardiovascular Risk Assessment at medscape.com.

b) Patients with diabetes mellitus: see Special Considerations, below.

2) DBP <90 mm Hg in all patients.

Lifestyle Modifications

1. Weight reduction in overweight patients and maintenance of a normal body weight (waist circumference ≤88 cm in women, ≤102 cm in men; body mass index <25 kg/m2).

2. A diet that emphasizes fruits and vegetables, low-fat dairy products, whole grains, and protein from plant sources that is reduced in saturated fat and cholesterol, including nuts, seeds, and legumes (the DASH [Dietary Approaches to Stop Hypertension] diet).

3. Reduction of sodium intake to ≤5 to 6 g of salt.

4. Limitation of and, ideally, abstinence from alcohol consumption.

5. Appropriate physical activity: Regular aerobic exercise, such as brisk walking for 30 to 45 minutes daily.

6. Smoking cessation.

Antihypertensive Treatment

1. The major classes of antihypertensive agents are diuretics (mainly thiazide and thiazide-like diuretics), beta-blockers, calcium channel blockers, ACEIs, and ARBs. Their BP-lowering efficacy is similar. Beta-blockers have been shown to be inferior to the other agents in their efficacy to reduce cardiovascular eventsEvidence 5 High Quality of Evidence (high confidence that we know true effects of the intervention). Ettehad D, Emdin CA, Kiran A, et al. Blood pressure lowering for prevention of cardiovascular disease and death: a systematic review and meta-analysis. Lancet. 2016 Mar 5;387(10022):957-967. doi: 10.1016/S0140-6736(15)01225-8. Epub 2015 Dec 24. Review. PubMed PMID: 26724178. and are generally not recommended as first-line therapy in North American guidelines anymore. Specific indications and contraindications: Table 3. Agents and dosage: Table 4.

2. Additional antihypertensive drugs: Angiotensin receptor blocker/neprilysin inhibitor combinations (ARNIs), alpha1-blockers (doxazosin, terazosin, prazosin), centrally acting sympathetic inhibitors (methyldopa, clonidine), direct vasodilators (hydralazine, minoxidil), diuretics other than thiazide or thiazide-like (see above). These agents are used in combination treatment and in special situations. Agents, dosage, specific indications and contraindications: Table 5.

3. Principles of pharmacotherapy: Depending on the cardiovascular risk as well as the baseline and target BP levels, start with 1 drug at a low dose (any agent of the main antihypertensive classes may be used, unless specific indications for or contraindications to any particular class exist), or 2 drugs at low doses (in patients with BP elevated by >20/10 mm Hg or at high cardiovascular risk; with a single-pill combination being preferred). Most agents produce the full antihypertensive effect after a few weeks of treatment, so their effectiveness should be assessed after 2 to 4 weeks.

If treatment with 1 drug at a low dose does not provide BP control (in a significant majority of patients treatment with ≥2 antihypertensive agents is necessary), you may:

1) Add a second drug (the preferred strategy).

2) Change to another drug (only if no hypotensive effects have been achieved or if adverse reactions occurred).

3) Increase the dose of the currently used drug (this increases the risk of adverse effects).

If treatment with 2 drugs at low doses (either from the beginning or at a subsequent phase of treatment) is not effective, you may:

1) Increase the doses of the currently used drugs; or

2) Add a third drug at a low dose.

Usually 2 or 3 antihypertensive agents are used; less commonly more drugs are necessary. The main benefits of a combination therapy are higher efficacy and fewer adverse effects (drug doses used in combinations are lower than those used in monotherapy). Preferred combinations include:

1) Thiazide/thiazide-like diuretic + ACEI.

2) Thiazide/thiazide-like diuretic + ARB.

3) Thiazide/thiazide-like diuretic + calcium channel blocker.

4) Calcium channel blocker + ACEI.

5) Calcium channel blocker + ARB.

The most rational triple-drug combination includes a drug acting on the RAAS (an ACEI or an ARB) + calcium channel blocker + thiazide/thiazide-like diuretic.

Timing of drug administration: Although not widely accepted and not introduced into clinical practice guidelines, there is some evidence that evening dosing may be associated with improved outcomes.Evidence 6Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to indirectness and the risk of bias. Hermida RC, Crespo JJ, Domínguez-Sardiña M, et al; Hygia Project Investigators. Bedtime hypertension treatment improves cardiovascular risk reduction: the Hygia Chronotherapy Trial. Eur Heart J. 2020 Dec 21;41(48):4565-4576. doi: 10.1093/eurheartj/ehz754. PMID: 31641769.

Follow-UpTop

The frequency of follow-up visits depends on the overall cardiovascular risk, BP level, and patient’s compliance (eg, regarding BP self-measurements at home). Once the target BP has been achieved and other risk factors have been adequately controlled, the frequency of visits can be significantly reduced. It may be of value to ask patients to record their resting BP, when possible, on several occasions prior to their follow-up visit.

Suggested schedule of follow-up visits in patients with hypertension:

1) After 2 to 4 weeks of starting antihypertensive treatment.

2) After 4 weeks of introducing a change in the treatment regimen.

3) Every 3 months after achieving the target BP.

Special ConsiderationsTop

Elderly Patients

1. In elderly patients (>65 years of age) the most common form of hypertension is isolated systolic hypertension. Additionally, orthostatic hypotension is frequent (BP must also be measured in the upright position).

2. General principles of antihypertensive treatment in the elderly:

1) Lower BP gradually, initially using low doses of drugs.

2) Note that interactions with other drugs may occur.

3) For many, a target SBP <140 mm Hg will be reasonable. In those who have been identified as potentially benefiting from an SBP target <120 mm Hg (see above), consider cautiously lowering SBP further while monitoring for adverse effects including orthostatic hypotension.

3. You can start treatment with a drug from any major antihypertensive class; however, in patients with isolated systolic hypertension start with a diuretic (thiazide or thiazide-like) or a calcium channel blocker. As comorbidities are frequent in patients with hypertension, these should be taken into consideration when choosing antihypertensive agents.

4. In a significant proportion of patients, it is necessary to use ≥2 antihypertensive drugs to achieve the target BP levels.

Patients with Diabetes Mellitus

1. There is currently some uncertainty as to the BP target, as demonstrated by differences in the most key clinical practice guidelines. SBP targets range between 130 and 140 mm Hg and DBP between 80 and 90 mm Hg. We suggest a BP target <130/80 mm Hg, particularly in those with diabetic nephropathy, if it can be achieved without undue treatment burden (see Diabetes Mellitus).

2. All the major classes of antihypertensive drugs have beneficial effects in this group of patients.

3. ACEIs and ARBs have renal protective effects, significantly reduce proteinuria, and are the preferred option in patients with albuminuria.

4. In a significant proportion of patients, the target BP values can only be achieved with ≥3 appropriately selected antihypertensive drugs.

5. BP should also be measured in the upright position due to the increased risk of orthostatic hypotension.

6. Intensive lifestyle modifications are of particular importance (see Lifestyle Modifications, above).

White Coat Hypertension

In patients with no additional cardiovascular risk factors, consider limiting the intervention to lifestyle changes, as long as careful follow-up is continued. In patients with a higher cardiovascular risk due to metabolic disturbances or asymptomatic target organ damage, you may consider adding antihypertensive pharmacotherapy.

Masked Hypertension

Consider introducing both lifestyle changes and antihypertensive drugs, as this category of hypertension is associated with a cardiovascular risk similar to that of hypertension observed in both office and home measurements.

Resistant Hypertension

Hypertension is defined as resistant if target BP values cannot be achieved despite the use of ≥3 antihypertensive drugs (including a diuretic) at optimal doses and in appropriate combinations.

Causes:

1) Noncompliance with the antihypertensive drug regimen and with lifestyle modifications (alcohol abuse, tobacco smoking, excessive sodium intake, persistent obesity).

2) Inappropriate drug combinations (failure to include a diuretic in treatment, using a diuretic at inadequate doses, or failure to adapt the type of the diuretic to the patient’s renal function).

3) Pseudoresistance to treatment (BP measurement errors, white coat hypertension [see White Coat Hypertension, above]).

4) Pseudohypertension (see Differential Diagnosis, above).

5) Obstructive sleep apnea.

6) Drug interactions reducing the efficacy of antihypertensive drugs (nonsteroidal anti-inflammatory drugs [NSAIDs]).

7) Treatment with drugs that increase BP.

8) Metabolic syndrome (insulin resistance).

9) Chronic kidney disease.

10) Unrecognized secondary hypertension.

Management:

1) Resistance to treatment is confirmed in patients in whom target office BP levels are not achieved despite treatment with ≥3 antihypertensive drugs at optimal doses, including a diuretic.

2) Exclude pseudoresistance: Determine whether the patient is compliant with the recommended treatment and exclude white coat hypertension (if the patient has abnormal office BP levels with normal BP levels in self-measurement or ABPM, pseudoresistance to treatment is confirmed).

3) Identify and attempt to modify adverse lifestyle factors, such as obesity, excessive alcohol consumption, or high sodium intake.

4) Eliminate or minimize the effect of substances that increase blood pressure, such as NSAIDs, sympathomimetic agents (appetite suppressants, decongestants), stimulants, and oral contraceptives.

5) Search for causes of secondary hypertension.

6) Modify pharmacotherapy: Maximize diuretic treatment (consider adding a mineralocorticoid receptor antagonist [MRA] or amiloride, use loop diuretics in patients with renal failure), use drugs with different mechanisms of action.

7) Refer the patient to a specialist in the case of a confirmed or suspected secondary hypertension, or if hypertension remains uncontrolled despite a sufficient duration of treatment.

Accelerated Hypertension

The most severe form of hypertension, characterized by a DBP >120 to 140 mm Hg, rapid progression of target organ complications, and particularly by the development of heart failure, renal failure, and severe lesions in the retinal vessels (transudates, ecchymoses, papilledema). This type of hypertension may develop in the course of hypertension of various etiologies, both essential and secondary, and is most common in patients with renal artery stenosis or glomerulonephritis. The term “malignant hypertension” was used in the past to indicate the very poor prognosis in such patients.

Symptoms are often present and can include weakness, headache, dizziness, dyspnea, chest pain, and less commonly abdominal pain (caused by abnormalities of intestinal vessels). Symptoms of rapidly progressive renal failure as well as central nervous system symptoms of varying severity, up to severe encephalopathy, may predominate. The patients are at increased risk of stroke and heart failure, often in the form of pulmonary edema.

Diagnosis is based on the clinical and laboratory manifestations.

TablesTop