Published online before print May 12, 2008, doi: 10.1161/HYPERTENSIONAHA.108.112334
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(Hypertension. 2008;52:107.)
© 2008 American Heart Association, Inc.
Original Articles |
Left Ventricular Filling Pressure by Doppler Echocardiography in Patients With End-Stage Renal Disease
From the Departments of Medicine and Therapeutics (A.Y-M.W., M.W., Y.Z., J.E.S.) and Chemical Pathology (C.W-K.L., I.H-S.C.), Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong. Current affiliations: Department of Medicine (A.Y-M.W., M.W.), Queen Mary Hospital, University of Hong Kong, Hong Kong; Department of Cardiovascular Medicine (J.E.S.), University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Correspondence to Angela Yee-Moon Wang, University Department of Medicine, University of Hong Kong, Queen Mary Hospital, 102 Pokfulam Rd, Pokfulam, Hong Kong. E-mail aymwang{at}hku.hk
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Abstract |
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Left ventricular hypertrophy and systolic dysfunction predict mortality in patients with end-stage renal disease. However, the prognostic value of left ventricular filling pressure has remained uncertain in this population. We evaluated whether the early mitral inflow velocity to peak mitral annulus velocity (E/Em) ratio, an estimate of left ventricular filling pressure by tissue Doppler imaging, has significant additional prognostic value to conventional echocardiographic parameters and other clinical and biochemical parameters in 220 patients with end-stage renal disease. The E/Em ratio was elevated (>15) in 62% of the patients. Multivariate analysis showed that an elevated E/Em ratio had the highest correlation with left ventricular volume index, followed by loss of residual glomerular filtration rate, increasing age, worsening ejection fraction, and diabetes. During the median follow-up of 48 months, the E/Em ratio emerged as an independent predictor of all-cause mortality (adjusted hazard ratio: 1.027; 95% CI: 1.003 to 1.051; P=0.026) and cardiovascular death (adjusted hazard ratio: 1.033; 95% CI: 1.002 to 1.065; P=0.035) in the multivariable Cox regression analysis. In addition, the E/Em ratio added significant incremental prognostic value for all-cause mortality (P=0.035) and cardiovascular death (P=0.035) beyond the standard clinical, biochemical, and dialysis parameters and echocardiographic measurements. In conclusion, the E/Em ratio displayed important additional long-term prognostic information above and beyond that of left ventricular mass and systolic function. Our data suggest that left ventricular filling pressure should be estimated during echocardiographic examination for additional prognostication in patients with end-stage renal disease.
Key Words: end-stage renal disease • mortality risk • tissue Doppler • left ventricular filling pressure
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Introduction |
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Cardiovascular disease is the leading cause of death in patients with end-stage renal disease (ESRD) and is partly attributed to the high prevalence of accelerated atherosclerosis and left ventricular (LV) hypertrophy. Of patients starting long-term dialysis therapy, LV hypertrophy was already present in nearly three quarters and was frequently complicated with LV dilatation and systolic dysfunction.1 Furthermore, progressive worsening of cardiac dilatation with compensatory hypertrophy continued with time on dialysis.2
In patients with ESRD, both LV hypertrophy and systolic dysfunction have been shown to be important predictors of outcome, and there is a high prevalence of circulatory congestion.1,3–5 Furthermore, patients with a history of heart failure at the initiation of dialysis were noted to have higher mortality.6 Thus, the ability to assess LV filling pressure noninvasively using echocardiography may serve as an important clinical tool and add important value for prognostication in this group of patients. Recently, the ratio of early transmitral flow velocity (E) to early diastolic mitral annular velocity (Em) (E/Em ratio) assessed using tissue Doppler imaging may be more accurate than other methods for estimating LV filling pressure7 and has been shown to be an excellent predictor of diastolic filling in different subsets of patients.8–11
Therefore, the objective of this study was to investigate whether the estimation of the E/Em ratio using tissue Doppler imaging adds significant long-term prognostic value beyond that of standard clinical, biochemical, dialysis, and echocardiographic parameters in patients with ESRD.
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Methods |
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Study Design and Subjects
This was a 4-year prospective study performed in 220 stable patients with ESRD receiving maintenance peritoneal dialysis (PD) at a regional dialysis center in Hong Kong. The study protocol complies with the Declaration of Helsinki and had full approval from the local clinical research ethics committee. All of the patients provided informed consent before study entry.
Patients were considered eligible for study inclusion if they had received continuous PD treatment for 
3 months. Exclusion criteria included severe valvular stenosis or regurgitation, hypertrophic cardiomyopathy, underlying malignancy, chronic liver disease, systemic lupus erythematosus, chronic rheumatic heart disease, congenital heart disease, patients who refusal to give consent, or incomplete data. Fifty patients were excluded by these criteria, representing 18.5% of the total PD population. All of the patients were continuously dialyzed using conventional lactate-buffered glucose-based PD solutions. In those who developed acute coronary syndrome, acute heart failure, peritonitis, exit site infections, or any other infective complications, assessments were deferred for 1 month after complete resolution of the complication.
Clinical and Demographic Data
Known clinical atherosclerotic vascular disease was defined as the presence of coronary artery disease (indicated by history of angina, previous myocardial infarction with or without history of coronary artery bypass surgery, or percutaneous intervention), cerebrovascular disease (indicated by history of cerebrovascular event or transient ischemic attack), and peripheral vascular disease (indicated by the presence of intermittent claudication or resting leg pain, together with clinical signs of peripheral vascular disease with or without a history of amputation or revascularization). With a mercury sphygmomanometer, systolic and diastolic blood pressures were measured once on every follow-up visit after the patient was rested for 15 minutes on either arm at 8-week intervals for 12 months preceding study entry and were then averaged to give the final systolic and diastolic blood pressure.
Echocardiography and Tissue Doppler Imaging
Echocardiography was performed at study entry using a GE-VingMed System 5 echocardiographic machine (GE-VingMed Sound AB) with a 3.3-mHz multiphase array probe in subjects lying in the left decubitus position by a single experienced cardiologist blinded to all of the clinical details of patients. The echocardiographic techniques and calculation of different cardiac dimensions and volumes were performed according to the guidelines of the American Society of Echocardiography.12 LV ejection fraction was obtained using a modified biplane Simpson’s method from apical 2- and 4-chamber views.13 Midwall fractional shortening (mwFS) was calculated according to the formula as described by Mayet et al.14 The LV mass was calculated using the modified American Society of Echocardiography cube formula proposed by Devereux et al15 and indexed by body surface area. LV hypertrophy was defined as LV mass indexed by body surface area >131 g/m2 in men and >100 g/m2 in women.16,17
Mitral inflow velocities were recorded using pulsed wave Doppler with the sample volume placed at the tip of the mitral valve tips from the apical 4-chamber view. From the mitral valve inflow velocity curve, the following measurements were made: peak E-wave velocity and its deceleration time, peak A-wave velocity, and the isovolumetric relaxation time were measured from the aortic valve closure to the mitral valve opening.18 A composite of these conventional Doppler measurements was used to define diastolic dysfunction.19,20 Abnormal diastolic function was further categorized into an abnormal relaxation filling pattern, restrictive filling pattern, and pseudonormal filling pattern.21
Myocardial velocities were recorded using the tissue Doppler technique, as described previously.9,22 Color-coded tissue Doppler images were acquired over a predetermined 2 consecutive cardiac cycles for each of the 4 mitral segments and were transferred to a workstation composed of a personal computer of which the software package provides customized image visualization, processing, and analysis (EchoPac, GE-VingMed). The sample volume was placed in the mitral annulus of septal and lateral myocardial segments from the 4-chamber view and inferior and anterior myocardial segments from the 2-chamber views. Mean velocities during systole, early diastole, and late diastole were measured. The final value represented the average of 4 sites.
Biochemical Analysis
EDTA and heparinized blood samples were collected at baseline for measurement of high-sensitivity C-reactive protein, serum albumin, blood hemoglobin, urea, creatinine, calcium, phosphorus, and intact parathyroid hormone. High-sensitivity C-reactive protein and albumin in heparin plasma were measured, respectively, using the Tina-quant C-reactive protein latex ultrasensitive assay and the bromocresol purple method on the Roche analyzer. Serum intact parathyroid hormone was measured by the IMMULITE 1000 Analyzer (Diagnostic Products Corporation).
Assessment of Residual Renal Function and Dialysis Indices
Twenty-four-hour urine and dialysate was collected for the measurement of residual glomerular filtration rate, total weekly urea, and creatinine clearance using standard methods.23,24
Outcome Measures
All of the patients were prospectively followed 
4 years from the day of baseline assessment or until death. The cause of death was determined by the attending physicians, who had no knowledge of the tissue Doppler imaging results. This information was identified from the computerized clinical management system of the Hong Kong Hospital Authority and the Renal Registry Database that keeps detailed records of all hospitalization episodes and causes of death. In case of death out of the hospital, family members were interviewed by telephone to ascertain the circumstances surrounding death. No patient was lost to follow-up.
The outcome measures evaluated were death from all causes and cardiovascular death. Cardiovascular death included death associated with a definite myocardial ischemic event, heart failure, cerebrovascular event, arrhythmia, and peripheral vascular accident, all of which were defined according to standard clinical criteria, as well as sudden cardiac death, which was defined as unexpected natural death within 1 hour from the symptom onset and without any previous condition that would appear fatal.25,26
Statistical Analysis
Continuous data were expressed as means±SDs or median (interquartile range) and categorical data as percentages. Comparisons between groups were done by the unpaired t test for mean data, Mann-Whitney U test for median data, or 
2 test for categorical data. Comparisons of baseline characteristics among patients who remained alive on dialysis at the end of 4 years and those who died from cardiovascular and noncardiovascular causes were done by the 1-way ANOVA, Kruskal-Wallis test, or 2 test, where appropriate. Multivariate logistic regression of the E/Em ratio 15 was performed by considering factors with P<0.25 in the univariate analysis.
Cumulative survival curves were generated by the Kaplan-Meier method, and between-group survival was compared by the log-rank test. In this analysis, patients who underwent kidney transplant or were transferred to hemodialysis during follow-up were censored at the time of transfer to alternative renal replacement therapy. If a patient died within 3 months of transfer to hemodialysis, then he or she was not censored, because the early mortality was considered to reflect the health status during the period of failing PD treatment. We used a Cox proportional hazards model to estimate the hazard ratios of all-cause mortality and cardiovascular death in relation to the E/Em ratio and other variables. We checked that all of the variables considered in the regression analysis met the assumption of proportional hazards. Variables that showed significant difference between patients who remained alive on dialysis and those who died from cardiovascular or noncardiovascular causes were considered in the multivariable Cox regression analysis. To have adequate confounder control, important covariates, such as gender, duration of dialysis, and presence of hypertension, were retained in all of the models regardless of their statistical significance.
The incremental value of E/Em ratio over other clinical, demographic, biochemical, dialysis, and conventional echocardiographic parameters was assessed by a modified stepwise procedure in 4 modeling steps. The first model consisted of baseline clinical, demographic, biochemical, and dialysis risk factors. The second model consisted of adding LV mass index. The third step consisted of adding mwFS. The final step was entering either E/Em ratio or conventional Doppler-defined diastolic dysfunction into the model. A significant improvement in model prediction was based on the –2 log likelihood ratio statistic, which follows a 2 distribution, and the P value was based on the incremental value compared with the previous model. A risk score for each subject based on each model was calculated by multiplying the coefficient estimate for each variable from the fully adjusted Cox model by the value of the variable for each patient and then adding these figures for each patient. This risk score was then used to calculate the predictive value of each model using the receiver-operator characteristics curve analysis. Statistical analysis was performed using SPSS version 14.0 (SPSS, Inc).
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Results |
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The baseline characteristics of the study population are shown in Table 1. Of the 222 patients, 2 patients (0.9%) had E/Em ratios <8, 81 patients (36.8%) had E/Em ratios of 8 to 15, and 137 patients (62.3%) had E/Em ratios >15 (which identifies an abnormally elevated LV filling pressure).7 Because there were only 2 patients with E/Em ratios <8, the group with E/Em ratios <8 and 8 to 15 were merged together for analysis. The baseline characteristics of patients with E/Em ratios >15 versus those with E/Em ratios
15 are compared in Table 1. The differences in echocardiographic parameters between the 2 groups of patients are presented in Table 2. Using multiple logistic regression analysis, an elevated E/Em ratio >15 showed the strongest correlation with LV volume index, followed by residual glomular filtration rate, age, LV ejection fraction, and diabetes (Table 3).
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During the 48-month follow-up, 84 patients had died, 27 patients underwent kidney transplantation, and 24 patients were switched to long-term hemodialysis. Fifty-three deaths (63%) were of cardiovascular causes, and 31 deaths were because of noncardiovascular causes. The cardiovascular deaths included ischemic heart disease/acute myocardial infarction in 7 patients, cerebrovascular events in 14 patients, sudden cardiac death in 22 patients, heart failure in 4 patients, peripheral vascular disease in 5 patients, and arrhythmia in 1 patient. The noncardiovascular deaths included peritonitis in 12 patients, other infective complications in 13 patients, malignancy in 1 patient, and termination of dialysis in 5 patients. The baseline characteristics of patients who remained alive on PD and patients who died from cardiovascular and noncardiovascular causes are presented in Figure S1 (please see http://hyper.ahajournals.org). The baseline E/Em ratio was the highest among patients who died from cardiovascular causes.
Figures 1A and 1B show the Kaplan-Meier estimates of overall survival and cardiovascular event-free survival probability for patients stratified by tertiles of the E/Em ratio. On univariate analysis, the hazard ratios associated with E/Em ratio in relation to all-cause mortality and cardiovascular death were 1.051 (95% CI: 1.033 to 1.069; P<0.001) and 1.055 (95% CI: 1.034 to 1.076; P<0.001), respectively. In the multivariable Cox regression analysis, the E/Em ratio was associated with an increased risk of all-cause mortality (adjusted hazard ratio: 1.027; 95% CI: 1.003 to 1.051; P=0.026; Figure S2) and cardiovascular death (adjusted hazard ratio: 1.033; 95% CI: 1.002 to 1.065; P=0.035; Figure S3).
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The predictive value for all-cause mortality and cardiovascular death was the highest in the model, including demographic, clinical, biochemical, and dialysis risk factors, as well as LV mass index, mwFS, and E/Em ratio (model 4B; Table 4). Including conventional Doppler-defined diastolic dysfunction did not increase the predictive value for all-cause mortality and cardiovascular death (model 4A; Table 4).
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The incremental value of the E/Em ratio and conventional Doppler-defined diastolic dysfunction in outcome prediction is shown in Figure 2A and 2B. E/Em ratio improved the prognostic value for all-cause mortality (P=0.035; model 4B, Figure 2A) and cardiovascular death (P=0.035; model 4B, Figure 2B) in a model including clinical, demographic, biochemical, and dialysis risk factors, as well as LV mass index and mwFS. However, conventional Doppler-defined diastolic dysfunction had no significant incremental value in predicting all cause mortality (model 4A; Figure 2A) and cardiovascular death (model 4A; Figure 2B).
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Discussion |
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In this study, we showed that >60% of our patients with ESRD had elevated LV filling pressure. More importantly, we demonstrated that combining the transmitral flow velocity with annular velocity (E/Em ratio) provides independent and additional prognostic value for long-term (4 years) mortality and cardiovascular death in patients with ESRD above and beyond that of clinical, biochemical, dialysis, and echocardiographic parameters, including LV mass and systolic function. Studies have shown that E/Em ratio is the single best Doppler predictor of elevated LV filling pressure7 and a powerful independent predictor of all-cause mortality in a general cardiac population in those with LV systolic dysfunction and after acute myocardial infarction27–29 and correlates better with pulmonary capillary wedge pressure than brain natriuretic peptide.30 More recently, a study in the ESRD population showed that an E/Em ratio of
15 has a sensitivity of 82% and a specificity of 88% in predicting LV end-diastolic pressure >15 mm Hg,31 suggesting that an E/Em ratio >15 is a reliable marker of increased LV filling pressure in this population. Taken together with our current data, this suggests that the additional prognostic value contributed by the E/Em ratio beyond that of LV mass and mwFS is most likely explained because it is reflecting an increased LV filling pressure in the patients with ESRD. Notably, the E/Em ratio appeared to be a more significant predictor of long-term mortality and cardiovascular death compared with mwFS. A higher E/Em ratio, indicating a higher LV diastolic filling pressure, was associated with greater LV hypertrophy and dilatation and more systolic dysfunction. However, only the E/Em ratio retained independent significance in the multivariable Cox regression model for cardiovascular death. We stratified patients by the E/Em ratio of 15. As shown in the general population, this is the optimum cutoff value above which patients are considered to have an elevated LV filling pressure, as determined by measuring the mean LV end-diastolic pressure at cardiac catheterization and also as currently recommended by the European Society of Cardiology.7,20 It is worth noting that only 2 patients in our cohort had E/Em ratios <8. The finding that an E/Em ratio >15 showed the strongest correlation with LV volume index provides additional evidence that increased LV filling pressure of patients with ESRD may be partly attributed to extracellular volume expansion. Our observation is in keeping with an earlier study suggesting that volume loads and ventricular distensibility modifications are the primary factors that influence LV filling pressure in uremic patients.32 Loss of residual renal function was second to LV volume index as the most significant factor associated with an increased E/Em ratio in our patients. This well accords with our previous data showing an important link between residual renal function and cardiac hypertrophy33 in PD patients and suggests that an increased LV filling pressure is reflecting the degree of LV hypertrophy.
In addition, an E/Em ratio >15 appeared to identify the sickest patients with ESRD as evidenced by the greater prevalence of diabetes, atherosclerotic vascular disease and heart failure, higher systolic blood pressure, greater inflammation, more anemia and hypoalbuminemia, and lower residual renal function compared with those with E/Em 15. This is consistent with studies showing that LV hypertrophy, reduced aortic distensibility, diabetes, and coronary artery disease may all contribute to an increased LV filling pressure in ESRD.28,34,35 Furthermore, a higher E/Em ratio was associated with a worse echocardiographic profile. Indeed, systolic dysfunction emerged as one of the significant factors associated with an elevated E/Em ratio. Thus, the E/Em ratio should not be considered only as a measure of volume status but rather as surrogate marker of LV filling pressure, which may be elevated from multiple causes, including extracellular volume expansion.
Our study has several limitations. First, only prevalent dialysis patients were included, which may introduce survival bias. Second, all of the parameters were measured at a single time point and did not reflect changes over time. Third, invasive measurement of LV filling pressure was not performed simultaneously. However, as shown by other studies, the E/Em ratio correlates well with LV filling pressure.7,9,30 Fourth, volume status was not directly assessed in our patients, and it is not known whether an E/Em ratio may vary according to the volume status. It was reported previously that volume reduction affects mitral inflow velocities in hemodialysis patients.36 Mitral annular velocity was also volume dependent, yet, to a lesser extent than mitral inflow velocities.22,37,38 However, there is currently no similar data in PD patients.
Perspectives
This study demonstrates the incremental value of measuring the ratio of early mitral inflow velocity to peak mitral annulus velocity (E/Em ratio), an estimate of LV filling pressure, over other standard clinical, biochemical, and dialysis risk factors and conventional echocardiographic and Doppler-derived measures for prognostication in patients with ESRD. Our data suggest that LV filling pressure should be assessed during echocardiographic examination of patients with ESRD for additional prognostication and cardiovascular risk stratification.
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Acknowledgments |
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Sources of Funding
This study was supported by the Hong Kong Health Service Research Fund (project code 6901023), of which A.Y-M.W. was the principal investigator.
Disclosures
None.
Received February 20, 2008; first decision March 10, 2008; accepted April 21, 2008.
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