Impact Of Aortic Stiffness Research Articles

Relations of aortic stiffness with arterial damage beyond brachial pressure are both dependent and independent of central arterial pulsatile load.

We aimed to determine whether the impact of aortic stiffness on atherosclerotic or small vessel end organ damage beyond brachial blood pressure depends in-part on stiffness-induced increases in central arterial pressures produced by an enhanced resistance to flow (characteristic impedance, Zc). We studied 1021 participants, 287 with stroke or critical limb ischaemia, and 734 from a community sample with atherosclerotic or small vessel end organ measures. Central arterial haemodynamics were determined from arterial pressure (SphygmoCor) and velocity and diameter assessments in the outflow tract (echocardiography). Although Zc and carotid-femoral pulse wave velocity (PWV) were correlated (P < 0.0001), these relations were not independent of confounders (P = 0.90). Both Zc and hence central arterial pressures generated by the product of Zc and aortic flow (Q) (PQxZc), as well as PWV were independently associated with carotid intima-media thickness, estimated glomerular filtration rate (eGFR), endothelial activation markers [vascular cell adhesion molecule-1 (V-CAM-1)] and events. With further adjustments for brachial pulse pressure (PP) or SBP, PWV and PQxZc were both associated with eGFR and V-CAM-1. Relationships between PWV and eGFR or V-CAM-1 were independent of PQxZc (P < 0.05) and relationships between PQxZc and eGFR and V-CAM-1 were independent of PWV (P < 0.005). Similarly, with adjustments for confounders and brachial PP or SBP, across the full adult lifespan, both aortic PWV and PQxZc were increased in those with arterial events (P < 0.005). Relationships between PWV and events were again independent of PQxZc (P < 0.005) and between PQxZc and events were independent of PWV (P < 0.0001). Beyond brachial blood pressure, the impact of aortic stiffness on arterial damage involves effects that are both dependent (proximal aortic Zc and hence PQxZc) and independent (full aortic length indexed by PWV) of central arterial pulsatile load. Hence, PWV and brachial PP may be insufficient to account for all of the damage mediated by increases in aortic stiffness.

Impact of aortic stiffness by velocity-encoded magnetic resonance imaging on late gadolinium enhancement to predict cardiovascular events.

BackgroundIncreased aortic stiffness has been established as a marker in various cardiovascular diseases. Previous reports revealed a significant correlation between aortic stiffness and myocardial scarring using the late gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR). However, prognostic data concerning aortic stiffness combining myocardial scarring remains limited.MethodA total of 402 patients who had undergone clinical CMR for the evaluation of cardiac function, LGE, and aortic pulse wave velocity (PWV) using velocity encoded-CMR (VE-CMR) were included. Patients were classified into 4 groups using mean PWV and the presence of LGE as elevated or non-elevated PWV and positive or negative LGE. Patients received follow-up for major adverse cardiovascular events (MACE) comprising cardiovascular death, non-fatal myocardial infarction, hospitalization for heart failure, coronary revascularization, and ischemic stroke. Predictors of MACE and hard cardiac events (cardiovascular death or non-fatal myocardial infarction) were evaluated.ResultsDuring the average follow-up period of 47.7 months, 58 MACE occurred. Patients who had elevated PWV and positive LGE experienced the highest rate of MACE compared to the group with non-elevated PWV and negative LGE (HR 11.90, p < 0.001). Among patients who had LGE, those who had elevated PWV experienced a 2.4-times higher rate of MACE compared to those who had non-elevated PWV. Multivariate analysis showed that PWV and LGE were independent predictors of MACE and hard cardiac events. PWV had excellent intra- and inter-observer reproducibility (intra-: ICC = 0.98, p < 0.001, inter-: ICC = 0.97, p < 0.001).ConclusionAortic stiffness using VE-CMR had prognostic value to predict cardiovascular events, with the added benefits of LGE.

&lt;p&gt;The Possible Impact of Aortic Stiffness on Quality of Late Life: An Exploratory Study&lt;/p&gt;

PurposeAortic stiffness (AS) is associated with cardiovascular events and all-cause mortality in the older population. AS might also influence the health-related quality of life (HRQOL) as a result of the negative effects of AS on cognitive and physical morbidity. We aimed to investigate the possible association between AS and HRQOL in people aged 75 years and over.Patients and MethodsThis cross-sectional study was part of the SCOPE study, an international multicenter cohort observational study. The indicators for AS were aortic pulse wave velocity (aPWV) and central pulse pressure (cPP). HRQOL was assessed using the EQ-5D index and the EQ-5D visual analog scale (VAS). ANCOVA and multivariate regression models were used to investigate possible associations.ResultsWe included 280 Dutch participants of the SCOPE study. Median age was 79 years (IQR 76–83) and 42.1% were women. Participants reporting any problem on the EQ-5D index (n=214) had higher values of aPWV (12.6 vs 12.2 m/s, p = 0.024) than participants not experiencing any problem (n=66) and comparable values of cPP (44.4 vs 42.0 mmHg, p = 0.119). Estimates only slightly changed after adjustments. No association was found between indicators of AS and EQ-5D VAS.ConclusionAortic stiffness was associated with impaired quality of late life. This association could be mediated by subclinical vascular pathology affecting mental and physical health.

Impact of aortic stiffness on myocardial ischaemia in non-obstructive coronary artery disease

ObjectiveHigh aortic stiffness may reduce myocardial perfusion pressure and contribute to development of myocardial ischaemia. Whether high aortic stiffness is associated with myocardial ischaemia in patients with stable angina and...

Evaluation of Peak Wall Stress in an Ascending Thoracic Aortic Aneurysm Using FSI Simulations: Effects of Aortic Stiffness and Peripheral Resistance.

It has been reported clinically that rupture or dissections in thoracic aortic aneurysms (TAA) often occur due to hypertension which may be modelled with sudden increase of peripheral resistance, inducing acute changes of blood volumes in the aorta. There is clinical evidence that more compliant aneurysms are less prone to rupture as they can sustain such changes of volume. The aim of the current paper is to verify this paradigm by evaluating computationally the role played by the variation of peripheral resistance and the impact of aortic stiffness onto peak wall stress in ascending TAA. Fluid-structure interaction (FSI) analyses were performed using patient-specific geometries and boundary conditions derived from 4D MRI datasets acquired on a patient. Blood was assumed incompressible and was treated as a non-Newtonian fluid using the Carreau model while the wall mechanical properties were obtained from the bulge inflation tests carried out in vitro after surgical repair. The Navier-Stokes equations were solved in ANSYS Fluent. The Arbitrary Lagrangian-Eulerian formulation was used to account for the wall deformations. At the interface between the solid domain and the fluid domain, the fluid pressure was transferred to the wall and the displacement of the wall was transferred to the fluid. The two systems were connected by the System Coupling component which controls the solver execution of fluid and solid simulations in ANSYS. Fluid and solid domains were solved sequentially starting from the fluid simulations. Distributions of blood flow, wall shear stress and wall stress were evaluated in the ascending thoracic aorta using the FSI analyses. We always observed a significant flow eccentricity in the simulations, in very good agreement with velocity profiles measured using 4D MRI. The results also showed significant increase of peak wall stress due to the increase of peripheral resistance and aortic stiffness. In the worst case scenario, the largest peripheral resistance (1010kgsm-4) and stiffness (10MPa) resulted in a maximal principal stress equal to 702kPa, whereas it was only 77kPa in normal conditions. This is the first time that the risk of rupture of an aTAA is quantified in case of the combined effects of hypertension and aortic stiffness increase. Our findings suggest that a stiffer TAA may have the most altered distribution of wall stress and an acute change of peripheral vascular resistance could significantly increase the risk of rupture for a stiffer aneurysm.

AORTIC-BRACHIAL STIFFNESS MISMATCH IN PATIENTS WITH ARTERIAL HYPERTENSION AND TYPE 2 DIABETES MELLITUS

Objective: Aortic stiffness (AS) is a strong predictor of cardiovascular (CV) mortality in various clinical conditions. The impact of AS on CV outcomes is mediated by the reversal of the AS gradient. Its negative prognostic significance has been studied only in the dialysis population. Aim of the study: to assess AS gradient in patients with arterial hypertension (AH) and type 2 diabetes mellitus (T2DM). Design and method: The study group included 90 patients (39% males,mean age 63,8 ± 11,6 years, 44% smokers, 80% with dyslipidemia, mean office BP 146 ± 23/86 ± 10 mmHg); control group included 42 patients with AH matched by basic parameters. Median duration of diabetes was 8,5 years (IQR 2;13). All patients received combined antihypertensive therapy, target BP < 140/85 mmHg was achieved in 29 (52,7%) patients. BP was measured with a validated oscillometric device. Parameters of arterial stiffness (AS) were assessed by applanation tonometry. AS gradient was calculated as carotid-femoral (cf)PWV/carotid-radial (cr)PWV and its elevation > 1 was considered as AS mismatch. p < 0,05 was considered significant. Results: Mean cfPWV was 10,5 ± 2,4 vs 9,5 ± 1,8 m/s (p = 0,04), crPWV – 8,5 ± 1,4 vs 10,4 ± 1,7 m/s (p = 0,001), AS gradient – 1,2 ± 0,3 vs 0,9 ± 0,1 (p = 0,04). Incidence of AS mismatch in the study group was 93% vs 19% in the control group (χ2 = 59,5, p < 0,001) and 70% vs 9% in the group with PWV < 10 m/s respectively (χ2 = 37,1, p < 0,05). Patients with AS gradient > 1,0 were older (65,2 ± 10,7 vs 59,1 ± 10,7 years), had longer median duration of DM (10 vs 3 years), higher creatinine (96,8 ± 21,1 vs 91,3 ± 22,1 μmol/l) and lower GFR (62 ± 18 vs 70 ± 20 ml/min/1,73m2), p < 0,05 for trend. Spearmen analysis revealed significant correlations between AS gradient and age (r = 0,4), DM duration (r = 0,3), creatinine (r = 0,2) and GFR (r = −0,2), p < 0,05 for trend. Age and DM duration were significant predictors of aortic-brachial stiffness mismatch (β = 0,4, p = 0,0002 and β = 0,3, p = 0,004, respectively). ROC analysis showed that presence of DM was an early factor of AS mismatch with AUC 0,849, sensitivity of 98% and specificity of 58%, p < 0,05. Conclusions: In diabetic patients with arterial hypertension AS mismatch is highly prevalent and in patients with normal PWV may be regarded as an early marker of arteriolosclerosis.

Aortic-Brachial Pulse Wave Velocity Ratio: A Blood Pressure-Independent Index of Vascular Aging.

Aortic stiffness, a cardiovascular risk factor, depends on the operating mean arterial pressure (MAP). The impact of aortic stiffness on cardiovascular outcomes is proposed to be mediated by the attenuation or the reversal of the arterial stiffness gradient. We hypothesized that arterial stiffness gradient is less influenced by changes in MAP. We aimed to study the relationship between MAP and aortic stiffness, brachial stiffness, and arterial stiffness gradient. In a cross-sectional study of a dialysis cohort (group A, n=304) and a cohort of hypertensive or kidney transplant recipient with an estimated glomerular filtration rate of >45 mL/min/1.73 m2 (group B, n=114), we assessed aortic and brachial stiffness by measuring carotid-femoral and carotid-radial pulse wave velocities (PWV). We used aortic-brachial PWV ratio as a measure of arterial stiffness gradient. Although there was a positive relationship between MAP and carotid-femoral PWV (R2=0.10 and 0.08; P<0.001 and P=0.003) and MAP and carotid-radial PWV (R2=0.22 and 0.12; P<0.001 and P<0.001), there was no statistically or clinically significant relationship between MAP and aortic-brachial PWV ratio (R2=0.0002 and 0.0001; P=0.8 and P=0.9) in group A and B, respectively. Dialysis status and increasing age increased the slope of the relationship between MAP and cf-PWV. However, we found no modifying factor (age, sex, dialysis status, diabetes mellitus, cardiovascular disease, and class of antihypertensive drugs) that could affect the lack of relationship between MAP and aortic-brachial PWV ratio. In conclusion, these results suggest that aortic-brachial PWV ratio could be considered as a blood pressure-independent measure of vascular aging.

Impact of Aortic Stiffness on Exercise Tolerance and Left Ventricular Filling Pressure after Percutaneous Coronary Intervention for Patients with Chronic Stable Coronary Artery Disease

Background and Aim: In patients with stable coronary artery disease aortic rigidity may contribute to exercise intolerance and impaired left ventricular (LV) function after coronary intervention. However, this relationship has not yet been investigated. We aimed to assess the impact of aortic stiffness on both exercise tolerance and left ventricular diastolic filling pressure after percutaneous coronary intervention (PCI). Methods: A percutaneous coronary intervention and stenting was performed in 98 consecutive patients with stable coronary artery disease (CAD) and positive exercise ECG. Before and after PCI, echocardiographic study, exercise stress test and aortic stiffness indices were calculated. Results: Aortic stiffness index was significantly higher in patients with CAD (19.5 ± 4.9vs 5.6 ± 2.1; P<0.0001), and still elevated even after successful PCI (11.5 ± 2.7; P<0.002). METs was significantly correlated with Aortic beta index (r = 0.64, P< 0.0001), LAVI (r= 0.49, P<0.001) and E/E? (r = 0.53, P < 0.001). ASI of <15 and < 16.5 were the best cut-off values for prediction of improved exercise tolerance and LV filling pressure after PCI. The AUROC was calculated as 0.93 and 0.94 respectively (P<0.001). Conclusion: In patients with stable coronary artery disease, increase in aortic rigidity, as assessed by aortic beta index, was independently correlated with reduced exercise tolerance and increased LV filling pressures, after PCI. ASI<15 and <16.5 were powerful predictors for improved exercise tolerance and decreased LV filling pressures after PCI.

Abstract 19533: The Relationship Between Aortic-brachial Stiffness Mismatch and Mean Blood Pressure

Background: Carotid-femoral pulse wave velocity (cf-PWV) is considered to be the gold standard for assessment of aortic stiffness. The impact of aortic stiffness on peripheral end-organ damage is explained by the loss or reversal of physiological impedance mismatch between aorta and medium-sized muscular conduit arteries. The main limitation of cf-PWV is its positive relationship with mean blood pressure. Recently, we have shown that assessment of aortic-brachial stiffness mismatch (PWV ratio) outperforms cf-PWV for the prediction of mortality in dialysis population. As both carotid-radial PWV (cr-PWV) and cf-PWV depend on blood pressure, we hypothesized that PWV ratio is not influenced by mean blood pressure. Method: In 310 dialysis patients (median age of 67 years [25 th -75 th percentiles: 56 - 76], 185(60%) men, 134 (43%) diabetes and 162 (52%) cardiovascular disease), cf-PWV and cr-PWV were measured using direct distance (Complior) and maximal upstroke algorithm. Mean blood pressure was obtained using arterial tonometry calibrated with brachial systolic and diastolic blood pressures in a controlled environment. In a linear regression analysis, we examined the relationship between MBP and cf-PWV, cr-PWV and PWV ratio. Results: The mean cf-PWV, cr-PWV, PWV ratio and MBP were respectively 13.52±4.06 m/s, 8.76±1.68 m/s, 1.59±0.52 and 92±16 mmHg. The linear relationships between MBP, cf-PWV and cr-PWV are shown in figures 1A-B. However, there were no relationship between MBP and PWV ratio (Figure 1C). There were no interaction between age, gender and the absence of a relationship between MBP and PWV ratio. Conclusion: As PWV ratio is mechanistically a logical parameter for explaining target organ damage and it has no significant relationship with MBP, it seems to be an ideal index for macro-circulatory disease. These findings need to be validated in independent cohorts.

Impact of aortic stiff ness on the frequency of paroxysmal atrial fi brillation recurrences

Background The relationship between arterial stiff ness (AS) and atrial fi brillation (AF) incidence is well-known. In this study we aimed to investigate the relationship between AS parameters and AF occurence as well as AF recurrence post catheter ablation (CA) in patients with paroxysmal AF (PAF).Methods We enrolled 103 patients with PAF diagnosis and 103 control subjects with similar demographic characteristics. We measured AS parameters and central aortic pressure (CAP) parameters by an oscillometric device in both groups. In the patient group 51 patients underwent CA for AF and recurrence rates at 3 and 6 months postprocedurally were recorded. AS parameters were compared between patients with and without AF recurrence.Results In the PAF patient group central systolic pressure, central diastolic pressure, central pulse pressure, augmentation pressure, augmentation index, and pulse wave velocity were signifi cantly higher than in the control group (for each listed parameter P < 0.05). AS parameters were not associated with AF recurrence post CA. Left atrial size (LAS) was found as an independent predictor for recurrence in multivariate analysis (β: 2.30; P= 0.02; OR: 9.97; 95% CI [1.28-77.48]).Conclusion Increased AS is associated with PAF occurence. Nevertheless, LAS, a traditional risk factor, was the most powerful predictor for recurrence post CA; whereas AS or CAP were not associated with recurrence.

OP-110 Impact of Aortic Stiffness on Paroxysmal Atrial Fibrillation Frequency and Recurrence

OP-110 Impact of Aortic Stiffness on Paroxysmal Atrial Fibrillation Frequency and Recurrence

Relationship between aortic valve stenosis, its replacement, and aortic function

The paper of Rosca et al. 1 was read with great interest entitled ‘ Impact of aortic stiffness on left ventricular function and B-type natriuretic peptide release in severe aortic stenosis ’. The major finding of this study was that in patients with severe aortic valve stenosis (AS) and preserved left ventricular (LV) ejection fraction, independently of the valvular load, an increase in aortic rigidity, as assessed by aortic stiffness …

Increased Aortic Stiffness Can Predict Perioperative Cardiovascular Outcomes in Patients Undergoing Noncardiac, Nonvascular Surgery

Aortic stiffness is an early marker of arteriosclerosis and associated with cardiovascular mortality. However, the impact of aortic stiffness on perioperative cardiovascular outcomes in patients undergoing noncardiac surgery is unknown. The study population was composed of 660 consecutive adults aged 18 years and over (mean age = 65.3 ± 14 years) who underwent intermediate-risk (nonvascular), noncardiac surgery between January 2010 and February 2011. Nonemergency, non-day-case, open surgical procedures were enrolled. Aortic stiffness indices were calculated from the aortic diameters measured by echocardiography. Electrocardiography and cardiac biomarkers were evaluated 1 day before surgery, and on days 1, 3, and 7 after surgery. Eighty patients (12.1%) experienced perioperative cardiovascular events (PCE). Preoperative aortic distensibility (AD) (2 ± 1.3 vs. 2.9 ± 1.1 cm2/dyn/10(3), P < 0.001) and aortic strain (AS) (4.4 ± 2.4 vs. 6.4 ± 1.9, P < 0.001) of the patients with PCE were significantly lower than in patients without PCE. Univariate analysis showed a significant association between age, diabetes mellitus (DM), coronary artery disease, preoperative atrial fibrillation, American Society of Anesthesiologists (ASA) status, Revised Cardiac Risk Index, left ventricle ejection fraction (LVEF), AD, aortic strain, and in-hospital PCE. However, on multivariate logistic regression analysis, only AD (OR: 1.94, 95% CI: 1.1-3.4; P = 0.02), AS (OR: 0.45, 95% CI: 0.3-0.6; P < 0.001), DM (OR: 2.28, 95% CI: 1.08-4.82; P = 0.03), and LVEF (OR: 0.96, 95% CI: 0.93-0.99; P = 0.03) remained as significant variables associated with PCE. Impaired elastic properties of the aorta are associated with increased PCE rates in patients undergoing noncardiac, nonvascular surgery.

Impact of Aortic Stiffness on Cardiovascular Disease in Patients With Chest Pain: Assessment With Direct Intra-Arterial Measurement

Aortic stiffness is an independent risk factor for cardiovascular (CV) events and mortality. However, there are few studies about the predictive role of aortic stiffness. We investigated the association between aortic pulse-wave velocity (aPWV), using direct intra-arterial measurement and future CV events, in patients with chest pain. Aortic pulse-wave velocity was measured through an aorto-femoral, fluid-filled system at baseline in 1004 patients with chest pain. Among these patients, 497 (237 male) were enrolled in the study. Aortic pulse-wave velocity was examined using tertiles. Tertiles were defined as follows: tertile 1, <9.20 m/sec; tertile 2, 9.21 to 12.49 m/sec; and tertile 3, >12.50 m/sec. The impact of aPWV on newly developed CV events, coronary artery disease (CAD), stroke, and congestive heart failure was evaluated. A higher aPWV was associated with new CV events (odds ratio, 2.18 for tertile 3 v tertile 1; 95% confidence interval [CI], 1.32 to 3.60) and new CAD (odds ratio, 1.87 for tertile 3 v tertile 1; 95% CI, 1.10 to 3.18) in univariate analysis. In multivariate analysis, aPWV was associated with new CV events (odds ratio, 2.05 for tertile 3 v tertile 1; 95% CI, 1.18 to 3.55) and new CAD (odds ratio, 1.86 for tertile 3 v tertile 1; 95% CI, 1.03 to 3.35). Aortic pulse-wave velocity was not associated with either new stroke (P = .096) or congestive heart failure (P = .63). These results suggest that aPWV is an independent risk factor for future CV events and CAD in patients with chest pain.

At the Beginning of Stiffening

Brachial cuff blood pressure (BP) continues to guide almost every decision related to the clinical management of the hypertensive patient. However, the BP within the central aorta (ie, aortic pressure) is receiving growing attention for 2 main reasons. First, brachial BP does not necessarily predict aortic pressure, and subjects with equal values of brachial cuff pressure may differ markedly in their aortic pressure.1 Second, aortic pressure may be superior to brachial BP for the prediction of several vascular complications, including the degree of carotid atherosclerosis,2 the extent of coronary artery disease,3 the likelihood of reocclusion after angioplasty,4 and, more important, the risk of major cardiovascular events.1,5 Aortic BP may be estimated noninvasively from analysis of peripheral radial artery waveforms with applanation tonometry. Although the reliability of derived aortic BP is crucially dependent on the validity of the transfer function used to generate the central aortic waveforms, the correspondence between estimated central aortic and intra-arterial systolic BP and pulse pressure (PP) seems to be quite close.6 In addition to central PP, pulse …

Nitric oxide and the regulation of large artery stiffness: from physiology to pharmacology.

The association between arterial stiffening and aging is well described and can be observed in almost all populations worldwide. A number of other cardiovascular risk factors including diabetes and cigarette smoking are also associated with increased large artery stiffness, often referred to as “premature arterial stiffening.” It is now apparent that the aortic pulse wave velocity (PWV), a measure of arterial distensibility, predicts outcome in a variety of different populations, including hypertensives,1 diabetics,2 individuals with end-stage renal disease (ESRD),3 and even in older adults.4 Indeed, in some populations, aortic PWV is a better predictor of future events than peripheral blood pressure.4 Moreover, arterial stiffening may be more than just a marker of cardiovascular risk; stiffening may also play a more direct role in the development of atherosclerotic plaques. Thus, arterial stiffness would appear to be a novel therapeutic target for the prevention of excess cardiovascular morbidity and mortality. To exploit such an exciting prospect fully, it is necessary to understand the factors regulating arterial stiffness. Traditionally, the stiffness of a vessel was viewed as simply a function of the structural elements of the vessel wall and distending (mean arterial) pressure. However, the large arteries also have a generous coat of smooth muscle, which can alter the distribution of stresses between the elastic and collagenous fibers of the vessel wall and thus alter arterial stiffness. Because smooth muscle tone is influenced by a number of circulating and local vasoactive mediators, arterial stiffness may be actively regulated, and indeed modifiable, at least in the short-term. The muscular arteries have a rich sympathetic innervation, and catecholamines are known to alter smooth muscle tone. Moreover, removal of the vascular endothelium in animals alters large artery stiffness,5,6 suggesting that endothelial-derived substances regulate arterial stiffness in vivo. However, the endothelium …

Impact of aortic stiffness on the risk of ischemic stroke in elder patients

Impact of aortic stiffness on the risk of ischemic stroke in elder patients

Diabetes mellitus, aortic stiffness, and cardiovascular mortality in end-stage renal disease.

Cardiovascular mortality is elevated in patients with end-stage renal disease (ESRD), especially in those with diabetes mellitus. Although the higher cardiovascular death rate in diabetic ESRD patients may be the result of more advanced atherosclerotic changes of the arterial wall, this has not been documented previously. Aortic stiffness was compared between ESRD patients with and without diabetes, and the impact of aortic stiffness on cardiovascular mortality was examined in a prospective, observational cohort study. The cohort consisted of 265 ESRD patients on hemodialysis, including 50 diabetic patients studied between June 1992 and December 1998. At baseline, the diabetic ESRD patients had significantly higher aortic pulse wave velocity (PWV), a noninvasive measure of aortic stiffness, than the nondiabetic patients. During a mean follow-up period of 63 mo, 81 deaths, including 36 cardiovascular deaths, were recorded. Kaplan-Meier analysis revealed higher all-cause or cardiovascular mortality rates in the diabetic as compared with the nondiabetic patients and also in those with higher aortic PWV than those with lower aortic PWV. The effect of diabetes on cardiovascular death was significant in the Cox model, including age, years on hemodialysis, gender, smoking, C-reactive protein, hematocrit, and body mass index as covariates. However, when aortic PWV was included as a covariate, the impact of diabetes was no longer significant, whereas aortic PWV was a significant predictor. In a model including 13 covariates, aortic PWV remained a significant predictor for cardiovascular and overall mortality but not for non-cardiovascular death. These results demonstrate that the increased aortic stiffness of the ESRD patients with diabetes mellitus contributed to the higher all-cause and cardiovascular mortality rates.

Impact of aortic stiffness on survival in end-stage renal disease.

Damage to large arteries is a major factor in the high cardiovascular morbidity and mortality of patients with end-stage renal disease (ESRD). Increased arterial stiffness and intima-media thickness, together with increased pulse pressure, are the principal arterial alterations. Whether increased aortic pulse-wave velocity (PWV), a classic marker of increased arterial stiffness, may predict all-cause and/or cardiovascular mortality has never been investigated. A cohort of 241 patients with ESRD undergoing hemodialysis was studied between April 1987 and April 1998. The mean duration of follow-up was 72+/-41 months (mean+/-SD). Mean age at entry was 51.5+/-16.3 years. Seventy-three deaths occurred, including 48 cardiovascular and 25 noncardiovascular fatal events. At entry, together with standard clinical and biochemical analyses, patients underwent echocardiography and aortic PWV measured by Doppler ultrasonography. On the basis of Cox analyses, 2 factors emerged as predictors of all-cause and cardiovascular mortality: age and aortic PWV. Hemoglobin and low diastolic pressure interfered to a smaller extent. After adjustment for all the confounding factors, an OR for PWV >12. 0 versus <9.4 m/s was 5.4 (95% CI, 2.4 to 11.9) for all-cause mortality and 5.9 (95% CI, 2.3 to 15.5) for cardiovascular mortality. For each PWV increase of 1 m/s in our study population, all-cause mortality-adjusted OR was 1.39 (95% CI, 1.19 to 1.62). These results provide the first direct evidence that in patients with ESRD, increased aortic stiffness determined by measurement of aortic PWV is a strong independent predictor of all-cause and mainly cardiovascular mortality.

K026 Impact of aortic stiffness on survival in end-stage renal failure

K026 Impact of aortic stiffness on survival in end-stage renal failure