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(Hypertension. 1997;30:809-816.)
© 1997 American Heart Association, Inc.
Articles |
Diastolic Pressure Underestimates Age-Related Hemodynamic Impairment
From the Unidad de Fisiología Clínica e Hipertensión Arterial, Servicio de Clínica Médica, Hospital Italiano de Buenos Aires and Instituto de Investigaciones Clínicas and Mesa Nacional de Residentes de Clínica Médica, Sociedad Argentina de Medicina.
Correspondence to Dr Carlos R. Galarza, Unidad de Hipertensión Arterial, Servicio de Clínica Médica, Hospital Italiano de Buenos Aires, Gascón 450 (1181), Buenos Aires, Argentina. E-mail galarza{at}connmed.com.ar
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Abstract |
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Abstract It has been hypothesized that as large arteries become more rigid with age, the pattern of hypertension changes from diastolic to systolic. Thus, diastolic blood pressure (DBP) may lose its ability to reflect the increase in vascular resistance with age. To assess this, we studied the age-related changes in blood pressure pattern and its steady-state and pulsatile determinants. We performed an epidemiological analysis based on a national survey of 10 462 subjects from Argentina. A hemodynamic analysis (impedance cardiography) was then carried out in 636 consecutive hypertensive patients (age, 25 to 74 years). Whereas the rate of increment in the prevalence of mild to moderate hypertension (MMH) reached a plateau after the sixth decade, isolated and borderline systolic forms of hypertension began a steep and sustained rise. Among patients with MMH, DBP remained stable from the third to the seventh decade, whereas SBP maintained a sustained increase. Despite similar DBP, the systemic vascular resistance index increased 47% (P<.01) and the cardiac index decreased 27% (P<.01), whereas the ratio of stroke volume to pulse pressure, an index of arterial compliance, decreased 45% (P<.01). However, there were no significant differences between older patients with MMH and those with isolated systolic hypertension in the level of SBP, vascular resistance, stroke volume, and cardiac index. Compared with age-matched normotensive control subjects, the ratio of stroke volume to pulse pressure was much more reduced in isolated systolic hypertension (48%) than in MMH (30%). In summary, the present study, carried out in a large sample of hypertensive subjects with a wide age range, showed a simultaneous impairment in vascular resistance and arterial compliance associated with aging in different patterns of hypertension. The magnitude of these changes, with opposite effects on DBP but additive effects on SBP, suggests that a hemodynamic mechanism could determine the transition in the prevalence of diastolic hypertension toward a systolic pattern of hypertension with aging. Also, the results suggest that SBP, but not DBP, is a reliable indicator of the underlying hemodynamic abnormalities (high resistance and low arterial compliance) in the elderly.
Key Words: hemodynamics • arterial compliance • blood pressure • hypertension, systolic • vascular resistance • age
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Introduction |
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Conventionally, it has been assumed that high vascular resistance, the major hemodynamic abnormality in essential hypertension, is reflected by elevated DBP, whereas SBP is determined by SV and AC. However, the contribution of vascular resistance, CO, and AC for a given level of DBP and SBP varies from patient to patient, and the physiological significance of both pressures could change with aging. Epidemiological data show that SBP increases continuously with age, whereas DBP tends to decrease after the seventh decade. To explain this, it has been hypothesized that as large arteries become more rigid with aging, SBP will be higher and DBP lower for a given level of vascular resistance and blood flow.1 2 3 In a preliminary analysis in MMH, however, we observed that despite similar DBP, SVR and SBP showed a consistent rise with age.4 These data suggest that DBP may progressively lose its ability to reflect the age-related increase in vascular resistance, whereas SBP does not. Experimental data on animals showed that the effect of an isolated decrease in arterial compliance causes an increase in SBP as well as a decrease in DBP pressure of similar magnitude without a change in MAP. Therefore, although a decreased compliance may be found, this change alone cannot explain ISH.5 As a result, it would be expected that as the pattern of hypertension changes with age from diastolic to predominantly systolic, associated with a decrease in AC, an increase in vascular resistance takes place.
To assess this hypothesis and to gain insight concerning the change in BP pattern throughout the aging process in hypertensive subjects, we performed a cross-sectional epidemiological and hemodynamic study. The analysis included the steady state and pulsatile hemodynamic changes underlying the age-related transition in BP pattern and the hemodynamic differences between diastolic and isolated systolic forms of hypertension in older subjects.
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Methods |
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Epidemiological Analysis
Epidemiological data were based on the Argentine Blood Pressure Study.6 A national sample of 10 462 noninstitutionalized subjects (age, 15 to 99 years) from the general population of 16 Argentine regions was studied during a 6-month period in 1990. BP was measured by physicians, with a standard aneroid sphygmomanometer, on two different days at an interval no greater than 1 week (three measurements each day). DBP was measured after Korotkoff's phase V. The average BP measurement was used to classify hypertension severity (in agreement with the Joint National Committee IV7 ).
Prevalence was adjusted by age and sex by taking into account the last population census. Subjects were grouped for decades beginning at 5 years (ie, first decade from 5 to 14 years).
We analyzed the (1) age-related trend in BP in the overall population, (2) age-related trends in BP in mild to moderate hypertensive and normotensive subjects, and (3) changes in MMH, BSH, and ISH prevalence with age.
Hemodynamic Analysis
After the completion of the epidemiological study,
hemodynamic evaluations were performed in 636
consecutive hypertensive patients who were seen throughout a 2-year
period. All subjects gave informed consent, and the study was approved
by an institutional review committee. The procedures followed were in
accordance with institutional guidelines. Patients were grouped as
described below.
MMH Group
This group included 199 untreated mild to moderate hypertensive
patients. The entry criteria included (1) no previous treatment of
their hypertension or withdrawal from antihypertensive drugs at least 2
weeks (4 weeks in the case of diuretics) before the study, (2)
DBP >89 and <115 mm Hg (six recordings averaged during
two visits), (3) no use of sedative or hypnotic drugs, (4) no clinical
or routine laboratory evidence of secondary causes of hypertension, (5)
absence of any known condition that could invalidate the assessment of
cardiac output by impedance cardiography (see "Methods"), (6) no
clinical evidence of complicated hypertensive disease or other major
illness, and (7) age range from 25 to 74 years.
Treated Group
Three hundred fifty-four treated hypertensive patients,
irrespective of their current BP level, composed this group. The entry
criteria adopted were the same as those in the MMH group, with the
exception of items 1 and 2.
ISH Group
This group consisted of 32 ISH patients (SBP >159 mm Hg,
DBP <90 mm Hg). With the exception of items 2 and 7, entry
criteria were similar to those used for the MMH group. The entry
criterion for age was 55 to 74 years.
BSH Group
Fifty-one borderline systolic hypertensive patients
(SBP >139 and <160 mm Hg, DBP <90 mm Hg) composed this
group. Entry criteria were similar to those used for the ISH group.
We analyzed age-related trends in steady state and pulsatile hemodynamic variables in untreated mild to moderate hypertensive patients and treated patients, and we compared hemodynamic variables among older patients with ISH, BSH, and MMH and normotensive subjects of similar age and same sex.
Procedures
All hemodynamic measurements were performed in
basal conditions during the morning. After all recording
devices were attached, patients rested for 15 minutes and then BP and
impedance cardiography recordings were made three
times.8
Cardiac output was measured by a Minnesota 304 B Impedance Cardiograph (Surcom Inc) by use of Kubicek's technique and equation.9 10 At the time of a short apnea after a passive expiration, avoiding Valsalva, simultaneous recordings of the first temporal derivative of impedance change during the cardiac cycle (dZ/dt) and phonocardiograms (Hewlett Packard 21050A transducer) were made with a recorder (model RG, Dyne) for manual measurement at a paper speed of 50 mm/s.9 10 11 12
The following formula was used to calculate ventricular SV
in milliliters: SV=
(L/Z0)2 · T
· (dZ/dt)max, where is electrical resistance of blood
at 100 kHz13 (
/cm), L is mean distance between the
inner electrodes (cm), Z0 is mean impedance of the thorax
(), (dZ/dt)max is peak value of the first derivative of
thoracic impedance occurring during ventricular ejection
(/s), and T is ventricular ejection time (s).
Heart rate (HR, bpm) was obtained from the interbeat interval. CO was calculated as CO=SVxHR.
BP was determined by a mercury sphygmomanometer with the auscultatory method on the right brachial artery. Korotkoff's phase V was used as an indicator of DBP. MAP was calculated as DBP+(SBP-DBP)/3.
SVR was calculated by conventional formulas assuming a mean right atrial pressure of 4 mm Hg as SVR=[(MAP-4)/CO]x80, where 80 was used to convert the SVR from arbitrary units (mm Hg · L-1 · min-1) to the metric international system (dyne · s · cm-5).
SAC was estimated by the ratio of SV to PP (mL · mm Hg).14 15 16 17 18 19 20 Although this indicator of SAC depends on the BP at the end of diastole, it was possible to compare values obtained in groups with similar DBP values. The determination of the SV to PP ratio has shown a close correlation with other invasive and noninvasive techniques used to measure AC and has been used to estimate AC in population groups.15 16 17 18 19 20
Validation of Impedance Cardiography
Reliability of impedance cardiography for CO measurement has
been questioned primarily because of concerns about the equation put
forward by Kubicek et al9 rather than because of adverse
results in selected populations. At present, a consensus is
developing concerning the qualitative accuracy of this technique
because of increased knowledge of the technique and its clinical
limitations.10 11 12 13 21 22 In addition, before beginning this
study, we observed and analyzed the tracings of impedance
cardiography in different cardiovascular diseases in
the catheterization laboratory for 2
years.21 We, as well as others, have verified that the
method provides aberrant measurement of CO in several conditions, such
as (1) cardiac diseases that modify blood flow directions during
ventricular systole (valvular
regurgitation or congenital shunts), (2) pathological
thoracic conditions that modify the electric field of the thorax
(pericardial or pleural effusion and hemopneumothorax), and (3)
abnormal recordings of dZ/dt during ventricular
systole (bicuspid wave).21 Therefore, excluding these
conditions, several reports have shown that impedance cardiography is a
reliable and reproducible method to estimate CO. The absolute value of
CO determined by this method is usually higher than that of reference
invasive methods.10 11 12 21 22 23 24 25 26 27 28 29 30 31 In our work, the correlation
coefficient between simultaneous impedance cardiography and
thermodilution determinations of CO in patients with coronary
artery disease, severe hypertension, aortic stenosis, mitral
stenosis, and congestive heart failure was .94, and the mean
paired difference was 0.08 L/min (95% CI, -0.12 to 0.27 L/min). The
regression equation for the two methods was
y=-0.76+1.17x, where y=CO by impedance
cardiography and x=CO by thermodilution.21 In
our laboratory, the variation coefficient between two consecutive
measurements of CO was 3.9%.30 In addition, we evaluated
the long-term interassay variation of CO in 35 hypertensive patients
(1-month interval). The mean paired difference was -0.05 L/min (95%
CI, -0.16 to 0.05 L/min).31
Statistical Methods
Epidemiological Data
Statistical analysis of data from the survey was
performed with an SAS program at the Cardiovascular
Branch of the Centers for Disease Control and Prevention at
Atlanta.
Hemodynamic Data
For statistical purposes, patients in the MMH group and treated
MMH group were grouped by decades in the same way as the subjects in
the survey. Results were expressed as mean±SD. Comparisons were made
by a one-way ANOVA. When statistically significant differences were
found, multiple comparisons were performed by Bonferroni's
t test.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Epidemiological Findings
When the entire population (n=10 462) was analyzed, both DBP and SBP rose progressively with age until the sixth decade. Then, the SBP continued a sustained and progressive increase, whereas DBP reached a plateau and even decreased slightly after the seventh decade (Fig 1A
).
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However, when mild to moderate hypertensive subjects (n=1561) were
analyzed separately (Fig 1B
), the mean DBP remained stable (93
to 97 mm Hg) throughout the age range, whereas the SBP increased
a mean of 24 mm Hg from the 25th through the 34th year to the
65th through the 74th year, reaching levels similar to those observed
in ISH patients of similar age. Normotensive subjects experienced a
similar age-related tendency in their BP profile with a smaller
increase in SBP (7 mm Hg) throughout the five decades (Fig 1B).
Hypertension prevalence increased in a sustained and progressive way
throughout the range of ages (Fig 2). The
MMH prevalence increased substantially until the sixth decade, after
which a significant decrease took place in the following decades. In
contrast, ISH and BSH prevalence experienced a steep rise after the
sixth decade.
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Hemodynamic Results
Systemic Hemodynamics and Age in the MMH
Group
Anthropometric variables of MMH and sex were similar among the
five decades. Mean DBP was similar over the five decades (range, 94±5
to 96±5 mm Hg), whereas mean SBP rose significantly (19%,
P<.05). There was a mild and nonsignificant rise in MAP
(Table 1). The SVRI increased 47% (P<.01) and CI decreased
27% (P<.01) from the third decade (25 to 34 years) to the
seventh decade (65 to 74 years).
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The ratio of SV to PP decreased 45% (P<.01) from the
third to the seventh decade (Fig 3). There was a mild and
nonsignificant decrease in stroke index and HR
(7%).
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Systemic Hemodynamics and Age in Treated
Patients
These patients were under treatment with ACE
inhibitors (n=224), calcium channel blockers (n=89),
ß-blockers (n=65), diuretics (n=37), and other drugs (n=17).
The trends in BP and hemodynamic variables with age
were similar to the untreated mild to moderate hypertensive patients
(Table 2). Diastolic BP did
not change significantly with age (range, 82±12 to 91±12
mm Hg), whereas mean SBP rose significantly (27%) throughout the 5
decades. In addition, SVRI increased 58% (P<.05) and mean
CI decreased 37% (P<.05) with a mild and nonsignificant
rise in MAP over the third to seventh decade. The mean ratio of SV to
PP decreased 52% (P<.05) over the five decades.
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Hemodynamic Difference Between Systolic
(BSH and ISH) and Diastolic (MMH) Patterns of
Hypertension
Whereas ISH and BSH are more common after the sixth decade of
life, the hemodynamic analysis was confined to
the 55- to 74-year age range (Table 3).
Compared with normotensive control subjects, the three hypertensive
groups had higher SVRI (48% in MMH, 35% in ISH, and 30% in BSH;
P<.05) and lower ratios of SV to PP (30% in MMH, 48% in
ISH, and 34% in BSH; P<.05). However, the CI was similar
among the four groups.
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Compared with MMH, ISH showed a lower ratio of SV to PP (25%, P<.05), whereas BSH showed an intermediate value. SVRI was lower in BSH than in MMH, and the difference did not attain statistical significance in the ISH group (ANOVA and t test).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In these studies, we combined epidemiological and hemodynamic data to learn more about the hemodynamic changes that underlie age-related BP patterns. As in previous studies performed in other occidental countries, data from the present survey showed that the prevalence of MMH increased with age and reached a plateau beyond the sixth decade.6 32 In contrast, the prevalence of ISH showed a steep rise in elderly people. In addition to the increased prevalence of systolic subtypes of hypertension, diastolic hypertension demonstrates a transition toward a disproportionate systolic pattern with aging. After the sixth decade, the MMH pattern exhibits SBP levels in the range seen in ISH.
The age-related change in steady state and pulsatile in hemodynamic determinants of BP reported here agrees with previous results.33 34 35 36 The primary value of this study is the measurement of the concurrent changes in steady-state as well as pulsatile hemodynamic parameters among hypertensive subjects with similar DBP over a wide age range (25 to 75 years). In untreated patients with MMH, SVR increased 47% from the third to the seventh decades despite similar DBP. This hemodynamic phenomenon could be explained by the concurrent decrease in both CO and AC (27% and 45%, respectively). In contrast, SBP increased on average from 143 to 170 mm Hg, reaching a level comparable to that of ISH. A similar trend was observed in treated hypertensive subjects and in the BP survey.
In addition, our older patients with isolated systolic and borderline systolic hypertension showed 35% and 30% higher SVR and 48% and 34% lower AC (the ratio of SV to PP), respectively, compared with age-matched normotensive control subjects. Interestingly, there was no significant difference in the level of SVR between older patients with MMH and those with ISH despite the normal DBP level in the latter group.
The contribution of low AC to ISH pattern has been demonstrated by Simon et al.37 This study confirms that both high SVR and low AC are common features of hypertension in the elderly, either with the diastolic or the isolated systolic form. Also, our results performed in a large population of systolic hypertension (ISH and BSH) confirm previous invasive studies based on smaller samples comparing ISH and normal subjects.38
The hemodynamic data described above are consistent with results obtained with circulation models. These models provide experimental evidence about the effect of isolated changes in a given hemodynamic parameter on systolic and diastolic BP.5 18 19 34 35 36 37 38 39 40 41 Using closed-chest animals, Randall et al showed the effect of isolated changes in AC. Whereas decreased AC caused an increase in systolic pressure and a decrease in diastolic pressure by the same magnitude, the effect on mean pressure was minimal. A significant decrease in CO occurred only when the decrease in compliance was large.5 Based on an electrical model of circulation, Berger and Li39 estimated that under constant flow, the vascular change needed to obtain DBP and SBP levels in the range of ISH could be obtained with a 25% rise in SVR combined with a 50% to 75% reduction in SAC. According to our data, we can speculate that after 4 decades, a young patient with MMH would experience a 19% fall in CI associated with a 36% increase in SVR and a 45% decrease in SAC, remaining within the same DBP range. However, a pattern of ISH could be reached with a 23% increase in SVRI and a 55% decrease in the ratio of SV to PP.
Thus, a reduction in AC with age may offset the predicted effect of the SVR increment on the DBP.5 18 19 39 40 41 The latter, though generally known, is not considered frequently by physicians. In contrast, both the rise in vascular resistance and the reduction in AC have an additive effect on SBP.
Although the increase in SBP, which is included in the computation of SVR through MAP, could exaggerate the increase in SVR, the change in vascular resistance in 78% of mild to moderate hypertensive patients over the 5 decades is attributable to a decrease in systemic blood flow. Only the remaining percentage (22%) can be attributed to a mild, though not a significant, increase in MAP, which is related to the rise in SBP. Furthermore, recent studies support the hypothesis that PP may be one of the major determinants of the structural changes in small vessels during long-term hypertension.43 44 James et al44 showed a significant relation between the media-lumen ratio and the PP independently of the age, MAP, and BP variability in a group of untreated elderly subjects, most of whom were hypertensive. Therefore, the rise in SVR could be the result of structural adaptive changes of resistance of vessels to the high PP. It is also likely that in the presence of low AC and wide PP, SVR may increase to maintain a constant flow in peripheral circulation.
Other possible limitations of the present study are the
assumed value of the right atrial pressure and the determination of PP
from the humeral artery. Even though a mild pulmonary
arterial pressure increases with age in hypertensive
patients, the use of a constant value for right atrial pressure in the
calculation of SVR should attenuate slightly the observed age-related
increase in SVR.42 As underscored by O'Rourke et
al,45 there is a progressive increase in PP and SBP
between the proximal aorta and peripheral arteries as a
consequence of the wave reflection. The difference between central and
peripheral arteries depends on age and results in a
decrease in pulse amplification. Therefore, the true relative
difference in the SV to PP ratio between age groups would probably be
much greater than that reported in this study if the PP had been
obtained from the aorta.45 An invasive study in the aortic
arch, performed primarily in normotensive subjects, found similar
trends in SBP, DBP, and SVR over the age range of 20 to 60
years.46 Aortic systolic pressure increased 25%
and SVR 37% without changes in aortic DBP. The rise in the
characteristic aortic impedance (137%) was much greater than the
change in the ratio of SV to PP observed in our noninvasive study. With
this exception, the study agrees with ours in that it shows that aortic
DBP remains unchanged despite a significant increase in SVR. Thus, it
is unlikely that the stable DBP across the age range depended on the
anatomic site of BP measurement. Our epidemiological data confirm that
auscultatory DBP remains relatively unchanged with age in both
normotensive and MMH subgroups (Fig 1B). This pattern differs from that
observed in the overall population, in which DBP rises until the sixth
decade and then decreases after the seventh decade despite a continuous
increase in SBP (Fig 1A). As shown in Fig 2, the increasing number of
individuals with diastolic hypertension explains the
age-related rise in DBP in the overall population, whereas the increase
in the prevalence of BSH and ISH underlies the later fall in
DBP.
Clinical-Epidemiological Implications
This study provides confirmatory evidence of the limitations
of diastolic pressure to characterize arterial
hypertension, especially in the elderly. Because an increase in SVR and
a decrease in AC have opposite effects on DBP but an additive effect on
SBP, the latter better reflects the underlying circulatory impairment.
This finding agrees with morphological studies that describe in older
subjects an association between subclinical
arteriosclerotic disease and lower DBP and higher
SBP.47 48 49 Therefore, as patients get older, DBP becomes
progressively less related to vascular resistance. This concept is in
contrast to the old clinical management of hypertension based on DBP
values and guided by the assumption that vascular resistance is
positively related to DBP level, without consideration being given to
the patient's age.
As experimental studies suggest, an isolated decrease in AC reduces DBP and increases SBP.5 This change could determine by a reduction in DBP a transition of MMH toward a systolic pattern of hypertension. The size and age ranges of the subjects studied in the present analysis lend support to the hypothesis that the transition in the hypertension pattern from diastolic to systolic may be explained by a change in hemodynamic forces associated with age. The study shows (1) that as mild to moderate hypertensive patients get older, vascular resistance and SBP become higher without change in DBP and (2) that patients with ISH have similar vascular resistance and SBP but lower AC and DBP than older mild to moderate hypertensive patients. On the basis of these findings, it is possible that as patients with MMH get older, DBP decreases below 90 mm Hg.
In addition, in the presence of lower SAC, new hypertensive subjects may emerge as purely systolic despite high SVR, as we documented in BSH and ISH.
This could partially explain why the rise in the prevalence of MMH stops after the sixth decade and is "replaced" by a simultaneous increase in the prevalence of isolated systolic forms of hypertension.
An alternative explanation of why the prevalence of diastolic hypertension tends to be lower with aging is the classic "demographic" interpretation; patients with diastolic hypertension die earlier than patients with ISH because the latter enjoy a better medical condition. However, recent studies have demonstrated that untreated ISH patients are associated with a high rate of morbidity.50 51 The hypothesis that the increase in the prevalence of diastolic hypertension becomes blunted after the sixth decade because of an age-related hemodynamic transition52 is reinforced by the analysis of long-term longitudinal hemodynamic studies.35 53 Examination of the data from the Bergen study shows that those patients aged 17 to 29 years at entry time showed a mild increase in DBP and SBP after 20 years of follow-up. In contrast, the group aged 40 to 49 years at entry showed a transition from the diastolic to the systolic pattern of hypertension. This age-related change in BP pattern at follow-up was associated with a reduction in AC and CI and a rise in vascular resistance.
Furthermore, a recent report documented that a considerable proportion of patients with ISH (treated and untreated) had previous (burned-out) diastolic hypertension.54 Therefore, it is possible that with the passing of time, DBP in some patients could decrease because of worsened circulatory homeostasis instead of a positive response to treatment.
The clinical significance of this observation is reinforced by data from the Multiple Risk Intervention Trial when the relation between mortality from ischemic heart disease and BP parameters are compared at different ages. This study shows that with increasing age, DBP decreases its predictor value for coronary heart disease mortality whereas there is no reduction in the positive relation between ischemic heart disease mortality and SBP with age, and SBP is a stronger predictive factor than DBP in subjects >39 years old.50
In summary, the present results show a simultaneous age-related impairment in vascular resistance and AC in different types of hypertension. These hemodynamic changes could underlie the transition in the prevalence of diastolic and systolic forms of hypertension. Also, our results suggest that SBP, but not DBP, is a reliable indicator of the underlying hemodynamic abnormalities (high resistance and low arterial compliance) in the elderly.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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The authors are grateful to Silvia Yeha for her secretarial assistance.
Received September 9, 1996; first decision October 3, 1996; accepted March 4, 1997.
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References |
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