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Perit Dial Int 29(2): 163-170
2009
© 2009 International Society for Peritoneal Dialysis
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Clinical

ASSOCIATION BETWEEN PULSE PRESSURE AND MORTALITY IN PATIENTS UNDERGOING PERITONEAL DIALYSIS

Wei Fang1,2, Xiao Yang1,3, Joanne M. Bargman1 and Dimitrios G. Oreopoulos1

Peritoneal Dialysis Program,1 University Health Network and University of Toronto, Toronto, Ontario, Canada; Renal Division,2 Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai; Department of Nephrology,3 the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China

Correspondence to: D.G. Oreopoulos, University Health Network, Toronto, and University of Toronto, 399 Bathurst Street, Toronto, Ontario M5T 2S8 Canada. dgo{at}teleglobal.ca


   ABSTRACT
TOP
 ABSTRACT
SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 DISCLOSURE
 REFERENCES
 

{diamondsuit} Background: Pulse pressure has been shown to be associated with adverse outcomes in the general population and in patients on hemodialysis (HD). However, the significance of pulse pressure has not been studied in peritoneal dialysis (PD) patients. This study examined the association between pulse pressure and mortality in patients undergoing chronic PD.

{diamondsuit} Methods: All patients aged 18 years or older that commenced PD between 1 January 2000 and 31 December 2005 at the University Health Network, Toronto, were included. The association between pulse pressure and mortality was assessed using the Cox proportional hazards model.

{diamondsuit} Results: A total of 306 patients were included in the study. Mean pulse pressure of the study cohort was 56.8 ± 17.8 mmHg. Age and diabetes were significant predictors of elevated pulse pressure (p < 0.001). After adjusting for the level of systolic blood pressure and other demographic and clinical parameters, multivariable Cox proportional hazards modeling showed a direct and consistent association between pulse pressure and death risk. Each increment of 1 mmHg in pulse pressure was associated with a 2.7% increased hazard of all-cause death [95% confidence interval (CI) 1.001 – 1.054, p = 0.039] and a 4.1% increase in risk for cardiovascular mortality (hazard ratio 1.041, 95% CI 1.003 – 1.081; p = 0.035).

{diamondsuit} Conclusion: Elevated pulse pressure is associated with an increased risk of all-cause and cardiovascular death in patients on PD. Recognition of this characteristic as an important predictor of mortality suggests that one goal of antihypertensive therapy in PD patients should be to decrease elevated pulse pressure.

KEY WORDS: Arterial stiffness; mortality risk; pulse pressure.

Hypertension is an important predictor of subsequent adverse clinical outcomes in the general population (1,2); however, in patients with end-stage renal disease (ESRD), blood pressure has a paradoxical association with clinical outcome. A number of observational cohort studies have reported U-shaped or reverse-J-shaped relationships between conventional blood pressure measurements (systolic, diastolic, and mean arterial) and mortality in hemodialysis (HD) patients (3–5). These studies report that HD patients with higher systolic pressures have improved survival compared with those whose systolic pressures are lower.

Blood pressure propagates through the arterial tree as a repetitive continuous wave and is more accurately described as consisting of a pulsatile component and a steady component. There is increasing evidence that the pulsatile aspect can provide important information about the cardiovascular risk conferred by hypertension, particularly in middle-aged and elderly populations (6–11). Pulse pressure is an index of the pulsatile component of the cardiac cycle (12) and is governed by the relationship between ventricular ejection and the elastic properties of large arteries (arterial stiffness), as well as the indirect effect of arterial-wave reflection from periphery back to central conduit arteries. Large prospective cohort and interventional trials that investigated the association between pulse pressure and clinical events in non-ESRD populations found a positive correlation between increased pulse pressure and heart failure, myocardial infarction, and all-cause and cardiovascular death (6–10).

Patients with ESRD exhibit vascular abnormalities that contribute to elevated pulse pressure, especially medial vascular calcification — which leads to increased arterial stiffness — increased pulse-wave velocity, and early wave reflection (13,14). Recently, it was shown that pulse pressure has a consistent association with higher mortality in patients on maintenance HD (15,16). However, in peritoneal dialysis (PD), where there are no significant fluctuations of blood pressure associated with the treatment and where initiation of this form of dialysis produces early improvement of hypertension (17), the significance of pulse pressure has not been studied. The present study examined the association between pulse pressure and mortality in patients undergoing chronic PD.


   SUBJECTS AND METHODS
TOP
 ABSTRACT
 SUBJECTS AND METHODS
RESULTS
 DISCUSSION
 DISCLOSURE
 REFERENCES
 
PATIENTS AND DATA COLLECTION
All patients aged 18 years or older that started on PD between 1 January 2000 and 31 December 2005 at the University Health Network, Toronto, were identified from administrative records and included in our study. Demographic and clinical data were extracted from clinical charts. Blood pressure was measured in the PD clinic by trained nurses using a standard mercury sphygmomanometer with the patient in the supine position. Systolic and diastolic blood pressures were collected serially every 3 months. Pulse pressure was quantified as the difference between systolic pressure and diastolic pressure. The numbers and details of antihypertensive medications [angiotensin-converting enzyme inhibitors (ACEIs)/angiotensin II-receptor blockers (ARBs), calcium channel blockers, beta-blockers, and others] and the use of statins were also collected.

The following demographic and comorbidity characteristics were collected at initiation of PD: age, gender, race, underlying cause of ESRD, height, weight, presence of diabetes mellitus (defined either as a comorbid condition or the etiology of ESRD), history of hypertension, previous congestive heart failure (defined as episode of congestive heart failure during the 6 months before PD commencement), coronary artery disease, peripheral vascular disease, cerebrovascular disease, smoking status, and details about renal transplantation. Cardiovascular disease (CVD) was defined as a previous history of coronary artery disease, peripheral vascular disease, or cerebrovascular disease. Body mass index was calculated as weight (in kilograms) divided by the square of height (in meters). The following laboratory parameters were collected: hemoglobin, serum albumin, calcium, phosphate, intact parathyroid hormone (iPTH), and lipids. Other clinical data collected at initiation of PD included the presence of left ventricular hypertrophy (LVH), residual renal function, urine output, PD prescription, peritoneal transport characteristics measured by the dialysate-to-plasma creatinine ratio (D/Pcr) at 4 hours in a standard peritoneal equilibration test, and total Kt/V urea. Left ventricular hypertrophy was defined by mass indexed to body surface area of greater than 131 g/m2 in men and 100 g/m2 in women, or by electrocardiogram in case of echocardiography data not being available. All patients were followed up from PD initiation until death, cessation of PD, transfer to other centers, or to the end of the study (31 December 2006). Detailed causes of death were recorded from clinical charts. Causes of death were grouped as follows: cardiovascular, including cardiac, cerebrovascular, peripheral vascular, and sudden death; ad non-cardiovascular, including infection, other, and unknown causes.

STATISTICAL ANALYSES
All data are expressed as mean ± SD for normally distributed data, median and range for skewed data, and frequency (%) for categorical data. Univariate associations between pulse pressure and demographic, clinical, and laboratory parameters were estimated using the t-test and linear regression for categorical and continuous parameters, respectively. To determine independent associations, multivariable linear regression estimated the relationship between pulse pressure and the parameters described above.

Associations with mortality were examined using univariate and multivariate Cox proportional hazards regression by backward stepwise elimination based on the likelihood ratio. Pulse pressure was analyzed as both a categorical variable and a continuous variable. Data for survival analysis were censored at the time of renal transplantation, transfer to HD, transfer to another center, cessation of PD, or 31 December 2006. Statistical analysis was performed using SPSS version 13.0 (SPSS Inc., Chicago, IL, USA). A p value less than 0.05 was considered statistically significant.


   RESULTS
TOP
 ABSTRACT
 SUBJECTS AND METHODS
 RESULTS
DISCUSSION
 DISCLOSURE
 REFERENCES
 
CHARACTERISTICS OF THE COHORT
We included in the present study 306 patients that started PD between 1 January 2000 and 31 December 2005. The main baseline demographic characteristics of the study population are presented in Table 1. Our study cohort had a mean age of 59.4 ± 17.4 years and 53.6% were male. The underlying renal diagnosis was diabetic nephropathy in 88 (28.8%), glomerulonephritis or autoimmune disease in 85 (27.8%), hypertensive nephrosclerosis in 41 (13.4%), polycystic kidney disease in 23 (7.5%), and other miscellaneous causes in 69 patients (22.5%). Among the 306 patients, 115 (37.6%) had diabetes mellitus either as their primary renal disease or as a comorbidity, 66 (21.6%) had previous congestive heart failure, 135 (44.1%) had a history of CVD, 41 (13.4%) were failed transplants, and 54 (17.6%) had a history of smoking. Most patients (87.9%) had preexisting hypertension; 255 (83.3%) were taking at least 1 hypertensive medication and 165 (53.9%) were being treated with an ACEI or an ARB. Table 2 shows the clinical characteristics of the study patients. During follow-up, the PD modality was continuous ambulatory PD in 119 (38.9%) and continuous cycling PD in 187 (61.1%); icodextrin solution was being used in 94 (30.7%) patients.


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  		TABLE 1 Baseline Demographic Characteristics of the Study Patients

 

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  		TABLE 2 Baseline Clinical Characteristics of the Study Patients

 

The study population had mean systolic pressure of 134.1 ± 22.6 mmHg and diastolic pressure of 77.3 ± 13.6 mmHg at initiation of PD. Mean baseline pulse pressure was 56.8 ± 17.8 mmHg.

FACTORS ASSOCIATED WITH PULSE PRESSURE
Univariate analysis showed that pulse pressure rose with increasing age: pulse pressure increased by 2.2 mmHg for every 10-year increase in age (p < 0.001). Mean pulse pressure for men was higher than for women (58.8 ± 17.6 vs 54.5 ± 17.8 mmHg, p < 0.05). A higher pulse pressure was seen among patients with diabetes compared with those without diabetes (62.5 ± 19.2 vs 53.3 ± 16.0 mmHg, p < 0.001). Patients with a history of CVD and hypertension had a higher pulse pressure than that of patients without CVD (61.1 ± 19.3 vs 53.4 ± 15.8 mmHg, p < 0.001) and without hypertension (57.8 ± 17.8 vs 49.6 ± 16.0 mmHg, p < 0.01). Patients with LVH had a higher pulse pressure than those without LVH (61.2 ± 18.4 vs 54.3 ± 17.3 mmHg, p < 0.01). Left ventricular mass index (LVMi) was associated with pulse pressure: an increase of 10 g/m2 in LVMi for every increment of 0.7 mmHg pulse pressure (p < 0.05). Peritoneal permeability was associated positively with pulse pressure: an elevation of 2.6 mmHg for every 0.1 increase in D/Pcr (p < 0.05). A higher pulse pressure was seen among patients receiving antihypertensive treatment compared with patients not receiving them (58.4 ± 17.8 vs 48.9 ± 15.9 mmHg, p < 0.01). History of smoking, residual renal function, body mass index, hemoglobin, calcium, phosphate, iPTH, and lipids were not associated with pulse pressure. Variability in pulse pressure between patients was driven primarily by variations in systolic pressure, as evidenced by a significant R square in linear regression for the relationship between systolic pressure and pulse pressure (r2 = 0.636, p < 0.001), but not for diastolic pressure (r2 = 0.000, p > 0.05).

Because systolic blood pressure correlated highly with pulse pressure in univariate analysis, the level of systolic pressure may have influenced the associations between pulse pressure and other parameters. Therefore, we included systolic pressure as a covariate in a multivariable regression analysis of pulse pressure (Table 3). After adjustment for the level of systolic pressure, important variables independently associated with elevated pulse pressure were age (2.5 mmHg per 10-year increase) and the presence of diabetes mellitus (4.9 mmHg).


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  		TABLE 3 Multivariable Linear Regression Analysis of Pulse Pressure in Peritoneal Dialysis Patientsa

 

OUTCOME
Median duration of follow-up of the study population was 21.1 (0.6 – 83.5) months. During a total follow-up of 8422 patient-months, 74 patients died (35 cardiovascular deaths and 39 non-cardiovascular deaths), 46 patients transferred to HD, 47 patients received a transplant, 20 patients transferred to other centers, and 8 patients spontaneously recovered renal function and ceased dialysis. There was no significant difference in baseline pulse pressure among the patients that received transplant, switched to HD, recovered, or transferred to another center. Transplant patients had fewer baseline CVD comorbidities compared to other censored patients, they were younger, and had higher serum albumin than patients that transferred to HD or another center.

ASSOCIATION BETWEEN PULSE PRESSURE AND MORTALITY
Unadjusted Cox proportional hazards model showed that the association between pulse pressure and mortality was not statistically significant [hazard ratio (HR) 1.008, 95% CI 0.995 – 1.021; p = 0.223]. Because pulse pressure has a strong association with systolic blood pressure, examining the independent association between pulse pressure and mortality required an adjustment for the level of systolic pressure. After controlling for the level of systolic pressure, a direct and consistent association was seen between increasing pulse pressure and increasing risk of mortality (HR 1.051, 95% CI 1.028 – 1.076; p < 0.001). After these patients were classified into five categories according to quintiles of baseline pulse pressure (<40 mmHg, 40 – 49 mmHg, 50 – 59 mmHg, 60 – 69 mmHg, and ≥70 mmHg), the results showed that the hazard for death increased with increasing pulse pressure category after adjustment for systolic pressure (Figure 1). Compared with subjects in the reference category 40 – 49 mmHg, patients with pulse pressure >60 mmHg experienced significantly increased mortality. After adjustment for level of systolic blood pressure, pulse pressure was a function solely of diastolic pressure. For any given level of systolic pressure, lower diastolic pressure was associated with increased risk of death (HR 0.951, 95% CI 0.930 – 0.973; p < 0.001). Compared with the patients in the reference category 70 – 79 mmHg, patients with diastolic pressure <60 mmHg had significantly higher risk for death after correction for systolic pressure (Figure 2).


Figure 1
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  		Figure 1 — Hazard ratios for mortality associated with pulse pressure after adjustment for systolic pressure. The category with pulse pressure 40 – 49 mmHg served as reference.

 

Figure 2
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  		Figure 2 — Hazard ratios for mortality associated with diastolic blood pressure after adjustment for systolic pressure. The category with diastolic pressure 70 – 79 mmHg served as reference.

 

The results of a full mortality model adjusted for other variables known to influence either pulse pressure or death are shown in Table 4. After adjustments for systolic pressure and other demographic and clinical parameters, pulse pressure remained significantly associated with all-cause mortality: each increment of 1 mmHg in pulse pressure was associated with a 2.7% increased hazard of death (95% CI 1.001 – 1.054, p = 0.039). In this model, systolic pressure was inversely related to mortality: 2.2% decreased death hazard for each elevation of 1 mmHg in systolic pressure (95% CI 0.959 – 0.998, p = 0.03). Mortality risk increased with age and presence of previous congestive heart failure. Mortality risk decreased with higher serum albumin. In this model, pulse pressure was a function solely of diastolic pressure. We further introduced diastolic pressure into the multivariate Cox model instead of pulse pressure and the results showed that lower diastolic pressure was associated with increased mortality (HR 0.979, 95% CI 0.960 – 0.999; p = 0.036). Further analysis showed that pulse pressure was independently associated with cardiovascular mortality (HR 1.041, 95% CI 1.003 – 1.081; p = 0.035) but was not associated with non-cardiovascular death (HR 1.01, 95% CI 0.974 – 1.048, p = 0.583) (Table 5).


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  		TABLE 4 Multivariable Cox Proportional Hazards Model of All-Cause Mortality

 

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  		TABLE 5 Multivariable Cox Proportional Hazards Model of Cardiovascular and Non-Cardiovascular Mortality

 

Subgroup analyses were performed by stratifying patients by the presence or absence of previous CVD and diabetes. Table 6 shows that elevated pulse pressure is associated with mortality only in subjects without known CVD (HR 1.063, 95% CI 1.015 – 1.112; p = 0.009) and not in patients with CVD. Similarly, pulse pressure tended to have an association with death in nondiabetic patients but not in patients with diabetes. The risk attributed to pulse pressure in the mortality model differed among individuals with different levels of systolic pressure: p = 0.011 for the interaction term between systolic pressure and pulse pressure. We did not do further stratification analysis because the number of patients in each systolic pressure category was too small.


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  		TABLE 6 Hazard Ratios for Death Associated with Pulse Pressure Stratified by Cardiovascular Disease (CVD) or Diabetes

 


   DISCUSSION
TOP
 ABSTRACT
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
DISCLOSURE
 REFERENCES
 
To our knowledge, this study is the first to demonstrate the association between pulse pressure and increased death risk in ESRD patients receiving PD. Since variability of pulse pressure in the study population was largely accounted for by variation in systolic blood pressure, a model examining mortality and pulse pressure alone could be confounded by the independent relationship between mortality and systolic pressure. For this reason we adjusted the level of systolic pressure in mortality, an approach used in recent studies of both general and ESRD populations (7,9,15,16). Because pulse pressure correlated with systolic pressure in the current study, there was concern of multicollinearity in our regression analysis. To assess this concern, we examined the tolerance and the variation inflation factor of these two variables and the results showed that the tolerance was 0.346 and the variation inflation factor was 2.7. Therefore, multicollinearity was not likely a problem in our mortality analysis.

By adjusting for systolic pressure and other important demographic and clinical parameters in the final multivariable Cox proportional hazards model, we showed that, for a given level of systolic pressure, an increment of 1 mmHg in pulse pressure was associated with a 2.7% increase in the hazard for all-cause death and a 4.1% increase in the hazard for cardiovascular mortality. Moreover, although pulse pressure is more likely to be elevated in patients with CVD, the risk attributed to pulse pressure actually is driven by patients without this comorbidity. Arterial stiffness is strongly associated with CVD (18); therefore, a widening pulse pressure would be expected in patients with CVD, as was seen in present study. A possible explanation for this observation is that there are risk factors other than arterial stiffness more associated with mortality in patients with clinically recognized CVD. It is also possible that patients with CVD susceptible to a high pulse pressure already died and the remaining patients may have been protected against a higher pulse pressure. As Figure 2 illustrates, when adjusting for systolic pressure, the magnitude of pulse pressure is determined solely by diastolic blood pressure. In essence, this indicates that, for any given level of systolic blood pressure, the lower the diastolic pressure the greater the risk of death.

Pulse pressure is a simple mathematical difference between systolic and diastolic blood pressure and therefore is an easily measured index of pulsatile hemodynamic load during the cardiac cycle. Early return of reflected arterial waves increases afterload at end-systole and decreases coronary perfusion pressure during diastole (19). Such dynamic stress may be particularly important when underlying cardiac dysfunction is present, as is often the case in ESRD patients (20,21). Studies in non-ESRD populations have shown that death and cardiac disease may be related more to pulsatile stress than to small vessel resistance reflected in static measures of blood pressure, such as systolic, diastolic, or mean arterial pressure (7–11).

A stepwise increase in arterial stiffness with increasing stages of chronic kidney disease has been reported recently (22). Compared with age- and blood pressure-matched controls with normal renal function, ESRD is associated with elevated arterial stiffness, pulse wave velocity, and early wave reflections (13,14). Also, prolonged uremia aggravates stiffening of the arterial wall (23). The mechanisms underlying these changes are incompletely understood but may be a reflection of the abnormal vascular biology seen in chronic kidney disease. The atherogenic environment of chronic kidney disease includes contributions from hypertension, hypervolemia, qualitative and quantitative lipid abnormalities, divalent ion changes, aberrant inflammatory responses, and hyperhomocysteinemia, among other putative disturbances (24).

Banerjee et al. recently reported that elevated pulse pressure is related to high risk of death in predialysis patients (25). Pulse pressure has also been shown to be a reliable indicator of increased mortality in HD patients. Tozawa et al. followed 1243 HD patients for 9 years and reported that high pulse pressure is associated with all-cause mortality and that, as a predictor of death, it is superior to systolic and diastolic blood pressure in nondiabetic Japanese HD patients (16). Foley et al., who examined outcomes of 11142 HD patients from USRDS Waves 3 and 4 Study with an average follow-up period of 3.8 years, reported that both higher systolic pressure and lower diastolic pressure had independent associations with mortality in a pattern suggesting wider pulse pressure (26). Klassen et al. analyzed data from 37069 HD patients and found a direct and consistent relationship between increasing pulse pressure and increasing death risk after adjustment for systolic pressure: there was a 1.2% increased hazard for death for each 1-mmHg increase in pulse pressure (15). The present study showed a similar positive association between pulse pressure and mortality in PD patients. With high pulse pressure being an indicator of pathology, PD patients may bear the burden of increased afterload and decreased coronary perfusion pressure. It is conceivable that such a burden contributes to the high prevalence of LVH and CVD seen in patients with ESRD. This is consistent with our observation that higher pulse pressure is an independent predictor of cardiovascular death.

Pulse pressure in the present PD cohort was lower than that reported in HD patients: 70 – 75 mmHg predialysis and 66 – 72 mmHg postdialysis (15,16,27). The lower pulse pressure might partially explain our observation that, in our patients, each increment in pulse pressure was associated with a higher risk for death than Klassen et al. found in their HD patients. The mechanisms of the lower pulse pressure in PD patients are not fully understood. Some contributing factors may be better fluid volume control and greater clearance of vasoconstrictor factors compared with HD (28); the presence of an arteriovenous fistula in HD patients, which increases cardiac preload and stroke volume and is associated with progression of LVH (29); and the fluctuations of blood pressure associated with a HD session. Peritoneal permeability (D/Pcr) was found to be associated positively with pulse pressure in the univariate regression analysis. The mechanism of this observation is not clear but may relate partially to impaired ultrafiltration and fluid overload in patients with high peritoneal permeability. Similarly to previous reports in HD patients (15,16,27), age and diabetes were significant predictors of elevated pulse pressure in PD patients in our study (Table 3).

The present study showed that elevated pulse pressure increases the risk of mortality in PD patients. Therefore, we suggest that the goal of antihypertensive therapy in PD patients should be not only to reduce blood pressure but also to decrease pulse pressure. Abnormalities in arterial stiffness can be modified by aerobic exercise, reduced salt intake, cessation of smoking, and a healthy diet (30–32). Among antihypertensive agents, ACEIs and calcium channel blockers could decrease arterial wave reflection and pulse-wave velocity and increase arterial compliance in certain populations (33–35). The potential therapeutic implications of these medications for arterial stiffness in PD patients need further investigation.

Our study has several limitations. It is a retrospective study. Univariate analysis showed only an insignificant trend to increased risk for death with elevated pulse pressure; however, once the data were adjusted for systolic pressure and other important parameters, we saw a statistically significant association. We believe that the multivariate model more accurately represents the truth because univariate analysis is incomplete and contains potential confounders. In Tozawa et al.'s study (16), only 17% of patients had diabetes, whereas 37.6% of patients in our study had diabetes; this might partially explain why we did not observe an association between pulse pressure and mortality in the univariate analysis. The interaction between systolic pressure and pulse pressure was significant; however, further analysis was not done because of the small number of patients in each category. Compared to studies of HD patients and based on registry data, our study has a small sample size; however, we included more detailed information about patients' comorbidities and clinical and laboratory data, allowing us to make appropriate adjustments to examine the relationship between pulse pressure and mortality. Furthermore, our data originate from the same care provider and hence uniform patient management practices, thereby avoiding many potentially confounding factors compared to studies using contributions from different centers.

In conclusion, elevated pulse pressure is associated with risk of all-cause and cardiovascular death in PD patients. The recognition of pulse pressure as an important predictor of mortality in PD patients suggests that one goal of antihypertensive therapy should be to decrease elevated pulse pressure. Also, this highlights the need to investigate the potential therapeutic implications of measures that would lessen arterial stiffness and thus improve clinical outcomes in PD patients.


   DISCLOSURE
TOP
 ABSTRACT
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 DISCLOSURE
REFERENCES
 
None declared.

Received 20 November 2007; accepted 4 June 2008.


   REFERENCES
TOP
 ABSTRACT
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 DISCLOSURE
 REFERENCES
 

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