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NDT Advance Access published online on August 17, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm484
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Pulse wave velocity—a useful tool for cardiovascular surveillance in pre-dialysis patients

Marcelo M. Lemos1, Alessandra D. B. Jancikic1, Fabiana M. R. Sanches1, Dejaldo M. Christofalo2, Sérgio A. Ajzen2, Márcio H. Miname3, Raul D. Santos3, Fernando C. Fachini4, Aluízio B. Carvalho1, Sérgio A. Draibe1 and Maria Eugênia F. Canziani1

1Department of Internal Medicine, Division of Nephrology, 2Department of Radiology, Hospital do Rim e Hipertensão, Federal University of São Paulo, São Paulo, Brazil, 3Lipid Clinic Heart Institute (InCor), University of São Paulo, Medical School Hospital and 4Centro de Diagnóstico Brasil, São Paulo, Brazil

Correspondence and offprint requests to: Maria Eugênia F. Canziani, Rua Pedro de Toledo 282, ZIP 04039-000, São Paulo, Brazil. Email: dialisefor{at}uol.com.br



   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 
Background. Cardiovascular mortality is high among patients with chronic kidney disease. Pulse wave velocity (PWV) is a simple method used for arterial distensibility evaluation. Few data are available concerning PWV in pre-dialysis patients. The aim of this study was to evaluate the association between PWV and cardiovascular disease in pre-dialysis.

Methods. One hundred and four patients were submitted to PWV analysis, coronary artery calcium (CAC) determination with a multi-slice CT scan of the coronary arteries, echocardiogram and a carotid intima-media thickness (IMT) evaluation, with a high resolution ultrasound. The demographic characteristics and laboratory tests results were studied.

Results. The mean age of those studied was 54.4 ± 11.5 years, 60% were males and the mean creatinine clearance was 40 ml/min/1.73 m2. The mean PWV was 12.2 ± 3.4 m/s and it was significantly higher in males, diabetics, those with creatinine clearance <60 ml/min and proteinuria ≥1 g/24 h. PWV was correlated with systolic blood pressure, age, triglycerides, total cholesterol and 24 h proteinuria. In the multiple regression analysis, PWV was significantly associated with diabetes, age, systolic blood pressure and cholesterol. Fifty-eight patients (56%) presented coronary calcification and PWV correlated with coronary calcium score (R = 0.48; P < 0.001) and calcium volume (R = 0.50; P < 0.001). Moreover, PWV was higher in patients with coronary calcification (13.4 ± 3.6 m/s vs 10.7 ± 2.4 m/s; P < 0.001). The mean left ventricular mass index (LVMI) was 106 ± 31 g/m2 and 24% of patients had left ventricular hypertrophy, while 19 (18.3%) patients had left ventricular dysfunction. PVW was correlated with LVMI (R = 0.25; P = 0.01) while no association could be seen between PWV and the ejection fraction or left ventricular dysfunction. A correlation between the IMT and PWV was observed (R = 0.27; P = 0.005). In addition, those with a thicker IMT had a higher PWV (13.2 ± 3.4 m/s vs 11. 2 ± 3.2 m/s; P = 0.003).

Conclusion. PWV is associated with cardiovascular disease in pre-dialysis patients and can be a useful tool to identify patients with increased cardiovascular risk.

Keywords: arterial stiffness; cardiovascular disease; coronary calcification; pulse wave velocity



   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Acknowledgements
 References
 
Cardiovascular mortality is greater in patients with renal disease than in the general population [1]. This excess of cardiovascular risk has been reported since very early stages of chronic kidney disease (CKD) [2,3] and persists even after transplantation. Not surprisingly, among patients with CKD stage 4, the mortality rate overcomes the proportion of patients starting on dialysis [4].

Clearly, the potential for changing the burden of cardiovascular morbidity in this population is based on early recognition of cardiovascular disease and risk stratification. Pulse wave velocity (PWV) has been used for arterial stiffness evaluation and seems to be a good predictor of cardiovascular events and mortality in the general as well as dialysis population [5–7]. Recent data have shown that dialysis patients have stiffer arteries than non-uraemic subjects [8]. In addition, PWV measurement is a very simple test that can be performed by any trained professional, in an out-patient setting, with low costs and no radiation exposure.

In CKD patients, both coronary artery calcification (CAC) and carotid intima-media thickness (IMT) have been used as surrogate markers of atherosclerosis and were associated with increased risk of cardiovascular events. Few studies evaluated PWV among pre-dialysis patients; therefore, the aim of the present study was to evaluate arterial stiffness and to analyse its association with cardiovascular disease in pre-dialysis patients.



   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Acknowledgements
 References
 
Patients
A total of 104 pre-dialysis patients were recruited from the out-patient clinic at the São Paulo Hospital, Federal University of São Paulo. Screened patients were older than 18 years and had been followed for at least 3 months. Exclusion criteria included the presence of chronic inflammatory disease, active malignancy, human immunodeficiency virus (HIV), viral hepatitis and chronic use of steroids. Before enrolment, 86 (82.7%) patients were on regular use of angiotensin-converting enzyme (ACE) inhibitors, 23 (22.1%) angiotensin receptor blockers, 44 (42.3%) ß-blockers, 42 (40.4%) calcium channel blockers, three (2.9%) nitrates and 81 (77.9%) patients were taking diuretics. In addition, six (5.8%) patients were taking calcium-based phosphate binders and six (5.8%) patients were taking calcitriol, four (3.8%) were on human recombinant erythropoietin therapy and none of them were taking statins or fibrates. This study was approved by the University Ethical Advisory Committee and written informed consent was obtained from all participants.

Study protocol
All patients were evaluated by laboratory tests, PWV determination, 24 h ambulatory blood pressure monitoring (ABPM), CAC quantification by coronary multi-slice computed tomography, IMT determination by high resolution ultrasound and Doppler echocardiogram. The exams were performed within 1 month from the enrolment date.

Anamneses focusing on demographics, clinical characteristics, comorbidities, familiar and personal disease history, previous cardiovascular events and/or surgical procedures were obtained. The nutritional status of the subjects was assessed, body mass index was calculated for all patients and the waist circumference was determined as well.

Laboratory analysis
A whole-blood sample was drawn at the clinic by vein puncture from every patient in a 12 h fasting state. Laboratorial evaluation included determinations of haemoglobin, urea, creatinine, ionized calcium, phosphate, alkaline phosphatase, intact parathyroid hormone [(iPTH); chemiluminescence immunoassay (Immulite; DPC-Biermann, Bad Nauheim, Germany)], bicarbonate, sodium, potassium, lipid profile, albumin and C-reactive protein (CRP) levels determined by chemiluminescence immunoassay. Twenty-four-hour urine samples were obtained for the determination of proteinuria. Abnormal proteinuria was defined as urinary protein excretion >150 mg/24 h. For descriptive purposes, proteinuria was categorized in ≥1 g/24 h or <1 g/24 h. The creatinine clearance (CrCl) was estimated with the formula described by Cockcroft and Gault [9]. The diagnosis and classification of CKD were established according to the criteria from the Clinical Practice Guidelines for Chronic Kidney Disease Outcomes Quality Initiative [10]. Anaemia and metabolic acidosis were defined as haemoglobin <11 g/dl and bicarbonate <22 mEq/l, respectively. Hyperparathyroidism, hyperphosphataemia and hypercalcaemia were defined according to bone metabolism K/DOQI guidelines [11]. Metabolic syndrome was defined according to the guidelines of the National Cholesterol Education Program (Adult Treatment Panel III) [12].

Cardiovascular evaluation
PWV was determined by recording the carotid and femoral waveforms consecutively by using the Complior SP apparatus (Artech Medical, Pantin, France) and applying the foot-to-foot method, as previously published and validated [13]. The exams were performed early in the morning by a single-blinded operator. The intraobserver error for PWV was previously determined in 16 health volunteers (3.9%). The paired-samples t-test was used to compare first and second PWV determination and no significant difference was observed (t = 1.7; P = 0.11).

A 24 h ambulatory blood pressure monitoring was performed using the equipment Dyna-MAPA (Cardios, São Paulo, Brazil; approved by the Association for the Advancement of Medical Instrumentation, AAMI) according to an ongoing consensus [14].

Patients underwent CAC quantification by a multi-slice computed tomography scanner (LightSpeed Pro16, GE Healthcare, Milwaukee, USA), using a gantry rotation of 0.4 s; collimation: 2.5 mm (slice thickness); reconstruction time: 6 frames per second. A calcium threshold of 130 or more Hounsfield units (HU) was used. The images were scored by a single radiologist blinded to all clinical and biochemical aspects of the patient. As described by Agatston, the calcium score was determined by multiplying the area of each calcified lesion by a weighting factor corresponding to the peak pixel intensity for each lesion [15]. The sum of each lesion of all coronary arteries was used for analysis.

Carotid IMT was determined in all patients by high-resolution ultrasound [Ultramark HDI 3000, ATL Ultrasound Incorporation, Bothwell, WA, USA, (linear probe, 7.0 mhz, digital, with variable focal point)], according to the methodology described and validated elsewhere [16,17].

A 2D colour Doppler echocardiogram was performed in each patient according to the recommendations of the American Society of Echocardiography [18] using the equipment Philips HDI 5000 (Royal Philips Electronics, Netherlands). Left ventricular hypertrophy (LVH) was defined as a left ventricular mass index (LVMI) of 134 g/m2 or higher among men and 110 g/m2 or higher among women. Left ventricular dysfunction was defined by an ejection fraction ≤55%.

Statistical analysis
Data were analysed using SPSS 11.0 for Windows and all values were expressed as mean ± SD, median (range) and frequency, unless stated. Chi-square or Fisher's exact test were used for categorical variables, whereas Student's t-test or Mann–Whitney was used for continuous variables while comparing groups when appropriate. ANOVA was used for the comparison of three or more groups. The correlation between PWV and biochemical or cardiovascular variables was obtained by the Pearson correlation. The correlation between PWV and CAC was determined by the Spearman correlation. Multiple regression analysis was conducted to determine variables independently associated with PWV. Statistical significance was considered when P-value < 0.05.



   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Acknowledgements
 References
 
The characteristics of the 104 patients are shown in Table 1. The population was mostly composed of middle-aged male patients. Hypertension and diabetes were the main causes of CKD. According to CKD stages, three patients (2.9%) were in stage 1, 14 patients (13.4%) in stage 2, 53 patients (51%) in stage 3, 32 patients (30.8%) in stage 4 and two patients (1.9%) in stage 5. Abnormal proteinuria was observed in 58 (56%) patients and was ≥ 1 g/24 h in 19 (18%) patients. The prevalence of metabolic syndrome was 43.3%.


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  		Table 1. General characteristics of the patients (n = 104)

 
The mean PWV was 12.2 ± 3.4 m/s, and it was higher in diabetic patients (15.2 ± 3.7 m/s vs 11.0 ± 2.4 m/s; P < 0.001), males (13.0 ± 3.7 m/s vs 11.1 ± 2.6 m/s; P = 0.005), in those with CrCl <60 ml/min (12.4 ± 3.6 m/s vs 11.2 ± 1.5 m/s; P = 0.022) and those with proteinuria ≥1 g/24 h (14.4 ± 5.0 m/s vs 11.7 ± 3.0 m/s; P = 0.009) as shown in Figure 1. No differences in PWV were observed in patients with anaemia, metabolic acidosis or abnormal iPTH.


Figure 1
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  		Fig. 1. PWV vs cardiovascular risk factors.

 
PWV was positively correlated with systolic blood pressure (R = 0.42; P < 0.001), age (R = 0.42; P < 0.001), triglycerides (R = 0.31; P = 0.002), total cholesterol (R = 0.27; P = 0.005) and 24 h proteinuria (R = 0.21; P = 0.038). There were no correlations between PWV and waist circumference, diastolic blood pressure, body mass index, HDL-cholesterol, LDL-cholesterol, haemoglobin, iPTH, ionized calcium, phosphate, CRP and CrCl. In the multiple regression model, which included age, total cholesterol, triglycerides, 24 h proteinuria, mean systolic blood pressure, diabetes, CrCl <60 ml/min and male gender, the independent determinants of PWV were diabetes, age, total cholesterol and systolic blood pressure (Table 2).


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  		Table 2. Multiple linear regression: determinants of PWV

 
There were 58 (56%) patients with CAC in whom the median calcium score was 230AU (1–2500) and 22 (21%) patients had severe calcification (calcium score >400AU). PWV was correlated with coronary calcium score (R = 0.48; P < 0.001) and calcium volume (R = 0.50; P < 0.001). Moreover, PWV was higher in patients presenting CAC compared with those that had no CAC (13.4 ± 3.6 vs 10.7 ± 2.4; P < 0.001), as can be seen in Figure 2.


Figure 2
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  		Fig. 2. PWV in patients with coronary calcification vs no calcification.

 
The mean LVMI was 106 ± 31 g/m2, and 25 (24%) patients had LVH, while 19 (18.3%) patients had left ventricular dysfunction. PWV was correlated positively with LVMI (R = 0.25; P = 0.01) and tended to be higher among patients with LVH (13.2 ± 4.3 m/s vs 11.8 ± 3.0 m/s; P = 0.08). No association could be noted between PWV and the ejection fraction or with the presence of left ventricular dysfunction.

There were only two (1.9%) patients with a carotid IMT >0.1 cm (upper limit of reference range). A correlation between IMT and PWV was observed (R = 0.27; P = 0.005) and, when divided by the median (0.058 cm), those patients with a thicker IMT complex had a higher PWV (13.2 ± 3.4 m/s vs 11.2 ± 3.2 m/s; P = 0.003).



   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Acknowledgements
 References
 
This study demonstrated the association between arterial stiffness and cardiovascular disease among pre-dialysis patients. In addition, traditional risk factors for cardiovascular disease were the main determinants of PWV in these patients.

Among the several traditional risk factors, age and male gender were associated with PWV in the present study, in agreement with previous studies [19–22]. Actually, arterial stiffening is a hallmark of the ageing process, due to changes in the artery wall structure and remodelling [23]. Regarding gender, the differences between males and females concerning central obesity prevalence, smoking and blood pressure have been considered as possible explanations for the higher PWV in males. In addition, there might be other interactions between traditional cardiovascular risk factors and sex hormones, capable of modifying the elastic properties of large arteries [24].

It is already established that systolic blood pressure determines a mechanical stimulus to arterial wall remodelling through an excessive collagen production, leading to changes in the viscoelastic properties of aorta and branches [25]. Nevertheless, former studies have shown that increasing arterial stiffness might be also a primer, since it compromises the arterial ‘mechanical stress buffering’, leading to isolated systolic hypertension. Although the present study design did not allow causal determination, it has once more demonstrated the association between the mean systolic 24 h blood pressure and PWV.

Previous studies have reported an association between PWV and diabetes as well as hyperlipidaemia [26]. Accordingly, in this trial, multivariate analysis indicated that diabetes and total cholesterol were independent determinants of PWV, which could suggest an addictive effect, leading to arterial stiffening. Factors like advanced glycation end-products, endothelial dysfunction and atherosclerotic processes are probably included in this process [26].

Notably, PWV was associated with renal dysfunction and proteinuria. Despite study design limitations, this observation permits one to speculate that arterial stiffening could be leading to a predominant systolic hypertensive state, with consequent renal damage. Alternatively, arterial stiffening might have been increased merely as a consequence of CKD metabolic disturbances [19,27].

Beyond the association between arterial stiffness and several cardiovascular risk factors, the present study demonstrated that PWV has been a surrogate marker of cardiovascular disease. Whether arterial stiffening is a risk factor for the development of cardiovascular disease or is simply a marker of established cardiovascular disease is controversial and a matter of debate [28].

It has been demonstrated that the association between arterial stiffness and vascular calcification could probably be explained by age and other atherosclerosis-associated factors, such as diabetes and lipid profile disorders [29]. Moreover, vascular calcification has a direct effect on arterial stiffness, once calcified median lesions compromise the elastic properties of the arterial tree [30]. CAC probably develops in parallel with other large artery calcification, because risk factors are similar for both, justifying why PWV associates with either CAC, as shown in the present study, or large arteries (non-coronary) calcification, as demonstrated previously [31]. Therefore, carotid-femoral PWV, as an aortic artery distensibility index, could be a useful indicator of CAC.

As previously seen [32], PWV was linked to LVH. This association could be partially explained by the haemodynamic changes that follow arterial stiffening, increasing cardiac after-load, which in turn leads to development of LVH. Despite the lack of association between PWV and the ejection fraction or the presence of left ventricular dysfunction, which could be due to the heterogeneity of aetiologies of heart failure in the studied population, which included valve disorders, ischaemic heart disease, Chagas cardiopathy and many others that could not be entirely explained or associated with haemodynamic parameters such as PWV, these aspects remain to be studied.

Despite the very low prevalence of patients with abnormal IMT, PWV was correlated with carotid IMT, and it was higher among those with a thicker intima-media complex. This is in agreement with a previous study, that reported a linear correlation between IMT and arterial stiffness in dialysis patients [33]. Therefore, PWV could be useful even in cases of subtle modifications in carotid artery morphology, when IMT is still in the normal range. Nevertheless, further studies addressing the upper limit of normal for carotid IMT are necessary.

The present study provides a suggestion that a common pathway might justify the presence of multiple factors as independent determinants of the PWV and the association between PWV and cardiovascular disease. Laurent et al. [5] were the first researchers to report a direct relationship between aortic stiffness and cardiovascular and all-cause mortality in hypertensive patients without kidney disease, and several mechanisms that might explain this association, including LVH and atherosclerosis, are in agreement with the present study findings. These aspects and this hypothetical common pathway remain to be investigated.

In conclusion, this study pointed out factors associated with arterial stiffening and demonstrated that PWV seems to be a useful tool for cardiovascular surveillance in pre-dialysis patients. PWV is a simple, easy to perform, cheap and non-invasive method that identifies subgroups of pre-dialysis patients in whom cardiovascular disease evaluation should be even more prompt and detailed. This is very relevant, since early recognition of cardiovascular disease is essential to lower the unacceptably high mortality rates in CKD population.



   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
References
 
The authors thank Dr Robert Guiberteau, Genzyme Corporation, for providing the equipment for PWV measurement. Ambulatory blood pressure monitors were provided by Cardios Sistemas. The investigators were solely responsible for the design, conduct, analysis and publication of the trial. There were no restrictions on publication, and all data were maintained and analysed solely by the authors.

Conflict of interest statement. None declared.



   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 

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Received for publication: 10. 2.07
Accepted in revised form: 26. 6.07


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