Original Article
Pulse Pressure Within 3 Months After Ischemic Stroke Is
Associated With Long-Term Stroke Outcomes
Ning Su,1,* Fei-Fei Zhai,1,* Jun Ni,1 Li-Xin Zhou,1 Ming Yao,1 Bin Peng,1 Yi-Cheng Zhu,1,†
and Li-Ying Cui1,†
BACKGROUND
Pulse pressure (PP) is a surrogate marker of arterial stiffness. Studies on
baseline PP and long-term outcomes in patients with stroke are limited.
We aimed to evaluate whether PP within 3 months after ischemic stroke
was associated with long-term stroke outcomes.
METHODS
A total of 4,195 patients (61.2 ± 11.6 years, 68.4% men) with first-ever
ischemic stroke in 3  months had baseline blood pressure (BP) meas-
ured. Study end-points were the combined end-points (recurrent vas-
cular events and all-cause mortality) and recurrent stroke.
RESULTS
In the group <60 years of age, the BP components of systolic BP
(SBP), diastolic BP (DBP), mean arterial pressure (MAP), or PP did not
Pulse pressure (PP) as a pulsatile component of blood
pressure (BP), is a surrogate marker of arterial stiffness.1,2
Accumulating evidence has indicated that PP was superior
to either systolic BP (SBP) or diastolic BP (DBP) in predict-
ing the risk of coronary heart disease (CHD).3–6 In prospec-
tive cohorts, PP was associated with myocardial infarction
(MI) and mortality in normotensive and hypertensive
populations.7 PP has also been linked to incident stroke.8–11
A  recent meta-analysis summarizing 11 studies demon-
strated an association between the increase in PP and the
risk of stroke occurrence.11
Unlike the established role of PP as a risk factor for stroke,
the prognostic importance of PP in determining the outcome
after stroke is still unknown because most related studies
focused on short-term outcomes and reported controversial
results.12–14 Aslanyan et al.13 reported that elevated PP during
the first 60 hours of acute ischemic stroke was associated with
poor short-term functional outcome and mortality, while
Dawson et al.15 found that PP within 72 hours of ictus had
no prognostic impact on short-term death or dependence. In
Correspondence: Li-Ying Cui (pumchcuily@sina.com).
Initially submitted June 1, 2017; date of first revision June 16, 2017;
accepted for publication July 12, 2017.
significantly correlate with long-term stroke outcomes. In the group ≥60
years of age, PP was significantly associated with combined end-points
(hazards ratio [HR] = 1.35; 95% confidence interval [CI], 1.18–1.54) and
recurrent stroke (HR = 1.46; 95% CI, 1.24–1.72). Combination of SBP and
PP, DBP and PP, or MAP and PP, respectively, showed no incremental
value of SBP, DBP, or MAP in predicting long-term stroke outcomes.
CONCLUSIONS
PP was significantly associated with long-term stroke outcomes, and
this association was prominent in patients with stroke older than
60 years of age.
Keywords: blood pressure; hypertension; ischemic stroke; long-term
outcome; pulse pressure.
doi:10.1093/ajh/hpx121
these studies, BP within 24–72 hours after stroke onset was
commonly applied. However, an acute hypertensive response
occurs within 24 hours in up to 80% of patients with acute
stroke and spontaneously declines afterward within days
to weeks.16,17 Thus, PP in the acute stage of stroke may not
be a proper measurement for investigating the association
between arterial stiffness and stroke outcomes.
Based on previous findings, we conducted a national,
multicenter, prospective, observational study. Patients hav-
ing ischemic stroke were recruited, and BP levels were meas-
ured. We aimed to investigate the relationship of PP within
3 months after stroke with long-term stoke outcomes.
METHODS
Study population
The Standard Medical Management in Secondary
Prevention of Ischemic Stroke in China (SMART) study
had revealed that a guideline-based structured program,
1Department of Neurology, Peking Union Medical College Hospital,
Chinese Academy of Medical Sciences and Peking Union Medical College,
Beijing 100730, China.
*Both authors contributed equally to this work.
†Both authors contributed equally to this work.
© American Journal of Hypertension, Ltd 2017. All rights reserved.
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American Journal of Hypertension  1
Su et al.
combination of pharmaceutical treatment, lifestyle modifi-
cation, and patient education could improve the adherence
to secondary prevention of ischemic stroke during 1-year
follow-up in China.18,19 In order to implement SMART pro-
gram in more patients with ischemic stroke, we performed
the SMART-II study in 91 medical centers in China. Patients
having ischemic stroke within 3  months, aged 18  years or
older, and functionally independent before stroke (modi-
fied Rankin scale < 3), were enrolled between July 2012
and February 2014. Those with severe handicaps (modified
Rankin scale = 5) after stroke, severe comorbid illness, unsta-
ble medical condition, such as congestive cardiac failure,
severe liver dysfunction, renal failure, or expected life span
less than 2  years were excluded. All participants provided
their written informed consent to participate. The study was
approved by the central ethics committee of the principal
study center at Peking Union Medical College Hospital and
by the ethics committees at the participating study sites.
A total of 4,487 patients of the SMART-II study with first-
ever ischemic stroke were enrolled in the current study. We
excluded 24 patients with missing baseline BP measure-
ments, and 268 patients lost to follow-up. Thus, the final
analysis of the present study was performed with 4,159
patients. The baseline characteristics of all patients with first-
ever ischemic stroke, both included and not included in this
study, were comparable (Supplementary Table S1).
BP measurement and clinical assessments
BP measurements were made using conventional meth-
ods.20–22 The SBP and DBP were measured in the sitting
position with a sphygmomanometer on the left arm of the
patients after sitting for 5 minutes. The mean of the 3 record-
ings was used in the analysis. The mean arterial pressure
(MAP) was calculated as two-thirds DBP plus one-third
SBP.23 PP was calculated as SBP minus DBP.
Baseline data on demographics, cardiovascular risk fac-
tors, and medical history were collected through a struc-
tured questionnaire by trained neurologists. Body mass
index was calculated as weight in kilograms divided by the
height in meters squared. Cardiovascular risk factors were
defined as follows: (i) hypertension was defined as SBP
≥140  mm Hg or DBP ≥90  mm Hg, self-reported hyper-
tension, or treatment with antihypertensive medication;
(ii) diabetes mellitus (DM) was defined as fasting serum
glucose ≥7.0 mmol/l, self-reported diabetes, or use of oral
blood sugar-lowering drugs or insulin; (iii) hyperlipidemia
was defined as total cholesterol >5.2  mmol/l or low-den-
sity lipoprotein-cholesterol >2.58  mmol/l, or self-reported
hyperlipidemia; (iv) atrial fibrillation was identified on
electrocardiogram or continuous electrocardiographic
recording; (v) CHD included any history of MI, angina, or
asymptomatic MI; and (vi) current smoker was defined as
one who smoked at least one cigarette per day for more than
6 months before the stroke onset.
Follow-up process and outcomes assessment
The registered patients were followed up at 3 months and
6  months after recruitment and then every half-year until
2  American Journal of Hypertension
2  years after recruitment to assess the clinical outcomes.
Follow-up evaluations were conducted at the medical center
or by telephone interviews.
The combined end-points were recurrent vascular events
and all-cause mortality. The recurrent vascular events were a
composite of recurrence of ischemic or hemorrhagic stroke,
transient ischemic stroke, acute coronary syndrome, or
peripheral vascular disease. A recurrent stroke was defined
as new-onset focal neurologic deficits persisting longer than
24 hours. The ST elevation MI, non-ST elevation MI, and
unstable angina were defined as acute coronary syndrome.
The peripheral vascular disease was defined as new-onset
ischemic symptoms in the lower limbs. All-cause mortality
was also recorded.
Statistical analysis
Demographic and clinical characteristics of the sample
were compared among the PP quartiles, using the analysis of
variance for continuous variables and the chi-squared tests
for categorical variables. Kaplan–Meier survival analysis
with log–rank test was conducted to compare the survival
rates across the 4 PP quartiles.
The multivariable Cox proportional hazards regression
model was used to assess the relations of combined end-
points and recurrent stroke with BP components as continu-
ous variables. Hazards ratios (HRs) with 95% confidence
interval (CI) were estimated for 1-SD increment in each BP
component, adjusted for age, sex, current smoking, obesity
(body mass index ≥ 30), DM, hyperlipidemia, atrial fibril-
lation, history of CHD, antihypertensive medication, anti-
platelet medication, and lipid-lowering medication. Single
BP components (SBP, DBP, MAP, PP) were initially entered
in separate multivariable models. With results from the
Framingham study that age-related changes of SBP and DBP
leading to steep rise of PP after the 6th decade,24 and find-
ings from Costa Rican Study that wide PP was associated
with higher risk of cardiovascular death in those aged 60
or more years,25 while under age 60, PP became not predic-
tive,26 as well as the lower age boundary of 60 years in sev-
eral randomized clinical trials on antihypertensive treatment
in the elderly,27 we stratified our participants by 60 years of
age to explore the association between BP levels and out-
come events in the respective age subgroups. Furthermore,
in order to assess the independent relationships of PP with
other BP indices, the dual BP components of SBP + PP, DBP
+ PP, or MAP + PP were entered simultaneously in the same
model to adjust for each other in each age subgroup. Similar
statistical method has been used in previous studies for
community populations.3,8,10,28 A  2-sided P value of <0.05
indicated statistical significance. All statistical analyses were
performed using SAS version 9.4 (SAS Institute, Cary, NC).
RESULTS
Demographic and clinical characteristics
A total of 4,195 patients with first-ever ischemic stroke
were enrolled in the present study, of which 2,869 were
men (68.4%). The mean age (SD) was 61.2  years (11.6),
 Association of PP With Stroke Outcome

with 1,847 (44.0%) patients younger than 60  years of age.
Prevalent conditions at baseline included hypertension
(82.4%), DM (33.0%), hyperlipidemia (65.2%), and atrial
fibrillation (5.8%). Most of the patients with hypertension
(70.6%) were taking antihypertensive medications. Mean
(SD) BP parameters included SBP of 144.4 (20.4), DBP of
85.7 (12.3), MAP of 105.2 (13.7), and PP of 58.7 (15.2) mm
Hg. The patients with high PP levels tended to be older at
inclusion, included a higher proportion of male and current
smoker participants, had histories of hypertension, hyper-
lipidemia, and DM, and received antihypertensive and anti-
platelet treatment. In addition to the increased MAP values,
patients with high PP values also had higher SBP and DBP
values (P < 0.01; Table 1).
Follow-up and outcomes
The median follow-up time was 23.5 months (interquar-
tile range, 16.8–25.6 months). During follow-up, 371 (8.8%)
patients had combined end-points, of whom 302 (7.2%)
experienced recurrent vascular events and 69 (1.6%) patients
died. Among those patients, 236 (5.6%) had a recurrent
stroke. Patients having the highest quartile of PP had a com-
bined end-point rate of 11% and a recurrent stroke rate of
6.8%, compared to 7.2% and 4.2%, respectively, in the lowest
category (Table 1). Figure 1 shows the Kaplan–Meier curves
for each point. Analysis of the survival curves demonstrated
that patients in the higher PP quartiles were at a higher risk
of combined end-points and recurrent stroke than those in
the lower PP quartiles (log–rank test, P = 0.008 and 0.035,
respectively; Figure 1a and b).
Association of PP with long-term outcomes in single BP
component models
The associations between PP and long-term stroke
outcomes (combined end-points and recurrent stroke)
are summarized in Table  2. The multivariate Cox pro-
portional-hazards model adjusted by age, sex, current
smoking, obesity, DM, hyperlipidemia, atrial fibrillation,
history of CHD, antihypertensive medication, antiplatelet
medication, and lipid-lowering medication showed that
every 1-SD increment in PP was associated with a 26%
increase in the risk of combined end-points (HR, 1.26;
95% CI, 1.12–1.41; P < 0.01) and 33% increase in the risk
of recurrent stroke (HR, 1.33; 95% CI, 1.16–1.53; P < 0.01;
Table 2).
In order to assess whether the association of stroke out-
comes and BP components was influenced by age, the sample
was then stratified by age (<60 years, ≥60 years). There were
no associations between BP components (SBP, DBP, MAP,
or PP) and the combined end-points or recurrent stroke in
the group <60 years of age (Table 2). In the group ≥60 years
of age, PP was significantly associated with combined end-
points (HR, 1.35; 95% CI, 1.18–1.54; P < 0.01) and recurrent
stroke (HR, 1.46; 95% CI, 1.24–1.72; P < 0.01; Table 2).

Table 1.  Demographic and clinical characteristics of whole sample and subgroups by quartiles of pulse pressure

Quartiles of pulse pressure

<50 mm Hg 50–58 mm Hg 59–69 mm Hg >69 mm Hg

Characteristic Overall (n = 4,195) (n = 881) (n = 1,204) (n = 1,039) (n = 1,071) P value

Age, years, mean (SD) 61.2 (11.6) 57.5 (11.9) 59.5 (11.2) 62.6 (11.1) 64.9 (11.0) <0.01
Male, n (%) 2,869 (68.4) 632 (71.7) 856 (71.1) 706 (67.9) 675 (63.0) <0.01
Current smoker, n (%) 1,578 (37.6) 375 (42.6) 473 (39.3) 358 (34.5) 372 (34.7) <0.01
Obesity (BMI ≥ 30), n (%) 266 (6.5) 47 (5.5) 78 (6.6) 70 (6.9) 71 (6.8) 0.59
Blood pressure, mean (SD)
  SBP (mm Hg) 144.4 (20.4) 124.9 (13.2) 136.2 (10.9) 147.4 (12.1) 166.5 (17.9) <0.01
  DBP (mm Hg) 85.7 (12.3) 84.5 (12.4) 84.6 (10.8) 86.1 (11.9) 87.5 (13.7) <0.01
  MAP (mm Hg) 105.2 (13.7) 98.0 (12.4) 101.8 (10.8) 106.5 (11.9) 113.8 (14.4) <0.01
  PP (mm Hg) 58.7 (15.2) 40.5 (5.3) 51.6 (2.5) 61.4 (2.6) 79.0 (10.8)
Hypertension, n (%) 3,456 (82.4) 539 (61.2) 894 (74.3) 962 (92.6) 1,061 (99.1) <0.01
Diabetes mellitus, n (%) 1,384 (33.0) 256 (29.1) 376 (31.2) 363 (34.9) 389 (36.3) <0.01
Hyperlipidemia, n (%) 2,733 (65.2) 535 (60.8) 801 (66.5) 686 (66.0) 711 (66.4) 0.02
Atrial fibrillation, n (%) 243 (5.8) 58 (6.6) 66 (5.5) 62 (6.0) 57 (5.3) 0.63
Outcome events, n (%)
  Combined end-pointsa 371 (8.8) 63 (7.2) 94 (7.8) 96 (9.2) 118 (11.0) 0.01
  Recurrent stroke 236 (5.6) 37 (4.2) 60 (5.0) 66 (6.4) 73 (6.8) 0.04

Abbreviations: BMI, body mass index; DBP, diastolic blood pressure; MAP, mean arterial blood pressure; PP, pulse pressure; SBP, systolic
blood pressure.
aCombined end-points include new-onset ischemic and hemorrhagic stroke, transient ischemic stroke, acute coronary syndrome, peripheral

vascular disease, and all-cause mortality.

American Journal of Hypertension  3

Su et al.

Figure 1.  Kaplan–Meier curves of long-term outcomes by quartiles of pulse pressure. Kaplan–Meier curves of the cumulative risk for combined end-
points (a) and recurrent stroke (b) in patients with first-ever ischemic stroke stratified into quartiles of pulse pressure. The P values were calculated with
the log–rank test.

Table 2.  Association of single blood pressure component with combined end-points and recurrent stroke

Combined end-points Recurrent stroke

BP components/per SD increment HRa (95% CI) P value HRa (95% CI) P value

Total patients (n = 4,195) (n = 371, 8.8%) (n = 236, 5.6%)

 SBP 1.24 (1.11, 1.40) <0.01 1.34 (1.16, 1.54) <0.01
 DBP 1.07 (0.94, 1.21) 0.31 1.14 (0.98, 1.33) 0.08
 MAP 1.16 (1.03, 1.31) 0.02 1.26 (1.09, 1.45) <0.01
 PP 1.26 (1.12, 1.41) <0.01 1.33 (1.16, 1.53) <0.01
Age <60 years (n = 1,847) (n = 120, 6.5%) (n = 76, 4.1%)
 SBP 1.05 (0.86, 1.29) 0.61 1.08 (0.84, 1.38) 0.54
 DBP 0.97 (0.79, 1.20) 0.81 1.04 (0.81, 1.34) 0.76
 MAP 1.01 (0.83, 1.23) 0.92 1.06 (0.83, 1.36) 0.64
 PP 1.11 (0.90, 1.37) 0.34 1.09 (0.83, 1.43) 0.53
Age ≥60 years (n = 2,348) (n = 251, 10.7%) (n = 160, 6.9%)
 SBP 1.36 (1.18, 1.57) <0.01 1.49 (1.26, 1.76) <0.01
 DBP 1.11 (0.95, 1.29) 0.19 1.18 (0.98, 1.42) 0.09
 MAP 1.25 (1.08, 1.46) <0.01 1.36 (1.14, 1.64) <0.01
 PP 1.35 (1.18, 1.54) <0.01 1.46 (1.24, 1.72) <0.01

SBP, DBP, MAP, and PP entered in separate model, adjusted for age, sex, current smoking, obesity (BMI ≥ 30), diabetes mellitus, hyperlipi-
demia, atrial fibrillation, history of coronary heart disease, antihypertensive medication, antiplatelet medication, and lipid-lowering medication.
Abbreviations: BMI, body mass index; CI, confidence interval; DBP, diastolic blood pressure; HR, hazards ratio; MAP, mean arterial blood pres-
sure; PP, pulse pressure; SBP, systolic blood pressure.
aHR was calculated by 1-SD increase in corresponding blood pressure component.

Association of PP with long-term outcomes in dual BP
component models
We further addressed the relative importance of PP, SBP,
DBP, and MAP in predicting stroke outcomes using the mul-
tivariate Cox proportional-hazards model to examine the BP
parameters in combination. In the group <60 years of age,
dual BP components of SBP + PP, DBP + PP, MAP + PP were
analyzed separately using the same model. Neither of these
BP components showed an association with combined end-
points or recurrent stroke (Table 3). When SBP and PP were
examined in the same model in the group ≥60 years of age,
PP, but not SBP, was significantly associated with combined
end-points (HR, 1.29; 95% CI, 1.02–1.64; P  =  0.03) and

4  American Journal of Hypertension

 Association of PP With Stroke Outcome

Table 3.  Association of dual blood pressure components with combined end-points and recurrent stroke stratified

Combined end-points Recurrent stroke

BP components/per SD increment HRa (95% CI) P value HRa (95% CI) P value

Age <60 years (n = 1,847)

  SBP and PP
  SBP 0.91 (0.64, 1.28) 0.58 1.02 (0.67, 1.56) 0.92
  PP 1.22 (0.85, 1.77) 0.28 1.08 (0.68, 1.71) 0.75
  DBP and PP
  DBP 0.94 (0.77, 1.16) 0.58 1.01 (0.78, 1.31) 0.92
  PP 1.14 (0.92, 1.41) 0.25 1.09 (0.83, 1.44) 0.52
  MAP and PP
  MAP 0.94 (0.74, 1.18) 0.58 1.01 (0.76, 1.35) 0.92
  PP 1.16 (0.91, 1.49) 0.23 1.09 (0.80, 1.49) 0.59
Age ≥60 years (n = 2,348)
  SBP and PP
  SBP 1.09 (0.85, 1.40) 0.50 1.18 (0.87, 1.59) 0.29
  PP 1.29 (1.02, 1.64) 0.03 1.32 (0.99, 1.75) 0.06
  DBP and PP
  DBP 1.05 (0.91, 1.22) 0.50 1.10 (0.92, 1.32) 0.29
  PP 1.38 (1.20, 1.58) <0.01 1.48 (1.26, 1.75) <0.01
  MAP and PP
  MAP 1.06 (0.90, 1.25) 0.50 1.11 (0.91, 1.36) 0.29
  PP 1.35 (1.16, 1.57) <0.01 1.43 (1.18, 1.71) <0.01

Dual BP measurements entered in the same model, additionally adjusted for age, sex, current smoking, obesity (BMI ≥ 30), diabetes mel-
litus, hyperlipidemia, atrial fibrillation, history of coronary heart disease, antihypertensive medication, antiplatelet medication, and lipid-lowering
medication. Abbreviations: BMI, body mass index; CI, confidence interval; DBP, diastolic blood pressure; HR, hazards ratio; MAP, mean arterial
blood pressure; PP, pulse pressure; SBP, systolic blood pressure.
aHR was calculated by 1-SD increase in corresponding blood pressure component.

marginally associated with recurrent stroke. In a separate
multivariate model of DBP and PP, the effect of PP on com-
bined end-points (HR, 1.38; 95% CI, 1.20–1.58, P  <  0.01)
and recurrent stroke (HR, 1.48; 95% CI, 1.26–1.75, P < 0.01)
was independent of DBP. Similarly, the effect of PP on com-
bined end-points (HR, 1.35; 95% CI, 1.16–1.57; P  <  0.01)
and recurrent stroke (HR, 1.43; 95% CI, 1.18–1.71, P < 0.01)
was independent of MAP (Table 3).
DISCUSSION
The present study investigated the association of PP with
long-term stroke outcomes in 4,195 patients with ischemic
stroke in a multicenter prospective cohort study. We found
that PP within 3-month after ischemic stroke was associ-
ated with 2-year-outcomes of combined end-points and
recurrent stroke, and that this association was prominent in
patients older than 60 years of age. For every 1-SD increase
in PP, there was a 35% increase in the risk of recurrent vascu-
lar events and all-cause mortality and a 46% increase in the
risk of recurrent stroke.
The superiority of PP as a cardiac risk predictor in hyper-
tension has been well-established. Moreover, a physiologically
plausible mechanism that explains the link between raised PP
and cardiac risk has been described. However, the association
between PP and stroke risk or prognosis is less understood.
A  study with 198 patients with acute stroke demonstrated
that for every 10-mm Hg increase of PP, mortality at 1-year
post-stroke increased by 40%.29 Another study with 219
patients with acute stroke reported no association between
PP and mortality at 2.5 years post-stroke.30 The present find-
ings indicated that PP within 3 months after ischemic stroke
was positively related to 2-year post-stroke recurrence and
death rates. This may offer further evidence of large artery
stiffness contributing to poor outcomes of cerebral vascular
diseases. Unlike in our study, most previous studies assessing
the predicting value of BP parameters for stroke outcomes
initiated the BP measurement 24 hours of ictus. Since BP
increases following acute stroke and spontaneously decreases
over a period of days to weeks, studies on BP measures in
this period may be influenced by stress response and disease
severity. Hence, we investigated BP within 3  months after
stroke in order to eliminate the acute phase response.
In this study, the predictive effect of PP was prominent in
the stroke population aged 60 years or older, thus manifesting
a possible modification of PP effect by age. This is consistent

American Journal of Hypertension  5

Su et al.
with previous evidence demonstrating that, with advancing
age, the predictor of CHD shifts from DBP to SBP and then
to PP as a consequence.8 This may be because the large vessel
stiffness is a dominant risk factor of CHD in the aging popula-
tion, whereas the resistance of peripheral arteries is dominant
in the younger population. Indeed, the changing patterns of
BP with increasing age have been widely accepted. SBP con-
tinues to rise throughout life in comparison to DBP, which
rises until 50 years of age, levels off over the next decade, and
remains constant or falls after 60  years of age. In line with
recent findings that PP dose not substantially contribute to the
cardiovascular risk stratification below the age of 60 years,31,32
our study further indicated that this age difference might also
be true in predicting the stroke outcomes. Further investiga-
tion is warranted to study the relationship of age-modified PP
effects with long-term outcomes in patients with stroke.
Our present study has several points of strength. First, it is a
multicenter, prospective, observational study with a large sam-
ple size, designed with objectivity, and its end-points are easy
to be evaluated. Second, BP measures were performed within
3 months of ischemic stroke, thus diminishing the influence
of the acute hypertensive response and reflecting a rela-
tively stable PP in predicting the long-term stroke outcomes.
Nevertheless, several limitations regarding our study should
be addressed. First, brachial BP by sphygmomanometer is less
accurate in measuring the central pressure than other more
invasive or technologically advanced methods. However, this
type of BP measurement is easily obtained in a clinical setting.
Second, a lower stroke recurrence rate (5.6% in our current
study) compared with 14.1% reported before was obtained.33
The exclusion of patients with severe comorbid diseases could
explain the limited event rate. Third, different antihyperten-
sive medications might have differential influence on differ-
ent components of BP, and changes in BP-lowering treatment
during follow-up might affect the association between PP
and long-term stroke outcomes. In addition, the value of PP
in clinical intervention may be limited and needed to be fur-
ther investigated in future prospective studies, though PP was
observed to be independently associated with long-term stroke
outcomes after adjustment of SBP, DBP, or MAP in the present
study. Finally, the current study was designed to improve the
secondary prevention of ischemic stroke in a Chinese patient
population. As previous reported, Chinese stroke patients had
higher prevalence of small vessel occlusion and large­artery
atherosclerosis, whereas prevalence of cardioembolic stroke
were lower than that in Caucasian.34,35 Therefore, the present
results might not directly apply to the broad populations, thus
limiting the generalizability of our findings.
In conclusion, our study demonstrated that in the elderly
ischemic stroke patients, PP was associated with long-term
stroke outcomes in a 2-year spectrum. Higher PP, considered
as an indicator or consequence of aortic stiffening, might
deteriorate the long-term prognosis under stroke conditions.
SUPPLEMENTARY DATA
Supplementary data are available at American Journal of
Hypertension online.
6  American Journal of Hypertension
ACKNOWLEDGMENTS
This study was supported by the 11th and 12th Five-Year
National Science and Technology Support Program (grant
number: 2006BAI01A10, 2011BAI08B03), and the National
Natural Science Foundation of China (grant number:
81173663).
DISCLOSURE
The authors declared no conflict of interest.
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