Mind the gap: prevalence and pathophysiology of isolated systolic hypertension: In reply

Mind the gap: prevalence and pathophysiology of isolated systolic hypertension: In reply

AJH 2001; 14:980 –981 Letter to the Editor Mind the Gap: Prevalence and Pathophysiology of Isolated Systolic Hypertension 5. To the Editor: In the...

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AJH

2001; 14:980 –981

Letter to the Editor Mind the Gap: Prevalence and Pathophysiology of Isolated Systolic Hypertension

5.

To the Editor: In the otherwise excellent editorial,1 Wilkinson and Cockroft make a few unfounded assertions:

In Reply: We are pleased that Dr. Bursztyn enjoyed our editorial on isolated systolic hypertension.1 We believe it highlighted the importance of a serious medical condition that is both underdiagnosed and undertreated. We would agree that the true prevalence of isolated systolic hypertension will vary between populations and also with the definition one uses. From the Framingham cohort,2 defining isolated systolic hypertension as a systolic pressure ⬎160 and diastolic ⬍90 mm Hg yields a prevalence of ⬃14% for men and 23% for women aged more than 60 years. However, using the Joint National Committee on Detection, Prevention, Evaluation and Treatment of High Blood Pressure definition of systolic ⱖ140 and diastolic ⬍90 mm Hg, Franklin et al3 found that ⬃51% of subjects aged more than 50 years in the National Health and Nutrition Examination Survey study had isolated systolic hypertension. Moreover, given that the prevalence of isolated systolic hypertension increases considerably with age,2 it might be expected that a substantially larger proportion of the individuals aged over 70 years would be affected. Therefore, it is somewhat surprising that Bursztyn et al4 only reported an incidence of 5% for isolated systolic hypertension in an Israeli population. A number of explanations for this disparity exist, including the rather small sample size, 448 of the Israeli study, ethnic considerations, and perhaps the unusual method of blood pressure assessment—averaging lying and standing pressures— used by Bursztyn et al. Although peripheral vascular resistance was assessed in 23 patients with systolic hypertension in the study by Vardan et al,5 to which Dr. Bursztyn refers, no direct comparative measurements whatsoever were undertaken in age-matched normotensive subjects. Therefore, it is difficult to draw any conclusion regarding differences in peripheral vascular resistance between those with isolated systolic hypertension and those older individuals who remain normotensive. However, in a well-controlled study involving both older and younger patients with systolic hypertension, Simon et al6 demonstrated that peripheral vascular resistance was no different between patients and controls. Nevertheless, arterial stiffness was increased in the older subjects with systolic hypertension, which may, in part, explain why isolated systolic hypertension is often resistant to therapy with conventional antihypertensive agents targeted at resistance vessels. Dr. Bursztyn’s final criticism centers on whether isolated systolic hypertension and essential hypertension are different entities. We stand by our assertion that they are

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That more than half of those aged ⬎60 years have isolated systolic hypertension. This is not true in our population2 and probably not in any other population, unless treated hypertensives with complete diastolic blood pressure response and partial systolic response are considered; the large number of patients screened for the Systolic Hypertension in the Elderly Program (447,921 subjects aged 60 years and older) yielding only 4736 participants is only one indication.3 They claim that in isolated systolic hypertension in the elderly there is no increase in peripheral resistance, yet the opposite was shown.4 Thus, the conclusion that “. . . isolated systolic hypertension and essential hypertension can no longer be viewed as the same condition . . .” is in contradiction to Framingham’s study findings that at least 40% of subjects with isolated systolic hypertension had had diastolic hypertension in previous years.5

Although everyone would (and should) agree with most of their editorial, these points are unfounded and overrated. MICHAEL BURSZTYN Department of Medicine Hadassah University Hospital, Mount Scopus Jerusalem 91240 Israel e-mail: [email protected] PII S0895-7061(01)02184-7 Address correspondence and reprint requests to Dr. Michael Bursztyn, Department of Medicine, Hadassah University Hospital, Mount Scopus, P.O. Box 24035, Jerusalem 91240, Israel.

References 1.

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Wilkinson IB, Cockroft JR: Mind the gap: Pulse pressure, cardiovascular risk and isolated systolic hypertension. Am J Hypertens 2000;13:1315–1317. Bursztyn M, Spillberg O, Ginsberg G, Cohen AA, Stessman J: Hypertension in the Jerusalem 70-year-old population: Prevalence, awareness, treatment and control. Isr J Med Sci 1996;32:629– 633. SHEP Cooperative Research Group: Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. JAMA 1991;265:3255–3264. Varden S, Mukherje S, Warner R, Smulyan H: Systolic hypertension in the elderly: Hemodynamic response to long term thiazide therapy and its side effects. JAMA 1983;250:2807–2813.

0895-7061/01/$20.00

Wilking SV, Belanger A, Kannel WB, D’Agostino RBC, Steel K: Determinants of isolated systolic hypertension. JAMA 1988;260: 3451–3455.

© 2001 by the American Journal of Hypertension, Ltd. Published by Elsevier Science Inc.

AJH–September 2001–VOL. 14, NO. 9, Part 1

indeed separate conditions. Isolated systolic hypertension is predominantly a disease of older individuals and is associated with arterial stiffing, whereas essential hypertension tends to occur in younger subjects.3 Stiffening of the large arteries is an age-dependent process7,8 and is accelerated in subjects with essential hypertension.9 Therefore, one might consider that individuals with essential hypertension are more likely to develop isolated systolic hypertension in later life. Although recent data suggest that systolic pressure increases with age in subjects with essential hypertension, diastolic pressure actually changes little between the third and seventh decades of life.10 Such observations do not necessarily mean that isolated systolic hypertension and essential hypertension are the same condition, just that the latter may increase the risk of the former, as indeed essential hypertension increases the risk of developing renal impairment. Moreover, although the Framingham study suggests that ⬃40% of patients with isolated systolic hypertension previously had elevated diastolic pressures,2 a population-based study conducted in the UK reported a figure of only ⬃16%.11 Therefore, a substantial number of elderly individuals will develop isolated systolic hypertension despite never having been hypertensive in earlier life. IAN B. WILKINSON Clinical Pharmacology Unit University of Cambridge, Addenbrooke’s Hospital Cambridge, UK JOHN R. COCKCROFT Department of Cardiology Wales Heart Research Institute University Wales College of Medicine Heath Park Cardiff, UK e-mail: [email protected] PII S0895-7061(01)02182-3

LETTER TO THE EDITOR

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Address correspondence and reprint requests to Dr. John Cockcroft, Department of Cardiology, Wales Heart Research Institute, University Wales College of Medicine, Heath Park, Cardiff, UK.

References 1.

Wilkinson IB, Cockcroft JR: Mind the gap: Pulse pressure, cardiovascular risk, and isolated systolic hypertension. Am J Hypertens 2000;13:1315–1317. 2. Wilking SV, Belanger A, Kannel WB, D’Agostino RB, Steel K: Determinants of isolated systolic hypertension. JAMA 1988;260: 3451–3455. 3. Franklin SS, Jacobs MJ, Wong ND, L’Italien GJ, Lapuerta P: Predominance of isolated systolic hypertension among middle-aged and elderly US hypertensives: Analysis based on national health and nutrition examination survey (NHANES)III. Hypertension 2001;37: 869– 874. 4. Bursztyn M, Shpilberg O, Ginsberg GM, Cohen A, Stessman J: Hypertension in the Jerusalem 70 year olds study population: Prevalence, awareness, treatment and control. Isr J Med Sci 1996;32: 629– 633. 5. Vardan S, Mookherjee S, Warner R, Smulyan H: Systolic hypertension in the elderly. Hemodynamic response to long-term thiazide diuretic therapy and its side effects. JAMA 1983;250:2807–2813. 6. Simon AC, Safar MA, Levenson JA, Kheder AM, Levy BI: Systolic hypertension: Hemodynamic mechanism and choice of antihypertensive treatment. Am J Cardiol 1979;44:505–511. 7. Bramwell JC, Hill AV: Velocity of transmission of the pulse-wave and elasticity of the arteries. Lancet 1922;i:891– 892. 8. Avolio AP, Fa-Quan D, Wei-Qiang L, Yao-Fei L, Zhen-Dong H, Lian-Fen X, O’Rourke MF: Effects of aging on arterial distensibility in populations with high and low prevalence of hypertension: comparison between urban and rural communities in China. Circulation 1985; 71:202–210. 9. Nichols W, Avolio AP, Kelly RP, O’Rourke MF: Effects of age and of hypertension on wave travel and reflections, London, Edward Arnold, 1993. 10. Galarza CR, Alfie J, Waisman GD, Mayorga LM, Camera LA, del Rio M, Vasvari F, Limansky R, Farias J, Tessler J, Camera MI: Diastolic pressure underestimates age-related hemodynamic impairment. Hypertension 1997;30:809– 816. 11. Bulpitt CJ, Palmer AJ, Fletcher AE, Bradley IC, Broxton JS, Davis AJ, Ganvir PL, Gostick NK, Mayhew SR, Mukerji D: Proportion of patients with isolated systolic hypertension who have burned-out diastolic hypertension. J Hum Hypertens 1995;9:675– 678.