Abstract
The association between single measurements of carotid‐femoral pulse wave velocity (cfPWV) and cardiovascular (CV) events is driven by late events beyond 12 months of follow‐up. This prospective study compares single measurements of cfPWV vs the 2‐year delta cfPWV and the association with short‐term development of CV events in hemodialysis patients. cfPWV was performed at t=0 and t=1 two years later, and patients were followed‐up for development of CV events through 12 months (n=66). In Cox regression models adjusted for CV risk factors, history of CV events and delta cfPWV remained associated with the development of CV events (hazard ratio for prior CV events=8.9, P=.03; hazard ratio for delta cfPWV=1.14; P=.002). When delta cfPWV was substituted for single cfPWV measurement, none of the single measures were associated with new CV events. The change in cfPWV, but not single measurements of cfPWV, was associated with the development of CV events through 12 months.
Cardiovascular (CV) complications are the leading cause of death among patients with end‐stage renal disease (ESRD). Approximately, 20% to 50% of patients with ESRD die from CV disease, 10‐ to 15‐fold higher than the age‐adjusted CV mortality in the general population.1, 2 Conventional CV risk factors studied in the general population seem to account only partially for the increased morbidity and mortality in the hemodialysis (HD) population. Vascular calcification and arterial stiffness are highly prevalent in this population and may have a pathophysiologic role in the elevated risk of CV events.3, 4
Carotid‐femoral pulse wave velocity (cfPWV) is a simple, noninvasive, and reproducible measure of large artery stiffness and calcification.5 cfPWV has been frequently used as a surrogate for CV events and CV mortality in the general population, and in special populations such as diabetic patients, hypertensive patients, and patients undergoing HD.5 It has previously been demonstrated that single elevated measurements of cfPWV are associated with an increased risk of fatal and nonfatal CV events among ESRD patients. Nonetheless, this association was mostly driven by the high incidence of late CV events beyond 12 months of follow‐up, with no significant changes observed in the early period following cfPWV measurements.4, 6, 7
Furthermore, the progression or change in cfPWV (delta cfPWV) by means of two time‐separated measurements, a more dynamic parameter of structural and functional arterial changes, has recently gained interest, mainly when considering the directionality of the relationship between stiffness and blood pressure (BP). Several cohort studies have investigated factors associated with the progression of cfPWV, which was used as a surrogate marker of CV risk.8, 9, 10 However, the validity of delta cfPWV as a CV risk surrogate has not been well investigated. Although available studies provide insight into the association between cfPWV progression and CV risk, they do not truly test the association between that progression and the subsequent development of future CV events, particularly in the short term and in special patient populations such as those undergoing HD. The present prospective study aims to evaluate the association between delta cfPWV over 2 years and the subsequent development of CV events through a 12‐month follow‐up period in a cohort of HD patients.
Methods
Study Population
Between March and April 2012, 82 patients with ESRD undergoing HD at the North Hospital Center in Zgharta, Lebanon, and who had been stable for at least 3 months were invited to participate in the study. All participants provided written informed consent. The study protocol was approved by the North Hospital Center institutional review board and was in accordance with the Helsinki Declaration.
Measurements and Definitions
Aortic stiffness was evaluated by measurement of cfPWV using the Complior SP automated device (Alam Medical, Vincennes, France). The totality of measurements was obtained 1 hour following an adequate HD session (urea reduction ratio >70%) by the same trained operator. Simultaneously recorded pulse waveforms were obtained transcutaneously over the common carotid and femoral arteries. cfPWV was then calculated automatically by the device using the distance between the carotid and femoral artery recording sites divided by the time interval of the pressure waves (averaged over 10 cardiac cycles). The detailed technique of cfPWV has been previously described.11, 12 A first measurement of cfPWV (cfPWVt=0) was obtained at enrollment. The second measurement (cfPWVt=1) was obtained 2 years ± 1 month after the initial measurement in order to calculate the change in cfPWV (delta cfPWV=cfPWVt=1 – cfPWVt=0). Following cfPWVt=1 measurement and calculation of delta cfPWV, baseline characteristics were obtained and patients were followed up for an additional 12 months for the development of new CV events (CV death, acute coronary syndrome, acute ischemic peripheral event necessitating intervention, or stroke) (Figure 1).
Figure 1.
Study design. Cardiovascular (CV) event was defined as the composite of CV death, acute coronary syndrome, significant acute ischemic peripheral arterial event necessitating intervention, or stroke. cfPWV indicates carotid‐femoral pulse wave velocity.
CV death was defined as any death occurring as a result of cardiac or vascular origin. Cardiac deaths included deaths as a result of proximate cardiac cause (eg, myocardial infarction, output failure, fatal arrhythmia), unwitnessed death, and death of unknown cause. Vascular deaths included those caused by noncoronary vascular causes, such as cerebrovascular causes, pulmonary embolism, aneurysmal rupture or dissection, or other vascular etiologies. Acute coronary syndrome (ACS) was defined as unstable angina, ST‐segment elevation myocardial infarction (STEMI), or non‐STEMI. Unstable angina was defined as suggestive symptoms that persisted for at least 10 minutes at rest with findings suggestive of ischemia on electrocardiography. Myocardial infarction was defined according to the third universal definition of myocardial infarction.13 Acute ischemic peripheral event was defined as acute limb ischemia that developed in the context of chronic limb ischemia and necessitated intervention. Peripheral ischemic events caused by traumatic and wound‐related causes were not included. Stroke was defined as either ischemic, hemorrhagic, or stroke of uncertain cause. All events in this study were identified independently by two investigators who had access to the source documentation and all hospital medical records. If the decisions of the two investigators were not consistent, a third investigator was consulted.
Medical records of all participating patients were reviewed at baseline (at the time of cfPWVt=1 measurement) for personal and family histories and current medications. Information regarding baseline kidney disease, CV risk factors and history of CV events, age at onset of kidney disease, age at HD initiation, type of vascular access, and information relating to HD sessions, such as weekly hours undergoing HD, was also obtained from patients' medical records and confirmed by means of patient interviews. A complete physical examination was also performed for all participating patients during all patient encounters. Hypertension was defined as a systolic BP (SBP) ≥140 mm Hg and/or a diastolic BP (DBP) ≥90 mm Hg (mean of six consecutive measurements) or current intake of antihypertensive agents. SBP and DBP values were measured with patients in the supine position in the arm not containing the vascular access after 15 minutes of rest. Mean BP (MBP) was calculated from the following equation: MBP=(SBP + 2 DBP)/3. Diabetes mellitus was defined as either glycated hemoglobin >6.4% or current intake of antidiabetic agents. Mean interdialytic weight gain was defined as the average weight gain between two consecutive HD sessions during the 10 sessions prior to cfPWVt=1 measurement (baseline).
Blood samples were drawn at the time of cfPWVt=0 measurement, cfPWVt=1 measurement (baseline), and at the end of follow‐up (12 months). All blood samples were obtained prior to an HD session and were immediately processed within 3 hours of withdrawal for complete blood cell count, glucose, calcium, phosphate, intact parathyroid hormone level, lipid profile, and C‐reactive protein.
Statistical Analysis
Data were analyzed using Stata 13 (StataCorp, College Station, Tx). Characteristics of the study population were evaluated using descriptive statistics. Data were expressed as frequencies and percentages for categorical variables, means±standard deviations for parametric continuous variables, and medians (interquartile ranges [IQRs]) for nonparametric continuous variables. The outcome variable, delta cfPWV, was evaluated as a nonparametric continuous variable. Spearman rank sum test was performed for the associations between delta cfPWV and other continuous variables, and Kruskal‐Wallis test was performed for the association between delta cfPWV and categorical variables. All variables with a P value <.10 in the univariate analysis were held for inclusion in the multiple regression model, in addition to parameters of interest, and those with a historical or biologically plausible correlation with arterial stiffness. Multiple regression analysis was performed to identify the variables independently associated with delta cfPWV. Survival analysis with right censorship was performed to identify variables associated with the development of new CV events through 12 months following the measurement of delta cfPWV. The time to first event was analyzed using Cox proportional hazards regression model with adjustments for variables associated with increased risk of CV events. All tests were double‐sided. A P value <.05 was considered significant.
Results
Patient Characteristics
A total of 82 patients were recruited for a first cfPWV measurement (cfPWVt=0), 66 of whom were evaluated again for a second measurement (cfPWVt=1) at the 2‐year ± 1‐month mark. Notably, nine patients (11%) died during the course of the study prior to the second measurement (cfPWVt=1), of which four (44%) died of CV causes (Figure 2). Baseline characteristics are summarized in Table 1. All patients were of Caucasian ethnicity. The mean age at baseline was 51.2±18.0 years and the median duration on dialysis was 71.8 (48.5–116.4) months; 56% of patients were men, 71% were hypertensive, 23% were diabetic, and 39% had a history of prior CV event. For the 66 patients who were enrolled in the study, median cfPWVt=1 was significantly higher compared with cfPWVt=0 (median cfPWVt=0: 10.6 [8.9–13.8] m/s vs median cfPWVt=1: 11.4 [9.7–15.1] m/s [P<.001]). Accordingly, median delta cfPWV was 1.1 (−0.3 to 2.6) m/s. During the 12‐month follow‐up period, 13 patients developed a total of 15 events, almost half (7 of 15) of which were fatal, four of 15 were attributed to ACS, and four of 15 were attributed to acute ischemic peripheral artery disease (PAD) necessitating intervention (Figure 3). No stroke events were recorded during the 12‐month follow‐up duration. In addition, two patients died of non‐CV causes, namely active malignancy and overwhelming infection.
Figure 2.
CONSORT diagram. Note: Cardiovascular (CV) event was defined as the composite of CV death, acute coronary syndrome, significant acute ischemic peripheral arterial event necessitating intervention, or stroke. cfPWV indicates carotid‐femoral pulse wave velocity.
Table 1.
Baseline Characteristics of the Study Population at the time of cfPWVt=1
| Characteristics | Value (N=66) | Univariate Association With Delta cfPWV, m/s P Value |
|---|---|---|
| Age, mean±SD, y | 53.2±18.0 | .15 |
| Male sex, No. (%) | 37 (56.1) | .04 |
| Body mass index, mean±SD, kg/m2 | 25.1±5.2 | .28 |
| Age at dialysis initiation, mean±SD, y | 47.9±18.7 | .26 |
| Duration on dialysis, median (IQR), mo | 71.8 (48.5–116.4) | .93 |
| Mean interdialytic weight gain, mean±SD, kg | 2.9±1.3 | .09 |
| Consanguinity, No. (%) | 26 (39.4) | .68 |
| Systolic blood pressure, median (IQR) | 123.8 (114.6–138.9) | .10 |
| Diastolic blood pressure, median (IQR) | 69.2 (65.0–76.7) | .51 |
| Pulse pressure, median (IQR) | 52.6 (48.6–63.9) | .10 |
| Hypertension, No. (%) | 47 (71.2) | .06 |
| Diabetes mellitus, No. (%) | 15 (22.7) | .76 |
| History of cardiovascular events,a No. (%) | 23 (34.9) | .08 |
| History of coronary artery disease, No. (%) | 20 (30.3) | .09 |
| History of stroke, No. (%) | 5 (7.6) | .93 |
| History of symptomatic PAD, No. (%) | 8 (12.1) | .004 |
| Hypercholesterolemia, No. (%) | 37 (56.1) | .54 |
| Hypertriglyceridemia, No. (%) | 12 (18.2) | .68 |
| Active smoking, No. (%) | 24 (36.4) | .31 |
Abbreviations: cfPWV, carotid‐femoral pulse wave velocity; IQR, interquartile range; PAD, peripheral artery disease; SD, standard deviation. aHistory of cardiovascular event was defined as history of acute coronary syndrome, cerebrovascular event, or acute peripheral ischemic event.
Figure 3.
Kaplan‐Meier cumulative incidence of cardiovascular (CV) events. Note: CV event was defined as the composite of CV death, acute coronary syndrome, significant acute ischemic peripheral arterial event necessitating intervention, or stroke. Cox model was adjusted for age, sex, average systolic and diastolic blood pressures, diabetes mellitus, hypercholesterolemia, smoking, and history of CV events. HR indicates hazard ratio; CI, confidence interval. cfPWV indicates carotid‐femoral pulse wave velocity.
Association Between Delta cfPWV and Clinical Parameters
On univariate analysis, delta cfPWV was significantly higher among male patients (P=.04) and among patients who had a history of symptomatic PAD (P=.004) (Table 1). Multivariate linear regression analysis was performed to identify independent factors associated with delta cfPWV. Variables with an association P value <.10 included age, sex, mean arterial pressure, mean interdialytic weight gain, baseline serum phosphate concentration, history of diabetes mellitus, history of hypertension, history of coronary artery disease, history of symptomatic PAD, and history of prior CV events. Delta cfPWV remained independently associated with sex (P=.025) and history of hypertension (P=.007) and was closely associated with history of symptomatic PAD (P=.050).
Delta cfPWV and Development of New CV Events
The association between delta cfPWV and the development of CV events during 12 months was evaluated in a Cox proportional hazards regression model (Table 2). A total of 13 first‐time events were recorded during the 12‐month follow‐up period, with no patients lost to follow‐up. Delta cfPWV was significantly associated with the development of CV events through 12 months (hazard ratio [HR], 1.22; P<.001). When adjusted for other risk factors for CV events, namely age, sex, either the combination of SBP and DBP or the combination of mean arterial pressure and pulse pressure (PP), diabetes mellitus, hypercholesterolemia, active smoking, and history of CV events, delta cfPWV remained significantly and independently associated with the development of new CV events through 12 months (HR, 1.14; P=.002). Compared with patients who did not develop any CV event, the median delta cfPWV was numerically but nonsignificantly higher among patients who developed CV events during the 12‐month follow‐up period (median delta cfPWV: 0.96 vs 2.47; P=.09) (Table 3). The same Cox regression model also identified history of CV events as the strongest independent correlate of new CV events (HR, 8.90; P=.03). Finally, when delta cfPWV was substituted for any of the single measurements of cfPWV (either cfPWVt=0 alone or cfPWVt=1 alone) in both the unadjusted model and the model adjusted for age, sex, active smoking, systolic and diastolic BPs, and history of diabetes mellitus, hypercholesterolemia, and prior CV events, none of the single measures (neither cfPWVt=0 alone nor cfPWVt=1 alone) was significantly associated with the development of new CV events through 12 months (Table 4).
Table 2.
Cox Proportional Hazards Regression Model Demonstrating Factors Associated With the Development of New Cardiovascular Events and CV Death and With New Acute Coronary Syndrome and New Acute Ischemic PAD Through 12 Months
| Delta cfPWV, m/s N=66 | ||||||
|---|---|---|---|---|---|---|
| Unadjusted | Adjusted for Age and Sex | Adjusted for Age, Sex, SBP, and DBP | Adjusted for Age, Sex, PP, and MAP | Adjusted for Age, Sex, SBP, DBP, and CV Risk Factors (DM, Hypercholesterolemia, and Smoking) | Adjusted for Age, Sex, SBP, DBP, CV Risk Factors (DM, Hypercholesterolemia, and Smoking), and Prior CV Events | |
| HR (95% CI) | HR (95% CI) | HR (95% CI) | HR (95% CI) | HR (95% CI) | HR (95% CI) | |
| New CV event | 1.22 (1.12–1.33)a | 1.20 (1.09–1.31)a | 1.21 (1.12–1.31)a | 1.21 (1.12–1.31)a | 1.19 (1.08–1.30)a | 1.14 (1.05–1.25)b |
| CV death | 1.22 (1.11–1.33)a | 1.21 (1.08–1.34)a | 1.22 (1.11–1.34)a | 1.22 (1.11–1.34)a | 1.17 (1.04–1.31)b | 1.13 (1.01–1.27)c |
| ACS | 1.37 (1.22–1.53)a | 1.34 (1.15–1.57)a | 1.30 (1.14–1.49)a | 1.30 (1.14–1.49)a | 1.38 (1.05–1.82)b | 1.38 (1.08–1.78)c |
| Acute ischemic PAD | 1.28 (0.91–1.80) | 1.27 (0.97–1.66) | 1.40 (1.09–1.80)b | 1.40 (1.09–1.80)b | 1.86 (1.13–3.06)c | N/A |
Abbreviations: cfPWV, carotid‐femoral pulse wave velocity; CI, confidence interval; DBP, diastolic blood pressure; DM, diabetes mellitus; HR, hazard ratio; MAP, mean arterial pressure; PAD, peripheral artery disease; SBP, systolic blood pressure. New cardiovascular (CV) event was defined as the composite of either CV death, acute coronary syndrome (ACS), significant acute ischemic peripheral arterial events necessitating intervention, or stroke. There were no stroke events in the cohort during the 12‐month follow‐up period. Not available (N/A) indicates that P value, hazard ratio, and confidence intervals could not be computed because of a small number of events. a P≤.001. b P≤.01. c P<.05.
Table 3.
Delta cfPWV Among Patients Who Developed vs Patients Who Did Not Develop CV Events During the 12‐Month Follow‐Up Period
| Clinical Event | Delta cfPWV, Median (IQR), m/s N=66 | P Value | |
|---|---|---|---|
| No Event | Event | ||
| New CV eventa | 0.96 (−0.36 to 2.31) (n=53) | 2.47 (0.96–6.00) (n=13) | .09 |
| CV death | 1.07 (−0.25 to 2.60) (n=59) | 2.47 (−1.47 to 15.06) (n=7) | .20 |
| ACS | 1.01 (−0.37 to 2.60) (n=62) | 2.06 (1.29–9.77) (n=4) | .37 |
| Acute ischemic PAD | 1.10 (−0.37 to 2.60) (n=62) | 2.62 (0.46–5.26) (n=4) | .49 |
Abbreviations: cfPWV, carotid‐femoral pulse wave velocity; IQR, interquartile range; PAD, peripheral arterial disease. aNew cardiovascular (CV) event was defined as the composite of either CV death, acute coronary syndrome (ACS), significant acute ischemic peripheral arterial events necessitating intervention, or stroke. There were no stroke events in the cohort during the 12‐month follow‐up period.
Table 4.
Association Between the Development of CV Events During 12 Months of Follow‐Up and Either Delta cfPWV or Single Measurements of cfPWV
| Measurement | Development of CV Events | ||
|---|---|---|---|
| Hazard Ratio | 95% CI | P Value | |
| Delta cfPWV | 1.14 | 1.05–1.25 | .002 |
| cfPWVt=0 | 0.92 | 0.72–1.19 | .53 |
| cfPWVt=1 | 1.06 | 0.96–1.17 | .26 |
Abbreviations: cfPWV, carotid‐femoral pulse wave velocity; CI, confidence interval. Cox model was adjusted for age, sex, average systolic and diastolic blood pressures, diabetes mellitus, hypercholesterolemia, smoking, and prior history of cardiovascular (CV) events.
During the 2‐year period prior to enrollment, not only did cfPWV change over time, but PP changes were also noted. When PP at t=0 was evaluated for the 66 patients who were then enrolled in the study, the median PP was 50 (40–60)mm Hg. Two years later at the time of enrollment t=1, the median PP for these patients was significantly higher, measuring 52.6 (48.6–63.9)mm Hg (P<.001). The two PP measures at t=0 and t=1 were very well correlated (Spearman's rho=.65). Consequently, the findings may help provide additional insight into the hemodynamic changes that affect HD patients during a 2‐year period, where changes observed by measurement of cfPWV may also be reflected by changes in PP.
In a separate Cox regression analysis that retrospectively evaluated the development of nonfatal CV events over the 2‐year period between cfPWVt=0 and cfPWVt=1 measurements (total of 12 nonfatal events), delta cfPWV was likewise significantly associated with the development of new nonfatal CV events (data not shown). The results were similar for both nonadjusted and adjusted Cox regression models (nonadjusted: HR, 1.17 [P<.001] vs adjusted: HR, 1.17 [P=.001]). Similarly, there was a trend towards a higher median delta cfPWV among the patients who developed CV events compared with those who did not, but it was not statistically significant (median delta cfPWV: 1.00 vs 2.08; P=.13). Paralleling the prospective analysis, history of CV events was also associated with an increased risk of new CV events (HR, 6.80; P=.03). Exclusively in this retrospective analysis, CV death was not evaluated as part of the composite outcome because of the unavailability of the follow‐up cfPWVt=1 measurement.
Specific Changes Related to ACS and PAD
In the present study, not only was delta cfPWV correlated with new CV events and death, but also with ACS and PAD, two diseases usually associated with atherosclerosis. Adjustments, mostly those related to hypercholesterolemia and smoking, were less significant (Table 2). These findings suggest that ACS and PAD may have different phenotypes from cfPWV, the first contributing to narrowing the vessel lumen and the second favoring plaque progression and enlargement.14
Discussion
The present prospective study demonstrates that the rate of progression of arterial stiffness in the HD population, measured by the change in cfPWV during a period of 2 years, may be closely associated with the incidence of CV events during that same period, and may be a significant independent risk factor for the development of CV events through 12 months. While single measurements of central PWV have been previously demonstrated to be associated with the development of CV events,4 the current findings demonstrate that compared with single measurements of cfPWV, a more dynamic, time‐dependent interpretation of PWV progression may be more clinically relevant for the short‐term evaluation of CV risk.
Notably, neither the first cfPWV measurement (cfPWVt=0) nor the second one at baseline (cfPWVt=1) was significantly associated with an increased risk of CV events through 12 months. When single measurements of cfPWV were analyzed in the past, the significant divergence between high vs low cfPWV and development of CV events was mostly observed late during the follow‐up duration, and the development of CV events was more pronounced beyond 1 year of follow‐up.4, 6, 7 Compared with single measurements of cfPWV, the current study demonstrates that delta cfPWV may be more strongly associated with the short‐term development of CV events. Interestingly, the 2‐year change in cfPWV was mirrored by a similar change in PP, another known measure of arterial stiffness and surrogate for CV disease. The findings highlight the magnitude of the temporal increase in cfPWV as possibly a more pertinent surrogate for worsening arterial stiffness and short‐term development of CV events compared with single cfPWV measurements.
The exact mechanism of arterial stiffness is not fully understood, but its progression is thought to occur more rapidly in HD patients than in the general population. Among HD patients, arterial stiffness is attributed to conventional risk factors (such as those related to aging, diabetes mellitus, smoking, and hypertension), as well as factors unique to ESRD and HD. Hyperphosphatemia and uremia classically associated with ESRD have been demonstrated to cause structural changes in the vascular bed, resulting in changes related to increased intimal and medial vascular calcification.15 In addition, accelerated dyslipidemia and subsequent arteriosclerosis in large and medium elastic and muscular arteries among patients undergoing HD are thought to contribute to the development of morphological derangements and the progression of arterial stiffness.16, 17 In addition to structural abnormalities, functional changes resulting from hypervolemia, vasoconstriction, and increased angiotensin II activity have also been described.18, 19 Thus, it is not unusual that HD patients experience rapid worsening of arterial stiffness over 2 years. Accordingly, the evaluation of short‐term progression of arterial stiffness and close follow‐up for the development of CV events may be warranted in this high‐risk patient population.
Consistent with prior literature in the general and HD populations, a history of CV events was the most significant correlate of future CV events during the 12‐month follow‐up period.20, 21, 22, 23 Despite the major risk levied by the history of prior CV events, the change in cfPWV during 2 years retained significant association with the incidence of CV events. This association was consistently observed for both the time span between the two cfPWV measurements and the 1‐year follow‐up period, even following the adjustment for major CV risk factors including age, sex, active smoking, BP parameters, diabetes mellitus, hypercholesterolemia, and history of CV events. When the association between delta cfPWV and individual CV events was analyzed, delta cfPWV was similarly significantly associated with development of each of CV death, ACS, and PAD when adjusted for other CV risk factors.
Notably, the independent association between delta cfPWV and CV events was linear during the follow‐up period, and the results were not significantly driven by either early or late events alone (data not shown). In general, the incidence of stroke events in the patient population was little, with only three incidents observed during the 2‐year period between the cfPWVt=0 and cfPWVt=1 measurements. No stroke events were reported during the 12‐month period following the calculation of delta cfPWV, and an association between the development of stroke and delta cfPWV was not possible prospectively.
Interestingly, compared with patients who did not develop any CV event during the 12‐month follow‐up period, the delta cfPWV of patients who developed new events tended to be approximately two‐fold higher (P=.09). The difference was even more pronounced among patients who had acute ischemic peripheral arterial events, with a four‐fold higher median delta cfPWV as compared with those who did not develop any acute ischemic peripheral arterial events, although this did not reach statistical significance. These findings further highlight that a more rapid rate of increase of central PWV is more closely associated with the short‐term risk of CV events.
Study Limitations
The current study was limited by the small sample size and the monocentric model of the investigation, which make these results only hypothesis‐generating, requiring larger‐scale investigations to confirm. Furthermore, given that 82 patients were recruited for initial cfPWVt=0 measurement, and that nine patients died before the second measurement could be undertaken, a possible survival bias may be present, making the study population for which the analysis was conducted a survivor population. Given that this population was generally characterized by well‐controlled BP, low frequency of diabetes, and a prolonged median duration on dialysis (median 71.8 months), the findings of this study are not necessarily generalizable to individuals who are initiating HD or those with markedly uncontrolled CV risk factors. In addition, there was no racial variation in the patient population (all patients were of Caucasian race), which may also limit the generalizability of the results among other ethnically diverse populations. Finally, given the observational, nonrandomized nature of the study, not all confounding factors could be accounted for in the study analyses.
Conclusions
The change in cfPWV (delta cfPWV) is significantly associated with short‐term development of CV events through 12 months. This association was not significant when single cfPWV measurements were analyzed. Compared with single measurements of cfPWV, the temporal change in cfPWV is possibly a more clinically relevant surrogate for worsening arterial stiffness and short‐term development of CV events.
Acknowledgments
None.
Conflict of Interest/Disclosure Statement
The authors report no specific funding in relation to this research and no conflicts of interest to disclose.
J Clin Hypertens (Greenwich). 2016;18:857–863. DOI: 10.1111/jch.12843. © 2016 Wiley Periodicals, Inc.
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