How do we best define hypertension? It is still uncertain whether it better defined (say) as a systolic blood pressure (SBP) ⩾140 mm Hg, a diastolic blood pressure (DBP) ⩾90 mm Hg, either or both. Applying either criteria or both, implies the existence of different ‘types’ of hypertension, such as systolic-diastolic hypertension, isolated systolic hypertension or isolated diastolic hypertension.
An added sub-definition is the ‘stage’ of hypertension. For example, the 1997 United States Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High blood Pressure (JNC) report (JNC-VI)1 and the 1999 World Health Organization (WHO) guidelines2 which try to classify hypertension into stages, based on levels of SBP and DBP, recommend that when an individual's SBP and DBP fall into separate stages that they be classified into the higher stage, referred to as ‘upstaging’. A reclassification that incorporates SBP would have marked implications on the prevalence of hypertension and eligibility for treatment, and studies from the United States would suggest that systolic hypertension is the main factor in determining staging.3,4 For example, when subjects in the Harlem Hospital Hypertension Clinic database were re-evaluated using the new criteria, 23.7% of the subjects were upstaged due to disparately higher SBP, whilst more than a fifth of subjects had underestimation of their blood pressure risk due to the previous emphasis on DBP.5 Furthermore, those who were upstaged had more evidence of end-organ damage.
In this issue of Journal of Human Hypertension, Banegas and colleagues6 report on the differential impact of SBP and DBP on blood pressure staging in a representative sample of the middle-aged population in Spain, a population with a high incidence of cardiovascular disease. In this study, the prevalence of SBP ⩾140 mm Hg was 34.1% and that of DBP ⩾90 mm Hg, 30.9%: 12% had isolated systolic hypertension, whilst 8.7% had isolated diastolic hypertension. As expected, only a third of their cohort had blood pressure controlled. Their data should be put into perspective in relation to current evidence-based practice.
Evolution of importance of SBP
For a long time, guidelines, clinical trials and clinical practice have based greater importance on DBP levels. The first JNC report in 1977 defined DBP as the basis for detection and treatment.7 For example, an individual with blood pressure of 180/85 mm Hg was not eligible for treatment under the old guidelines. In fact, it was felt that systolic hypertension, due to hardening and loss of elasticity of the major arteries was an unavoidable consequence of aging and augmented by hypertension, in contrast to DBP which was thought to be a function of peripheral resistance. Therefore SBP continues to rise with advancing age while DBP stabilizes or declines,8 giving rise to isolated systolic hypertension (ISH). For example, Silagy et al9 found that the prevalence of ISH increased from 0.8% in 50-year-old subjects, 5% in 60 year olds, 12.6% in 70 year olds, and up to 23.6% in 80 year olds. Certainly one of us remembers a story of an eminent geriatrician lecturing that SBP should not be reduced in the elderly, as these patients would fall over from reduced cerebral perfusion and sustain strokes!
In 1969, the Framingham Heart study first noted that systolic hypertension was related to increased cardiovascular risk.8 It was probably not possible to ‘dissect out’ the relative importance of SBP vs DBP until the use of statistical methods such as the Cox proportional hazards analysis and multivariate analyses, on the appropriate computer software/ hardware. Perhaps we can forgive our teachers of old for telling us ‘the DBP rules OK!’ (But they were wrong!) Indeed, it was not until the publication of the 5th JNC guidelines in 1993 that SBP was incorporated into blood pressure staging.10 Indeed, rather than a benign effect of again, ISH poses a strong and independent risk of cardiovascular mortality.11 In a meta-analysis of outcome trials in hypertension consisting of patients over 60 years, Staessen et al12 found that a 10 mm Hg rise in systolic hypertension was correlated with a 10% increase in all fatal and non-fatal cardiovascular complications. DBP, on the other hand, was inversely correlated with total and cardiovascular mortality. Similarly, the meta-analysis of several prospective cohort studies by He and Whelton13 indicated that the association between SBP and risk of coronary heart disease, stroke and end-stage renal disease was continuous, graded, and independent, and importantly, the association of SBP with these outcomes is stronger than that of DBP. Pooling of the data available from randomised controlled trials indicates that an average reduction of 12–13 mm Hg in SBP over 4 years of follow-up was associated with a 21% reduction in coronary heart disease, a 37% reduction in stroke, a 25% reduction in total cardiovascular mortality, and a 13% reduction in all-cause mortality.
Examination of data from Framingham and Framingham Offspring studies showed that DBP vastly underestimates the number of patients requiring treatment.4 For example, Lloyd-Jones et al,3 when evaluating blood pressure staging in 4962 patients, Framingham Heart Study subjects found that 94% had an elevated SBP but only 33% had elevated DBP. The older age of the Framingham subjects may explain why the percentages differ from the study Banegas et al6 where the prevalence of systolic hypertension was 34.1% and diastolic hypertension, 30.9%.
Is diastolic hypertension irrelevant in the new millennium?
In accordance with current guidelines, as well as in clinical practice, we measure and treat both systolic and diastolic blood pressure and aim for the recommended ideal of <140/85 mm Hg. However, due to the overwhelming evidence of the importance of systolic hypertension, it has even been suggested that one should not even bother measuring DBP.14,15 The personal view in the BMJ by Peter Sever14 even recommends that we abandon measuring DBP, except in cases where diastolic hypertension was suspected. Perhaps a society for the abolishment of measurement of DBP should be established!
Indeed, there is little published evidence of significant risk posed by isolated diastolic hypertension (IDH). The Copenhagen Heart Study did not find an association between IDH and risk of stroke after a 12 year follow-up of 6545 patients.16 The Multiple Risk Factor Intervention Trial found that for any level of DBP, SBP was the major determinant of cardiovascular risk.17 It has to be noted that in both these studies most of the study subjects were white Caucasians and in the Copenhagen Heart Study, aged over 50 years of age.
Older trials that showed benefits of treating diastolic hypertension, such as the Veterans Administration Study on Antihypertensive Agents,18 did not take into account the effect of elevated systolic hypertension. However, Perry and colleagues11 who found that in subjects aged under 40 years, pretreatment DBP was still a stronger predictor of cardiovascular risk than SBP. It is perhaps interesting that 47% of the subjects in this study were African-American. It seems the jury is still out on IDH and risk, at least in younger (aged <40 years) and non-Caucasian hypertensives.
Is pulse pressure a better predictor of risk?
One reason DBP cannot be ignored is that recently pulse pressure (PP), defined as the difference between SBP and DBP, has received some attention as an independent predictor of cardiovascular risk.12,19,20,21 With age, as SBP rises and DBP stabilizes or falls, and thus, PP widens.
Mechanistically, this is thought to be due to an increase in large artery stiffness and the increased amplitude of reflection of the wave caused by ventricular ejection.4 Pulse waves are generated in the left ventricle and the great vessels during systole. In the presence of aortic stiffness, the pulse waves reflect more quickly off the peripheral resistance vessels. Therefore instead of the pulse waves returning during diastole and augmenting DBP, they reach the large vessels during late systole, increasing SBP and widening pulse pressure.22
In the Framingham study, amongst the middle-aged and elderly, the cardiovascular risk was inversely related to DBP at any given SBP over 120 mm Hg. Furthermore, there was a higher risk with increments in PP without a change in SBP than with increments in SBP without a change in PP.4 Similarly, Vaccarino and colleagues21 reported that risk posed by PP for myocardial infarction and heart failure in the over 65s was unchanged even after adjustments for hypertension stage and importantly, was also seen among the normotensive population. In the first National Health and Nutrition Examination Survey (NHANES 1) a 10 mm Hg increase in pulse pressure in persons 25 to 45 was associated with a 26% increase in risk of cardiovascular death and a 10% increase in those aged 46 to 77 years.19 Analysis of data from the Systolic Hypertension in the Elderly Program (SHEP), pulse pressure was an independent predictor of heart failure in patients who were treated, after adjusting for SBP and DBP.20 The SHEP investigators felt that since this effect was seen even after adjusting for DBP that the effect of lowering DBP by treatment was not on the whole responsible for the risk posed by widened PP.
However there is some evidence to the contrary. The Chicago Heart Association Study which followed up 28 360 patients for prediction of 25-year mortality rates23 that SBP and mean arterial pressure were better predictors of cardiovascular mortality than pulse pressure, which was a view also held by Antikainen and colleagues.24
Is the future systolic?
Should there be a greater emphasis on SBP in the light of current evidence? JNC-VI states that ‘optimal’ SBP is below 120 mm Hg and that there is a strictly linear correlation between increasing SBP and risk (a dose-response effect?). Such aggressive approach to treatment has raised some concerns, not least amongst the health economists! It is estimated that at least 50% of the population would have SBPs between 120 and 140 mm Hg.25
However, the correlation between risk of death and coronary heart disease with SBP may be non-linear.26 Certainly, a single cut-off point of 140 mm Hg did not take into account that there is an age and sex-dependent threshold for hypertension and that the current recommendations which rely on a direct linear relation between SBP and risk over-estimates risk in those with mid-range blood pressures (130–170 mm Hg).26 Gender-related differences must also be taken into account. For example, in a recent study in middle-aged and elderly French men and women,27 elevated DBP was associated with higher mortality even after adjusting for age and SBP, in contrast to men in whom SBP determined prognosis.
In the survey by Banegas et al,6 60.8% of untreated subjects had parallel staging of SBP and DBP, whilst 22.5% were upstaged on the basis of their SBP, and 16.7% on the basis of DBP: thus, if SBP criteria were applied, 83.3% would be correctly staged according to JNC-VI, compared with 77.5% using DBP criteria. Furthermore, SBP control was worse than DBP control, and SBP represents a greater impact on blood pressure staging as well as a substantial community burden than does DBP.
By letting 22 years pass between doubts raised over emphasis on DBP and publication of recommendations that take into account both SBP and DBP, the medical profession may have denied treatment to many who required it. Further work needs to be done on pathogenesis and risk caused by high or low DBP before it can be convincingly dismissed. Perhaps PP may be the ultimate compromise,28 which at least reflects both SBP and DBP, as well as having the evidence showing the relationship to cardiovascular risk.
The Sixth Report of the Joint National Committee on Prevention, Evaluation, and Treatment of High Blood Pressure Arch Int Med 1997 157: 2413–2446
Chalmers J et al. 1999 World Health Organization-International Society of Hypertension Guidelines for the management of hypertension. Guidelines sub-committee of the World Health Organization Clin Exp Hypertens 1999 21: 1009–1060
Lloyd-Jones DM et al. Differential impact of systolic and diastolic blood pressure level on JNC-VI staging. Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure Hypertension 1999 34: 381–385
Franklin SS et al. Predominance of isolated systolic hypertension among middle-aged and elderly US hypertensives Hypertension 2001 37: 869–873
Pogue VA, Ellis C, Michel J, Francis CK . New staging system of the fifth Joint National Committee Report on the Detection, Evaluation, and Treatment of High Blood Pressure alters assessment of the severity and treatment of hypertension Hypertension 1996 28: 713–718
Banegas JR et al. Systolic versus diastolic blood pressure: community burden and impact on blood pressure staging J Hum Hypertens 2002 16: 163–167
Report of the Joint National Committee on detection, Evaluation, and Treatment of High Blood Pressure: a cooperative study JAMA 1977 237: 255–261
Kannel WB . Elevated systolic blood pressure as a cardiovascular risk factor Am J Cardiol 2000 85: 251–255
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The Fifth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure Arch Intern Med 1993 153: 154–183
Perry MP et al. Pretreatment blood pressure as a predictor of 21 year mortality Am J Hypertens 2000 13: 724–733
Staessen JA et al. Risks of untreated and treated isolated systolic hypertension in the elderly: metaanalysis of outcome trials The Lancet 2000 355: 865–872
He J, Whelton PK . Elevated systolic blood pressure as a risk factor for cardiovascular and renal disease J Hypertens Suppl 1999 17: S7–S13
Sever P . Abandoning Diastole BMJ 1999 318: 1773–1776
Swales JD . Systolic versus diastolic pressure: paradigm shift or cycle? J Hum Hypertens 2000 14: 477–479
Nielsen WB, Lindenstrom E, Vestbo J, Jensen GB . Is diastolic hypertension an independent risk factor for stroke in the presence of normal blood pressure in the middle-aged and elderly? Am J Hypertens 1997 10: 634–639
Leonetti G, Cuspidi C, Facchini M, Stramba-Badiale M . Is systolic pressure a better target for antihypertensive treatment than diastolic pressure? J Hypertens Suppl 2000 18: S13–S20
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Domanski M et al. Cardiovascular risk assessment using pulse pressure in the First National Health and Nutrition Examination Survey (NHANES 1) Hypertension 2000 38: 793
Vaccarino V et al. Pulse pressure and risk of cardiovascular events in the Systolic Hypertension in the Elderly Program Am J Cardiol 2001 88: 980–986
Vaccarino V, Holford T, Krumholtz HM . Pulse pressure and risk for myocardial infarction and heart failure in the elderly J Am Coll Cardiol 2000 36: 130–137
White WB . The systolic blood pressure versus pulse pressure controversy Am J Cardiol 2001 87: 1278–1281
Miura K et al. Pulse pressure compared with other blood pressure indexes in the prediction of 25-year cardiovascular and all-cause mortality rates: The Chicago Heart Association Detection Project in Industry Study Hypertension 2001 38: 232–237
Antikainen RL, Jousilahti P, Vanhanen H, Ruomilehto J . Excess mortality associated with increased pulse pressure among middle-aged men and women is explained by high systolic blood pressure J Hypertens 2000 18: 417–423
O'Brien E, Staessen J . What is hypertension? Lancet 1999 353: 1541–1542
Port S et al. Systolic blood pressure and mortality The Lancet 2000 355: 175–179
Benetos A et al. Should diastolic and systolic blood pressure be considered for cardiovascular risk evaluation: A study in middle-aged men and women J Am Coll Cardiol 2001 37: 163–168
Franklin SS et al. Is pulse pressure useful in predicting risk for heart disease? Circulation 1999 100: 354–360
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Cite this article
Tin, L., Beevers, D. & Lip, G. Systolic vs diastolic blood pressure and the burden of hypertension. J Hum Hypertens 16, 147–150 (2002). https://doi.org/10.1038/sj.jhh.1001373
- systolic hypertension
- blood pressure staging
- blood pressure upstaging
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