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Logo of thijTexas Heart Institute JournalSee also Cardiovascular Diseases Journal in PMCSubscribeSubmissionsTHI Journal Website
Tex Heart Inst J. 2010; 37(4): 439–441.
PMCID: PMC2929868

On Redefining Hypertension

Michel Accad, MD and Herbert L. Fred, MD, MACP

Any definition is inadequate and defective, unless itdoes really define, or describe, the disease.

— Elisha Bartlett (1804–1855), Philosophy of Medical Science

An elevated blood pressure can be a normal physiologic reaction, an abnormality of uncertain significance, a marker of cardiovascular risk, or the cardinal sign of a disease with potentially serious immediate or long-term complications. Depending on the clinical circumstances, therefore, the physician can ignore the finding, extend the scope of observation, engage the patient in a conversation on statistical risk, or initiate antihypertensive therapy. From our observations in the private practice and academic settings, most physicians facing these possibilities initiate therapy reflexively, on the spot. The “decision to treat” almost certainly stems from the current dogma that defines and classifies systemic hypertension solely on the basis of arbitrary cutoff numbers.1,2 Mindless adherence to these numbers prompts us to emphasize several points.

First, the blood pressure is inherently labile. When monitored indirectly by cuff devices in ambulatory patients, it varies substantially in response to changes in physical activity or the environment.3 This lability is strikingly evident during direct intra-arterial monitoring, wherein the highest pressures are often at least double the lowest pressures.4

Second, when the blood pressure is measured in the resting state as part of a screening procedure, the value obtained indicates a statistical risk of future cardiovascular events or death for that individual.5 This risk worsens in a graded manner with the systolic pressure: the higher the systolic pressure, the greater the risk.1 But no definitive threshold for risk has been identified to date.6,7 As for the diastolic pressure, regardless of the controversies concerning a “J-curve” phenomenon,8,9 cutoff numbers do not conform to any of the observed risk curves.10–12

Third, in addition to the normal lability of the blood pressure and the absence of a threshold value for risk, the phenomena of white-coat hypertension,13 masked hypertension,14 and pseudohypertension15 pose further difficulties in diagnosing hypertension by means of cutoff numbers alone. Moreover, defining hypertension on the basis of numbers alone makes it particularly difficult to differentiate a clinically important elevation in blood pressure from an incidental elevation. For instance, in many hospitalized patients, an elevated blood pressure simply represents a reaction to their concurrent illness or to the anxiety-provoking environment, or both. Such elevation rarely signals impending danger to those patients—yet physicians often rush to reduce the blood pressure, seemingly oblivious to the potential danger of doing so.16–20 This lack of perspective is widespread and is particularly evident in recent proposals that advocate screening for hypertension in the emergency department.21

Fourth, defining and classifying hypertension solely on the basis of cutoff numbers facilitates the treatment of populations but overlooks the individual patient. For example, because mild hypertension, however defined,11,22 is highly prevalent, it is a target for intervention to decrease the burden of cardiovascular risk to the community.23–25 But because this risk is minimal for the individual patient,26,27 the great majority of people so treated will not derive benefit, and some may actually be harmed.28 The harm results not only from the direct costs and side effects of therapy, but also from the psychosomatic sequelae associated with the diagnosis of hypertension—the so-called “labeling effect.”29–32

Fifth, experts do not always agree on the specific cutoff numbers.33–35 Furthermore, those numbers have enormous socioeconomic and public health implications.22,35,36 Millions of individuals worldwide who are deemed normal today can literally be turned into patients tomorrow, simply by selecting new numbers.22 And the recently defined category of “prehypertension”1 converts millions more.37–39 Sir George Pickering aptly warned of the “fallacy of the dividing line” throughout his distinguished career, but to no avail.40 Decades later, we are still treating patients by the numbers for their numbers.

Clinically important hypertension is sometimes called “the silent killer.” While it may be silent, it is not necessarily invisible. Early signs of its effect, if carefully sought, can be seen before the disease becomes clinically manifest. The funduscopic examination, for example, can identify early vascular abnormalities that might be reversed by treatment of hypertension.41,42 Many other noninvasive techniques are available to help determine the early impact of blood pressure elevation on different parts of the vascular tree.43–48 And comorbid conditions such as diabetes, hypercholesterolemia, and cigarette smoking can magnify the effect of hypertension on various organs.1,2,49

In 1957, William Evans published an observational study on patients with elevated blood pressure whom he had monitored for up to 10 years.50 He found that signs of target organ damage at the first visit indicated a high risk of future cardiovascular events, but the absence of such signs portended a generally benign prognosis. Consequently, he proposed the term “hypertonia” for an elevated blood pressure without signs of target organ damage, and “arterial hypertension” for an elevated blood pressure with such signs.

Almost 50 years after Evans's publication, the Hypertension Writing Group—a panel of experts from around the country—noted that the current threshold-based definition of hypertension fails to identify a large group of individuals who have subclinical cardiovascular disease before blood pressure elevation becomes chronic or manifest.51 Accordingly, the group proposed that target organ damage be incorporated into the definition and classification of hypertension. In a subsequent report published in 2009, the group made a distinction between high blood pressure (one manifestation of the disease—a biomarker) and hypertension (the disease).52

In conclusion, we join Evans and the Hypertension Writing Group in recommending that the definition of hypertension as a disease include a description of the associated pathologic manifestations. Such definition would spur the creation of new tools for detecting those manifestations53–58 and would foster a better understanding of the natural history of the disease. It would also promote a public-health approach that targets persons most likely to benefit from intervention. And for physicians who must deal with elevated blood pressures in the course of daily clinical work, the revised definition would encourage the circumspection and due diligence consistent with Mutton's Law of optimal patient care: “Know what to do and when to do it.”59


Address for reprints: Michel Accad, MD, 1800 Sullivan Ave., Suite 304, Daly City, CA 94015

E-mail: moc.detneirodnatrela@afm


1. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42(6):1206–52. [PubMed]
2. Whitworth JA; World Health Organization, International Society of Hypertension Writing Group. 2003 World Health Organization (WHO)/International Society of Hypertension (ISH) statement on management of hypertension. J Hypertens 2003;21(11):1983–92. [PubMed]
3. Richardson DW, Honour AJ, Fenton GW, Stott FH, Pickering GW. Variation in arterial pressure throughout the day and night. Clin Sci 1964;26:445–60. [PubMed]
4. Bevan AT, Honour AJ, Stott FH. Direct arterial pressure recording in unrestricted man. Clin Sci 1969;36(2):329–44. [PubMed]
5. Brackenridge RDC. Blood pressure. In: Medical selection of life risks: a comprehensive guide to life expectancy for underwriters & clinicians. 2nd ed. New York: Nature Press; 1985. p. 160–87.
6. Kannel WB, Vasan RS, Levy D. Is the relation of systolic blood pressure to risk of cardiovascular disease continuous and graded, or are there critical values? Hypertension 2003;42(4):453–6. [PubMed]
7. Port S, Demer L, Jennrich R, Walter D, Garfinkel A. Systolic blood pressure and mortality. Lancet 2000;355(9199):175–80. [PubMed]
8. Messerli FH, Panjrath GS. The J-curve between blood pressure and coronary artery disease or essential hypertension: exactly how essential? J Am Coll Cardiol 2009;54(20):1827–34. [PubMed]
9. Williams B. Hypertension and the “J-curve”. J Am Coll Cardiol 2009;54(20):1835–6. [PubMed]
10. Lewington S, Clarke R, Qizilbash N, Peto R, Collins R; Prospective Studies Collaboration. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies [published erratum appears in Lancet 2003;361(9362):1060]. Lancet 2002;360(9349):1903–13. [PubMed]
11. Vasan RS, Larson MG, Leip EP, Evans JC, O'Donnell CJ, Kannel WB, Levy D. Impact of high-normal blood pressure on the risk of cardiovascular disease. N Engl J Med 2001;345 (18):1291–7. [PubMed]
12. Pastor-Barriuso R, Banegas JR, Damian J, Appel LJ, Guallar E. Systolic blood pressure, diastolic blood pressure, and pulse pressure: an evaluation of their joint effect on mortality. Ann Intern Med 2003;139(9):731–9. [PubMed]
13. Verdecchia P, Staessen JA, White WB, Imai Y, O'Brien ET. Properly defining white coat hypertension. Eur Heart J 2002; 23(2):106–9. [PubMed]
14. Pickering TG, Davidson K, Gerin W, Schwartz JE. Masked hypertension. Hypertension 2002;40(6):795–6. [PubMed]
15. Littenberg B, Wolfberg C. Pseudohypertension masquerading as malignant hypertension. Case report and review of the literature. Am J Med 1988;84(3 Pt 1):539–42. [PubMed]
16. Morton C, Hickey-Dwyer M. Cortical blindness after nifedipine treatment. BMJ 1992;305(6855):693. [PMC free article] [PubMed]
17. Fischberg GM, Lozano E, Rajamani K, Ameriso S, Fisher MJ. Stroke precipitated by moderate blood pressure reduction. J Emerg Med 2000;19(4):339–46. [PubMed]
18. Stewart IM. Relation of reduction in pressure to first myocardial infarction in patients receiving treatment for severe hypertension. Lancet 1979;1(8121):861–5. [PubMed]
19. Farnett L, Mulrow CD, Linn WD, Lucey CR, Tuley MR. The J-curve phenomenon and the treatment of hypertension. Is there a point beyond which pressure reduction is dangerous? JAMA 1991;265(4):489–95. [PubMed]
20. Messerli FH, Mancia G, Conti CR, Hewkin AC, Kupfer S, Champion A, et al. Dogma disputed: can aggressively lowering blood pressure in hypertensive patients with coronary artery disease be dangerous? Ann Intern Med 2006;144(12):884–93. [PubMed]
21. Decker WW, Godwin SA, Hess EP, Lenamond CC, Jagoda AS. Clinical policy: critical issues in the evaluation and management of adult patients with asymptomatic hypertension in the emergency department. Ann Emerg Med 2006;47(3): 237–49. [PubMed]
22. Ramsay LE, Wallis EJ, Yeo WW, Jackson PR. The rationale for differing national recommendations for the treatment of hypertension. Am J Hypertens 1998;11(6 Pt 2):79S-88S. [PubMed]
23. Moser M, Gifford RW Jr. Why less severe degrees of hypertension should be treated. J Hypertens 1985;3(5):437–47. [PubMed]
24. Grimm RH Jr. Should mild hypertension be treated? Early intervention. Med Clin North Am 1984;68(2):477–90. [PubMed]
25. Chobanian AV. Shattuck Lecture. The hypertension paradox–more uncontrolled disease despite improved therapy [published erratum appears in N Engl J Med 2009;361(15):1516]. N Engl J Med 2009;361(9):878–87. [PubMed]
26. Collins R, Peto R, MacMahon S, Hebert P, Fiebach NH, Eberlein KA, et al. Blood pressure, stroke, and coronary heart disease. Part 2, Short-term reductions in blood pressure: overview of randomised drug trials in their epidemiological context. Lancet 1990;335(8693):827–38. [PubMed]
27. Cook RJ, Sackett DL. The number needed to treat: a clinically useful measure of treatment effect [published erratum appears in BMJ 1995;310(6986):1056]. BMJ 1995;310(6977):452–4. [PMC free article] [PubMed]
28. Ramsay LE. Mild hypertension: treat patients, not populations. J Hypertens 1985;3(5):449–55. [PubMed]
29. Stewart IM. Headache and hypertension. Lancet 1953;1 (6774):1261–6. [PubMed]
30. Haynes RB, Sackett DL, Taylor DW, Gibson ES, Johnson AL. Increased absenteeism from work after detection and labeling of hypertensive patients. N Engl J Med 1978;299(14):741–4. [PubMed]
31. Mena-Martin FJ, Martin-Escudero JC, Simal-Blanco F, Carretero-Ares JL, Arzua-Mouronte D, Herreros-Fernandez V. Health-related quality of life of subjects with known and unknown hypertension: results from the population-based Hortega study. J Hypertens 2003;21(7):1283–9. [PubMed]
32. Pickering TG. Now we are sick: labeling and hypertension. J Clin Hypertens (Greenwich) 2006;8(1):57–60. [PubMed]
33. O'Brien E, Staessen JA. A plea for harmonising guidelines. Int J Cardiol 2001;79(2–3):129–32. [PubMed]
34. Hopkins Tanne J. US guidelines say blood pressure of 120/80 mm Hg is not “normal”. BMJ 2003;326(7399):1104. [PMC free article] [PubMed]
35. A pressure to agree. Lancet 1999;354(9181):787. [PubMed]
36. Muntner P, He J, Roccella EJ, Whelton PK. The impact of JNC-VI guidelines on treatment recommendations in the US population. Hypertension 2002;39(4):897–902. [PubMed]
37. Sica DA. JNC 7: has the definition of hypertension changed? Heart Dis 2003;5(5):305–7. [PubMed]
38. Agnvall E. Making us (nearly) sick: a majority of Americans are now considered to have at least one ‘pre-disease’ or ‘borderline’ condition. Is this any way to treat us? The Washington Post. 2004 Feb 10;Sect. F:1.
39. Weber MA. Expanding the scope of hypertension: are we creating new diseases? J Clin Hypertens (Greenwich) 2006;8(9): 615–8. [PubMed]
40. Laragh JH, Brenner BM, editors. Hypertension: pathophysiology, diagnosis, and management. New York: Raven Press; 1990. p. 3–14.
41. Wong TY, Mitchell P. Hypertensive retinopathy. N Engl J Med 2004;351(22):2310–7. [PubMed]
42. Pose-Reino A, Rodriguez-Fernandez M, Hayik B, Gomez-Ulla F, Carrera-Nouche MJ, Gude-Sampedro F, Estevez-Nunez JC. Regression of alterations in retinal microcirculation following treatment for arterial hypertension. J Clin Hypertens (Greenwich) 2006;8(8):590–5. [PubMed]
43. Jensen JS, Feldt-Rasmussen B, Strandgaard S, Schroll M, Borch-Johnsen K. Arterial hypertension, microalbuminuria, and risk of ischemic heart disease. Hypertension 2000;35(4): 898–903. [PubMed]
44. Maisel AS. Cardiovascular and renal surrogate markers in the clinical management of hypertension. Cardiovasc Drugs Ther 2009;23(4):317–26. [PubMed]
45. Laurent S, Boutouyrie P. Arterial stiffness: a new surrogate end point for cardiovascular disease? J Nephrol 2007;20 Suppl 12:S45–50. [PubMed]
46. Devereux RB, Alderman MH. Role of preclinical cardiovascular disease in the evolution from risk factor exposure to development of morbid events. Circulation 1993;88(4 Pt 1):1444–55. [PubMed]
47. Rosei EA, Muiesan ML. Early target organ damage and its reversibility: the heart. Clin Exp Hypertens 2004;26(7–8):673–87. [PubMed]
48. Leoncini G, Viazzi F, Parodi D, Vettoretti S, Ratto E, Ravera M, et al. Mild renal dysfunction and subclinical cardiovascular damage in primary hypertension. Hypertension 2003;42 (1):14–8. [PubMed]
49. Volpe M, Tocci G. 2007 ESH/ESC Guidelines for the management of hypertension, from theory to practice: global cardiovascular risk concept. J Hypertens 2009;27 Suppl 3:S3–11. [PubMed]
50. Evans W. Hypertonia or uneventful high blood pressure. Lancet 1957;273(6985):53–9. [PubMed]
51. Giles TD, Berk BC, Black HR, Cohn JN, Kostis JB, Izzo JL Jr, Weber MA. Expanding the definition and classification of hypertension. J Clin Hypertens (Greenwich) 2005;7(9):505–12. [PubMed]
52. Giles TD, Materson BJ, Cohn JN, Kostis JB. Definition and classification of hypertension: an update [published erratum appears in J Clin Hypertens (Greenwich) 2010;12(1):13]. J Clin Hypertens (Greenwich) 2009;11(11):611–4. [PubMed]
53. Pose-Reino A, Gomez-Ulla F, Hayik B, Rodriguez-Fernandez M, Carreira-Nouche MJ, Mosquera-Gonzalez A, et al. Computerized measurement of retinal blood vessel calibre: description, validation and use to determine the influence of ageing and hypertension. J Hypertens 2005;23(4):843–50. [PubMed]
54. Duprez DA, Kaiser DR, Whitwam W, Finkelstein S, Belalcazar A, Patterson R, et al. Determinants of radial artery pulse wave analysis in asymptomatic individuals. Am J Hypertens 2004;17(8):647–53. [PubMed]
55. Anderson TJ. Prognostic significance of brachial flow-mediated vasodilation. Circulation 2007;115(18):2373–5. [PubMed]
56. Cohn JN, Duprez DA, Grandits GA. Arterial elasticity as part of a comprehensive assessment of cardiovascular risk and drug treatment. Hypertension 2005;46(1):217–20. [PubMed]
57. Stein JH, Korcarz CE, Hurst RT, Lonn E, Kendall CB, Mohler ER, et al. Use of carotid ultrasound to identify subclinical vascular disease and evaluate cardiovascular disease risk: a consensus statement from the American Society of Echocardiography Carotid Intima-Media Thickness Task Force. Endorsed by the Society for Vascular Medicine [published erratum appears in J Am Soc Echocardiogr 2008;21(4):376]. J Am Soc Echocardiogr 2008;21(2):93–111. [PubMed]
58. Harazny JM, Ritt M, Baleanu D, Ott C, Heckmann J, Schlaich MP, et al. Increased wall:lumen ratio of retinal arterioles in male patients with a history of a cerebrovascular event. Hypertension 2007;50(4):623–9. [PubMed]
59. Fred HL. Milton + Sutton = Mutton: “know what to do and when to do it”. Tex Heart Inst J 2009;36(4):272. [PMC free article] [PubMed]

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