Download Determinants of Arterial Stiffness progression in Peritoneal Dialysis

Impact of Mean Arterial Pressure on Progression of Arterial Stiffness in
Peritoneal Dialysis Patients under Strict Volume Control Strategy
Meltem Sezis Demirci 1, Ozkan Gungor 1, Fatih Kircelli 1, Juan Jesus Carrero 2,
Erhan Tatar 1, Cenk Demirci 1, Meral Kayikcioglu 3, Gulay Asci 1, Huseyin Toz
1
,
Mehmet Ozkahya 1, Ercan Ok 1
1 Ege
University School of Medicine, Division of Nephrology, Izmir, Turkey
2 Divisions
of Renal Medicine and Baxter Novum, Center for Gender Medicine and
Center for Molecular Medicine, Karolinska Institute, Sweden
3
Ege University School of Medicine, Division of Cardiology, Izmir, Turkey
Running Title: Arterial stiffness progression in peritoneal dialysis patients
Corresponding Author:
Ozkan Gungor
Ege University School of Medicine, Division of Nephrology
35100, Bornova, Izmir
Phone: ++90.232.3904254
Email: [email protected]
ABSTRACT
Introduction: Arterial stiffness is an important contributor to the increased
cardiovascular burden of uremia. The aim of the study was to identify determinants of
arterial stiffness progression in peritoneal dialysis (PD) patients with strict volume
control.
Patients-Methods: Eighty-nine prevalent PD patients were enrolled. Assessment of
arterial stiffness was performed at baseline and after nine months on average (range
8-12 month) by carotid-femoral pulse wave velocity (cf-PWV).
Results: Mean age was 51±13 years; preceeding time on PD was 40±34 months.
Fifty-seven percent of the patients were men and 9% were diabetic. At baseline,
mean cf-PWV was 8.7±2.7 m/s and was significantly higher in patients with diabetes
and on automated PD therapy. Cf-PWV was positively correlated with age, history of
cardiovascular disease, mean arterial pressure (MAP), blood glucose, left atrium
diameter and left ventricular mass index. Sixty patients underwent a second cf-PWV
measurement. Thirty-six percent had progression of arterial stiffness. Delta cf-PWV
value was 2.08±1.89 m/s for progressors and -1.25 ± 1.43 m/s p<0.01 for nonprogressors (p<0.01). In logistic regression analysis, the change in MAP was the only
predictor for progression of arterial stiffness.
Conclusions: MAP is the main determinant of arterial stiffness progression. Our
results lead us to suggest that efficient blood pressure control may contribute to
preserved or reduced arterial stiffness in PD patients.
Keywords: Peritoneal dialysis, blood pressure, arterial stiffness, mean arterial
pressure.
1
Introduction
Peritoneal dialysis (PD) patients have increased cardiovascular (CV) burden, and CV
disease is in fact the most frequent cause of death [1, 2]. Problems in control of
blood volume, dyslipidemia and greater oxidative stress caused by glucose-based
PD solutions are factors specific to PD therapy that have been suggested to affect
these adverse outcomes [3]. Arterial stiffness (AS) has also been depicted as an
important contributor to the increased CV burden [4,5]. The underlying mechanisms
of AS are, nevertheless, not well defined, but elevated levels of oxidative stress and
inflammation markers, hypervolemia, arterial calcification, activation of the renin–
angiotensin–aldosterone system, sympathetic nervous system overactivity are all
anticipated to play a role in stiffening of the arterial bed [6]. Increased left ventricular
stress and reduced coronary perfusion (which are both consequences of arterial
stiffness) lead to cardiac hypertrophy and myopathy resulting in congestive heart
failure and sudden death in dialysis patients [7].
Hypertension is an important contributor to the increased cardiovascular morbidity
and mortality of dialysis patients, and we have previously shown that a strict volume
control strategy may be an effective method to reach better control of hypertension
and preservation of cardiac functions in both PD and hemodialysis patients [8-10].
Strong associations between mean arterial pressure (MAP) and arterial stiffness
have been reported in both dialysis and renal transplant patients [11-13]. However,
the determinants of arterial stiffness and its progression in PD patients are not welldefined. In this study we evaluated the changes of carotid-femoral pulse wave
velocity (cf-PWV) during 9 months on PD as an attempt to elucidate factors
associated PWV progression in a cohort of patients under strict volume control.
2
Materials and Methods
Patients
Of the ninety-five patients undergoing PD at our institution, eighty-nine PD patients
being treated at our unit for at least 6 months were enrolled in this study (3 patients
did not want to participate, 2 had atrial fibrillation and 1 had a new onset peritonitis),
which included a second examination on average 9 months after (range 8-12
months). Seventy-three patients were on Continuous Ambulatory PD (CAPD) and 16
on automated PD (APD). CAPD patients were dialyzed using Baxter Twin Bag
(Baxter Healthcare SA, Castlebar, County Mayo, Ireland) and Fresenius A.N.D.Y
Plus or Stay-safe systems. (Fresenius Medical Care GmbH, Bad Homburg,
Germany). APD patients were treated with Baxter Home-Choice or Fresenius PD
Night cyclers.
Baseline data including age, sex, body mass index (BMI), systolic and diastolic blood
pressure, weekly creatinine clearance, and peritoneal Kt/V urea, type of PD therapy
and duration of PD therapy, medications and biochemical parameters were recorded
from patients’ charts. Blood chemistry parameters were assayed by standardized and
automated techniques in the Hospital’s analytical laboratory, which is adhered to
several external quality control programs. Blood pressure and biochemical
parameters (fasting) were measured at 2-month intervals during the follow-up and
time-averaged values were calculated. Blood pressures were measured during the
clinic visits by the same physician using an Erka sphygmomanometer in the morning
period and while the patient was sitting/resting at least for 5 minutes. The reported
measurement measurements are the average of two measurements taken 5 minutes
apart. Mean arterial pressure was calculated by adding the systolic pressure reading
3
to two times the diastolic reading and dividing the sum by 3. Fifty healthy individuals
with a similar age and sex distribution were used as controls.
The study was approved by Local Ethics Committee, informed consent was obtained
from all patients and was performed according to the recommendations of the
Declaration of Helsinki.
Center’s Strict Volume Control Strategy
Our center applies a strict volume control strategy consisting of dietary salt restriction
and ultrafiltration in order to reach blood pressure levels below 130/85 mmHg and
cardiothoracic index below 0.50. To reach these targets, detailed oral and written
information on moderate salt restriction (NaCl intake 4-5 g/day) is given to the
patients. Patients are allowed to drink as much as their thirst requires, as long as
their salt intake is restricted. Visits are scheduled according to their clinical and
laboratory data; monthly during the first 6 months and thereafter every 2 months. If
necessary, more frequent visits are performed. At every visit, patient is questioned
about salt intake and physical examination was performed to assess volume status. If
necessary, hypertonic PD solutions (2.27% or 3.86% glucose) were used to remove
excess volume. When in doubt, a ‘’captopril test’’ is performed as previously
described [7,8]. In hypervolemic patients furosemide is added. Those not responding
to diuretics or having a positive captopril test are treated with appropriate
antihypertensive drugs.
Echocardiographic Measurements
At baseline, patients underwent echocardiography at the time of arterial stiffness
investigation by the same operator. All echocardiographical measurements were
4
performed according to American Society of Echocardiography recommendations
(14). The following assessments were recorded: left atrium diameter (LAD), left
ventricular end-diastolic (LVEDD) and end-systolic diameters (LVESD), right
ventricular end-diastolic diameter, thickness of the posterior wall and the
interventricular septum. Left ventricular mass (LVM) was calculated using the
equation described by Devereux [14]. Left ventricular mass index (LVMI) was
calculated by dividing LVM by body surface area. Intra-operator variability was less
than % 8.
Carotid İntima Media Thickness Measurement
Common carotid artery intima-media thickness (CA-IMT) was assessed by highresolution color Doppler ultrasound (HDI 5000, Philips, Bothell, WA, USA) with 5–12MHz broadband electronic linear-array transducer. The intra-observer variability of
measurement was 4% (mean difference, 0.02).
Bioimpedance Analysis
Volume status was determined by bioimpedance analysis (Bodystat Quadscan 4000
(Isle of Man, British Isles). Extracellular water corrected for height was assessed.
Arterial Stiffness Measurements
Arterial stiffness was assessed by carotid-femoral PWV with the SphygmoCor device
(Atcor Medical, Sydney, Australia). Assessments were done by sequential recordings
of the arterial pressure wave at the carotid and femoral arteries, and by
measurement of the distance from the carotid sampling site to the suprasternal notch
and from the suprasternal notch to the femoral sampling site [15]. With a
5
simultaneous ECG recording of the R-wave as reference, the integral software
calculated the pulse wave transit time. Measurements were performed in fasting
status with an empty abdomen after 5-10 minutes of resting. If used, antihypertensive
medications were stopped at least 24 hours prior to evaluation. Arterial stiffness was
measured by the same operator at both time-points. Intra-operator variability was
less than %5. Progression of arterial stiffness was defined as an increase in the cfPWV> 5% (to rule out possible intra-observer effect) in the second measurement at
the end of the follow-up. Patients were grouped as progressors and non-progressors
on the basis of having a change of cf-PWV higher or equal lower than 5%,
respectively.
Statistical analysis
All parameters were expressed as mean ± SD. A P value less than 0.05 was
considered statistically significant. Comparisons between two groups were assessed
by independent t-test analysis. Pearson’s rank correlation was used to assess
correlations of arterial stiffness and other variables. Multivariate logistic regression
analysis was used to study the predictive factors for arterial stiffness progression.
Data of patients who did not undergo the second examination due to transfer to
another dialysis center, switch of dialysis modality or transplantation were included in
all analyses in order to minimize selection bias. Time-averaged data were used to
evaluate the relation between laboratory data and changes in arterial stiffness.
Calculations were performed using SPSS 15.0 (Chicago, IL, USA). In linear
regression analysis for predictors of arterial stiffness 2 models were used: in model
1: Age, sex, body mass index, diabetes, history of CVD, mean blood pressure, PD
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modality, LVMI and ECW/height was included in the model. In model 2, CA-IMT was
added to model 1.
Results
Baseline data
Demographical characteristics of the patients are listed on Table 1. Mean age was 51
± 13 years and the preceeding time on PD was 40 ± 34 months (median 37
months). Fifty seven percent were women and 9% were diabetic. Eighteen percent
of the patients were on APD. CVD history was present in 7% of the cases and 16%
were on antihypertensive drugs. Thirty six percent of the patients were anuric. 4
patients were on 3.86 (or 4.25) % glucose PD solution and the remaining patients
were on 2.27 (or 2.5) % or 1.36 (or 1.5) % glucose PD solution. A comparison with 50
healthy controls of similar age and sex distribution (mean age 51±9 years and 58%
were women) showed that despite similar blood pressure levels (mean systolic and
diastolic blood pressures were 128±18 mmHg and 78±9 mmHg, respectively), cfPWV was higher in the PD patients (8.7±2.7 vs. 7.5±1.4 m/s; p=0.003).
At baseline, cf-PWV was positively correlated with age, blood glucose, history of
CVD and diabetes, MAP, pulse pressure (PP), waist-hip ratio, CA-IMT, LAD, LVMI
and extracellular water corrected for height (ECW/height). There was no correlation
between arterial stiffness and dialysis duration in our study (r=0.107, p=0.317).
Diabetic patients (11.9±4.6 & 8.2±2.2 m/s, p=0.01) and patients on APD (10.9±3.7 &
8.0±2.1 m/s, p= 0.01) had higher cf-PWV values compared to those who were not.
We performed multiple linear regression analysis predicting cf-PWV with variables
selected from univariate analysis. Age, diabetes, MAP, being on APD and LVMI were
7
predictors for cf-PWV in model 1. CA-IMT, MAP and APD modality were predictors in
model 2, which included model 1 and CA-IMT (Table 2).
Follow-up Data
All patients were invited to undergo a second examination 9 months on average after
baseline determinations. Twenty nine patients did not undergo a second
measurement due to the following reasons: 4 patients were transferred to other
institutions, 3 patients died, 6 patients received kidney transplantation and 14 were
switched to hemodialysis due to ultrafiltration failure and/or hypervolemia. Of the
sixty-two patients, two patients were excluded a posteriori due to new onset
arrhythmia which disabled cf-PWV measurements. Second arterial stiffness
evaluation could be performed in 60 PD patients.
Of these patients, mean percentage change in cf-PWV from baseline was 1.6%.
This would be not considered to be clinically significant and to rule out possible intraobserver effect (less than 5%), patients were grouped as progressors and nonprogressors on the basis of having a change of cf-PWV higher or equal lower than
5%, respectively. According to this definition, 22 patients had progression (81 % of
them having a change of cf-PWV higher than 10%) of cf-PWV and 38 had no
progression. Δ cf-PWV (2.08±1.89 m/s and -1.25 ± 1.43 m/s p<0.01, respectively)
and ΔMAP (10.8±13.6 and -6.7±16.4 mmHg, p<0.01, respectively) were significantly
higher in progressors than non-progressors (Figure 1). In univariate analysis, Δ cfPWV was correlated with change in MAP and pulse pressure (PP) (Figure 2, 3).
Baseline mean PTH was 422±373 pg/ml, CaxP=45±13 mg 2/dl2, CRP=1.09±1.39
mg/dl and final mean PTH was 424±366 pg/ml, CaxP was 43±12 mg 2/dl2,
CRP=0.84±1.18 mg/dl.
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When baseline and time-averaged characteristics were compared, there were
no significant differences in time-averaged serum levels of blood glucose,
albumin, hs-CRP, CaXP product, parathyroid hormone, cholesterol, and
triglyceride. In addition, time averaged values of weekly total creatinine
clearance, ultrafiltration volume and residual urine volume were not different
between progressors and non-progressors. However, progressors had higher use
of anti-hyperlipidemic agents than non-progressors. Comparisons of baseline vs 9month data (paired t-test) showed that progressors showed an increase in blood
glucose, systolic and diastolic blood pressure and decrease in residual diuresis,
whereas non-progressors showed an increase in serum triglyceride levels and
decrease in serum calcium level, systolic and diastolic blood pressure (Table 3).
Whereas the use of low-calcium dialysate did not differ between groups at baseline
(p=0.578; data not shown), it was significantly increased in non-progressors during
the follow-up (from 66% to 82%, p=0.012) and there was no significant difference in
progressors (from 73% to 86%, p=0.08). In a stepwise forward exclusion logistic
regression analysis, only delta MAP was associated with the progression of arterial
stiffness in PD patients (Table 4).
Discussion
Our study shows that PD patients have stiffer arteries than age- and sex-matched
controls. Both cross-sectionally and longitudinally, MAP significantly contributes to
the variance of arterial stiffness in PD patients under a strict blood pressure control
regime. The contribution of MAP to the changes in arterial stiffness could be
explained in part by functional changes of artery resulting from high blood pressure
(the load on the vessel) in our study. Additionally, in the presence of disease-induced
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structural changes, the stiffening is less dependent on lowering blood pressure. In
the study by Guerin et al. [16], it was shown that survival of end-stage renal failure
patients was significantly worse in whose aortic PWV did not decline in response to
blood pressure lowering. In accordance with this, when we divided patients according
to ΔMAP, (ΔMAP<0, n=23,and ΔMAP≥0 n=37), only two out of 23 patients within the
ΔMAP<0 group had stiffness progression (8.7%). Although these findings may
support the existence of disease-induced structural changes of the arteries, the
numbers of the patients who had progressed according to this definition are
inadequate to reached definitive conclusion. It is also possible that longer follow-up
may be needed to denote such changes. Altogether, these results may allow us to
speculate that blood pressure control could be helpful to therapeutically reduce
arterial stiffness in this population.
Hypertension is a major risk factor for the increased cardiovascular mortality rates of
PD patients [17-20]. Increases in systolic blood pressure cause elevations in endsystolic stress subsequently leading to cardiac hypertrophy and higher myocardial
oxygen requirement. On the other hand, a decrease in diastolic blood pressure alters
coronary perfusion and causes myocardial ischemia [21]. In our study, which
included patients with a good control of blood pressure (mean SBP and DBP of
121±24 and 77±14 mm/Hg, respectively), we found that per 1mmHg increment in
MAP, the risk of progression of AS increases by 12.4 %. This result emphasizes the
important effect of blood pressure changes on AS even in patients without evident
hypertension, and goes in line with recent data showing MAP as the main
determinant of IMT levels in pre-dialysis patients [22]. In our study, PP and changes
in PP (Δ PP) were significantly correlated with baseline f-c PWV and Δf-c PWV,
respectively. However, in multivariate analysis when ΔPP was added to the model for
10
prediction of arterial stiffness progression, ΔMAP was the only significant predictor.
This last observation disagrees with Kim. et al. [23], who reported that PP had the
strongest correlation with PWV among a variety of BP parameters.
In our study, the rate of progression of arterial stiffness was 1.6% and this rate
was lower than the recent study by Jung JY. et al. In this study, despite no
exact data on progression of arterial stiffness is given, derived from a
progression of 44±209 cm/s from the baseline value of 1022±276 cm/s,
approximately 4.3% change over a 1 year period was observed. They also
reported that “some” patients had a progression rate of more than 15%, which
was the median of annual increasing change in cf-PWV. The reason for this
difference between these 2 studies may be due to higher baseline mean arterial
blood pressure (106.6±16.8 vs. 93±17 mmHg, respectively), left ventricular
mass (127.4 ± 41.3 vs. 112±41 g/m2, respectively) and antihypertensive drug use
(76.1% vs. 16%, respectively) in the study of Jung JY. et al. compared to our
study; showing a population with a not so good volume control.
Cardiovascular disease is the leading cause of death for patients with end-stage
renal disease (ESRD). The increased risk of cardiovascular mortality may be
attributable to advanced atherosclerotic vascular changes and left ventricular
hypertrophy [24]. We also found that, increased carotid IMT and LVMI along with
older age and presences of diabetes were associated with increase in cf-PWV in our
patients. One of the most important factors commonly contributing to atherosclerosis
and LVH in dialysis patients may be increased end systolic stress, which has been
shown to result from increased stiffness of large arteries and augmentation of systolic
pressure in central arteries by wave reflection [25]. A raised pulse pressure due to
increased vascular stiffness may induce arterial remodeling, increasing wall
11
thickness, and the development of plaques. These mechanisms may also explain the
association between cf-PWV and LVMI and CA-IMT in our patients.
A recent study recently identified age, fetuin-A, MAP and TG as factors associated
with progression of AS in a cohort of 67 PD patients [26]. The fact that we didn’t
observe any association between TG and arterial stiffness progression may be the
consequence of a short follow-up. We found nevertheless that serum triglyceride
levels increased during follow-up in non-progressors, but time-averaged TG levels
were not different between groups. Two studies have reported that residual renal
function is associated with all-cause and cardiovascular mortality in both
hemodialysis and PD patients [27, 28]. Also, RRF related cross-sectionally to blood
pressure control, left ventricular hypertrophy, increased sodium removal, improved
fluid status and arterial stiffness [29]. However, despite a decrease in residual
diuresis in progressors by time, we did not find in our study any predictivity of
residual diuresis for progression of AS.
Increased arterial stiffness may be related to a high peritoneal permeability resulting
in fluid overload in PD patients [30]. In this study, we found that APD modality was
associated with increased arterial stiffness. Its explanation may be the use of more
glucose and lower clearance of glomerulotoxic middle molecules. In some reports it
has been suggested that the preservation of RRF was worse in APD patients.
Patients having high/high-average transport characteristics were treated with APD
modality in our study and their residual urine volume were significantly lower than on
CAPD patients (data not shown). These factors may have indirectly contributed to
development of arterial stiffness
In our previous study [31] we showed that dialysis with high dialysate Ca (1.75
mmol/L) was associated with increased arterial stiffness in PD patients. In this study,
12
despite non-significance in multivariate analysis, we found that decreases in serum
calcium level during follow-up in non-progressor group accompanied increased use
of low-calcium dialysate. On the basis of this observation, we suggest that it may be
a contributor to slowing down of progression of arterial stiffness together with control
of blood pressure.
Major limitations of our study are that we enrolled prevalent HD patients who have
been on peritoneal dialysis for an average of over 40 months and some of them for
many more months that we have a short follow-up of only 9 months, that we are
lacking a control group of patients who are having stage 5 CKD and that we have not
studied all other possible factors (oxidative stress, arterial calcification, activation of
the renin-angiotensin and sympathetic nervous system etc.) that may affect the
arterial stiffness. However, we should emphasize that we did not find any association
between PWV and inflammation marker (hs-CRP) and dialysis duration. Since we
found an association between PWV and volume parameters (ECW/height, LAD and
anti-hypertensive use), these results could support the relationship between arterial
stiffness and hypervolemia. We did not find association between arterial stiffness and
dialysis duration in our study.
Although our results should be interpreted with caution due to a relatively low number
of patients enrolled, this observational study shows that MAP was the main
determinant of AS and there was an association between MAP and AS and AS
progression in PD patients with strict volume control. Altogether, this may suggest
that efficient control of blood pressure could lead to reduced arterial stiffness,
particularly in PD patients.
13
Acknowledgments
J.J.C. obtained support from the Loo and Hans Osterman’s Foundation. We thank all
patients and staff for their help and support.
Disclosures
The authors declare no conflict of interest.
14
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