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(Circulation. 1997;96:4254-4260.)
© 1997 American Heart Association, Inc.
Articles |
Sphygmomanometrically Determined Pulse Pressure Is a Powerful Independent Predictor of Recurrent Events After Myocardial Infarction in Patients With Impaired Left Ventricular Function
From the Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (G.F.M., E.B., M.A.P.); the University of Texas Health Science Center and the School of Public Health, Houston (L.A.M.); the Institut de Cardiologie de Montreal, Québec (J.-L.R.), the University of British Columbia, Vancouver, British Columbia (V.B.); Washington University School of Medicine, St Louis, Mo (E.M.G.); and the University of Missouri Health Science Center, Columbia (G.C.F.).
Correspondence to Gary F. Mitchell, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail gfmitchell{at}bics.bwh.harvard.edu
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Abstract |
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Background There is increasing evidence of a link between conduit vessel stiffness and cardiovascular events, although the association has never been tested in a large post–myocardial infarction patient population.
Methods and Results We evaluated the relationship between baseline pulse pressure, measured by sphygmomanometry 3 to 16 days after myocardial infarction, and subsequent adverse clinical events in the 2231 patients enrolled in the SAVE Trial. Increased pulse pressure was associated with increased age, left ventricular ejection fraction, female sex, history of prior infarction, diabetes, and hypertension and use of digoxin and calcium channel blockers. Over a 42-month period, there were 503 deaths, 422 cardiovascular deaths, and 303 myocardial infarctions. Pulse pressure was significantly related to each of these end points as a univariate predictor. In a multivariate analysis, pulse pressure remained a significant predictor of total mortality (relative risk, 1.08 per 10 mm Hg increment in pulse pressure; 95% CI, 1.00 to 1.17; P<.05) and recurrent myocardial infarction (relative risk, 1.12; 95% CI, 1.01 to 1.23; P<.05) after control for age; left ventricular ejection fraction; mean arterial pressure; sex; treatment arm (captopril or placebo); smoking history; history of prior myocardial infarction, diabetes, or hypertension; and treatment with ß-blockers, calcium channel blockers, digoxin, aspirin, or thrombolytic therapy.
Conclusions These data provide strong evidence for a link between pulse pressure, which is related to conduit vessel stiffness, and subsequent cardiovascular events after myocardial infarction in patients with left ventricular dysfunction.
Key Words: hemodynamics • arteriosclerosis • risk factors • atherosclerosis • aging
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Introduction |
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There is increasing evidence of a link between stiffness of the conduit vessels and cardiovascular morbidity. Measures of aortic stiffness have been demonstrated to be associated with left ventricular hypertrophy,1 myocardial infarction,2,3 and stroke4 in normotensive and hypertensive populations. The association between conduit vessel stiffness and recurrent cardiac events after myocardial infarction has not been evaluated, despite a number of factors that suggest such an association. Stiffening of the conduit vessels increases pulse-wave velocity, which results in premature return of the reflected pressure wave to the heart during systole. The reflected pressure wave adds to the forward wave and increases load on the heart, whereas the reflected flow wave diminishes forward flow and stroke volume.5 The impaired ventricle, with a reduced end-systolic elastance, may be sensitized to this incremental late-systolic load, resulting in a reduction in stroke volume.6 Movement of the reflected wave from diastole into systole diminishes coronary perfusion pressure and has been shown to produce ischemia in animal models both with7 and without8 epicardial coronary stenoses. This is particularly important in impaired hearts, in which elevated filling pressures may further limit coronary perfusion pressure and vasodilatory reserve.9 Finally, increased levels of pulse pressure have been implicated in the development and progression of large-vessel atherosclerosis10 and small-vessel disease.11–13 The present study evaluates the relationship between pulse pressure determined by sphygmomanometry, a simple and readily obtainable correlate of conduit vessel stiffness, and recurrent cardiovascular events in a large, prospectively followed population of survivors of a myocardial infarction.
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Methods |
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The Survival and Ventricular Enlargement (SAVE) trial was a randomized, double-blind, placebo-controlled trial designed to determine whether long-term therapy with the ACE inhibitor captopril would improve survival in patients with significant left ventricular dysfunction but without overt heart failure after myocardial infarction.14 Patients 21 to 80 years of age with a radionuclide left ventricular ejection fraction of
40% were randomized 3
to 16 (mean, 11) days after infarction and followed for an average of
42 months. Prospectively defined end points of the study considered in
this analysis included mortality from all causes, mortality
from cardiovascular causes, and recurrence of a
myocardial infarction. A single seated blood pressure was measured by
sphygmomanometry at the time of randomization, and pulse pressure was
calculated as the difference between systolic and
diastolic pressures. A standard formula was used to
calculate mean arterial pressure from the sphygmomanometric
blood pressure: systolic pressure and twice
diastolic pressure were summed and then divided by three.
The relationship between calculated mean arterial pressure
and clinical outcome was then assessed. Clinical variables
considered as potential correlates of adverse events included a prior
history of hypertension, defined as a clinical history of elevation in
blood pressure sufficient to require drug therapy at some point before
the index infarction.
Statistical Analysis
The relationship between baseline characteristics and pulse
pressure was determined by a general linear model. Patients were
categorized by tertiles of systolic, diastolic, and
pulse pressures. The relationship between end points and tertiles of
systolic, diastolic, and pulse pressures was
determined by the 
2 test. The association
between pulse pressure as a continuous variable and time-dependent
end points was evaluated with Cox proportional-hazards models that
controlled first for mean arterial pressure alone and then
for all baseline characteristics found to influence pulse pressure as
well as other known predictors of outcome after myocardial
infarction.
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Results |
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Baseline Characteristics of the Study Population
Baseline characteristics of the study population according to level of pulse pressure are presented in Table 1
. Significant positive relationships
were found between pulse pressure and age, left ventricular
ejection fraction, and mean arterial pressure. There was no
relationship between pulse pressure tertile and heart rate or years of
smoking, although there was a weak linear correlation between pulse
pressure and years of smoking when both were treated as continuous
variables (r=.062, P<.01). The proportion of
the patients who were female increased with increasing pulse-pressure
tertile. In addition, there were significant linear trends across
tertiles of pulse pressure for increasing proportions of patients with
histories of prior myocardial infarction or diabetes or a history of
hypertension requiring drug therapy before the index infarction. There
were significant positive associations between pulse pressure and use
of calcium channel blockers, digoxin, diuretics, and nitrates
within the 24 hours before randomization, whereas there was a negative
association with use of ß-blockers. With increasing pulse pressure,
there was an unexpected decrease in the proportion of patients who were
smokers at the time of their index myocardial infarction.
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To evaluate the independent association of each of these covariates with pulse pressure, a general linear model was constructed that controlled for age, years of smoking, mean arterial pressure, and ejection fraction. Nonlinearity in the relationship between pulse pressure and age was evaluated by including a quadratic (age2) term. When the potential covariates were individually tested in this model, the associations with diuretic and nitrate use and current smoking status were not statistically significant. A final multivariate analysis of significant univariate correlates of pulse pressure revealed that use of digoxin (P=.01) or calcium channel blocking agents (P=.001), a history of diabetes (P<.001) or hypertension (P=.011), and female sex (P<.05) were independently associated with increased pulse pressure.
Adverse Cardiovascular Events
Patients were followed for an average of 42±10 months (range, 24
to 60 months), during which time there were 503 deaths, 422
cardiovascular deaths, and 303 recurrent myocardial
infarctions. Systolic and pulse pressures had positive linear
relationships with each of the end points
(Figure). In contrast,
diastolic pressure had no apparent relationship with any of
the end points. Whereas previous studies have focused on
systolic pressure as a prognostic indicator, from a
physiological and therapeutic perspective, it is
important to establish the relative effects of steady flow and
pulsatile load on adverse events. Mean pressure correlates with steady
flow load, which is a function of resistance vessel tone and cardiac
output, whereas pulse pressure is an indicator of conduit vessel
function and pulsatile load. Furthermore, because of the nonlinearity
of arterial stiffness, pulse pressure is somewhat dependent
on the level of mean arterial pressure. To determine which
components of load were related to time-dependent end points, a
proportional-hazards model was constructed that included both mean and
pulse pressure (Table 2). Pulse pressure
remained a highly significant predictor of each of the clinical end
points independent of the level of mean arterial pressure.
In contrast, mean arterial pressure remained independently
predictive of an adverse outcome only for recurrent myocardial
infarction.
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To determine whether pulse pressure provides independent prognostic
information in this already well-characterized patient population, a
proportional-hazards model was constructed that included the correlates
of pulse pressure identified above (age, years of smoking, ejection
fraction, mean arterial pressure, sex, history of diabetes
or hypertension, and use of calcium channel blockers or digoxin) as
well as several other factors known to influence survival after
myocardial infarction (use of aspirin, thrombolytic
therapy, or ß-blockers; history of prior myocardial infarction;
current smoking status; and randomization to captopril therapy). Pulse
pressure remained independently predictive of total mortality (Table 3) and recurrence of myocardial
infarction (Table 4).
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Discussion |
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The principal finding of this analysis is that a single, casual determination of pulse pressure, a readily obtainable correlate of pulsatile hemodynamic load, measured 3 to 16 days after myocardial infarction, was a powerful and independent predictor of adverse cardiovascular events in a large population of post–myocardial infarction patients with impaired left ventricular function. There were strong univariate associations between increased pulse pressure and total mortality, cardiovascular mortality, and recurrence of myocardial infarction. A multivariate analysis, which included an extensive list of factors thought or known to contribute to outcome after myocardial infarction, confirmed the independent prognostic implications of increased pulse pressure on total mortality and recurrence of myocardial infarction.
Pathophysiological Implications of Increased
Vascular Stiffness
There are several potential explanations for the association
between a higher pulse pressure and cardiac events in patients with
coronary artery disease. Because it is unlikely that stroke
volume or peak aortic flow was increased in these patients with left
ventricular dysfunction after myocardial infarction, it may
be presumed that the increased pulse pressure was a result of increased
conduit vessel stiffness. Furthermore, it is likely that the increased
load associated with conduit vessel stiffening contributed to a
reduction in stroke volume in the patients with elevated pulse
pressure. Conduit vessel stiffening increases the amplitude of the
pressure pulse produced by a given flow wave, resulting in higher
systolic and lower diastolic pressures for any
given mean pressure. Pulse-wave velocity is increased in stiffened
conduit vessels, and this shortens the time required for the forward
pressure wave to travel down the aorta and peripheral
conduits to the various reflecting sites and back to the heart. The
resulting movement of the reflected wave from diastole into
systole has no effect on mean arterial pressure. However,
the premature reflected wave further increases the systolic
pressure-time integral and decreases the diastolic
pressure-time integral, thereby increasing systolic load while
decreasing coronary perfusion pressure. The
diastolic perfusion pressure gradient is further
compromised if ventricular filling pressures are
elevated.9 The latter is exacerbated by premature
return of the reflected wave, which impairs left
ventricular relaxation.15
Animal models have confirmed the enhanced susceptibility to ischemia of ventricles coupled to stiff aortas, both in the presence7 and absence8 of epicardial stenoses. Furthermore, the functional implications of regional ischemia are enhanced in animals with artificially stiffened aortas, with threefold greater reductions in systolic pressure and ejection fraction after coronary artery occlusion.16 Ischemia adequate to impair ventricular function and reduce systolic pressure may have a direct and immediate impact on global coronary blood flow that would otherwise be moderated by a more compliant arterial system with a higher diastolic pressure and predominantly diastolic coronary flow. An associated increase in heart rate and filling pressures during an ischemic episode could further impair coronary flow17 and initiate a catastrophic vicious cycle in these patients.
In addition to increasing left ventricular load and diminishing coronary perfusion pressure, conduit vessel stiffness correlates with the presence and severity of atherosclerosis. Because atherosclerosis modifies the physical properties of the conduit vessel wall,18,19 increased pulse pressure may simply serve as a marker for advanced or rapidly advancing atherosclerotic disease. Alternatively, stiffening of the conduit vessels may play a primary role in the development and progression of atherosclerosis. Age-related increases in pulse-wave velocity occur in populations in which the prevalence of atherosclerosis is low,20 indicating that atherosclerosis is not a necessary precursor of arterial stiffening. Increased vascular stiffness, independent of the presence of clinically apparent atherosclerosis, is associated with several established risk factors for coronary artery disease, including diabetes,21 hypertension,20 age,4,22–24 and a family history of myocardial infarction.25 Arterial stiffening could represent a component of the association between these risk factors and development of atherosclerosis. Pulse pressure and pulsatile diameter changes from diastole to systole have been shown to be important in the development of atherosclerosis of the aorta in a primate model.10 A 41% reduction in pulse pressure at constant mean pressure decreased aortic diameter change by 52% and reduced intimal plaque area by 82%. Stiffening of the peripheral conduits reduces the transit time of the reflected wave, resulting in progressive overlap between forward and reflected waves in the proximal aorta. This produces a disproportionately large increase in pulse pressure and pulsatile strains in the proximal aorta22,26 and thus in the coronary and carotid arteries and may thereby favor development of atherosclerosis in these vascular beds.
Clinical Correlates of Increased Pulse Pressure
Well-known correlates of conduit vessel stiffness, including
age24,27 and a history of
diabetes21 or
hypertension,20 were found to be related to pulse
pressure in the present analysis. Two additional important
associations that deserve further comment were the finding of a higher
pulse pressure in women and in patients treated with calcium channel
blockers. The finding of a higher pulse pressure in the female patients
in this study is consistent with the observation that
systolic pressure increases more rapidly with age in women than
in men.4,27 Elevated pulse pressure may
represent one additional risk factor that must be considered
when differences in outcome in men and women with coronary
artery disease are compared.
The association between use of calcium channel blockers and increased pulse pressure is intriguing in light of recent controversies regarding an increased frequency of ischemic events in hypertensive patients treated with these agents.28 Calcium channel blockade has been shown to have a favorable short-term effect on conduit vessel function and pulsatile hemodynamics in hypertensive patients in some studies29 but not in others.30 Longer-term studies in animals31 and in humans32 have suggested that favorable acute effects of calcium channel blockade on conduit vessel function may be offset over time by compensatory changes in left ventricular contractility and arterial structure and function. It is important to note that calcium channel blockade in our patients was not randomized. Therefore, differences in pulse pressure may be related to a bias toward prescribing these agents in patients with refractory or long-standing hypertension. Ongoing randomized, double-blind clinical trials designed to evaluate the relationship between calcium channel blocker therapy and clinical events in hypertensive patients will provide an opportunity to determine whether pulse pressure is relatively higher in patients treated with calcium channel blockers as opposed to other antihypertensive agents.
Pulsatile Load and Adverse Clinical Events
A number of small studies have related left
ventricular mass to various measures of pulsatile
load.1,33–38 Because increased left
ventricular mass has been correlated with adverse
events,39–41 it may be hypothesized that
pulsatile load is related to clinical outcome, although few studies
have directly evaluated this relationship. A recently proposed vascular
overload index, which sums the increments in mean and pulse pressure
(relative to a normal blood pressure of 120/80 mm Hg), was shown
to have a direct linear relationship with adverse events that was
qualitatively superior to the relationship between events and
systolic or diastolic pressure
alone.42 In a study of nonhypertensive adults,
the pulsatile component index, a strong correlate of pulse pressure,
was derived by a principal-components analysis of
systolic and diastolic
pressures.2 An association between the pulsatile
component index and ECG evidence of left ventricular
hypertrophy was observed. During follow-up, the pulsatile
component index was associated with an increased risk of death from
coronary artery disease. However, a significant relationship
was found only in women >55 years old. In a prospective evaluation of
hypertensive patients, those in the highest tertile of pulse pressure
before the initiation of therapy (
63 mm Hg) had an increased
risk of myocardial infarction and stroke during an average follow-up of
5 years.3 In the latter study,
multivariate analysis revealed that pulse
pressure as a categorical variable (although not as a continuous
variable) was an independent predictor of myocardial
infarction.
The relative effects of diastolic, systolic, and pulse pressures on 5-year mortality were evaluated in the Hypertension Detection and Follow-up Program.43 Pulse pressure was shown to be a significant predictor of total mortality in a logistic regression model that included age, race, sex, randomized antihypertensive therapy, diabetes, hypertensive end-organ damage, and smoking. The relative risk of 1.11 per 10 mm Hg increment in pulse pressure exceeded that of diastolic (1.05) and systolic (1.08) pressures. In a model that included only patients who were untreated at baseline, pulse pressure remained significant even when the model included systolic pressure, although the two variables are highly correlated. Furthermore, in that model, pulse pressure had a relative risk (1.19) that was >1, whereas systolic pressure had a relative risk (0.93) that was quantitatively <1 after the effects of pulse pressure had been considered. These data suggest an important role for pulse pressure as a predictor of adverse outcome in hypertensive patients, even though the authors concluded that the data lent no strong support to such a notion. Our study adds to the foregoing observations and suggests an even stronger relationship between conduit vessel stiffness and adverse events in patients with known coronary artery disease and impaired left ventricular function.
Therapeutic Implications
Abnormalities in conduit vessel function are
modifiable.35,44–48 For example, a low-salt diet
followed for an average of 24.8 months by normotensive patients
produced a pressure-independent decrease in pulse-wave velocity,
suggesting a modification of the intrinsic properties of the
aorta.44 ACE inhibition has been shown to
decrease blood pressure, wave reflection, and pulse-wave velocity and
to increase arterial compliance and conduit vessel
diameter.35,45–48 Over the course of several
weeks, the effects on conduit function are enhanced, resulting in
normalization of conduit vessel function in a hypertensive patient
population. Further studies are needed to determine whether a reduction
in pulse pressure should be a goal of therapy in the postinfarction
patient population.
The observed reduction in recurrent myocardial infarction with ACE inhibition has been associated with only modest reductions in blood pressure, leading to investigation of potential nonhemodynamic effects of treatment.49 It is likely, however, that the change in peripheral blood pressure with therapy reported in the foregoing studies underestimated the reduction in central aortic systolic and pulse pressures, especially in patients with stiff conduit vessels. In young adults with highly compliant central conduits, there is considerable amplification of the pressure pulse as it propagates distally into the progressively stiffer peripheral conduits. As the central conduit vessels stiffen, the reflected wave returns to the heart prematurely and becomes an important determinant of peak systolic and pulse pressure in the central aorta. In contrast, peak systolic pressure in the brachial artery is determined by the primary pressure wave well into the eighth decade of age.22 This disproportionate increase in central aortic systolic pressure obscures normal amplification of the primary pressure pulse with distal propagation. Vasodilators decrease the amplitude and delay the return of the reflected wave and thereby decrease or eliminate the late systolic peak in central aortic pressure.50–55 The normal differences between central and peripheral pressures are thereby restored. Because the reflected wave determines neither systolic nor diastolic pressure in the peripheral artery, changes in the amplitude and timing of the reflected wave go unnoticed by sphygmomanometry. Consequently, vasodilators have been shown to reduce central systolic pressure an average of 5 to 10 mm Hg more than is indicated by the change in peripheral pressure, with discrepancies ranging as high as 40 mm Hg. Accounting for this discrepancy by use of more sophisticated measures of conduit vessel function in future studies should considerably narrow the gap between hemodynamic effect and clinical benefit.
Limitations
The dependence of pulse pressure on stroke volume and peak aortic
blood flow, both of which may be decreased after extensive infarction,
could potentially obscure a relationship between conduit vessel
stiffening and mortality after infarction. Despite this, we found a
relationship between pulse pressure as a continuous variable and
clinical events, including a reduction in event rate in patients with a
pulse pressure substantially below the median value of 40 mm Hg.
In contrast, the observed association between ß-blocker usage and
reduced pulse pressure should strengthen the relationship between the
latter and adverse events, because the selection bias for use of
ß-blockers in healthier patients and the protective effect of the
therapy are both likely to favorably impact prognosis. However, pulse
pressure remained independently predictive of events even after these
potentially confounding factors were controlled for. Heart rate might
also influence pulse pressure because of the inverse relationship with
stroke volume. However, we found no association between heart rate and
pulse pressure or between heart rate and subsequent events.
The dependence of pulse pressure on hemodynamic factors (stroke volume, peak aortic blood flow) other than aortic and peripheral conduit vessel stiffness per se makes this an imperfect indicator of conduit vessel function. Conversely, several important parameters are integrated into this single, easily obtainable measurement. Future studies will need to assess more direct measures of conduit vessel stiffness, such as pulse-wave velocity, proximal aortic compliance, characteristic impedance, and waveform morphology, to determine to what extent increased pulse pressure is a measure of conduit vessel stiffness. The transfer function (alteration in waveform morphology) between central aorta and radial artery has been shown to be remarkably consistent across a wide range of ages.56,57 As a result, calibrated noninvasive recordings of radial arterial pressure waveforms using arterial tonometry and a generalized transfer function may allow for accurate determination of central aortic pressure amplitude and morphology and their change under therapy.56
It is important to note that this analysis is exploratory in nature and was not a prespecified analysis of the SAVE study. As a result, prospective confirmation of our results is needed. These observations apply to a highly selected population of patients with a recent myocardial infarction and impaired left ventricular function.
Clinical Implications
The importance of risk stratification and targeted secondary
prevention after myocardial infarction is clear, although the proper
algorithm to optimize cost and benefit continues to evolve. In the
present era, the potential benefits of technologically advanced
evaluations must be balanced against their cost. It is interesting to
note that a century after the description by Riva-Rocci of the modern
sphygmomanometer,58 pulse pressure, a
long-overlooked measurement provided by this simple, cheap, and
universally available instrument, should prove so valuable in risk
stratification after myocardial infarction. Further studies will be
needed to establish whether pulse pressure and other measures of
conduit vessel function can be used as tools for targeting primary and
secondary prevention in a broader segment of the population.
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Acknowledgments |
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The SAVE study was supported by a grant from the Bristol-Myers Squibb Institute for Pharmaceutical Research, which was not involved in the acquisition or management of data and did not have access to unblinded information during the conduct of the study.
Received May 30, 1997; revision received September 1, 1997; accepted September 15, 1997.
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 X. Peng, F. A. Recchia, B. J. Byrne, I. S. Wittstein, R. C. Ziegelstein, and D. A. Kass In vitro system to study realistic pulsatile flow and stretch signaling in cultured vascular cells Am J Physiol Cell Physiol, September 1, 2000; 279(3): C797 - C805. [Abstract] [Full Text] [PDF]
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V. Vaccarino, T. R. Holford, and H. M. Krumholz Pulse pressure and risk for myocardial infarction and heart failure in the elderly J. Am. Coll. Cardiol., July 1, 2000; 36(1): 130 - 138. [Abstract] [Full Text] [PDF]
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J. Blacher, J. A. Staessen, X. Girerd, J. Gasowski, L. Thijs, L. Liu, J. G. Wang, R. H. Fagard, and M. E. Safar Pulse Pressure Not Mean Pressure Determines Cardiovascular Risk in Older Hypertensive Patients Arch Intern Med, April 24, 2000; 160(8): 1085 - 1089. [Abstract] [Full Text] [PDF]
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M. St. John Sutton Aortic stiffness: a predictor of acute coronary events? Eur. Heart J., March 1, 2000; 21(5): 342 - 344. [PDF]
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C Stefanadis, J Dernellis, E Tsiamis, C Stratos, L Diamantopoulos, A Michaelides, and P Toutouzas Aortic stiffness as a risk factor for recurrent acute coronary events in patients with ischaemic heart disease Eur. Heart J., March 1, 2000; 21(5): 390 - 396. [Abstract] [PDF]
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A. Benetos, M. Zureik, J. Morcet, F. Thomas, K. Bean, M. Safar, P. Ducimetiere, and L. Guize A decrease in diastolic blood pressure combined with an increase in systolic blood pressure is associated with a higher cardiovascular mortality in men J. Am. Coll. Cardiol., March 1, 2000; 35(3): 673 - 680. [Abstract] [Full Text] [PDF]
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H. Smulyan and M. E. Safar The Diastolic Blood Pressure in Systolic Hypertension Ann Intern Med, February 1, 2000; 132(3): 233 - 237. [Abstract] [Full Text] [PDF]
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O. A. Carretero and S. Oparil Essential Hypertension : Part II: Treatment Circulation, February 1, 2000; 101(4): 446 - 453. [Full Text] [PDF]
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N. Iwai, T. Katsuya, K. Ishikawa, T. Mannami, J. Ogata, J. Higaki, T. Ogihara, T. Tanabe, and S. Baba Human Prostacyclin Synthase Gene and Hypertension : The Suita Study Circulation, November 30, 1999; 100(22): 2231 - 2236. [Abstract] [Full Text] [PDF]
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M. O'Rourke and E. D. Frohlich Pulse Pressure : Is This a Clinically Useful Risk Factor? Hypertension, September 1, 1999; 34(3): 372 - 374. [Full Text] [PDF]
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M. J. Domanski, B. R. Davis, M. A. Pfeffer, M. Kastantin, and G. F. Mitchell Isolated Systolic Hypertension : Prognostic Information Provided by Pulse Pressure Hypertension, September 1, 1999; 34(3): 375 - 380. [Abstract] [Full Text] [PDF]
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S. S. Franklin, S. A. Khan, N. D. Wong, M. G. Larson, and D. Levy Is Pulse Pressure Useful in Predicting Risk for Coronary Heart Disease? : The Framingham Heart Study Circulation, July 27, 1999; 100(4): 354 - 360. [Abstract] [Full Text] [PDF]
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M. J. Domanski, G. F. Mitchell, J. E. Norman, D. V. Exner, B. Pitt, and M. A. Pfeffer Independent prognostic information provided by sphygmomanometrically determined pulse pressure and mean arterial pressure in patients with left ventricular dysfunction J. Am. Coll. Cardiol., March 15, 1999; 33(4): 951 - 958. [Abstract] [Full Text] [PDF]
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G. de Simone, M. J. Roman, M. J. Koren, G. A. Mensah, A. Ganau, and R. B. Devereux Stroke Volume/Pulse Pressure Ratio and Cardiovascular Risk in Arterial Hypertension Hypertension, March 1, 1999; 33(3): 800 - 805. [Abstract] [Full Text] [PDF]
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C. U. Chae, M. A. Pfeffer, R. J. Glynn, G. F. Mitchell, J. O. Taylor, and C. H. Hennekens Increased Pulse Pressure and Risk of Heart Failure in the Elderly JAMA, February 17, 1999; 281(7): 634 - 643. [Abstract] [Full Text] [PDF]
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 N. Stergiopulos, P. Segers, and N. Westerhof Use of pulse pressure method for estimating total arterial compliance in vivo Am J Physiol Heart Circ Physiol, February 1, 1999; 276(2): H424 - H428. [Abstract] [Full Text] [PDF]
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A. Benetos, A. Rudnichi, F. Thomas, M. Safar, and L. Guize Influence of Heart Rate on Mortality in a French Population : Role of Age, Gender, and Blood Pressure Hypertension, January 1, 1999; 33(1): 44 - 52. [Abstract] [Full Text] [PDF]
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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]
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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]
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N. Stergiopulos and N. Westerhof Determinants of Pulse Pressure Hypertension, September 1, 1998; 32(3): 556 - 559. [Abstract] [Full Text] [PDF]
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A. Benetos, A. Rudnichi, M. Safar, and L. Guize Pulse Pressure and Cardiovascular Mortality in Normotensive and Hypertensive Subjects Hypertension, September 1, 1998; 32(3): 560 - 564. [Abstract] [Full Text] [PDF]
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