scholarly journals MMP-2 gene silencing attenuates age-dependent carotid stiffness via reduction of elastin degradation and increased eNOS activation

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
Y M Puspitasari ◽  
C Diaz-Canestro ◽  
L Liberale ◽  
T J Guzik ◽  
A J Flammer ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Arterial Stiffness ◽  
Gene Silencing ◽  
Matrix Metalloproteinase 2 ◽  
Elderly Subjects ◽  
Breakdown Product ◽  
Elastin Degradation ◽  
Carotid Stiffness ◽  
Increased Risk ◽  
Age Dependent

Abstract Background and aims Arterial stiffness is a hallmark of vascular aging. Being characterized by a loss of elasticity of large arterial walls, arterial stiffness is associated with an increased risk of cardiovascular disease (CVD). The age-dependent arterial stiffness is primarily attributed to alterations in the elastic and collagen deposition that is regulated by a number of enzymes, including matrix metalloproteinase-2 (MMP-2). Nevertheless, the mechanistic link between age-dependent arterial stiffness and MMP-2 remains unclear. In this study, we investigated the effect and efficacy of therapeutic MMP-2 knockdown using small interfering RNA (siRNA) on age-dependent arterial stiffness. Methods Pulse wave velocity (PWV) was assessed in the right carotid artery of wild-type (WT) mice of different age groups. MMP-2 levels and activity in the carotid artery and plasma of young (3 months) and aged (20–25 months) WT mice were determined. Old WT mice (18–21 months) were treated for 4 weeks with either MMP-2 or scrambled siRNA, in which carotid PWV was assessed at baseline, 2 and 4 weeks after the start of the treatment. Elastin to collagen ratio, desmosin (DES) level, and endothelial nitric oxide synthase (eNOS) pathways were also evaluated and compared. Lastly, levels of circulating MMP-2 and DES, the breakdown product of elastin, were measured in a human cohort (23–86 years old), in whom carotid-femoral PWV was assessed. Results Carotid PWV, as well as both vascular and circulating MMP-2 levels, were elevated with increasing age in WT mice (Figure 1). Therapeutic MMP-2 knockdown in aged WT mice reduced the vascular MMP-2 expression and attenuated age-dependent carotid stiffness. Increased elastin to collagen ratio and a lower plasma DES level were observed on MMP-2 silenced treated animals (Figure 2). Moreover, siMMP-2 treated mice showed enhanced eNOS phosphorylation on Ser1177. A direct interaction between MMP-2 and eNOS was also observed, which, interestingly, is augmented with age. Finally, collected human data showed a higher level of circulating MMP-2 levels on the elderly subjects. In addition, plasma DES level is positively correlated with age and aortic PWV, indicating the involvement of vascular elastin catabolism on arterial stiffness. Conclusions Therapeutic MMP-2 gene silencing, specifically targeting vascular MMP-2, attenuates age-dependent carotid stiffness. This effect is mediated by augmenting eNOS activation and reducing elastin degradation. Thus, our findings indicate MMP-2 as a potential therapeutic target to mitigate age-dependent arterial stiffness and CVD. FUNDunding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Swiss National Science Foundation,Foundation for Cardiovascular Research–Zurich Heart House Figure 1

The role of matrix metalloproteinase-2 on age-dependent arterial stiffness

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y.M Puspitasari ◽  
C Diaz-Canestro ◽  
I Sudano ◽  
A Flammer ◽  
N.R Bonetti ◽  
...  
Keyword(s):  
Arterial Stiffness ◽  
Standard Technique ◽  
Matrix Metalloproteinase 2 ◽  
Elastic Fibers ◽  
Funding Source ◽  
Cardiovascular Research ◽  
Ecm Remodeling ◽  
Carotid Stiffness ◽  
Age Dependent

Abstract Introduction Arterial stiffness is a well-characterized sign of vascular aging. It strongly predicts the development of several cardiovascular diseases (CVD), such as hypertension, stroke and heart failure. The age-dependent stiffening of elastic arteries is primarily attributed to the loss of interlaminar elastic fibers and the increase of collagen fibers. This process is regulated by matrix metalloproteinases (MMPs), including MMP-2. A strong correlation between MMP-2 levels and arterial stiffness has been previously described. However, the causative link between age-dependent arterial stiffness and MMP-2 remains unclear. Purpose In this study, we aimed to prospectively investigate the effect of MMP-2 gene silencing on the development of age-dependent carotid stiffness in wild type (WT) mice. Methods Pulse Wave Velocity (PWV), as the gold standard technique to assess arterial stiffness, was assessed in the right common carotid artery (RCCA) of C57BL/6 WT mice of various ages ranging between 3 and 25 months. Plasma and vascular levels of MMP-2 on RCCA were also measured and correlate with PWV. Moreover, aged WT male mice (18–21-month-old) were treated for 4 weeks with either MMP-2 siRNA or Scr siRNA via tail vein injection every 4 days and PWV was assessed at baseline, 2 and 4 weeks. Results Mouse carotid PWV increased and was positively correlated with age in our in vivo longitudinal study. Increases of vascular and circulating MMP-2 levels were also observed in this study. MMP-2 knockdown by siRNA treatment reduced vascular MMP-2 level (Fig. 1), which in turn attenuated age-dependent carotid stiffening (data not shown). siMMP-2 treated animals also showed an increase of elastin to collagen ratio. Furthermore, enhanced phosphorylation of the activatory eNOS Ser1177 was observed in the siMMP-2 group without affecting the level of total eNOS and Akt phosphorylation. Interestingly, co-immunoprecipitation experiments demonstrated that MMP-2 directly interacts with eNOS and this interaction is augmented with age. Conclusion The silencing of MMP-2 attenuates age-dependent carotid stiffness by affecting elastin to collagen ratio and interfering with eNOS activation. Thus, MMP-2 may mediate ECM remodeling and endothelial-dependent vasorelaxation in the development of age-dependent vascular stiffness. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Swiss National Science Foundation, Foundation for Cardiovascular Research-Zurich Heart House

Arterial stiffness and carotid distensibility following acute formaldehyde exposure in female adults

2021 ◽  
pp. 074823372110316
Author(s):  
Nina L Stute ◽  
Jonathon L Stickford ◽  
Marc A Augenreich ◽  
Kyle C Kimball ◽  
Janet M Cope ◽  
...  
Keyword(s):  
Arterial Stiffness ◽  
Vascular Function ◽  
Intima Media Thickness ◽  
Human Cadaver ◽  
Media Thickness ◽  
Carotid Stiffness ◽  
Short Term Exposure ◽  
Increased Risk ◽  
Carotid Distensibility ◽  
The Impact

Formaldehyde (FA) is a ubiquitous organic preservative used in several industries and represents an occupational health hazard. Short-term exposure to FA can increase oxidative stress and cause a decrease in conduit vessel function. These decrements in vascular function may extend to the arterial architecture, predisposing individuals to increased risk of cardiovascular disease. The purpose of this study was to investigate the impact of an acute 90-minute FA exposure period (259 ± 95 ppb) on indices of arterial architecture. Arterial stiffness and carotid distensibility as determined by central pressures, augmentation index (AIx), and carotid-femoral pulse wave velocity (cfPWV) ( n=13F, 24 ± 1 year) as well as carotid stiffness and intima media thickness (IMT) ( n = 9F, 23 ± 1 year) were assessed prior to (Pre-FA) and immediately following (Post-FA) exposure to FA in human cadaver dissection laboratories. Central pressures and cfPWV (Pre-FA: 5.2 ± 0.8 m.s−1, Post-FA: 5.2 ± 1.1 m s−1) were unchanged by acute FA exposure ( p > 0.05). Carotid stiffness parameters and distension were unchanged by acute FA exposure ( p > 0.05), although distensibility (Pre-FA: 33.9 ± 10.5[10–3*kPa−1], Post-FA: 25.9 ± 5.5[10–3*kPa-1], p < 0.05), and IMT (Pre-FA: 0.42 ± 0.05 mm, Post-FA: 0.51 ± 0.11 mm, p < 0.05) decreased and increased, respectively. Individual Pre- to Post-FA changes in these markers of arterial architecture did not correlate with levels of FA exposure ([FA]: 20–473 ppb) ( p > 0.05). Our group previously found vascular function decrements following acute FA exposure in human cadaver laboratories; here we found that carotid distensibility and intima media thickness are altered following FA exposure.

Therapeutic MMP-2 knockdown blunts age-dependent carotid stiffness by decreasing elastin degradation and augmenting enos activation

2021 ◽  
Vol 331 ◽  
pp. e29-e30
Author(s):  
Y.M. Puspitasari ◽  
C. Diaz-Canestro ◽  
L. Liberale ◽  
T.J. Guzik ◽  
A.J. Flammer ◽  
...  
Keyword(s):  
Elastin Degradation ◽  
Carotid Stiffness ◽  
Age Dependent

Arterial stiffness as an ultrasound biomarker of radiation-induced carotid artery disease

VASA ◽  
2021 ◽  
pp. 1-8
Author(s):  
Veronica Fernández-Alvarez ◽  
Carlos Suárez Nieto ◽  
Fernando López Alvarez
Keyword(s):  
Carotid Artery ◽  
Arterial Stiffness ◽  
Background Radiation ◽  
Carotid Artery Disease ◽  
Stiffness Index ◽  
Control Group ◽  
Significant Group ◽  
Carotid Stiffness ◽  
Radiation Induced ◽  
Artery Disease

Summary: Background: Radiation-induced carotid artery disease (RICAD) is an important issue in head and neck cancer (HNC) survivors after radiotherapy (RT). The risk of cerebrovascular disease in these patients is doubled. The aim of this study was to assess the effect of RT on carotid artery stiffness in HNC patients. Patients and methods: Conventional arterial stiffness parameters were measured in a total of 50 HNC survivors treated with RT for at least 5 years and compared to 50 unirradiated HNC patients. Elastic modulus (Ep) and Beta stiffness index (β) were measured in proximal, mid and distal common carotid artery (CCA). Results: The mean age of the subjects was 68±9 years (range: 44–84) in the irradiated group and 67±10 years (range: 45–85) in the control group. The RT group was treated with a mean radiation exposure of 60.3±6.7 Gy (range: 44–72) in the neck. Carotid stiffness parameters showed significant group differences: Ep in the RT group was 2.329±1.222 vs 1.742±828 in the non-RT group (p=0.006) and β index in the RT group was 23±11 vs 15±8 in the non-RT group (p<0.001). Radiation-induced carotid stiffness was quantified and cervical exposure to RT increased Ep in 575 kPa (p=0.014) and β in 7 units (p<0.003). Conclusions: Ep and β index could be suitable ultrasound biomarkers of radiation-induced atherosclerosis in HNC survivors. Further prospective studies are needed to feature RICD in this setting.

scholarly journals Carotid artery wall stiffness is increased in patients with small vessel disease: A case-control study

2016 ◽  
Vol 144 (1-2) ◽  
pp. 6-9 ◽  
Author(s):  
Denisa Salihovic-Hajdarevic ◽  
Aleksandra Pavlovic ◽  
Dzevdet Smajlovic ◽  
Ana Podgorac ◽  
Zagorka Jovanovic ◽  
...  
Keyword(s):  
Risk Factors ◽  
Carotid Artery ◽  
Arterial Stiffness ◽  
Small Vessel Disease ◽  
Vascular Risk Factors ◽  
Small Vessel ◽  
Vascular Risk ◽  
Vessel Disease ◽  
Increased Risk ◽  
Atheromatous Plaques

Introduction. Cerebral ischemic small-vessel disease (SVD), causing lacunar infarcts and white matter hyperintensities on brain magnetic resonance imaging (MRI), is a progressive disease associated with an increased risk of stroke, dementia and death. Increased arterial stiffness has been associated with ischemic stroke and cerebral SVD independently of common vascular risk factors. Objective. The aim of the study was to analyze arterial stiffness in our patients with symptomatic SVD. Methods. In a cross-sectional study design we included 30 patients with clinical and MRI evidence of cerebral SVD and 30 age-, gender- and risk factor-matched control subjects with no neurological diseases. Patients were evaluated at the Ultrasound Laboratory at the Neurology Clinic, Clinical Center of Serbia in Belgrade, during a three-month period (from September 1st to December 1st 2012). Baseline demographic and vascular risk factors were recorded. All patients underwent standard carotid ultrasound scans with measuring of intima-media thickness (IMT) and analysis of atheromatous plaques. Internal carotid artery stiffness was evaluated with the use of e-tracking option as beta stiffness index (BSI) value. Results. There were no differences between study groups in regard to degree of carotid stenosis and type of carotid plaques (p>0.05). Patients in SVD group had significantly higher mean IMT (p=0.0093) and mean BSI (p<0.0001) than subjects in the control group. No significant correlation was detected between IMT and BSI in SVD group (r=0.168; p=0.376). Brain lesions severity correlated with BSI (r=0.733; p<0.0001). Conclusion. Arterial stiffness is increased in symptomatic patients with SVD, independently of vascular risk factors and IMT.

scholarly journals Augmentation Index Is Inversely Associated with Skeletal Muscle Mass, Muscle Strength, and Anaerobic Power in Young Male Adults: A Preliminary Study

2021 ◽  
Vol 11 (7) ◽  
pp. 3146
Author(s):  
Dongmin Lee ◽  
Kyengho Byun ◽  
Moon-Hyon Hwang ◽  
Sewon Lee
Keyword(s):  
Skeletal Muscle ◽  
Muscle Strength ◽  
Arterial Stiffness ◽  
Muscle Mass ◽  
Muscular Strength ◽  
Skeletal Muscle Mass ◽  
Augmentation Index ◽  
Anaerobic Power ◽  
Negatively Associated ◽  
Increased Risk

Arterial stiffness is associated with an increased risk of cardiovascular disease. Previous studies have shown that there is a negative correlation between arterial stiffness and variables such as skeletal muscle mass, muscular strength, and anaerobic power in older individuals. However, little research has been undertaken on relationships in healthy young adults. This study presents a preliminary research that investigates the association between arterial stiffness and muscular factors in healthy male college students. Twenty-three healthy young males (23.9 ± 0.5 years) participated in the study. The participants visited the laboratory, and variables including body composition, blood pressure, arterial stiffness, blood parameters, grip strength, and anaerobic power were measured. Measurements of augmentation index (AIx) and brachial-ankle pulse wave velocity (baPWV) were performed to determine arterial stiffness. There were significant positive correlations among skeletal muscle mass, muscle strength, and anaerobic power in healthy young adult males. AIx was negatively associated with a skeletal muscle mass (r = −0.785, p < 0.01), muscular strength (r = −0.500, p < 0.05), and anaerobic power (r = −0.469, p < 0.05), respectively. Likewise, AIx@75 corrected with a heart rate of 75 was negatively associated with skeletal muscle mass (r = −0.738, p < 0.01), muscular strength (r = −0.461, p < 0.05), and anaerobic power (r = −0.420, p < 0.05) respectively. However, the baPWV showed no correlation with all muscular factors. Our findings suggest that maintaining high levels of skeletal muscle mass, muscular strength, and anaerobic power from relatively young age may lower AIx.

scholarly journals Associations of markers of arterial stiffness and remodeling with new-onset type 2 diabetes mellitus

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
F Ahmadizar ◽  
K Wang ◽  
F Mattace Raso ◽  
MA Ikram ◽  
M Kavousi
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Blood Glucose ◽  
Arterial Stiffness ◽  
Wall Stress ◽  
Lipid Lowering ◽  
Circumferential Wall Stress ◽  
Increased Risk

Abstract Funding Acknowledgements Type of funding sources: None. Background. Arterial stiffness/remodeling results in impaired blood flow and, eventually, decreased glucose disposal in peripheral tissues and increased blood glucose. Besides, increased arterial stiffness/remodeling may lead to hypertension, as a potential reciprocal risk factor for type 2 diabetes mellitus (T2D). We, therefore, hypothesized that increased arterial stiffness/remodeling is associated with an increased risk of T2D. Purpose. To study the associations between arterial stiffness/remodeling and incident T2D. Methods. We used the prospective population-based Rotterdam Study. Common carotid arterial properties were ultrasonically determined in plaque-free areas. Aortic stiffness was estimated by carotid-femoral pulse wave velocity (cf_PWV), carotid stiffness was estimated by the carotid distensibility coefficient (carDC). Arterial remodeling was estimated by carotid artery lumen diameter (carDi), carotid intima-media thickness (cIMT), mean circumferential wall stress (CWSmean), and pulsatile circumferential wall stress (CWSpuls). Cox proportional hazard regression analysis was used to estimate the associations between arterial stiffness/remodeling and the risk of incident T2D, adjusted for age, sex, cohort, mean arterial pressure (MAP), antihypertensive medications, heart rate, non- high-density lipoprotein (HDL)-cholesterol, lipid-lowering medications, and smoking. We included interaction terms in the fully adjusted models to study whether any significant associations were modified by sex, age, blood glucose, or MAP. Spearman correlation analyses were applied to examine the correlations between measurements of arterial stiffness/remodeling and glycemic traits. Results. We included 3,055 individuals free of T2D at baseline (mean (SD) age, 67.2 (7.9) years). During a median follow-up of 14.0 years, 395 (12.9%) T2D occurred. After adjustments, higher cf_PWV (hazard ratio (HR),1.18; 95%CI:1.04-1.35), carDi (1.17; 1.04-1.32), cIMT (1.15; 1.01-1.32), and CWSpuls (1.28; 1.12-1.47) were associated with increased risk of incident T2D. After further adjustment for the baseline glucose, the associations attenuated but remained statistically significant. Sex, age, blood glucose, or MAP did not modify the associations between measurements of arterial stiffness/remodeling, and incident T2D. Among the population with prediabetes at baseline (n = 513) compared to the general population, larger cIMT was associated with a greater increase in the risk of T2D. Most measurements of arterial stiffness/remodeling significantly but weakly correlated with baseline glycemic traits, particularly with blood glucose.  Conclusions. Our study suggests that greater arterial stiffness/remodeling is independently associated with an increased risk of T2D development. Blood glucose and hypertension do not seem to play significant roles in these associations. Further studies should disentangle the underlying mechanism that links arterial stiffness/remodeling and T2D.

Association between Pre-Existing Coronary Artery Disease and 5-Year Mortality in Stroke Patients with High-Grade Carotid Artery Stenosis

2020 ◽  
pp. 1-7
Author(s):  
Ching-I Wu ◽  
Chia-Lun Wu ◽  
Feng-Chieh Su ◽  
Shun-Wen Lin ◽  
Wen-Yi Huang
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Carotid Artery ◽  
Carotid Artery Stenosis ◽  
Significant Risk ◽  
Cox Proportional Hazards Model ◽  
Artery Stenosis ◽  
High Grade ◽  
Increased Risk ◽  
Artery Disease

<b><i>Background:</i></b> The coincidence of coronary artery disease (CAD) and carotid artery stenosis (CAS) was observed. However, the association between pre-existing CAD and ischemic stroke (IS) outcome in patients with high-grade CAS remains unclear. We aimed to investigate the association between pre-existing CAD and outcomes of acute IS patients with high-grade CAS. <b><i>Methods:</i></b> From January 1, 2007, to April 30, 2012, we enrolled 372 acute IS patients with high-grade CAS and prospectively observed them for 5 years. Demographic features, vascular risk factors, comorbidities, and outcomes were compared between patients with and without pre-existing CAD. <b><i>Results:</i></b> Among 372 individuals, 75 (20.2%) patients had pre-existing CAD and 297 (79.8%) patients did not have pre-existing CAD. The prevalence rates of hypertension, congestive heart failure, chronic kidney disease, and gout in patients with pre-existing CAD were significantly higher than in those without pre-existing CAD (<i>p</i> = 0.017, <i>p</i> &#x3c; 0.001, <i>p</i> = 0.002, and <i>p</i> &#x3c; 0.001, respectively). The multivariate Cox proportional hazards model revealed that pre-existing CAD was a significant risk factor for a 5-year all-cause mortality in acute IS patients with high-grade CAS (hazard ratio = 2.26; 95% confidence interval = 1.35–3.79; <i>p</i> = 0.002). <b><i>Conclusion:</i></b> Pre-existing CAD was associated with an increased risk of 5-year mortality in acute IS patients with high-grade CAS. Intensive treatment for the pre-existing CAD may reduce long-term mortality in acute IS patients with high-grade CAS.

Increased Rates of Hemorrhages after Endovascular Stroke Treatment with Emergency Carotid Artery Stenting and Dual Antiplatelet Therapy

2021 ◽  
pp. 1-9
Author(s):  
Felix Hadler ◽  
Raveena Singh ◽  
Martin Wiesmann ◽  
Arno Reich ◽  
Omid Nikoubashman
Keyword(s):  
Risk Factors ◽  
Carotid Artery ◽  
Antiplatelet Therapy ◽  
Carotid Artery Stenting ◽  
Dual Antiplatelet Therapy ◽  
Stroke Treatment ◽  
Systemic Thrombolysis ◽  
Stroke Registry ◽  
Increased Risk ◽  
Arterial Thrombolysis

<b><i>Background:</i></b> While endovascular stroke treatment (EST) of large vessel occlusions in acute ischemic stroke (AIS) is proven to be safe and effective, there are subgroups of patients with increased rates of hemorrhages. Our goal was to identify risk factors for intracerebral hemorrhage and to assess whether acute carotid artery stenting (CAS) was associated with increased bleeding rates. <b><i>Methods:</i></b> We performed a retrospective analysis of our monocentric prospective stroke registry in the period from May 2010 to May 2018 and compared AIS patients receiving EST with (<i>n</i> = 73) versus without acute CAS (<i>n</i> = 548). Patients with intracranial stents, intra-arterial thrombolysis, or dissection of the carotid artery were excluded. <b><i>Results:</i></b> Parenchymal hemorrhage rates (PH2 according to the ECASS classification) and symptomatic hemorrhage (sICH) rates were increased in EST patients receiving CAS with odds being 6.3 (PH2) and 6.5 (sICH) times higher (PH2 17.8 vs. 3.3%, <i>p</i> &#x3c; 0.001 and sICH: 16.4 vs. 2.9%, <i>p</i> &#x3c; 0.001). Additional systemic thrombolysis with rtPA (IVRTPA) was no risk factor for cerebral hemorrhage (<i>p</i> = 0.213). <b><i>Conclusion:</i></b> AIS patients receiving EST with acute CAS and consecutive tirofiban or dual antiplatelet therapy suffered from an increased risk of relevant secondary intracranial bleeding. After adjusting for confounders, tirofiban and dual antiplatelet therapy were associated with higher bleeding rates.

MO570PULSE PRESSURE: A PREDICTOR OF CARDIOVASCULAR CALCIFICATION AND CARDIOVASCULAR MORTALITY IN HEMODIALYSIS PATIENTS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Merita Rroji (Molla) ◽  
Saimir Seferi ◽  
Majlinda Cafka ◽  
Erjola Likaj ◽  
Vilma Cadri ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Abdominal Aorta ◽  
Cardiovascular Mortality ◽  
Pulse Pressure ◽  
Univariate Analysis ◽  
Hemodialysis Patients ◽  
Case Series Study ◽  
Increased Risk ◽  
Elevated Systolic Blood Pressure

Abstract Background and Aims The mortality rate is extremely high in chronic kidney disease (CKD), primarily due to the high prevalence of cardiovascular disease (CVD). Increased pulse pressure (PP), defined as the difference between inappropriately elevated systolic blood pressure (SBP) and reduced diastolic blood pressure (DBP) at any value of mean arterial pressure (MAP), is a surrogate measure of increased arterial stiffness of central elastic arteries (aorta and its major branches). CKD-MBD anomalies leading to calcification contribute to increased arterial stiffness and pulse pressure. This study aimed to evaluate the relationship of pulse pressure parameter with valve calcification and abdominal aortic calcification in hemodialysis patients and its impact on cardiovascular mortality. Method We performed a prospective case series study with 3 years follow- up. Plain X-ray images of the lateral lumbar spine from all subjects were studied to obtain images of the lower abdominal aorta using semiquantitative scores as described by Kauppila et al. Cardiac valve calcifications were evaluated by two-dimensional echocardiography with an HDI 5000 Sono CT echocardiographic machine with a 3.3-MHz multiphase array probe in subjects lying in the left decubitus position an according to the recommendations of the European Association of Echocardiography. The patient was evaluated as having vascular calcification if he had the presence of calcification in at least one of the site examined: a mitral valve, aortic valve or abdominal aorta. Results We studied 85 chronic stable hemodialysis patients. Mean age and meantime is therapy was 49.9±12.4 years and 51.5±28.7 months, respectively. Mean pulse pressure was 55.72±14.2 mmHg. Fifty-nine patients (69.4%) were identified with aortic abdominal calcification, and the mean Kauppila score was 4.91 ± 4.05. Sixty patients (70.5%) had at least one valve calcified, while thirty-three patients (38.8%) had both valves calcified. Univariate analysis revealed that every 1 mmHg increase in pulse pressure was associated with increased cardiovascular calcification risk p=0.020. In multivariate analysis, after adjustment for age, gender, diabetes mellitus, cholesterol, and triglyceride serum levels, the association also remained strong, where every increase of 1 mm Hg in pulse pressure was associated with increased risk for cardiovascular calcification (HR 1.02, 95% CI (1.00-1.03), p= 0.038). Besides, pulse pressure was an independent predictor for cardiovascular mortality (HR 1.03, 95% CI (1.02-1.05), p=0.002). Conclusion Pulse pressure may identify hemodialysis patients with subclinical cardiovascular calcification who need further evaluation. Wide pulse pressure is associated with increased cardiovascular mortality.

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