How Is Hypertension Defined With Regard to Blood Pressure Readings?

Essential hypertension remains a major modifiable run a risk gene for cardiovascular illness (CVD) despite important advances in our understanding of its pathophysiology and the availability of effective treatment strategies. High blood pressure (BP) increases the risk of CVD for millions of people worldwide, and at that place is prove that the trouble is simply getting worse. In the past decade, age-adapted rates of stroke incidence have risen, and the slope of the historic period-adapted charge per unit of decline in coronary affliction has leveled off. The incidence of cease-stage renal disease and the prevalence of centre failure have too increased. A major correspondent to these trends is inadequate control of BP in the hypertensive population. This review of electric current concepts regarding the definition, etiology, and handling of essential hypertension is intended to aid the clinician in identifying those individuals at loftier risk who need to undergo evaluation and handling, too as in selecting optimal handling strategies for hypertensive patients with comorbid conditions and/or target organ harm. The part of the review that deals with the genetic ground of hypertension and the factor/environment interaction that may atomic number 82 to elevated BP is still a piece of work in progress. Information gained from the Human Genome Project and from ongoing studies of the genetic basis of hypertension both in animal models and human being populations may revolutionize the handling of hypertension by replacing current empirical therapy with more constructive, targeted treatments based on the genotype of the patient. Concepts introduced in this review form the basis for such "pharmacogenomic" approaches to antihypertensive therapy.

Definition of Essential or Primary Hypertension

BP is a quantitative trait that is highly variable¹ ; in population studies, BP has a normal distribution that is slightly skewed to the right. There is a strong positive and continuous correlation between BP and the take chances of CVD (stroke, myocardial infarction, heart failure), renal disease, and bloodshed, even in the normotensive range. This correlation is more robust with systolic than with diastolic BP.^two There is no specific level of BP where cardiovascular and renal complications start to occur; thus the definition of hypertension is arbitrary but needed for practical reasons in patient assessment and treatment.

The Sixth Study of the Articulation National Committee on Prevention, Detection, Evaluation, and Treatment of High Claret Pressure level (JNC VI) defined and classified hypertension in adults, every bit shown in Table 1.³ The diagnosis of hypertension is made when the average of 2 or more diastolic BP measurements on at least 2 subsequent visits is ≥ninety mm Hg or when the average of multiple systolic BP readings on 2 or more subsequent visits is consistently ≥140 mm Hg. Isolated systolic hypertension is divers as systolic BP ≥140 mm Hg and diastolic BP <xc mm Hg. Individuals with high normal BP tend to maintain pressures that are above average for the general population and are at greater take a chance for development of definite hypertension and cardiovascular events than the general population. With the use of these definitions, it is estimated that 43 million people in the United states have hypertension or are taking antihypertensive medication, which is ≈24% of the adult population. This proportion changes with (1) race, beingness higher in blacks (32.four%) and lower in whites (23.iii%) and Mexican Americans (22.6%); (2) age, considering in industrialized countries systolic BP rises throughout life, whereas diastolic BP rises until age 55 to sixty years and thus the greater increase in prevalence of hypertension among the elderly is mainly due to systolic hypertension; (three) geographic patterns, because hypertension is more prevalent in the southeastern United States; (iv) gender, considering hypertension is more prevalent in men (though menopause tends to abolish this deviation); and (5) socioeconomic status, which is an indicator of lifestyle attributes and is inversely related to the prevalence, morbidity, and mortality rates of hypertension.

Essential, primary, or idiopathic hypertension is defined as high BP in which secondary causes such as renovascular disease, renal failure, pheochromocytoma, aldosteronism, or other causes of secondary hypertension or mendelian forms (monogenic) are not nowadays. Essential hypertension accounts for 95% of all cases of hypertension. Essential hypertension is a heterogeneous disorder, with different patients having different causal factors that lead to high BP. Essential hypertension needs to exist separated into various syndromes because the causes of high BP in virtually patients presently classified as having essential hypertension can exist recognized.

Known Etiological Factors in Essential Hypertension

Although information technology has frequently been indicated that the causes of essential hypertension are not known, this is only partially true because nosotros have lilliputian information on genetic variations or genes that are overexpressed or underexpressed equally well as the intermediary phenotypes that they regulate to cause high BP.^iv A number of factors increase BP, including (1) obesity, (ii) insulin resistance, (three) high alcohol intake, (four) high salt intake (in salt-sensitive patients), (5) crumbling and perhaps (6) sedentary lifestyle, (7) stress, (8) depression potassium intake, and (ix) low calcium intake.^{5 six} Furthermore, many of these factors are additive, such as obesity and alcohol intake.

In this review, variations in BP that are genetically determined will be called "inherited BP," although nosotros do not know which genes crusade BP to vary; we know from family studies that inherited BP tin can range from low normal BP to severe hypertension. Factors that increase BP, such equally obesity and loftier alcohol and salt intake, will be called "hyperten-sinogenic factors." Some of these factors have inherited, behavioral, and environmental components. Inherited BP could be considered core BP, whereas hypertensinogenic factors crusade BP to increment above the range of inherited BPs, thus creating 4 main possibilities: (1) patients who have inherited BP in the optimal category (<120/<80 mm Hg); if 1 or more hypertensinogenic factors are added, BP would probably increase but remain in the normal range (<135/<85 mm Hg) (Effigy 1, beginning 2 columns); (2) patients who have inherited BP in the normal category (≤130/≤85 mm Hg); if 1 or more than hypertensinogenic factors are added, BP volition probably increase to the loftier normal range (130 to 139/85 to 89 mm Hg) or to stage 1 of the hypertensive category (140 to 159/ninety to 99 mm Hg) (Effigy 1, second ii columns); (3) patients who have inherited BP in the high normal category (130 to 139/85 to 89 mm Hg); if 1 or more hypertensinogenic factors are added, BP will increment to the hypertensive range (≥140/≥90 mm Hg) (Figure one, third 2 columns); and (iv) patients who take inherited BP in the hypertensive range; addition of 1 or more hypertensinogenic factors volition make hypertension more severe, changing it from stage 1 to stage 2 or 3 (Figure 1, 4th to sixth ii columns).

Theoretically, in a population unaffected past hypertensinogenic factors, BP will have a normal distribution; it will be skewed to the right and will have a narrow base of operations or less variance (Figure two, continuous line). When one hypertensinogenic factor is added to this population, such as increased body mass, one would expect the normal distribution curve to be farther skewed to the right; consequently the base volition exist wider (more than variance) and the curve will exist flatter (Effigy ii, broken line). If a second hypertensinogenic factor such every bit alcohol intake is added to increased torso mass, the curve will be skewed more to the right and the variance will increase further, with more subjects classified equally hypertensive (Figure two, dotted line).

Discovering which genetic variations place BP on the left or right side of the distribution curve is of both theoretical and applied importance because it could help the physician to better treat or cure hypertension.^vii Recognition of the hypertensinogenic factors may allow nonpharmacological prevention, treatment, or cure of hypertension. Hypertensinogenic factors such equally obesity, insulin resistance, or high alcohol intake also have an important genetic component. Furthermore, there are interactions between genetic and environmental factors (Figure 2) that influence intermediary phenotypes such as sympathetic nerve activity, the renin-angiotensin-aldosterone and renal kallikrein-kinin systems, and endothelial factors, which in turn influence other intermediary phenotypes such every bit sodium excretion, vascular reactivity, and cardiac contractility. These and many other intermediary phenotypes determine total vascular resistance and cardiac output and, consequently, BP. Recognition of the hypertensinogenic factor(s) and establishing that the patient's hypertension is the upshot of obesity (either alone or combined with other factors such as insulin resistance or high alcohol intake) or old age instead of essential hypertension may help the md also as the patient and his or her family to modify or eliminate these hypertensinogenic and CVD take chances factors when possible, which may cure the hypertension or at least facilitate command of BP. When the hypertensinogenic factor cannot be reduced or eliminated, as with systolic hypertension induced past aging (arteriosclerosis), recognition of the underlying cause of high BP will emphasize the need for (ane) farther studies to determine whether the patient has arteriosclerosis and/or atherosclerosis, the magnitude of the disease, and whether there are occlusive lesions; (2) treatment of the atherosclerosis with lifestyle and dietary changes and lipid-lowering agents if necessary; and (3) pharmacological treatment of systolic hypertension to decrease passive stiffness (arteriosclerosis) of the major key elastic arteries and decrease morbidity and bloodshed rates. Thus recognition of factors that induce hypertension is not only of theoretical but also of practical importance. In conclusion, as stated past Beilin,⁸ "it is no longer advisable to define essential hypertension as a rise in blood pressure without crusade," since a number of causes tin be clearly identified in about cases of so-called "essential hypertension." Every bit discussed afterwards in more particular, there is clear evidence that changes in lifestyle, including dietary changes that reduce trunk weight, fat, and alcohol intake and increment potassium and calcium intake,⁹ too equally practice,^{x eleven} reduce or normalize BP in many patients.

Inherited BP

The identification of variant (allelic) genes that contribute to the development of hypertension is complicated by the fact that the ii phenotypes that determine BP, cardiac output and total peripheral resistance, are controlled by intermediary phenotypes, including the autonomic nervous system, vasopressor/vasodepressor hormones, the structure of the cardiovascular system, body fluid volume and renal function, and many others. Furthermore, these intermediary phenotypes are also controlled by complex mechanisms including BP itself.¹² Thus there are many genes that could participate in the development of hypertension.

The influence of genes on BP has been suggested by family unit studies demonstrating associations of BP amid siblings and between parents and children. In that location is a better association amid BP values in biological children than in adopted children and in identical equally opposed to nonidentical twins. BP variability attributed to all genetic factors varies from 25% in full-blooded studies to 65% in twin studies. Furthermore, genetic factors also influence behavioral patterns, which might lead to BP summit. For example, a tendency toward obesity or alcoholism will be influenced by both genetic and environmental factors; thus the proportion of BP variability caused by inheritance is difficult to determine and may vary in different populations.

Mutations in at to the lowest degree ten genes have been shown to raise or lower BP through a common pathway by increasing or decreasing salt and water reabsorption by the nephron.^{13 14} The genetic mutations responsible for 3 rare forms of mendelian (monogenic) hypertensive syndromes−glucocorticoid-remediable aldosteronism (GRA), Liddle's syndrome, and credible mineralocorticoid excess−accept been identified, whereas in a fourth, autosomal ascendant hypertension with brachydactyly, the gene is non yet identified just has been mapped to chromosome 12 (12p). Subtle variations in ane of these genes may also cause some forms of "essential" hypertension. For a review of the mutations that cause a decrease in BP, see Lifton.¹³

Glucocorticoid-Remediable Aldosteronism

This is an autosomal ascendant form of monogenic hypertension in which aldosterone secretion is regulated by adrenocorticotropic hormone. Glucocorticoid handling causes BP to decrease and gives the syndrome its proper noun. The genetic mutation that causes GRA has been identified past Lifton¹⁴ every bit a chimeric gene fusing nucleotide sequences of the promoter-regulatory region of 11β-hydroxylase (controlled by adrenocorticotropic hormone) and the structural portion of the aldosterone synthase gene. The chimeric gene results from a meiotic mismatch and diff crossing over. The patients are normally thought to have main aldosteronism considering they exhibit book expansion, metabolic alkalosis with hypokalemia, low plasma renin, and loftier aldosterone. About of the patients first described equally having GRA showed astringent hypertension and died prematurely from stroke. However, with the evolution of straight genetic testing, the BP of patients with this syndrome was found to comprehend a wide range, including normotensive levels.^{15 16} In patients with GRA and normal BP, expression of the chimeric gene may exist variable, but because steroid levels are similar in patients with severe and balmy hypertension, this seems unlikely. It is as well possible that the genetic groundwork of the trait (other than the chimeric mutation), such as loftier renal kallikrein, places the inherited BP of these subjects in the depression or ideal normal range and the mutation causes BP to increase to high normal or hypertensive phase 1. Thus the final BP would be the combined event of the inherited BP (including the genetic mutation) and the increase in BP caused by hypertensinogenic factors such equally salt.

Liddle'due south Syndrome

This is an autosomal ascendant grade of monogenic hypertension that results from mutations in the amiloride-sensitive epithelial sodium channel, leading to increased channel activity.¹⁷ The mutations reported to appointment result in the elimination of 45 to 75 amino acids from the cytoplasmic carboxyl terminus of β- or γ-subunits of the channel; thus Liddle'southward syndrome is genetically heterogeneous. It is characterized by the early onset of hypertension with hypokalemia and suppression of both plasma renin activity and aldosterone, the latter differentiating this syndrome from chief aldosteronism. Both the hypertension and the hypokalemia vary in severity, raising the possibility that some patients classified as having salt-sensitive essential hypertension actually take Liddle's syndrome.¹⁸ It is as well possible that high BP in blacks, who are frequently table salt-sensitive, is due to a polymorphism in one of the sodium channel genes or in ane of the genes of systems that regulate information technology, causing its activity to increase.

Credible Mineralocorticoid Excess

This is an autosomal recessive form of monogenic juvenile hypertension that results from a mutation in the renal-specific isoform 11β-hydroxysteroid dehydrogenase gene.¹⁹ Unremarkably this enzyme converts cortisol to the inactive metabolite cortisone. In the distal nephron this is of import considering cortisol and aldosterone take a similar affinity for the mineralocorticoid receptor. The enzymatic deficiency allows the mineralocorticoid receptors in the nephron to exist occupied and activated by cortisol, causing sodium and water retentivity, volume expansion, low renin, low aldosterone, and more importantly, a salt-sensitive form of hypertension. Thus this gene may be a locus for salt-sensitive essential hypertension.

Autosomal Ascendant Hypertension With Brachydactyly

In this monogenic syndrome, hypertension and brachydactyly are e'er inherited together (100% cosegregation).⁴ Affected persons are shorter than nonaffected relatives. The gene for hypertension has been mapped to the short arm of chromosome 12 (12p) in a big Turkish kindred. Two other families with this syndrome have been reported, one in Canada and 1 in the United States. In addition, the written report of a Japanese child with hypertension and blazon Due east brachydactyly has immune the area on 12p containing the gene mutation to be pinpointed farther, although the gene responsible for this syndrome has not still been cloned. Unlike the other 3 autosomal forms of hypertension, BP is not affected by volume expansion and the underlying mechanism is non known. Thus identification of the gene responsible may assist clarify some of the genetic alterations in essential hypertension.

Essential or Primary Hypertension

The genetic alterations responsible for inherited "essential" hypertension remain largely unknown.⁴ Results from family studies propose several possible intermediary phenotypes (genetic traits) that may be related to inherited loftier BP, such as high sodium-lithium countertransport, depression urinary kallikrein excretion, loftier fasting plasma insulin concentrations, high-density LDL subfractions, fat blueprint alphabetize, and torso mass index (BMI).¹² Jeunemaitre et al^{20 21} outset reported a polymorphism in the angiotensinogen gene linked with essential hypertension in hypertensive siblings from Utah and France. This polymorphism consists of a substitution of thymidine for cytosine in nucleotide 704, which causes substitution of methionine for threonine at position 235 (M235T) and is associated with increased concentrations of plasma angiotensinogen. This variant appears to be in tight linkage disequilibrium with a promoter mutation in which adenine replaces guanine (-6A) upstream from the initiation side of transcription.²² Tests of promoter activeness advise that this nucleotide substitution increases the charge per unit of factor transcription, which may explicate the higher angiotensinogen concentration establish in subjects with the variant M235T.²² Many studies have been published on diverse racial groups with regard to the association betwixt allelic variations in angiotensinogen and hypertension.²³ Nonetheless, these variations explain only a small part of the BP variation (≈half dozen%). Furthermore, plasma angiotensinogen concentrations, though college in patients with the polymorphism, clearly overlap with normotensive patients.

Polymorphisms and mutations in other genes such as angiotensin-converting enzyme, β_ii-adrenergic receptor, α-adducin, angiotensinase C, renin-binding protein, G-protein β_iii-subunit, atrial natriuretic factor, and the insulin receptor take also been linked to the development of essential hypertension; withal, virtually of them evidence a weak clan if any, and most of these studies demand further confirmation. Thus these gene alterations volition not be discussed here because they go beyond the scope of this review (see Luft⁴ ).

Hypertensinogenic Factors

There is show that obesity, insulin resistance, high alcohol intake, high table salt intake, a sedentary lifestyle, stress, dyslipidemia, and depression potassium or calcium intake increase BP in susceptible subjects. Here we will briefly hash out obesity and insulin resistance; other hypertensinogenic factors will be discussed in the section "Lifestyle Modification."

Obesity and Insulin Resistance

Obesity, and especially intestinal obesity, is the main hypertensinogenic factor. It was estimated in the Framingham study that each 10% weight gain is associated with a half-dozen.5 mm Hg increase in systolic BP.²⁴ Obesity is also the cause of insulin resistance, developed-onset diabetes mellitus, left ventricular hypertrophy, hyperlipidemia, and atherosclerotic disease. Thus obesity is an of import cardiovascular health problem; its incidence and prevalence are rising in most industrialized societies and in the U.s.a. has reached epidemic proportions. The relationship betwixt BP and body fat is not restricted to the morbidly obese but is continuous throughout the entire range of body weight. A straight association betwixt hypertension and BMI (weight in kilograms divided by the foursquare height in meters) has been observed in cross-sectional and longitudinal population studies from early childhood to old historic period.²⁵ A BMI of <25 is considered normal or salubrious, whereas a BMI of 26 to 28 (equally compared with BMI <23) increases the risk of high BP by 180% and the run a risk of insulin resistance by >yard%. Thus insulin resistance is present in many patients with obesity and hypertension.

The mechanism by which obesity raises BP is not fully understood, merely increased BMI is associated with an increase in plasma volume and cardiac output; both these alterations and BP tin exist decreased by weight loss in both normotensive and hypertensive subjects,²⁶ even when sodium intake is kept relatively constant.²⁷ BP in obese adolescents is sodium-sensitive, and fasting insulin is the best predictor of this sensitivity.²⁶ In these adolescents, mean BP dropped by ten mm Hg later on changing from 2 weeks on a high-sodium nutrition (>250 mmol sodium/d) to a low-sodium diet (<30 mmol/d). When some of these subjects lost weight past dieting, BP decreased past x mm Hg and salt sensitivity was no longer present. The variables that best predicted sodium sensitivity were fasting plasma insulin, plasma aldosterone, and plasma norepinephrine, supporting the hypothesis that BP is sensitive to dietary sodium and that this sensitivity may be due to the combined issue of hyperinsulinemia, hyperaldosteronism, and increased activity of the sympathetic nervous arrangement. It is non clear whether body fatty by itself is a factor because in overweight women, exercise for 1 hour per day, three times per week lowered BP, and this subtract was observed mainly in those who initially had loftier fasting insulin and whose insulin levels fell in response to exercise. In this study weight loss was not a gene because the subjects were on a free diet and really gained an average of 2.6 pounds during the six-calendar month practise trial,¹⁰ which suggests that exercise decreases plasma insulin by a different mechanism than loss of body weight. These studies can exist interpreted as showing that high plasma insulin causes table salt sensitivity and that decreasing insulin resistance by losing weight or exercising reduces BP. Furthermore, nonobese hypertensive subjects are much more likely to exhibit insulin resistance than normotensive individuals.²⁸ On the other hand, insulin by itself has a vasodilator effect. In obese subjects with hypertension there is resistance to the furnishings of insulin on glucose uptake. However, in addition to this metabolic effect, insulin increases both sympathetic nervus activity and sodium and water retentiveness, and it could be that the hypertension is due to the lack of resistance to these secondary effects of insulin.²⁹ More recently, insulin-like growth factor I³⁰ and leptin,³¹ a neuropeptide that regulates ambition, have also been implicated in the pathogenesis of obesity-induced hypertension. Thus, although the mechanisms by which obesity and insulin resistance increase BP remain undefined, it is articulate that these increases in BP are overlain on the inherited BP.

Diagnosis of Hypertension

Initial Evaluation

The goals of the initial evaluation are to determine baseline BP; assess the presence and extent of target organ harm and concomitant CVD; screen for potentially curable specific causes of hypertension (secondary hypertension); identify hypertensinogenic factors and other CVD risk factors; and characterize the patient to facilitate the selection of therapy (especially drug selection) and define prognosis.

BP Measurement

The accurate and reproducible measurement of BP by the cuff technique is the about important part of the diagnostic evaluation and follow-up of the patient and should be carried out in a standardized fashion (Table 2) with the utilize of properly calibrated and certified equipment.^{3 32 33} A mercury sphygmomanometer is preferred; acceptable alternatives include a recently calibrated aneroid manometer or a validated electronic device attached to an arm cuff. Two or 3 measurements should exist taken at each visit, and at to the lowest degree two minutes should be allowed between readings. The diastolic reading is taken at the level when sounds disappear (Korotkoff phase V).

Measurement of BP by patients or family members and/or automated ambulatory BP monitoring often helps verify the diagnosis and appraise the severity of hypertension. BP values obtained outside the clinical setting are lower and correlate better with target organ impairment than BP measurements past healthcare personnel. Self-measurement of BP has several potential advantages, including distinguishing sustained hypertension from hypertension that occurs only in the healthcare setting ("white coat" hypertension); assessing the response to antihypertensive handling; improving adherence to handling by making the patient a "partner" in his or her own care; and lowering costs by reducing the demand for frequent part BP checks. Accordingly, convalescent or cocky-monitoring of BP is recommended for many patients with loftier BP, particularly those who appear to be resistant to antihypertensive treatment. A limitation of home or workplace BP measurements is that accurate and calibrated BP monitors must be used and that conscientious and repeated education in how to measure BP must be given.

Medical History and Physical Examination

A conscientious, complete history should be obtained and a physical examination performed in all patients before beginning treatment. The assessment should include the elements described in Table 3. Information technology should assistance to place known, remediable causes of high BP; establish the presence or absence of target organ damage and CVD; and identify other CVD or comorbid conditions that might affect prognosis or handling.

Laboratory Tests and Other Diagnostic Procedures

Routine tests include only urinalysis, consummate blood count, claret chemistry (potassium, sodium, creatinine, fasting glucose, total and high-density lipoprotein or HDL cholesterol), and a 12-atomic number 82 ECG. Optional tests indicated in selected patients for the diagnosis of secondary hypertension and/or comorbid conditions include creatinine clearance, 24-hr urinary protein, measurement of microalbuminuria, uric acid, calcium, glycosylated hemoglobin, fasting triglycerides, limited echocardiography,³⁴ and plasma renin activity/aldosterone measurements.

This is Office I of a two-function article. Part 2 of this article will be published in the February i, 2000 result of Apportionment.

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Figure ane. Additive issue of hypertensinogenic factors (hatched areas) such as obesity and alcohol intake on hereditary systolic (white areas) and diastolic BP (black areas). Abscissa indicates the stage of inherited BP co-ordinate to JNC Half-dozen without adding the effect of the hypertensinogenic factors. Patients with normal or loftier normal inherited BP become hypertensive phase 1 when BP is increased past a hypertensinogenic factor. In patients with inherited hypertension in stages one to 3, their hypertension becomes more than severe when hypertensinogenic factors are added.

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Effigy two. Interaction among genetic and ecology factors in the development of hypertension. Left side of figure shows how environmental factors and multiple genes responsible for high BP interact and affect intermediary phenotypes. The outcome of these intermediary phenotypes is blood pressure with a normal distribution skewed to the right. Continuous line indicates the theoretical BP of the population that is not affected by hypertensinogenic factors; shaded area indicates systolic BP in the hypertensive range. Cleaved and dotted lines indicate populations in which 1 (obesity) or 2 hypertensinogenic factors (obesity plus high booze intake) have been added. Observe that in these 2 populations the distribution curves are shifted to the right (loftier BP) and the number of hypertensive individuals is significantly increased when hypertensinogenic factors are added.

Table 1. Definitions and Classification of Claret Pressure Levels

Category	Systolic, mm Hg		Diastolic, mm Hg
Optimal	<120	and	<eighty
Normal	<130	and	<85
High normal	130–139	or	85–89
Hypertension
Stage 1 (balmy)	140–159	or	90–99
Subgroup: borderline	140–149	or	90–94
Phase 2 (moderate)	160–179	or	100–109
Stage 3 (severe)	≥180	or	≥110
Isolated systolic hypertension	≥140	and	<90
Subgroup: borderline	140–149	and	<90

Table 2. Blood Pressure Management

Patients should exist seated with back supported and arm bared and supported.

Patients should refrain from smoking or ingesting caffeine for thirty minutes earlier measurement.

Measurement should begin after at to the lowest degree 5 minutes of rest.

Advisable gage size and calibrated equipment should be used.

Both systolic BP and diastolic BP should be recorded.

Ii or more readings should be averaged.

Table iii. Medical History and Physical Examination

Medical history

• Duration and classification of hypertension

• Patient history of CVD

• Family history

• Symptoms suggesting causes of hypertension

• Lifestyle factors

• Current and previous medications

Physical exam

• Blood force per unit area readings (2 or more than), including the continuing position

• Verification in contralateral arm

• Height, weight, and waist circumference

• Funduscopic examination for hypertensive retinopathy

• Test of the neck, heart, lungs, abdomen, and extremities for evidence of target organ damage

This work was supported by National Institutes of Health grant HL-28982.

Footnotes

Correspondence to Oscar A. Carretero, MD, Hypertension and Vascular Research Partition, Henry Ford Hospital, 2799 W 1000 Blvd, Detroit, MI 48202. E-mail [electronic mail protected]

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Source: https://www.ahajournals.org/doi/10.1161/01.CIR.101.3.329

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