(Hypertension. 1995;26:301-306.)
© 1995 American Heart Association, Inc.
Articles |
Pulse Pressure and Resistance Artery Structure in the Elderly
From the University Departments of Medicine for the Elderly, Glenfield Hospital (M.A.J., J.F.P.), and Medicine and Therapeutics, Leicester Royal Infirmary (P.A.C.W., H.T., J.D.S.), Leicester, UK.
Correspondence to Dr Martin A. James, University Department of Medicine for the Elderly, Glenfield Hospital, Leicester, LE3 9QP, UK.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Abstract There has been recent interest in the possibility that resistance vessel structural adaptation in hypertension may be more closely related to pulse pressure than to other blood pressure parameters. We investigated the relation between blood pressure and resistance vessel structure in a group of subjects from an age group (older than 60 years) in which a widening of pulse pressure is a typical finding and characterized blood pressure parameters using 24-hour ambulatory blood pressure monitoring. We studied resistance vessels retrieved from biopsies of skin and subcutaneous fat taken from the gluteal region of 32 subjects under local anesthesia (age, 70±1 years [mean±SEM]), 21 of whom were hypertensive and 11 normotensive. Media-lumen ratio was higher in the hypertensive than the normotensive subjects (18.6±1.6% versus 12.8±1.2%, P<.01) and correlated with age (r=.44, P<.05), clinic systolic pressure (r=.35, P<.05), 24-hour systolic pressure (r=.40, P<.05), and 24-hour pulse pressure (r=.56, P<.001). Stepwise multivariate regression analysis identified clinic and 24-hour pulse pressure as the only significant predictors of media-lumen ratio independent of age, other parameters of clinic blood pressure, and blood pressure variability (R2=41%, P<.05). These findings confirm those from animal models of hypertension in demonstrating the importance of pulse pressure in relation to cardiovascular structural adaptation and have important implications for the goals of treatment of hypertension in the elderly.
Key Words: pulse • blood pressure monitoring • vascular resistance • blood vessels • hypertension, essential
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Blood pressure increases with age in all Westernized societies.1 However, over the age of 60 years, increasing SBP with age tends to be accompanied by a plateau or fall in DBP, so there is a progressive widening of PP while MAP remains relatively unchanged or rises only modestly.1 2 These trends result in an increased proportion of elderly subjects with hypertension having isolated or disproportionate systolic hypertension (SBP
160 mm Hg with DBP <90 or 95 mm Hg).3
Hemodynamically, the widening of PP is regarded as resulting from a
loss of compliance in large conduit arteries and increased wave
reflections from the periphery and less to increased resistance in
small peripheral arteries, which is associated with an increase in
MAP.2 4 Inevitably, therefore, previous studies of the
adaptive response of the resistance vasculature to hypertension have
tended to concentrate on the role of MAP.5 6 The increased peripheral resistance that characterizes hypertension, and remains a prominent feature of hypertension in the elderly even in the presence of an increased PP,7 8 9 is determined principally at the level of the small artery (internal diameter <300 µm) as distinct from large or conduit arteries. This increased resistance is associated with an increased ratio of the vessel wall to lumen, itself a result of increased pressure load.10 11 12 Increased wall-to-lumen ratio of the resistance vessels is therefore observed in both genetically hypertensive rats and essential hypertensive subjects. Augmented neurohumoral responses occur as a secondary effect.5 13 14 There has been recent interest regarding the possible influence of PP on resistance vessel structure and in particular on wall-lumen ratio.15 16 17 18 Christensen15 found that structural regression in treated SHR was greater in those rats with larger reductions in PP. He also demonstrated that the strongest correlation between BP and structure was that between PP (measured intra-arterially over 24 hours) and media-lumen ratio. Moreover, Baumbach and colleagues18 have shown that carotid clipping, which normalizes PP but raises MAP, prevents medial hypertrophy in the cerebral arteries of stroke-prone SHR.
Hypertension in the elderly therefore presents an opportunity for exploring the relationship between PP and resistance vessel structure in human subjects. Previously, we and others have demonstrated the considerable prevalence of cardiovascular structural adaptation in the form of left ventricular hypertrophy in elderly hypertensive individuals,19 20 21 including a relationship between 24-hour PP and increased left ventricular mass,22 but alterations of the resistance vasculature have not been described. Accordingly, we set out in this study to describe the relationship between resistance artery structure and BP in the elderly. Further clarification of the cardiovascular load imposed by different BP parameters can be obtained from the use of 24-hour ABPM, which has been used extensively in the assessment of elderly subjects with systolic hypertension.23 24 25
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
We studied 32 elderly (older than 60 years) subjects drawn from hospital referrals, friends and relatives of the hospital patients, and respondents to a newspaper advertisement. The study received the approval of the local ethics committee, and all subjects gave written informed consent. Subjects were selected so as to obtain a wide range of clinic BP values in the normotensive and hypertensive ranges. Clinic BP was measured with subjects supine after 5 minutes of rest, using a large cuff when necessary, with a standard mercury sphygmomanometer. A minimum of three clinic BP readings were taken on three separate occasions at least 2 weeks apart; the reported clinic BP is the average of the resultant nine or more readings. Those subjects with a clinic BP greater than or equal to 160 mm Hg systolic and/or 90 mm Hg diastolic (Korotkoff phase V) were defined as hypertensive. By these criteria, 21 subjects were hypertensive and 11 normotensive. None had previously received any antihypertensive medication. No subject had evidence of secondary hypertension or coronary artery disease by history and examination, electrocardiogram, and standard laboratory and radiological tests. Subjects with a previous history of angina, myocardial infarction, diabetes mellitus, or stroke were excluded. On the third visit to the clinic, a blood sample was taken for measurement of fasting cholesterol and triglyceride levels, and subjects were fitted with a BP monitor (model 90207, SpaceLabs Inc). The monitor was validated for each subject by the sequential same-arm comparison with BP measured by standard sphygmomanometry, monitor readings having to be within 5 mm Hg of manual BP readings. Subjects wore the monitor for 24 hours, with readings being obtained every 15 minutes during a notional daytime period of 7 AM to 10 PM and at 30-minute intervals during the nighttime of 10 PM to 7 AM. The monitor was removed the following day, and the data were downloaded to a personal computer without manual editing to avoid the introduction of bias. Any recording with less than 80% data capture was repeated. Mean SBP and DBP values were obtained for the full 24 hours and for the respective daytime and nighttime periods. Daytime BP variability was taken as the standard deviation of all the daytime readings taken at 15-minute intervals.26
Within 2 weeks of ABPM, subjects donated a biopsy of skin and subcutaneous fat from the gluteal region (approximately 2x0.5x1 cm) taken under local anesthesia (3 to 5 mL of 2% lidocaine hydrochloride). Resistance arteries were dissected from the biopsy and mounted as ring preparations on two parallel 40-µm stainless steel wires in a Mulvany-Halpern myograph6 27 (JP Trading). One wire was connected to a micrometer and the other to a force transducer for measurement of isometric tension. The vessels were held without tension in physiological salt solution composed of (mmol/L) NaCl 118, KCl 4.5, CaCl2 2.5, MgSO4 · 7H2O 1.0, KH2PO4 1.0, NaHCO3 25, and glucose 6 at 37°C and bubbled with 5% CO2/95% O2 to achieve a pH of 7.4. After mounting in the myograph, the vessels were equilibrated for 30 minutes before measurement of vessel length and media thickness by light microscopy. After a further 30 minutes of equilibration, the vessels were exposed to predetermined stepwise increases in tension for determination of the length-tension characteristic calculated from the Laplace equation (P=T/r, where P is transmural pressure, T the wall tension, and r the internal radius of the vessel). The internal diameter then was set to 0.9xL100, where L100 is the internal diameter that the vessel would have in vivo when relaxed at P=100 mm Hg. This is described as the normalized lumen diameter, L0.9, and is the diameter at which the generated isometric tension is greatest. Morphology measurements obtained for each vessel included length (millimeters), normalized lumen diameter (L0.9, micrometers), media cross-sectional area (micrometers squared), normalized media thickness (micrometers), and media-lumen ratio (percent).
Results are expressed as mean±SEM. Data were obtained from two vessels
in 24 subjects, and these data were averaged before analysis;
however, in 8 subjects only one vessel could be retrieved from the
biopsy. The results were analyzed in two ways. First, a
comparison between hypertensive and normotensive groups was made with
Student's two-tailed unpaired t test (after testing for
normality with the Shapiro-Wilks W test) and the
2 test. Over the entire study group BP
parameters were normally distributed, and BP within each
hypertensive or normotensive subgroup also satisfied the Shapiro-Wilks
test, enabling parametric comparisons. Second, Pearson's
correlation and least-squares regression analysis were used to
test for linear relationships between structural parameters
and continuous variables such as BP and age.
Simultaneous independent effects of these variables on
structure were assessed by stepwise multivariate linear
regression. A value of P<.05 was regarded as statistically
significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Of the 32 subjects recruited (mean age, 70±1 years), 17 (53%) were male. There were no differences in age, gender, smoking history, family history of hypertension, weight, alcohol intake, fasting cholesterol, or triglycerides between the hypertensive and normotensive groups. Eight of the hypertensive subjects had isolated systolic hypertension on the basis of their clinic BP. These subjects were of similar age, with 24-hour SBP similar to those with combined systodiastolic hypertension and 24-hour DBP similar to the normotensive subjects; however, 24-hour PP was not significantly different in subjects with isolated systolic hypertension compared with the combined hypertension subgroup (ANOVA with Tukey's post hoc correction; subgroup data not shown). Data comparison therefore was confined to that between the 21 hypertensive and 11 normotensive subjects. Clinic and 24-hour ambulatory BP measurements for the study groups, together with resistance vessel structure, are shown in Table 1. Clinic BP and heart rate and 24-hour BP were significantly lower in the normotensive group compared with the hypertensive group. Twenty-four-hour ambulatory BP was significantly lower than clinic BP (all P<.001), but there was no difference in heart rate. There were no BP differences with gender, with the exception of 24-hour PP, which was higher in women than men (68±3 versus 59±3 mm Hg, respectively, P<.05). PP was not related to height.
|
Media-lumen ratio was significantly greater in hypertensive compared with normotensive subjects. This was probably the result of the combined effects of nonsignificant trends toward decreased lumen diameter and increased media thickness in the hypertensive subjects (Table 1). There was a tendency for the media-lumen ratio to be higher in women than men (18.9±1.8% versus 14.6±1.6%, respectively, P=.08), but sex was not an independent predictor of media-lumen ratio after correction for the difference in PP.
Univariate correlation was performed between resistance vessel structure and age, the various measures of clinic and ambulatory BP, daytime BP variability, and heart rate. The correlation matrix is shown in Table 2. Increasing age was associated with a significant decrease in lumen diameter and increase in media-lumen ratio. Media-lumen ratio was weakly correlated with clinic and 24-hour SBP, but there was a stronger correlation between media-lumen ratio and 24-hour PP (r=.56, P<.001; Figure, A). Dividing the 24-hour BP record into daytime and nighttime periods resulted in similar correlations, again with only SBP (day: r=.39, P<.05; night: r=.42, P<.05) and PP (day: r=.53, P<.01; night: r=.41, P<.05) being significantly related to media-lumen ratio. Media-lumen ratio and normalized media thickness correlated significantly with daytime BP variability but not with either clinic or 24-hour heart rate.
|
|
There were significant positive associations between age and clinic SBP (r=.48, P<.01), clinic MAP (r=.37, P<.05), clinic PP (r=.54, P<.001), and 24-hour PP (r=.53, P<.01). There was no association between age and DBP or heart rate. There were also significant associations between BP variability and 24-hour SBP (SBP variability: r=.74, P<.001; DBP variability: r=.57, P<.001) and between BP variability and 24-hour PP (SBP variability: r=.77, P<.001; DBP variability: r=.62, P<.001). In a stepwise multiple linear regression model with media-lumen ratio as the dependent variable, 24-hour PP was significantly associated with media-lumen ratio independent of age, 24-hour SBP, 24-hour MAP, and BP variability (R2=31%, P<.05). Enlarging the model by the addition of clinic SBP, MAP, and PP as predictor variables indicated that only 24-hour PP and clinic PP were significant independent predictors of media-lumen ratio (R2=41%, P<.05). This would suggest that the relation between increasing age and increasing media-lumen ratio is mediated predominantly through increasing PP. The relation between media-lumen ratio and PP is shown in the Figure with and without adjustment for age. The relationship between media-lumen ratio and unadjusted PP is linear (media-lumen ratio=0.31 PP-2.98, R2=31%, P<.001; Figure, A), but after adjustment for age (adj) the relationship becomes curvilinear (media-lumen ratio=66.4-1.94 adjPP+0.018 adjPP2, R2=27%, P<.01; Figure, B). Thus there appears to be a threshold effect at a PP of approximately 55 mm Hg.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The present study has demonstrated a significant relationship between media-lumen ratio and PP independent of age, SBP, MAP, and BP variability in a group of untreated elderly subjects, most of whom were hypertensive. Media-lumen ratio is the principal parameter of interest when structural adaptation in the resistance vasculature is being examined, and the present findings lend further evidence to the hypothesis that cyclical alteration in BP acts as the main stimulus to vascular remodeling in human hypertension.15 16 17 18 After adjustment for age, our results suggest that PP has an important influence on media-lumen ratio above a threshold of approximately 55 mm Hg. Ideally we would have studied distinct hypertensive subgroups with either isolated systolic hypertension or combined hypertension to explore the hypothesis that if SBP were identical between the two groups, any differences in resistance artery structure may be attributable to differences in PP. However, the homogeneity of sustained hypertension in our elderly study group prevented us from doing this, with the combined hypertensive subjects having a tendency to higher SBP values, which equalized PP between the two subgroups. We have therefore largely avoided emphasis on data analysis by arbitrary groups and mainly confined our analysis to treating BP as a continuous variable.
We have demonstrated no significant increase in media cross-sectional area with BP, which, combined with trends toward increasing media thickness and, to a lesser extent, decreasing lumen diameter, suggests that remodeling is the main adaptation that leads to a higher media-lumen ratio.13 28 This is consistent with other studies of subcutaneous vessels in human essential hypertension, in which remodeling predominates over growth in the adaptive response of resistance vessels.29
Our results are largely in agreement with those obtained from studies of animal models of hypertension. In such experiments PP was reduced by treatment with hydralazine or the angiotensin-converting enzyme inhibitor cilazapril17 or with carotid clipping,18 which reduces PP but raises systolic and mean BP. Such treatments prevented hypertrophy of cerebral arterioles in the stroke-prone SHR. In another study, Christensen15 found that resistance vessel structural regression was greatest in SHR with the largest reductions in PP with treatment. In Christensen's study, an independent effect of heart rate on media-lumen ratio was also identified, but this observation has not been confirmed in the current study. Christensen's analysis has been criticized for failing to take account of treatment effects,30 and the study was interesting in that 24-hour heart rate in the rat was not reduced by ß-blocker treatment.
In the one other study that has examined the relationship between PP and vascular structure in human resistance arteries, Cooper et al31 did not find a significant relation between PP measured casually and media-lumen ratio in a larger but younger group of hypertensive subjects. In our older group of subjects we found consistently better correlations between media-lumen ratio and 24-hour rather than casual BP measurements, presumably arising from the greater reproducibility of 24-hour ABPM. Also it is likely that in a younger group of hypertensive subjects PP levels are lower, and this may diminish any effect.
Our study is the first to our knowledge to report on resistance vessel structure in the elderly. We were particularly interested in this age group for two reasons: first, no data are currently available for this age group, and second, this age group offers a more powerful opportunity for studying the differential effects of PP and MAP on arterial structure. In this context the use of ABPM could be regarded as obligatory because it has been shown to reveal large discrepancies between PP measured in the clinic and by ambulatory methods.23 24 25 Other studies have demonstrated a link between arteriosclerosis, smoking, hyperglycemia, and increased 24-hour but not casual PP.32 33 By the same token, the use of 24-hour ABPM in this study considerably strengthened the correlations between SBP, PP, and vascular structure.
Increasing age is accompanied by a number of important hemodynamic changes. Increasing large arterial rigidity with aging tends to increase SBP and, at a given level of peripheral resistance, to decrease DBP.2 34 35 36 Furthermore, although in young subjects PP in peripheral arteries tends to be higher than in central arteries, this difference declines with age so that older than age 50 PP tends to be similar in both central and peripheral arteries in both normotensive and hypertensive subjects.34 36 One effect of this in the young is to reduce the apparent contribution of PP to changes at the level of the resistance artery when BP is measured at the brachial artery. In the elderly, PP measured at the brachial artery may more closely reflect the level of PP in the resistance vasculature, and this has implications when the relationship between the two is being considered. However, brachial BP is only a substitute measure for the level of BP prevailing in the resistance vessels of the gluteal region from which the biopsies were taken, and in humans the brachial-gluteal BP difference is unquantified. Moreover, the small arteries may be an important site for the generation of reflected waves, which amplify the systolic peak and contribute to a widened PP and disproportionate systolic hypertension.2 35 Therefore, it remains plausible that an increased SBP and PP are a consequence of greater structural alteration at the level of the small arteries rather than its cause.
Comparison of our data with those from other studies that have included normotensive control subjects from younger age groups shows the media-lumen ratio in normotensive elderly subjects to be considerably increased, attaining the levels observed in younger hypertensive subjects.5 37 38 39 No subject in the normotensive group of the present study had any history of high BP, thus excluding as far as we are able any subject with "burned out" hypertension. BP levels in our normotensive control group are higher than in equivalent control groups of younger subjects, but not greatly so, and the difference in BP would be insufficient to solely explain the difference in media-lumen ratio. Thus, despite the hemodynamic considerations described above, this would tend to suggest an independent effect of age. However, this issue can be resolved only by a study of young and older subjects matched for BP.
The results of the present study have important clinical implications because PP has until recently not received the same attention as other BP parameters. However, increasing evidence indicates the importance of PP as a risk factor for future cardiovascular events, including myocardial infarction.40 41 Assessment of PP in the elderly is best performed with the use of ambulatory methods, and the present study emphasizes further the clinical value of ABPM in the elderly. Structural regression in the resistance vasculature is likely to become an important goal of antihypertensive therapy, particularly if it proves to be related to beneficial effects elsewhere, such as an improvement in coronary reserve and reduction in myocardial infarction.42 To achieve structural regression, antihypertensive treatment must reduce PP as well as MAP. This will be particularly relevant in those elderly subjects with disproportionate systolic hypertension, in which treatments that predominantly lower SBP and PP irrespective of their effects on MAP or DBP may be preferable. As the Systolic Hypertension in the Elderly Program (SHEP) study has shown,43 a reduction in SBP and PP can be achieved in the elderly with few of the previously perceived adverse consequences on quality of life and with considerable benefit, including significant reductions in coronary heart disease not achieved in studies of younger age groups. The ongoing Systolic Hypertension in the Elderly in Europe (SYST-EUR) study,44 which is using a calcium channel blocker and an angiotensin-converting enzyme inhibitor as well as a diuretic as first-line therapy for isolated systolic hypertension, will help to clarify these issues further.
In conclusion, the present study has demonstrated in a group of untreated elderly subjects that PP is principally associated with resistance vessel structural adaptation independent of age and other BP parameters. These findings may have important implications for the goals of treatment of hypertension in the elderly, an area of sharply increasing importance for the prevention of cardiovascular disability and death.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
This research was supported by a project grant from the Sir Jules Thorn Trust. P.A.C.W. was supported by a British Heart Foundation project grant.
Received February 2, 1995; first decision March 2, 1995; accepted April 24, 1995.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Rose GA. Hypertension in the community. In: Bulpitt CJ, ed. Handbook of Hypertension, Volume 6: Epidemiology of Hypertension. Amsterdam, Netherlands: Elsevier Science Publishers; 1985:1-14.
2. Safar ME. Hemodynamic changes in elderly hypertensive patients. Am J Hypertens. 1993;6:20S-23S. [Medline] [Order article via Infotrieve]
3.
Wilking SV, Blenager A, Kannel WB, D'Agostino RB,
Steel K. Determinants of isolated systolic hypertension.
JAMA. 1988;260:3451-3455.
4. Nichols WW, O'Rourke MF. McDonald's Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 3rd ed. London, UK: Edward Arnold; 1990:77-142.
5.
Aalkjær C, Heagerty AM, Petersen KK, Swales JD,
Mulvany MJ. Evidence for increased media thickness, increased
neuronal amine uptake, and depressed excitation-contraction coupling in
isolated resistance vessels from essential hypertensives.
Circ Res. 1987;61:181-186.
6. Aalkjær C. Investigations of isolated small arteries from patients with hypertension. J Hum Hypertens. 1993;7:183-185. [Medline] [Order article via Infotrieve]
7. McNeil JJ, Silagy CA. Hypertension in the elderly: epidemiology and pathophysiology. Cardiovasc Drugs Ther. 1990;4:1197-1202.
8. Koch-Weser J. Correlation of pathophysiology and pharmacotherapy in primary hypertension. Am J Cardiol. 1973;32:499-510.
9. Berger DS, Li JK-J. Concurrent compliance reduction and increased peripheral resistance in the manifestation of isolated systolic hypertension. Am J Cardiol. 1990;65:67-71. [Medline] [Order article via Infotrieve]
10. Folkow B, Grimby G, Thulesius O. Adaptive structural changes of the vascular walls in hypertension and their relation to the control of peripheral resistance. Acta Physiol Scand. 1958;44:255-272. [Medline] [Order article via Infotrieve]
11.
Folkow B. Physiological
aspects of primary hypertension. Physiol Rev. 1982;62:347-504.
12. Folkow B, Hällback M, Lundgren Y, Sivertsson R, Weiss L. Importance of adaptive changes in vascular design for establishment of primary hypertension studied in man and in spontaneously hypertensive rats. Circ Res. 1973;32(suppl I):I-2-I-16.
13. Mulvany MJ. The development and regression of vascular hypertrophy. J Cardiovasc Pharmacol. 1992;19:S22-S27.
14. Mulvany MJ. Resistance vessel structure and the pathogenesis of hypertension. J Hypertens. 1993;11:S7-S12.
15.
Christensen KL. Reducing pulse pressure in
hypertension may normalize small artery structure.
Hypertension. 1991;18:722-727.
16.
Baumbach GL. Is pulse pressure a stimulus for
altered vascular structure in chronic hypertension?
Hypertension. 1991;18:728-729.
17.
Hajdu MA, Heistad DD, Baumbach GL. Effects of
antihypertensive treatment on mechanics of cerebral arterioles in
rats. Hypertension. 1990;17:308-316.
18. Baumbach GL, Siems JE, Heistad DD. Effects of local reduction in pressure on distensibility and composition of cerebral arterioles. Circ Res. 1991;68:339-351.
19. James MA. Fotherby MD, Potter JF. Clinical correlates of left ventricular mass in elderly hypertensives. J Hum Hypertens. 1994;8:409-415. [Medline] [Order article via Infotrieve]
20. Jones E, Morgan TO, Califore P, Johns J. Prevalence of left ventricular hypertrophy in elderly patients with well controlled hypertension. Clin Exp Pharmacol Physiol. 1990;17:207-210. [Medline] [Order article via Infotrieve]
21. Devereux RB, Casale PN, Hammond IW, Savage DD, Alderman MH, Campo E, Alonso DR, Laragh JH. Echocardiographic detection of pressure-overload left ventricular hypertrophy: effect of criteria and patient population. J Clin Hypertens. 1987;3:66-78. [Medline] [Order article via Infotrieve]
22. Pannier B, Brunel P, El Aroussy W, Lacolley P, Safar ME. Pulse pressure and echocardiographic findings in essential hypertension. J Hypertens. 1989;7:127-132. [Medline] [Order article via Infotrieve]
23. Silagy CA, McNeill JJ, McGrath BP. Isolated systolic hypertension: does it really exist on ambulatory blood pressure monitoring? Clin Exp Pharmacol Physiol. 1990;17:203-206. [Medline] [Order article via Infotrieve]
24. Cox JP, Atkins N, O'Malley K, O'Brien E. Does isolated systolic hypertension occur with ambulatory blood pressure measurement? J Hypertens. 1991;9:S100-S101.
25. Thijs L, Amery A, Clement D, Cox J, de Cort P, Fagard R, Fowler G, Guo C, Mancia G, Marin F, O'Brien E, O'Malley K, Palatini P, Parati G, Petrie J, Ravogli A, Rosenfeld J, Staessen J, Webster J. Ambulatory blood pressure monitoring in elderly patients with isolated systolic hypertension. J Hypertens. 1992;10:693-699. [Medline] [Order article via Infotrieve]
26.
Di Rienzo M, Grassi G, Pedotti A, Mancia G.
Continuous vs intermittent blood pressure measurements in
estimating 24-hour average blood pressure.
Hypertension. 1983;5:264-269.
27.
Mulvany MJ, Halpern W. Contractile properties of
small arterial resistance vessels in spontaneously
hypertensive and normotensive rats. Circ
Res. 1977;41:19-26.
28.
Heagerty AM, Aalkjær C, Bund SJ, Korsgaard N, Mulvany
MJ. Small artery structure in hypertension: dual processes of
remodeling and growth. Hypertension. 1993;21:391-397.
29. Korsgaard N, Aalkjær C, Heagerty AM, Izzard A, Mulvany MJ. The increased media-lumen ratio in resistance arteries from essential hypertensives is not associated with media hypertrophy or cellular hyperplasia. Blood Vessels. 1991;28:303. Abstract.
30. Harrap SB, Forbes AB. Pulse pressure and microvessels. Hypertension. 1993:21;525-526. Letter.
31. Cooper A, Aalkjær C, Korsgaard N, Mulvany MJ, Heagerty AM. Structural changes in small arteries and arterial blood pressure: lack of correlation with pulse pressure. J Hypertens. 1993;11(suppl 5):S413. Abstract.
32. Asmar RG, Girerd XJ, Brahimi M, Safavian A, Safar ME. Ambulatory blood pressure measurement, smoking and abnormalities of glucose and lipid metabolism in essential hypertension. J Hypertens. 1992;10:181-187. [Medline] [Order article via Infotrieve]
33. Asmar RG, Julia PL, Mascarel VL, Fabiani JN, Benetos A, Safar ME. Ambulatory blood pressure profile after carotid endarterectomy in patients with ischaemic heart disease. J Hypertens. 1994;12:697-702. [Medline] [Order article via Infotrieve]
34. Safar ME, Laurent S. Behaviour of conduit arteries in hypertension. Clin Exp Hypertens. 1993;15:1033-1045.
35. Palatini P, Graniero GR. Isolated systolic hypertension in the elderly: new insights. Clin Exp Hypertens. 1993;15:103-116.
36.
O'Rourke M. Arterial stiffness,
systolic blood pressure and logical treatment of arterial
hypertension. Hypertension. 1990;15:339-347.
37. Heagerty AM, Bund SJ, Aalkjær C. Effect of drug treatment on human resistance arteriole morphology in essential hypertension: direct evidence for structural remodelling of resistance vessels. Lancet. 1988;2:1209-1212. [Medline] [Order article via Infotrieve]
38. Aalkjær C, Pedersen EB, Danielsen H, Fjeldborg O, Jespersen B, Kjaer T, Sorensen SS, Mulvany MJ. Morphological and functional characteristics of isolated resistance vessels in advanced uraemia. Clin Sci. 1986;71:657-663. [Medline] [Order article via Infotrieve]
39. Schiffrin EL. Reactivity of small blood vessels in hypertension: relation with structural changes. Hypertension. 1992;19(suppl II):II-1-II-9.
40.
Darne B, Girerd X, Safar M, Cambien F, Guize L.
Pulsatile versus steady component of blood pressure: a
cross-sectional analysis and a prospective analysis on
cardiovascular mortality.
Hypertension. 1989;13:392-400.
41.
Madhavan S, Ooi WL, Cohen H, Alderman MH.
Relation of pulse pressure and blood pressure reduction to the
incidence of myocardial infarction.
Hypertension. 1994;23:395-401.
42. Mulvany MJ. Are vascular abnormalities a primary cause or secondary consequence of hypertension? Hypertension. 1991;18(suppl I):I-52-I-57.
43.
SHEP Cooperative Research Group. Prevention of
stroke by anti-hypertensive drug treatment in older persons with
isolated systolic hypertension: final results of the Systolic
Hypertension in the Elderly Program (SHEP). JAMA. 1991;265:3255-3264.
44. Slovick DI, Amery A, Birkenhager W, Bulpitt CJ, Cox J, de Leeuw P, de Cort P, Fagard R, Fletcher AE, Forette F, Fowler G, Girerd X, Leonetti G, O'Brien ET, O'Malley K, Petrie J, Rodicio JL, Rosenfeld J, Staessen J, Terzoli L, Thijs L, Tuomilehto J, Webster J, Yodfat Y. SYST-EUR multicentre trial on the treatment of isolated systolic hypertension in the elderly: first interim report. J Hum Hypertens. 1993;7:201-203.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  S. Laurent, M. Briet, and P. Boutouyrie Large and Small Artery Cross-Talk and Recent Morbidity-Mortality Trials in Hypertension Hypertension, August 1, 2009; 54(2): 388 - 392. [Full Text] [PDF]
|
|
|
|
 |
|
 M. E. Widlansky Shear stress and flow-mediated dilation: all shear responses are not created equally Am J Physiol Heart Circ Physiol, January 1, 2009; 296(1): H31 - H32. [Full Text] [PDF]
|
|
|
|
 |
|
 G. F. Mitchell Effects of central arterial aging on the structure and function of the peripheral vasculature: implications for end-organ damage J Appl Physiol, November 1, 2008; 105(5): 1652 - 1660. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. F. Mitchell, P. R. Conlin, M. E. Dunlap, Y. Lacourciere, J. M. O. Arnold, R. I. Ogilvie, J. Neutel, J. L. Izzo Jr, and M. A. Pfeffer Aortic Diameter, Wall Stiffness, and Wave Reflection in Systolic Hypertension Hypertension, January 1, 2008; 51(1): 105 - 111. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. L. Huang, A. E. Silver, E. Shvenke, D. W. Schopfer, E. Jahangir, M. A. Titas, A. Shpilman, J. O. Menzoian, M. T. Watkins, J. D. Raffetto, et al. Predictive Value of Reactive Hyperemia for Cardiovascular Events in Patients With Peripheral Arterial Disease Undergoing Vascular Surgery Arterioscler Thromb Vasc Biol, October 1, 2007; 27(10): 2113 - 2119. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D Fukuda, M Yoshiyama, K Shimada, H Yamashita, S Ehara, Y Nakamura, K Kamimori, A Tanaka, T Kawarabayashi, and J Yoshikawa Relation between aortic stiffness and coronary flow reserve in patients with coronary artery disease Heart, June 1, 2006; 92(6): 759 - 762. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Tsakiris, M. Doumas, D. Lagatouras, G. Vyssoulis, E. Karpanou, N. Nearchou, C. Kouremenou, and P. Skoufas Microalbuminuria Is Determined by Systolic and Pulse Pressure Over a 12-Year Period and Related to Peripheral Artery Disease in Normotensive and Hypertensive Subjects: The Three Areas Study in Greece (TAS-GR) Angiology, May 1, 2006; 57(3): 313 - 320. [Abstract] [PDF]
|
|
|
|
 |
|
 G. F. Mitchell, J. A. Vita, M. G. Larson, H. Parise, M. J. Keyes, E. Warner, R. S. Vasan, D. Levy, and E. J. Benjamin Cross-Sectional Relations of Peripheral Microvascular Function, Cardiovascular Disease Risk Factors, and Aortic Stiffness: The Framingham Heart Study Circulation, December 13, 2005; 112(24): 3722 - 3728. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G Tsivgoulis, K Spengos, N Zakopoulos, E Manios, K Xinos, D Vassilopoulos, and K N Vemmos Twenty four hour pulse pressure predicts long term recurrence in acute stroke patients J. Neurol. Neurosurg. Psychiatry, October 1, 2005; 76(10): 1360 - 1365. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. H. Dao, R. Essalihi, C. Bouvet, and P. Moreau Evolution and modulation of age-related medial elastocalcinosis: Impact on large artery stiffness and isolated systolic hypertension Cardiovasc Res, May 1, 2005; 66(2): 307 - 317. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. F. Mitchell, H. Parise, J. A. Vita, M. G. Larson, E. Warner, J. F. Keaney Jr, M. J. Keyes, D. Levy, R. S. Vasan, and E. J. Benjamin Local Shear Stress and Brachial Artery Flow-Mediated Dilation: The Framingham Heart Study Hypertension, August 1, 2004; 44(2): 134 - 139. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. H. Endemann, Q. Pu, C. De Ciuceis, C. Savoia, A. Virdis, M. F. Neves, R. M. Touyz, and E. L. Schiffrin Persistent Remodeling of Resistance Arteries in Type 2 Diabetic Patients on Antihypertensive Treatment Hypertension, February 1, 2004; 43(2): 399 - 404. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Viazzi, G. Leoncini, D. Parodi, M. Ravera, E. Ratto, S. Vettoretti, C. Tomolillo, M. D. Sette, G. P. Bezante, G. Deferrari, et al. Pulse pressure and subclinical cardiovascular damage in primary hypertension Nephrol. Dial. Transplant., October 1, 2002; 17(10): 1779 - 1785. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Duprez, M. De Buyzere, L De Bruyne, D. Clement, and J. Cohn Small and large artery elasticity indices in peripheral arterial occlusive disease (PAOD) Vascular Medicine, November 1, 2001; 6(4): 211 - 214. [Abstract] [PDF]
|
|
|
|
|
|
R. G. Asmar, G. M. London, M. E. O'Rourke, and M. E. Safar Improvement in Blood Pressure, Arterial Stiffness and Wave Reflections With a Very-Low-Dose Perindopril/Indapamide Combination in Hypertensive Patient: A Comparison With Atenolol Hypertension, October 1, 2001; 38(4): 922 - 926. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. A Dinenno, H. Tanaka, K. D Monahan, C. M Clevenger, I. Eskurza, C. A DeSouza, and D. R Seals Regular endurance exercise induces expansive arterial remodelling in the trained limbs of healthy men J. Physiol., July 1, 2001; 534(1): 287 - 295. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Verdecchia, G. Schillaci, G. Reboldi, S. S. Franklin, and C. Porcellati Different Prognostic Impact of 24-Hour Mean Blood Pressure and Pulse Pressure on Stroke and Coronary Artery Disease in Essential Hypertension Circulation, May 29, 2001; 103(21): 2579 - 2584. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. M. Dart and B. A. Kingwell Pulse pressure--a review of mechanisms and clinical relevance J. Am. Coll. Cardiol., March 15, 2001; 37(4): 975 - 984. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. S. Franklin, M. J. Jacobs, N. D. Wong, G. J. L'Italien, and P. Lapuerta Predominance of Isolated Systolic Hypertension Among Middle-Aged and Elderly US Hypertensives : Analysis Based on National Health and Nutrition Examination Survey (NHANES) III Hypertension, March 1, 2001; 37(3): 869 - 874. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Pedrinelli, G. Dell'Omo, G. Penno, S. Bandinelli, A. Bertini, V. Di Bello, and M. Mariani Microalbuminuria and Pulse Pressure in Hypertensive and Atherosclerotic Men Hypertension, January 1, 2000; 35(1): 48 - 54. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Alfie, G. D. Waisman, C. R. Galarza, and M. I. Camera Contribution of Stroke Volume to the Change in Pulse Pressure Pattern With Age Hypertension, October 1, 1999; 34(4): 808 - 812. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. R. Seals, E. T. Stevenson, P. P. Jones, C. A. DeSouza, and H. Tanaka Lack of age-associated elevations in 24-h systolic and pulse pressures in women who exercise regularly Am J Physiol Heart Circ Physiol, September 1, 1999; 277(3): H947 - H955. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. E. McVeigh, C. W. Bratteli, D. J. Morgan, C. M. Alinder, S. P. Glasser, S. M. Finkelstein, and J. N. Cohn Age-Related Abnormalities in Arterial Compliance Identified by Pressure Pulse Contour Analysis : Aging and Arterial Compliance Hypertension, June 1, 1999; 33(6): 1392 - 1398. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Verdecchia, G. Schillaci, C. Borgioni, A. Ciucci, S. Pede, and C. Porcellati Ambulatory Pulse Pressure : A Potent Predictor of Total Cardiovascular Risk in Hypertension Hypertension, December 1, 1998; 32(6): 983 - 988. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.-H. Chen, M. Nakayama, E. Nevo, B. J. Fetics, W. L. Maughan, and D. A. Kass Coupled systolic-ventricular and vascular stiffening with age: Implications for pressure regulation and cardiac reserve in the elderly J. Am. Coll. Cardiol., November 1, 1998; 32(5): 1221 - 1227. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. F. Mitchell, L. A. Moye, E. Braunwald, J.-L. Rouleau, V. Bernstein, E. M. Geltman, G. C. Flaker, M. A. Pfeffer, and f. t. S. Investigators Sphygmomanometrically Determined Pulse Pressure Is a Powerful Independent Predictor of Recurrent Events After Myocardial Infarction in Patients With Impaired Left Ventricular Function Circulation, December 16, 1997; 96(12): 4254 - 4260. [Abstract] [Full Text]
|
|
|
|
|
|
C. R. Galarza, J. Alfie, G. D. Waisman, L. M. Mayorga, L. A. Camera, M. del Rio, F. Vasvari, R. Limansky, J. Farias, J. Tessler, et al. Diastolic Pressure Underestimates Age-Related Hemodynamic Impairment Hypertension, October 1, 1997; 30(4): 809 - 816. [Abstract] [Full Text]
|
|
|
|
|
|
H. R. Black and J.-Y. Yi A New Classification Scheme for Hypertension Based on Relative and Absolute Risk With Implications for Treatment and Reimbursement Hypertension, November 1, 1996; 28(5): 719 - 724. [Abstract] [Full Text]
|
|
|
|
|
|
A. F. Dominiczak, A. M. Devlin, W. K. Lee, N. H. Anderson, D. F. Bohr, and J. L. Reid Vascular Smooth Muscle Polyploidy and Cardiac Hypertrophy in Genetic Hypertension Hypertension, March 1, 1996; 27(3): 752 - 759. [Abstract] [Full Text]
|
|
|
|
|
|
R. Weber, N. Stergiopulos, H. R. Brunner, and D. Hayoz Contributions of Vascular Tone and Structure to Elastic Properties of a Medium-Sized Artery Hypertension, March 1, 1996; 27(3): 816 - 822. [Abstract] [Full Text]
|
|
|
|
|
|
H. Tanaka, D. R. Seals, K. D. Monahan, C. M. Clevenger, C. A. DeSouza, and F. A. Dinenno Regular aerobic exercise and the age-related increase in carotid artery intima-media thickness in healthy men J Appl Physiol, April 1, 2002; 92(4): 1458 - 1464. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||