HTN is a complex disease modified by environmental and genetic determinants.

1. Genetics. HTN does not follow the classic Mendelian rules of inheritance attributable to a single gene locus.

a. However, Liddle syndrome (mutation of chimeric 11-β-hydroxylase-aldosterone synthase gene) and variants in the angiotensinogen locus are documented exceptions that cause primary HTN among whites.

b. Other potential candidate genes include various components of the renin-angiotensin—aldosterone system, the kallikrein—kinin system, and the sympathetic nervous system.

2. Increased left ventricular (LV) mass and LV wall thickness and altered peripheral vascular capacity and responsiveness occur more frequently among patients with a family history of HTN.

3. Contributors to HTN include variations in sodium intake, alcohol intake, renal function, vascular function, the sympathetic nervous system, the renin-angiotensin system, hyperinsulinemia/insulin resistance, and prostaglandins.

1. Positive relationship between systolic and diastolic blood pressures and cardiovascular risk has long been recognized.

a. The Multiple Risk Factor Intervention Trial (MRFIT). Prospective study (11.6 years of average follow-up period) with more than 361,000 subjects demonstrated the relationship between blood pressure and CAD. Baseline blood pressure elevations increased risk for CAD. The relationship was
stronger for systolic blood pressure than for diastolic blood pressure. Death rate for men with systolic blood pressures of 140 to 149 (2.4/1,000) and 150 to 159 mm Hg (3.1/1,000) was 40% higher compared with men with a baseline systolic blood pressure <120 mm Hg.

b. Death rate at follow-up can be lowered by 36% with primary prevention of HTN in the general population. In addition, rates of stroke and CAD fall with antihypertensive therapy.

c. Subjects with blood pressure <120/< 80 mm Hg have the fewest cardiovascular events. The recommended treatment cutpoint is 140/90 mm Hg.

d. Prehypertension. This is defined as blood pressure within the high-normal range (120 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic) and which may confer some increased risk for cardiovascular disease. Risk ratios of 2.5 for women and 1.6 for men have been reported in patients in the prehypertensive range. These patients should undertake lifestyle modifications (e.g., diet, exercise, and weight loss) to help prevent or delay the development of frank HTN in the future.

e. The gradual rise in blood pressure over a person’s lifetime and the increased prevalence of HTN among the elderly are not benign. Epidemiologic studies of the elderly demonstrate a U-shaped relationship between blood pressure and mortality. After adjustment for deaths within the first 3 years of the follow-up period, there is a positive linear relationship between blood pressure, cardiovascular disease mortality, and all-cause mortality. Isolated systolic HTN increases as the population ages, which confers increased risk for morbidity and mortality.

(1) Systolic Hypertension in the Elderly Program (SHEP) showed that 8% of persons aged 60 to 69 years have isolated systolic HTN, defined as systolic blood pressure >160 mm Hg and diastolic blood pressure <90 mm Hg, as do 11% of those aged 70 to 79 years and 22% of those aged 80 years or older.

(2) The relationship between systolic and diastolic blood pressures and cardiovascular events is more pronounced among persons aged 65 years and older. The association is stronger and more consistent for systolic blood pressure than for diastolic blood pressure and is evident at levels considerably >140 mm Hg.

2. Rate of cardiovascular events. Elevations in diastolic or systolic blood pressure values translate into significant increases in cardiovascular events. Generally, the yearly percent risk of cardiovascular events (i.e., risk of event by end of study, divided by duration of study) is between 0.5% and 2.5% for hypertensive subjects aged 40 years or older. Beginning at 115/75 mm Hg, each increase in blood pressure of 20/10 mm Hg doubles the risk of cardiovascular disease.

3. Systolic blood pressure is a greater predictor of risk. Over the last few years, greater emphasis has been placed on systolic blood pressure in characterizing cardiovascular risk. Age-adjusted 10-year mortality in the MRFIT revealed systolic blood pressure to be a stronger predictor of events from CAD than diastolic blood pressure. High systolic blood pressure conferred a CAD risk regardless of diastolic blood pressure. A systolic blood pressure of 140 to 149 mm Hg confers greater CAD mortality risk than a diastolic blood pressure of 90 to 94 mm Hg. A systolic blood pressure of 150 to 159 mm Hg carries greater risk than a diastolic blood pressure of 95 to 100 mm Hg. According to the SHEP study, isolated systolic HTN, which accounts for 60% of cases of HTN among the elderly, is highly correlated with cardiovascular disease and it is important that it is controlled.

Detection of HTN begins with proper blood pressure measurements, which should be obtained at each health-care encounter.

1. Data for evaluation are acquired through the medical history, physical examination, laboratory tests, and other diagnostic procedures. Evaluation of patients with documented HTN has the following three objectives:

a. To identify known causes of high blood pressure

b. To assess the presence or absence of end-organ damage and cardiovascular disease, the extent of the disease, and response to therapy

c. To identify other cardiovascular risk factors or concomitant disorders that may define prognosis and guide treatment

2. A medical history should focus on identifying important risk factors or symptoms of HTN.

3. Repeated blood pressure measurements determine whether initial elevations persist and necessitate prompt attention, or the blood pressure has returned to normal and the patient needs only periodic surveillance. Ambulatory blood pressure monitoring is clinically helpful and is most commonly used to evaluate patients with suspected “office” or “white-coat HTN.” It is also helpful in the care of patients with apparent drug resistance, hypotensive symptoms with antihypertensive medications, episodic HTN, and autonomic dysfunction.

a. Office visits. Clinicians should explain to patients the meaning of their blood pressure readings and advise them of the need for periodic remeasurement. Blood pressure is measured in a standardized manner with equipment that meets certification criteria.

(1) The patient sits in a chair with her or his back supported and the arms bared and supported at heart level.

(2) Patients should refrain from smoking or ingesting caffeine during the 30 minutes preceding the measurement.

(3) Measurement should begin after at least 5 minutes of rest.

(4) The appropriate cuff size must be used to ensure accurate measurement. The bladder within the cuff should encircle at least 80% of the arm. Many adults need a large adult cuff.

(5) Measurements are taken preferably with a mercury sphygmomanometer. Otherwise, a recently calibrated aneroid manometer or a validated electronic device can be used.

(6) The systolic blood pressure and diastolic blood pressure are recorded. The first appearance of sound is used to define systolic blood pressure. The disappearance of sound is used to define diastolic blood pressure.

(7) Two or more readings separated by 2 minutes should be averaged. If the first two readings differ by >5 mm Hg, additional readings should be obtained and averaged.

b. Ambulatory blood pressure monitoring. A variety of commercially available monitors that are reliable, convenient, easy to use, and accurate are available. These monitors are typically programmed to take readings every 15 to 30 minutes throughout the day and night while patients go about their normal daily activities. The readings can be downloaded for computer analysis.

(1) Normal ambulatory blood pressure values are lower than clinical readings while patients are awake (< 135/< 85 mm Hg) and are even lower while patients are asleep (< 120/< 75 mm Hg). The blood pressure often falls by 10% to 20% during the night. This change is more closely related to patterns of sleep and wakefulness than to the time of day.

(2) Patients with HTN. Ambulatory blood pressure correlates more closely than clinical blood pressure with a variety of measures of end-organ damage or left ventricular hypertrophy (LVH). Prospective evidence suggests that among patients for whom an elevated clinic pressure is the only abnormality, ambulatory monitoring may help identify a group at relatively low risk for morbidity.

4. Physical examination should include the following components:

a. Funduscopic examination for hypertensive retinopathy (e.g., arteriolar narrowing, focal arteriolar constrictions, arteriovenous crossing changes, hemorrhages and exudates, and disk edema).

b. Examination of the neck for carotid bruits, distended veins, or an enlarged thyroid gland.

c. Examination of the heart for abnormalities in rate and rhythm, increased size, precordial heave, clicks, murmurs, and S₃ and S₄.

d. Examination of the lungs for rales and bronchospasm.

e. Examination of the abdomen for bruits, enlarged kidneys, masses, and abnormal aortic pulsation. Abdominal bruits, particularly those that lateralize to the renal area and/or have a diastolic component, suggest renovascular disease. Abdominal or flank masses may indicate polycystic kidneys.

f. Examination of the extremities for diminished or absent peripheral arterial pulsations, bruits, hair loss, and edema. Delayed or absent femoral arterial pulses and decreased blood pressure in the lower extremities may indicate aortic coarctation.

h. Other assessments. Labile HTN or paroxysms of HTN accompanied by any or all of the following symptoms and signs—chest discomfort (“pressure”), headache (“pain”), palpitations, pallor, and diaphoresis (“perspiration”)— may indicate the presence of a pheochromocytoma. Truncal obesity with purple striae suggests Cushing’s syndrome.

1. It is recommended that the clinician request routine laboratory tests before initiating therapy to determine the presence of end-organ damage and other risk factors. These include urinalysis, complete blood cell count, blood chemistry, and 12-lead electrocardiogram (ECG).

2. Additional diagnostic procedures may be indicated to seek causes of HTN: poor response to drug therapy, well-controlled patients whose blood pressures begin to increase, and those with sudden onset of HTN. Optional tests include creatinine clearance; microalbuminuria, 24-hour urinary protein, blood calcium, uric acid, fasting triglyceride, low-density-lipoprotein cholesterol (LDL-C), glycosylated hemoglobin, and thyroid-stimulating hormone levels; and limited echocardiography to determine the presence of LVH.

a. Clues from laboratory tests include unprovoked hypokalemia (i.e., primary aldosteronism), hypercalcemia (i.e., hyperparathyroidism), and elevated creatinine or abnormal urinalysis (i.e., renal parenchymal disease).

b. The presence of LVH as determined by ECG or echocardiography is an important risk factor for adverse cardiovascular events and an independent predictor of high risk for CAD, cardiovascular disease, and all-cause mortality. LVH, the consequence of chronic pressure or volume overload and obesity, seems to be a stronger predictor of MI and CAD death than the degree of HTN. LV mass, as assessed with echocardiography, is a powerful predictor of cardiovascular events, cardiovascular mortality, and all-cause mortality.

3. More complete assessment of cardiac anatomy and function by means of conventional echocardiography, examination of structural alterations in arteries by means of ultrasonography, measurement of ankle—arm index, and plasma renin activity and urinary sodium determinations may be useful in assessing cardiovascular status in select patients.

1. Classification of blood pressure is given in Table 44.1. The criteria are limited to patients not taking antihypertensive medication and without acute illness. Classification is based on the average of two or more blood pressure readings. When systolic blood pressure and diastolic blood pressure fall into different categories, the higher pressure should be selected to classify the patient’s blood pressure.

2. Risk for cardiovascular disease among patients with HTN is determined by the blood pressure level and by the presence or absence of end-organ damage or other disease-modifying risk factors (smoking, dyslipidemia, and diabetes). The presence or absence of these factors is determined during the routine evaluation of patients with HTN (e.g., history, physical examination, and laboratory tests). This classification stratifies patients with HTN into risk groups for therapeutic decisions. The World Health Organization Expert Committee on Hypertension Control recommends a similar approach. Obesity and physical inactivity are also predictors of cardiovascular risk and interact with other risk factors, but they are of less importance in the selection of antihypertensive drugs.

a. Risk group A includes patients with prehypertension or HTN at stage 1 or 2 who do not have clinical cardiovascular disease, end-organ damage, or other risk factors. Persons with stage 1 HTN in risk group A are candidates for a longer trial (up to 1 year) of vigorous lifestyle modification with vigilant blood pressure monitoring. If the desired blood pressure is not achieved, pharmacologic therapy is added. For those with stage 2 HTN, drug therapy is warranted.

b. Risk group B includes patients with HTN who do not have clinical cardiovascular disease or end-organ damage but have one or more of the risk factors except for diabetes mellitus. This group includes most patients with high blood pressure. If multiple risk factors are present, clinicians consider antihypertensive drugs as initial therapy. Lifestyle modification and management of reversible risk factors are strongly recommended.

c. Risk group C includes patients with HTN and clinically manifested cardiovascular disease or end-organ damage. According to Joint National Committee 7 (JNC 7) criteria, some patients who fall into the prehypertensive category and have renal insufficiency or diabetes mellitus should be considered for prompt pharmacologic therapy. Appropriate lifestyle modifications are always recommended as adjunct treatment.

d. Therapy. Antihypertensive treatment has proved beneficial in the prevention and reduction of the progression of HTN, CVAs, congestive heart failure (CHF), renal insufficiency, and renal failure. Among patients with mild to moderate HTN, antihypertensive therapy has not favorably influenced angina, MI, and other atherosclerotic diseases (e.g., PVD and aortic atherosclerosis). The lower-than-expected reduction in CAD risk in most trials of antihypertensive agents has been attributed to the choice of agents, such as thiazide diuretics and β-blockers, that might negatively influence risk for CAD and to the short duration of the trials. Overall, antihypertensive treatment markedly reduces the prevalence of CAD events: CAD mortality (by 16%), the rate of fatal stroke (by 40%), and the incidence of heart failure (by 50%), with similar numbers of deaths prevented.

a. Weight reduction reduces systolic and diastolic blood pressures. Most clinical trials have demonstrated that weight reduction is directly related to blood pressure reduction. A weight loss of approximately 10 lb (4.5 kg) may reduce both systolic and diastolic blood pressures by 2 to 3 mm Hg. Among patients with high-normal blood pressure, the need for medical therapy may be averted for one-half through weight reduction by means of physical activity and calorie restriction.

b. Exercise reduces blood pressure by means of decreasing resting heart rate and peripheral vascular resistance and by modifying serum norepinephrine and insulin levels. After an increase in physical activity, both systolic and diastolic blood pressures have been demonstrated to fall by 7 mm Hg with or without weight reduction. Moderate-intensity exercise is as effective as high-intensity exercise for reducing blood pressure.

c. Diet. A modest, independent benefit of salt reduction has been demonstrated. HTN is less common in societies that consume low-salt, high-potassium diets. Although the theory that excessive salt intake produces HTN has been difficult to prove in large clinical trials, most data support the role of dietary salt excess for some persons. In general, low-salt diets, such as the Dietary Approaches to Stop Hypertension (DASH; 2,300-and 1,500-mg sodium diets), are recommended to most patients with HTN. Pooled estimates have suggested that salt restriction is most important for older persons, those with higher baseline levels of blood pressure, and particularly those who are salt sensitive. Salt restriction reduces the need for combination antihypertensive medications.

d. Tobacco and immoderate alcohol use (more than two daily drinks for men and more than one daily drink for women) increase blood pressure. Cessation of smoking and excessive alcohol use markedly reduces blood pressure and further reduces cardiovascular risk.

(1) Therapy for most patients with uncomplicated HTN at stage 1 should begin with the lowest dose to prevent adverse effects. If blood pressure remains uncontrolled after 1 to 2 months, the next dose level may be prescribed. It may take months to adequately control HTN. Most antihypertensive agents may be taken once each day. To improve patient compliance, this regimen is used whenever possible.

(2) For patients at higher risk, those in risk group 2, or those at particularly high risk for CAD or CVA event, drug therapy to achieve maximum beneficial reductions in blood pressure should proceed without delay. If blood pressure is elevated by 20/10 mm Hg above the goal, guidelines recommend starting two agents simultaneously.

(3) There is no debate regarding the need for aggressive blood pressure reduction in patients with diastolic blood pressures > 115 mm Hg and systolic blood pressures > 160 mm Hg. JNC 7 aggressively targets the 140/90 mm Hg cut-point and incorporates hypertensive therapy into an algorithm of overall risk.

(4) In the setting of hypertensive emergency (HTN with end-organ damage, often with neurologic symptoms), patients with a systolic blood pressure > 200 mm Hg or a diastolic blood pressure > 120 mm Hg may need hospitalization for therapy.

(5) Although some patients may respond to single therapy, two or more drugs are often required. The intervals between changes in regimen should not be prolonged, and the maximum dose of some drugs may be increased.

b. Medication selection. Special considerations include concomitant disease, demographic characteristics, quality of life, cost, and use of other drugs that may cause drug interactions.

(1) Concomitant diseases

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