(Hypertension. 1999;33:800-805.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Stroke Volume/Pulse Pressure Ratio and Cardiovascular Risk in Arterial Hypertension
From the Division of Cardiology, The New York Presbyterian Hospital–Weill Medical College of Cornell University, New York, NY (G.d.S., M.J.R., M.J.K., G.A.M., R.B.D.); the Department of Clinical and Experimental Medicine, Federico II University Hospital, Naples, Italy (G.d.S.); and Institute of Clinical Medicine, University of Sassari (Italy) (A.G.).
Correspondence to Dr Giovanni de Simone, Division of Cardiology, The New York Presbyterian Hospital–Weill Medical College of Cornell University, 525 E 68th St, New York, NY 10021. E-mail simogi{at}unina.it
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Abstract |
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Abstract—Ratio of stroke volume (SV, M-mode echocardiography) to pulse pressure (PP) has been proposed as an estimate of total arterial compliance and has been shown to be related to body size, age, and heart rate in normal adults. SV/PP was estimated in 294 hypertensive patients (98 women) as a raw value by use of SV/body surface area (SVi) and by the ratio of SV/PP to the value predicted by a previously developed equation (%SV/PP). At baseline, the 50 patients who had cardiovascular events over the following 10 years exhibited higher PP and lower SV/PP, SVi/PP, and %SV/PP (all P<0.008) than patients without events. Crude risk of follow-up total and fatal cardiovascular events increased with increasing level of PP and decreasing SV/PP, SVi/PP, and %SV/PP (all P<0.002). In multivariate logistic regression models with continuous covariates, the risk of total cardiovascular events was independently related to increasing age (P<0.0001) and left ventricular (LV) mass index (P<0.003) and decreasing values of %SV/PP (P<0.006) but not to increasing systolic, pulse, or mean blood pressure or gender. Similar although less strong results were obtained with the use of SVi/PP (P<0.02), whereas SV/PP did not enter the model as an independent predictor. Risk of cardiovascular death was only predicted by age and LV mass index. The %SV/PP was also an independent predictor of total cardiovascular events in Cox proportional hazards analysis (exp[b]: 2.49, P<0.001) independent of age (exp[b]: 1.05, P<0.003) and LV mass index (exp[b]: 1.02, P<0.0003), whereas no effect was detected for height. Thus, in patients with arterial hypertension, a reduced ratio of M-mode echocardiographic SV/PP as a percentage of the value predicted by demographic variables is a predictor of cardiovascular morbid events independent of age and LV mass index.
Key Words: hypertension, arterial • echocardiography • cardiac hypertrophy • prognosis • pulse
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Introduction |
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The ratio of stroke volume to pulse pressure (SV/PP) has been proposed as an indirect measure of total arterial compliance,1 2 3 4 simple enough to be used in epidemiological studies, and based on the principle that in a steady-state condition, the arterial tree can be modeled as an elastic chamber with a constant compliance (2-element Windkessel model). This ratio has been recently shown to increase during body growth because of the increased size of the arterial tree, whereas it remains stable during early adulthood, after the end of body growth, and decreases during late adulthood to old age, possibly because of increased arterial stiffness.5
Decreased arterial compliance may be a stimulus for left ventricular (LV) hypertrophy,6 7 8 especially the concentric pattern.9 This association may play a role in the increase in cardiovascular risk associated with the presence of concentric LV hypertrophy.10 Although PP might independently predict cardiovascular risk,11 12 13 14 there is no information on the ability of SV/PP to predict risk or on whether this prediction is independent of LV hypertrophy. Accordingly, this study was designed to investigate whether SV/PP is an independent marker of cardiovascular risk in arterial hypertension.
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Methods |
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Study Population
Direct follow-up or contact with relatives or physicians of patients who died was possible in 294 (91%) of 322 patients initially evaluated by echocardiography at New York Hospital–Cornell Medical Center between 1976 and 1986 and found eligible for this longitudinal trial. Detailed information about this cohort has been reported extensively.9 15 16
Echocardiography
Two-dimensionally targeted M-mode echocardiograms were performed
as previously described.17 18 19 20 21 22 23 LV
end-diastolic and end-systolic volumes were
calculated with the Z-derived method,24
which exhibited a high accuracy for M-mode LV volume calculation even
in the presence of dilated LV cavities. SV was calculated in
milliliters per beat as end-diastolic minus
end-systolic volume and normalized for body surface area
(stroke index).25 Reproducibility of various
echocardiographic quantitative parameters
has been reported in previous works18 26 as well as more
recently.27 28 Reproducibility of PP was assessed with the
data set of the Reproducibility Echocardiographic
Study28 by single-measure intraclass correlation of
measurements performed by a single observer 3 to 10 days apart (n=261,
Ri=0.87).
SV/PP Estimation
Blood pressure (BP) was measured at the first and fifth
Korotkoff phases with the use of an arm-cuff sphygmomanometer at the
end of the initial echocardiograms. Brachial PP was calculated as the
difference between systolic and diastolic BP and
used as a raw inverse estimate of total arterial
compliance29 together with SV/PP and the ratios of stroke
index to pulse pressure (SVi/PP). The value of SV/PP (mL ·
beat-1 ·
mm Hg-1) was also compared with the value
predicted by a multiple regression equation developed in 393
normotensive, normal-weight adults previously studied with the use of
Teichholz's method to determine LV volumes.5 The new
equation developed with the use of the Z-derived method of
calculation of LV volumes in the same population24
was
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Because of the known decline with age of PP augmentation from the
central aorta to the peripheral arteries, the central PP
determined by carotid aplanation tonometry6 7 8 9 was
estimated with the use of a regression equation with brachial pressure
(in mm Hg) and age (in years) in 145 unmedicated hypertensive
patients and 85 normotensive subjects studied in our laboratory:
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Statistical Analysis
Data were analyzed with commercially available
statistical packages. Standard analyses were carried out with
the use of 1-way ANOVA with the step-down multiple-stage F
post hoc test (Ryan-Einot-Gabriel-Welsch F
test)30 and least-squares linear regression.
Differences between regression lines were tested by computing
F statistics of between-slopes sum of squares of
standardized variables.31
Discriminant analysis based on logistic regression was used to identify variables that independently predicted cardiovascular morbid events or death by computing the exponential of the coefficients of regression (which is equivalent to a relative risk) and the relative 95% confidence limit. A stepwise procedure (forward conditional) was adopted using continuous variables and gender as a discrete variable (1=women, 2=men). To compute positive coefficients of regression consistent with those obtained with the other variables, SV/PP, SVi/PP, and the ratio of observed-to-predicted SV/PP entered the models in the form of their inverse values (ie, 1/[SV/PP]=PP/SV).
Product-limit Kaplan-Meyer estimation of survival functions and Cox proportional hazard analysis were computed for patients with normal or reduced %predicted SV/PP.
The null hypothesis was rejected at a 2-tailed value of P<0.05
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Results |
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Hypertensive patients were followed through a mean 10-year period. During the follow-up, 50 (17%)subjects experienced at least 1 cardiovascular complication, and 14 of them died.16
Table 1 shows that the subgroup of patients who had fatal or nonfatal cardiovascular events were older (P<0.0001) and had higher body mass index (P<0.02), systolic, diastolic, and pulse pressures (all P<0.002), and lower SV/PP, SVi/PP, and %predicted SV/PP (P<0.007) than event-free patients. Only age and systolic and pulse pressure were higher in patients with follow-up fatal cardiovascular events (all P<0.0001).
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Unadjusted Relative Risk
Risk of cardiovascular morbidity or mortality
increased by 3% and 4%, respectively, for each mm Hg of
increase in PP[exp(b) (95% confidence interval)=1.03 (1.01 to 1.05)
and 1.04 (1.02 to 1.07), respectively, both P<0.001], by
5% and 6% for each 0.1 mL/mm Hg decrease in SV/PP ratio
[exp(b)=4.97 (2.07 to 11.92), P<0.0003, and 5.96 (1.88 to
18.89), P<0.002, respectively]. With the use of SVi/PP,
risk of both total cardiovascular events and fatal
events increased by 3% for each 0.1 mL ·
m2 · mm Hg-1
[exp(b)=3.02 (1.80 to 5.09), P<0.0001 and 3.04 (1.54 to
6.02), P<0.002, respectively]. Similarly, risk of
cardiovascular morbidity and mortality increased by
4% for each unit of decrease in %predicted SV/PP [exp(b)=3.74
(1.98 to 7.02), P<0.0001 and 4.13 (1.72 to 9.92),
P<0.002, respectively].
Multivariate Analysis for Prediction of
Cardiovascular Risk
Multiple logistic regression was used to detect the independent
effect of SV/PP, SVi/PP, and %predicted SV/PP in separate models that
also included systolic BP, age, gender, and LV mass
index. In addition to age
(P<0.0001) and LV mass index (P<0.005),
decrease in %predicted SV/PP was independently related to the risk of
all cardiovascular events (P<0.001) (Table 2). Similar results were attained with the SVi/PP [exp(b)=1.94/
mL · m2 ·
mm Hg-1 decrease (1.12 to 3.35),
P<0.02]. SV/PP did not remain an independent predictor of
total and fatal cardiovascular events after
consideration of age and LV mass index.
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Other discriminant models were also generated for SVi/PP and %predicted SV/PP, substituting systolic BP with PP or mean BP, and the results were identical as with systolic BP. In every model, the iteration history showed that after age, LV mass index entered as the second most powerful predictor, followed negatively by %predicted SV/PP, which exhibited a residual association with adverse events higher than either systolic, pulse, or mean pressure. For instance, after age and LV mass index, the r-to-enter of %predicted SV/PP was 0.13 (P<0.01), higher than that of systolic BP (r=0.09, P<0.04). After the entry of %predicted SV/PP into the model, the residual r-to-enter of systolic BP was close to 0, with P>0.5. Interestingly, the exp(b) of age and LV mass index were not reduced by the entry of %predicted SV/PP as the third variable into the model (1.07 and 1.03, respectively, in the model with systolic BP, before entry of %predicted SV/PP).
Risk of cardiovascular death was only predicted by age and LV mass index in all models including SVi/PP or %predicted SV/PP and also including systolic BP (or PP or mean BP) and gender.
Time-Dependent Procedures
The inverse of %predicted SV/PP was evaluated in Cox proportional
hazard analysis. Patients were classified in relation to the
5th percentile of the distribution in the reference
population5 to generate survival curves
(Figure). A low value of %predicted
SV/PP was found in 100 patients, and among them 26 had follow-up
adverse events (odds ratio=2.5 [1.3 to 4.6], P<0.005). As
shown in the Figure, after adjusting for age, LV mass, and
height (as another potential predictor of
cardiovascular risk), event-free survival was lower in
patients with %predicted SV/PP from 4 years after enrollment to the
end of follow-up. The inverse of %predicted SV/PP was used as a
continuous variable for final Cox model. The probability of future
cardiovascular events increased with decreasing
%predicted SV/PP [exp(b)=2.49 (1.37 to 4.54), P<0.003],
independent of age [exp(b)=1.05 (1.02 to 1.08), P<0.002]
and LV mass index [exp(b)=1.02 (1.01 to 1.03), P<0.0003],
whereas height did not enter the model.
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Relation to Measures of LV Geometry
LV mass index was related to systolic BP
(r=0.29, P<0.0001) and more weakly to PP
(r=0.16, P<0.005) but not to SV/PP, SVi/PP, or
%predicted SV/PP (all r<0.02). In contrast, relative wall
thickness was more closely related to SV/PP (r=-0.29,
P<0.0001), SVi/PP (r=-0.31,
P<0.0001), and %predicted SV/PP (r=-0.31,
P<0.0001) than to systolic BP (r=0.18,
standardized slope differences calculated with the inverse of
systolic BP: all P<0.005) or to PP
(r=0.03).
Table 3 shows that the severity of BP elevation was associated with the presence of LV hypertrophy, whereas reduced SV/PP-based measures were associated with concentric LV geometry either with or without an increase in LV mass. Eccentric LV hypertrophy was associated with higher levels of SV/PP-based measures. It is noteworthy that PP was not significantly different among patients with the 4 LV geometric patterns.
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Discussion |
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The SV/PP has a physiological basis in the 2-element Windkessel model.4 32 However, stroke volume includes part of blood ejected after that the pressure curve reaches its peak, whereas to reproduce the 2-element Windkessel model, only the part of blood ejected within the time of peak pressure should be measured. Because the value of SV is higher than the volume stored at each systole, the assumption made for use of SV/PP is that SV is closely related to the volume stored in the arterial tree at each systole.
Another limitation of the calculation of SV/PP is the use of
peripheral instead of central PP. We studied the relation
between central and peripheral PP by using age in the
regression model as the variable mostly affecting the difference.
However, only 40% of variance could be explained by that model, and
the extent of this relation did not change by adding height and gender
as independent correlates. Thus, other variables and/or method
error not considered in the regression model may influence differences
between central and peripheral pulse pressure. Accordingly,
a more direct measure of central PP may be needed to further improve
the predictive value of the index proposed in the current study.
Calibrated carotid tonometry merged with ultrasound
arterial wall identification provides more direct measures
of the compliance of conduit arteries than the simple calculation of
SV/PP.9 33 34 A major advantage of this direct method is
the elimination of the age-dependent decline in the overestimation of
central PP by peripheral measurements in young individuals,
which results in underestimation of systemic arterial
compliance by the SV/PP. In this study, this error has been in part
attenuated by using the multiple regression equation including age.
Keeping in mind the above considerations, in previous studies we demonstrated that in adults, body size is an important covariate of SV/PP,5 35 more important than gender, paralleling the known association between body size and the size of the aorta.36 Therefore, the physiological effect of body size on SV/PP needs to be taken into account when a clinical application of this ratio is attempted.
There are several studies addressing the potential independent negative prognostic implication of decreased arterial compliance. In addition to data suggesting an adverse effect of high PP,11 12 13 14 37 reduced arterial compliance measured through more direct methods has been reported to be related to concentric LV hypertrophy,9 cardiovascular risk factors,38 and prevalent cerebrovascular disease.39
SV/PP as an Independent Marker of Cardiovascular Risk
When the effects of age, body size, and heart rate on the
SV/PP ratio are taken into account, this measure was a marker of
cardiovascular risk independent of age, height, and LV
mass index in the present series of patients with
arterial hypertension. The predictive value of the adjusted
SV/PP was greater than that of systolic BP or PP, a biological
variable associated with SV/PP and measures of arterial
compliance.40 41 42
In the context of a limited range of BP as seen in a purely hypertensive population, SV/PP-based variables may be prognostically more important than isolated BP measurements because their variability has not been constrained by diagnostic criteria. The coefficient of variability of systolic BP in the whole study population was 13.9% compared with 33.5% for SV/PP as percentage of predicted (P<0.0001). Thus in hypertension, SV/PP-based measures may be more important for prediction of cardiovascular events than measures of arterial pressure because their biological variability is higher (in part because of the flow component). Accordingly, the present results should be interpreted in the context of the type of population studied and cannot be automatically generalized to unselected populations.
From the prognostic point of view, the use of SV/PP as a %predicted increased the prediction of cardiovascular complications of arterial hypertension compared with use of the simpler SVi/PP. The inclusion of age, body size, and heart rate in the computation of %predicted SV/PP might have strengthened the relation with adverse events because each of these covariates has been related to adverse outcome in patients with cardiovascular disease. Moreover, further adjustment for age may attenuate or eliminate the overestimation of central PP by peripheral measurements in young, disease-free individuals.
The finding of an independent relation of SV/PP-based measures to cardiovascular morbidity has not been previously reported but is not surprising. Interestingly, similar to previous studies,9 whereas BP is more associated with increased LV mass, SV/PP-based measures are more related to concentric LV geometric patterns43 and may contribute to explaining the relatively higher risk associated with these patterns.10 44 45 There was not a statistically independent effect of low %predicted SV/PP on cardiovascular mortality in our study population, but the lack of this association might be due to both the relatively small number of cardiovascular deaths and the strong association between LV hypertrophy and the occurrence of cardiovascular death that has been previously reported.10 16 46
Conclusions
Reduced values of the ratio between SV and PP as a percentage of
predicted by individual body size, age, and heart rate is a predictor
of cardiovascular morbidity independent of age and
presence of LV hypertrophy in arterial
hypertension. Studies on more direct indexes of arterial
stiffness should be advisable to detect the interest of this
parameter in the prediction of
cardiovascular risk.
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Acknowledgments |
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This study was supported in part by grant HL-18323 from the National Heart, Lung, and Blood Institute, Bethesda, Md.
Received August 4, 1998; first decision September 1, 1998; accepted November 30, 1998.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Tarazi RC, Magrini F, Dustan HP. The role of aortic distensibility in hypertension. In: Milliez P, Safar M, eds. Recent Advances in Hypertension. Reims, France: Laboratories Boerhinger Ingelheim; 1975:133–142.
2. Ferguson JJ, Julius S, Randall OS. Stroke volume-pulse pressure relationships in borderline hypertension: a possible indicator of decreased arterial compliance. J Hypertens. 1984;2(suppl):s397–s399.
3. Randall OS, Westerhof N, van den Bos GC, Alexander B. Reliability of stroke volume to pulse pressure ratio for estimating and detecting changes in arterial compliance. J Hypertens. 1986;4(suppl):s293–s296.
4.
Stergiopulos N, Meister JJ, Westerhof N. Evaluation of
methods for estimation of total arterial compliance.
Am J Physiol. 1995;268:H1540–H1548.
5.
de Simone G, Roman MJ, Daniels SR, Mureddu GF, Kimball
TR, Greco R, Devereux RB. Age-related changes in total
arterial capacitance from birth to maturity in a
normotensive population. Hypertension. 1997;29:1213–1217.
6.
Roman MJ, Saba PS, Pini R, Spitzer M, Pickering TG,
Rosen S, Alderman MH, Devereux RB. Parallel cardiac and vascular
adaptation in hypertension. Circulation. 1992;86:1909–1918.
7. Saba PS, Roman MJ, Pini R, Spitzer M, Ganau A, Devereux RB. Relation of arterial pressure waveform to LV and carotid anatomy in normotensive subjects. J Am Coll Cardiol. 1993;22:1873–1880.[Abstract]
8. Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Association of carotid atherosclerosis and left ventricular hypertrophy. J Am Coll Cardiol. 1995;25:83–90.[Abstract]
9. Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Relation of arterial structure and function to left ventricular geometric patterns in hypertensive adults. J Am Coll Cardiol. 1996;28:751–756.[Abstract]
10. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med. 1991;114:345–352.
11.
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.
12.
Selker HP, Beshansky JR, Schmid CH, Griffith JL,
Longstreth WT Jr, O'Connor CM, Caplan LR, Massey EW, D'Agostino RB,
Laks MM, Lee KL, Maynard C, Wagner GS, Weaver WD, Califf RM.
Presenting pulse pressure predicts thrombolytic
therapy–related intracranial hemorrhage:
Thrombolytic Predictive Instrument (TPI) Project
results. Circulation. 1994;90:1657–1661.
13. Franklin SS, Sutton-Tyrrell K, Belle SH, Weber MA, Kuller LH. The importance of pulsatile components of hypertension in predicting carotid stenosis in older adults. J Hypertens. 1997;15:1143–1150.[Medline] [Order article via Infotrieve]
14.
Mitchell GF, Moyè LA, Braunwald E, Rouleau JL,
Bernstein V, Geltman EM, Flaker GC, Pfeffer MA, for the SAVE
investigators. Sphygmomanometrically determined pulse pressure is a
powerful independent predictor of recurrent events after myocardial
infarction in patients with impaired left ventricular
function. Circulation. 1997;96:4254–4260.
15. Mensah GA, Pappas TW, Koren MJ, Ulin RJ, Laragh JH, Devereux RB. Comparison of classification of hypertension severity by blood pressure level and World Health Organization criteria for prediction of concurrent cardiac abnormalities and subsequent complications in essential hypertension. J Hypertens. 1993;11:1429–1440.[Medline] [Order article via Infotrieve]
16.
de Simone G, Devereux RB, Koren MH, Mensah GA, Casale
PN, Laragh JH. Midwall left ventricular mechanics: an
independent predictor of cardiovascular risk in
arterial hypertension. Circulation. 1996;93:259–265.
17.
Devereux RB, Savage DD, Drayer JIM, Laragh JH. Left
ventricular hypertrophy and function in
patients with high, normal and low-renin forms of essential
hypertension. Hypertension. 1982;4:524–531.
18. Wallerson DC, Devereux RB. Reproducibility of echocardiographic left ventricular measurements. Hypertension. 1987;9(suppl 2):6–18.
19. de Simone G, Devereux RB, Roman MJ, Ganau A, Saba PS, Alderman MH, Laragh JH. Assessment of left ventricular function by the midwall fractional shortening/end-systolic stress relation in human hypertension. J Am Coll Cardiol. 1994;23:1444–1451.[Abstract]
20.
Sahn DJ, DeMaria A, Kisslo J, Weyman A. The Committee
on M-Mode Standardization of the American Society of
Echocardiography: Recommendations regarding
quantitation in M-mode echocardiography: results of
a survey of echocardiographic measurements.
Circulation. 1978;58:1072–1083.
21.
Devereux RB, Reichek N.
Echocardiographic determination of left
ventricular mass in men: anatomic validation of the method.
Circulation. 1977;55:613–618.
22. de Simone G, Daniels SR, Devereux RB, Meyer RA, Roman MJ, de Divitiis O, Alderman MH. Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and of the impact of overweight. J Am Coll Cardiol. 1992;20:1251–1260.[Abstract]
23. Ganau A, Devereux RB, Roman MJ, de Simone G, Saba PS, Vargiu P, Simongini I, Laragh JH. Patterns of left ventricular hypertrophy and geometric remodeling in arterial hypertension. J Am Coll Cardiol. 1992;19:1550–1558.[Abstract]
24. de Simone G, Devereux RB, Ganau A, Hahn RT, Saba PS, Mureddu GF, Roman MJ, Howard BV. Estimation of left ventricular chamber and stroke volume by limited M-mode echocardiography: validation by 2-dimensional and Doppler-echocardiography. Am J Cardiol. 1996;78:801–807.[Medline] [Order article via Infotrieve]
25.
de Simone G, Devereux RB, Daniels SR, Mureddu GF, Roman
MJ, Kimball TR, Greco R, Witt S, Contaldo F. Stroke volume and cardiac
output in normotensive children and adults: assessment of relations
with body size and impact of obesity. Circulation. 1997;95:1837–1843.
26. de Simone G, Ganau A, Verdecchia P, Devereux RB. Echocardiography in arterial hypertension: when, why and how? J Hypertens. 1994;12(10):1129–1136.
27. Palmieri V, Bella LN, Fishman D, Paranicas M, Dahlof B, DeQuattro V, Sharpe N, de Simone G, Devereux RB. Intra-individual Reliability of Echocardiographic assessment of Left Ventricular (LV) mass, geometry and systolic function: the PRESERVE Trial. Circulation. 1998;17(suppl I):I-29. Abstract.
28. de Simone G, Muiesan ML, Ganau A, Longhini C, Verdecchia P, Palmieri V, Agabiti-Rosei E, Mancia G, on behalf of the Working Group on Heart and Hypertension of Italian Society of Hypertension. Reliability of measurements of left ventricular mass in single patients: the Reproducibility Echocardiographic Study (RES). High Blood Pressure. 1998;7(suppl 2):2. Abstract.
29. Stergiopulos N, Meister JJ, Westerhof N. Simple and accurate way for estimating total and segmental arterial compliance: the pulse pressure method. Ann Biomed Eng. 1994;22:392–397.[Medline] [Order article via Infotrieve]
30. SPSS Base System. Reference Guide. Release 6.0. Chicago, Ill: SPSS Inc; 1993.
31.
de Simone G, Devereux RB, Daniels SR, Meyer RA. Gender
differences in cardiac growth. Hypertension. 1995;26:979–983.
32. Madkour MA, Levenson J, Bravo EL, Simon A, Fouad-Tarazi FM. Preload, adrenergic activity and aortic compliance in normal and hypertensive patients. Am Heart J. 1989;118:1243–1247.[Medline] [Order article via Infotrieve]
33. Roman MJ, Pini R, Pickering TG, Devereux RB. Non-invasive measurements of arterial compliance in hypertensive compared with normotensive adults. J Hypertens. 1992;10(suppl):S115–S118.
34.
Chen CH, Ting CT, Nussbacher A, Nevo E, Kass DA, Pak P,
Wang SP, Chang MS, Yin FC. Validation of carotid artery tonometry as a
means of estimating augmentation index of ascending aortic pressure.
Hypertension. 1996;27:168–175.
35. Oren S, Grossman E, Frohlich ED. Arterial and venous compliance in obese and nonobese subjects. Am J Cardiol. 1996;77:665–667.[Medline] [Order article via Infotrieve]
36. Roman MJ, Devereux RB, Kramer-Fox R, O'Loughlin J, Spitzer M, Robins J. Two-dimensional echocardiographic aortic root dimensions in normal children and adults. Am J Cardiol. 1989;64:507–512.[Medline] [Order article via Infotrieve]
37.
Madhavan S, Ooi WL, Cohen H, Alderman MH. Relation of
pulse pressure and blood pressure reduction to the incidence of
myocardial infarction. Hypertension. 1996;23:395–401.
38. Taquet A, Bonithop-Kopp C, Simon A, Levenson J, Scarabin Y, Malmejac A, Dicimetiere P, Guize L. Relations of cardiovascular risk factors to aortic pulse wave velocity in asymptomatic middle-aged women. Eur J Epidemiol. 1993;9:298–306.[Medline] [Order article via Infotrieve]
39. Lehmann ED, Hopkins KD, Jones RL, Rudd AG, Gosling RG. Aortic distensibility in patients with cerebrovascular disease. Clin Sci. 1995;89:247–253.[Medline] [Order article via Infotrieve]
40. Reneman RS, Hoeks AP. Arterial distensibility and compliance in hypertension. Neth J Med. 1995;47:152–161.[Medline] [Order article via Infotrieve]
41. Li JK, Zhu Y. Arterial compliance and its pressure dependence in hypertension and vasodilation. Angiology. 1994;45:113–117.
42. Saba PS, Roman MJ, Ganau A, Pini R, Jones EC, Pickering TG, Devereux RB. Relationship of effective arterial elastance to demographic and arterial characteristics in normotensive and hypertensive adults. J Hypertens. 1995;13:971–977.[Medline] [Order article via Infotrieve]
43. Roman MJ, Saba PS, Ganau A, Pini R, Pickering TG, Devereux RB. Arterial stiffening results in remodeling but not hypertrophy of the left ventricle. Circulation. 1997;96(suppl I):I-600. Abstract.
44. Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Gattobigio R, Zampi I, Santucci A, Santucci C, Reboldi G, Porcellati C. Prognostic value of left ventricular mass and geometry in systemic hypertension with left ventricular hypertrophy. Am J Cardiol. 1996;78:197–202.[Medline] [Order article via Infotrieve]
45. Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Battistelli M, Bartoccini C, Santucci A, Santucci C, Reboldi G, Porcellati C. Adverse prognostic significance of concentric remodeling of the left ventricle in hypertensive patients with normal left ventricular mass. J Am Coll Cardiol. 1995;25:871–878.[Abstract]
46.
Liao Y, Cooper RS, McGee DL, Mensah GA, Ghali JK. The
relative effects of left ventricular
hypertrophy, coronary artery disease, and
ventricular dysfunction on survival among black adults.
JAMA. 1995;273:1592–1597.
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 F. Antonini-Canterin, S. Carerj, V. Di Bello, G. Di Salvo, S. La Carrubba, O. Vriz, D. Pavan, A. Balbarini, G. L. Nicolosi, and On behalf of the Research Group of the Italian Soc Arterial stiffness and ventricular stiffness: a couple of diseases or a coupling disease? A review from the cardiologist's point of view Eur J Echocardiogr, January 1, 2009; 10(1): 36 - 43. [Abstract] [Full Text] [PDF]
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 L. F. Drager, L. A. Bortolotto, E. M. Krieger, and G. Lorenzi-Filho Additive Effects of Obstructive Sleep Apnea and Hypertension on Early Markers of Carotid Atherosclerosis Hypertension, January 1, 2009; 53(1): 64 - 69. [Abstract] [Full Text] [PDF]
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L. H.G. Henskens, A. A. Kroon, R. J. van Oostenbrugge, E. H.B.M. Gronenschild, M. M.J.J. Fuss-Lejeune, P. A.M. Hofman, J. Lodder, and P. W. de Leeuw Increased Aortic Pulse Wave Velocity Is Associated With Silent Cerebral Small-Vessel Disease in Hypertensive Patients Hypertension, December 1, 2008; 52(6): 1120 - 1126. [Abstract] [Full Text] [PDF]
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 H. Qiu, C. Depre, K. Ghosh, R. G. Resuello, F. F. Natividad, F. Rossi, A. Peppas, Y.-T. Shen, D. E. Vatner, and S. F. Vatner Mechanism of Gender-Specific Differences in Aortic Stiffness With Aging in Nonhuman Primates Circulation, August 7, 2007; 116(6): 669 - 676. [Abstract] [Full Text] [PDF]
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 L. F. Drager, L. A. Bortolotto, A. C. Figueiredo, B. C. Silva, E. M. Krieger, and G. Lorenzi-Filho Obstructive Sleep Apnea, Hypertension, and Their Interaction on Arterial Stiffness and Heart Remodeling Chest, May 1, 2007; 131(5): 1379 - 1386. [Abstract] [Full Text] [PDF]
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 K. Noma, C. Goto, K. Nishioka, D. Jitsuiki, T. Umemura, K. Ueda, M. Kimura, K. Nakagawa, T. Oshima, K. Chayama, et al. Roles of Rho-Associated Kinase and Oxidative Stress in the Pathogenesis of Aortic Stiffness J. Am. Coll. Cardiol., February 13, 2007; 49(6): 698 - 705. [Abstract] [Full Text] [PDF]
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 S. Laurent, J. Cockcroft, L. Van Bortel, P. Boutouyrie, C. Giannattasio, D. Hayoz, B. Pannier, C. Vlachopoulos, I. Wilkinson, H. Struijker-Boudier, et al. Expert consensus document on arterial stiffness: methodological issues and clinical applications Eur. Heart J., November 1, 2006; 27(21): 2588 - 2605. [Abstract] [Full Text] [PDF]
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 D. Jegger, R. da Silva, X. Jeanrenaud, M. Nasratullah, H. Tevaearai, L. K. von Segesser, P. Segers, V. Gaillard, J. Atkinson, I. Lartaud, et al. Ventricular-arterial coupling in a rat model of reduced arterial compliance provoked by hypervitaminosis D and nicotine Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1942 - H1951. [Abstract] [Full Text] [PDF]
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E. Dolan, L. Thijs, Y. Li, N. Atkins, P. McCormack, S. McClory, E. O'Brien, J. A. Staessen, and A. V. Stanton Ambulatory Arterial Stiffness Index as a Predictor of Cardiovascular Mortality in the Dublin Outcome Study Hypertension, March 1, 2006; 47(3): 365 - 370. [Abstract] [Full Text] [PDF]
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 L. F. Drager, L. A. Bortolotto, M. C. Lorenzi, A. C. Figueiredo, E. M. Krieger, and G. Lorenzi-Filho Early Signs of Atherosclerosis in Obstructive Sleep Apnea Am. J. Respir. Crit. Care Med., September 1, 2005; 172(5): 613 - 618. [Abstract] [Full Text] [PDF]
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M. Briand, J. G. Dumesnil, L. Kadem, A. G. Tongue, R. Rieu, D. Garcia, and P. Pibarot Reduced Systemic Arterial Compliance Impacts Significantly on Left Ventricular Afterload and Function in Aortic Stenosis: Implications for Diagnosis and Treatment J. Am. Coll. Cardiol., July 19, 2005; 46(2): 291 - 298. [Abstract] [Full Text] [PDF]
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D. Chemla, A. Nitenberg, and G. de Simone Can We Afford Crude Estimates of Central Pulse Pressure? Hypertension, June 1, 2005; 45(6): e22 - e22. [Full Text] [PDF]
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H. Senzaki, C.-H. Chen, H. Ishido, S. Masutani, T. Matsunaga, M. Taketazu, T. Kobayashi, N. Sasaki, S. Kyo, and Y. Yokote Arterial Hemodynamics in Patients After Kawasaki Disease Circulation, April 26, 2005; 111(16): 2119 - 2125. [Abstract] [Full Text] [PDF]
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G. de Simone, M. J. Roman, M. H. Alderman, M. Galderisi, O. de Divitiis, and R. B. Devereux Is High Pulse Pressure a Marker of Preclinical Cardiovascular Disease? Hypertension, April 1, 2005; 45(4): 575 - 579. [Abstract] [Full Text] [PDF]
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 L Kadem, J G Dumesnil, R Rieu, L-G Durand, D Garcia, and P Pibarot Impact of systemic hypertension on the assessment of aortic stenosis Heart, March 1, 2005; 91(3): 354 - 361. [Abstract] [Full Text] [PDF]
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 M. R. Rinder, R. J. Spina, L. R. Peterson, C. J. Koenig, C. R. Florence, and A. A. Ehsani Comparison of effects of exercise and diuretic on left ventricular geometry, mass, and insulin resistance in older hypertensive adults Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2004; 287(2): R360 - R368. [Abstract] [Full Text] [PDF]
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A. Y. Bagrov and E. G. Lakatta The Dietary Sodium-Blood Pressure Plot "Stiffens" Hypertension, July 1, 2004; 44(1): 22 - 24. [Full Text] [PDF]
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A. Scuteri, S. S. Najjar, D. C. Muller, R. Andres, H. Hougaku, E. J. Metter, and E. G. Lakatta Metabolic syndrome amplifies the age-associated increases in vascular thickness and stiffness J. Am. Coll. Cardiol., April 21, 2004; 43(8): 1388 - 1395. [Abstract] [Full Text] [PDF]
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P. Fesler, G. du Cailar, J. Ribstein, and A. Mimran Heterogeneity of Cardiorenal Characteristics in Normotensive Subjects Hypertension, February 1, 2004; 43(2): 219 - 223. [Abstract] [Full Text] [PDF]
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E. G. Lakatta and D. Levy Arterial and Cardiac Aging: Major Shareholders in Cardiovascular Disease Enterprises: Part I: Aging Arteries: A "Set Up" for Vascular Disease Circulation, January 7, 2003; 107(1): 139 - 146. [Full Text] [PDF]
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 K. E. North, J. W. MacCluer, R. B. Devereux, B. V. Howard, T. K. Welty, L. G. Best, E. T. Lee, R. R. Fabsitz, and M. J. Roman Heritability of Carotid Artery Structure and Function: The Strong Heart Family Study Arterioscler. Thromb. Vasc. Biol., October 1, 2002; 22(10): 1698 - 1703. [Abstract] [Full Text] [PDF]
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P. Boutouyrie, A. I. Tropeano, R. Asmar, I. Gautier, A. Benetos, P. Lacolley, and S. Laurent Aortic Stiffness Is an Independent Predictor of Primary Coronary Events in Hypertensive Patients: A Longitudinal Study Hypertension, January 1, 2002; 39(1): 10 - 15. [Abstract] [Full Text] [PDF]
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V. Palmieri, A. Celentano, M. J. Roman, G. de Simone, M. R. Lewis, L. Best, E. T. Lee, D. C. Robbins, B. V. Howard, and R. B. Devereux Fibrinogen and Preclinical Echocardiographic Target Organ Damage: The Strong Heart Study Hypertension, November 1, 2001; 38(5): 1068 - 1074. [Abstract] [Full Text] [PDF]
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L. M.A.B. Van Bortel, H. A.J. Struijker-Boudier, and M. E. Safar Pulse Pressure, Arterial Stiffness, and Drug Treatment of Hypertension Hypertension, October 1, 2001; 38(4): 914 - 921. [Abstract] [Full Text] [PDF]
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R. H. Fagard, K. Pardaens, J. A. Staessen, and L. Thijs The pulse pressure-to-stroke index ratio predicts cardiovascular events and death in uncomplicated hypertension J. Am. Coll. Cardiol., July 1, 2001; 38(1): 227 - 231. [Abstract] [Full Text] [PDF]
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S. Laurent, P. Boutouyrie, R. Asmar, I. Gautier, B. Laloux, L. Guize, P. Ducimetiere, and A. Benetos Aortic Stiffness Is an Independent Predictor of All-Cause and Cardiovascular Mortality in Hypertensive Patients Hypertension, May 1, 2001; 37(5): 1236 - 1241. [Abstract] [Full Text] [PDF]
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M. A. Weber, J. M. Neutel, and D. H. G. Smith Contrasting clinical properties and exercise responses in obese and lean hypertensive patients J. Am. Coll. Cardiol., January 1, 2001; 37(1): 169 - 174. [Abstract] [Full Text] [PDF]
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