Value of systemic inflammation-response index in predicting contrast-induced nephropathy in patients with ST-elevation myocardial infarction.

BACKGROUND: Contrast induced nephropathy (CIN) is one of the feared complications of contrast medium-using procedures. Present study was conducted in order to evaluate the value of systemic inflammatory-response index (SIRI) for development of CIN among patients who underwent primary percutaneous intervention. METHODS: Six hundred seventy-six patients with the diagnosis of ST elevation myocardial infarction were included. The patients were divided into two groups according to the presence of CIN. Patients without (n = 530) and with (n = 146) CIN constituted group 0 and group 1, respectively. Clinical and biochemical features of the patients were recorded. Calculation of SIRI was made for each patient. RESULT: CIN patients were older, had higher prevalence of hyperlipidaemia, higher values of pre- and post-procedural creatinine levels, neutrophil and monocyte counts, neutrophil/lymphocyte ratio (NLR) and monocyte/lymphocyte ratio (MLR) and SIRI. They had lower values of left ventricular ejection fraction (LVEF), haemoglobin and high-density lipoprotein-cholesterol levels. SIRI had the highest area under the curve (AUC) for prediction of CIN. Pairwise analyses of the AUC's demonstrated that SIRI had statistically significantly higher AUC compared to NLR and MLR. Multivariate logistic regression analysis showed that besides from LVEF and pre-procedural creatinine, NLR and SIRI were the independent predictors of CIN. SIRI had a higher odds ratio compared to NLR. CONCLUSION: SIRI had greater diagnostic power than NLR and MLR and it can easily be used by physicians for the identification of high-risk patients for the occurrence of CIN.

The Relationship between Extracellular Volume Compartments and Matrix Metalloproteinases-2 in Left Ventricular Remodeling after Myocardial Infarction. / A Relação entre Compartimentos de Volume Extracelular e Matriz Metaloproteinase 2 na Remodelação do Ventrículo Esquerdo após o Infarto do Miocárdio.

BACKGROUND: Matrix metalloproteinases (MMPs) can affect myocardial extracellular volume (ECV) and its compartments, and this can provide more detailed information about the mechanism of adverse left ventricular (LV) remodeling (AR) after acute myocardial infarction (MI). OBJECTIVES: To investigate the role of changes (Δ) in ECV compartments (matrix volume (MVi) and cell volume (CVi)) in the development of AR after MI, and their relationship with MMP-2 expressions. METHODS: Ninety-two first MI patients who underwent 3 Tesla cardiovascular magnetic resonance imaging performed 2 weeks (baseline) and 6 months post-MI. We measured T1 mapping with MOLLI sequences. ECV was performed post-gadolinium enhancement. ECV and LV mass were used to calculate MVi and CVi. AR was defined as an increase of ≥ 12% in LV end-diastolic volume in 6 months. MMPs were measured using a bead-based multiplex immunoassay system at first day (baseline) and 2 weeks post-MI. P <0.05 was accepted as statistically significant. RESULTS: Mean ECV and mean MVi baseline levels were higher in AR group compared to without AR group (42.9±6.4 vs 39.3±8.2%, p= 0.037; 65.2±13.7 vs 56.7±14.7 mL/m2, p=0.010; respectively). CVi levels was similar between groups. A positive correlation was found between baseline levels of MMP-2 and baseline levels of ECV (r=0.535, p<0.001) and MVi (r=0.549, p<0.001). Increased ΔMVi levels was independently predictor of AR (OR=1.03, p=0.010). ΔMVi had superior diagnostic performance compared to ΔECV in predicting AR (ΔAUC: 0.215±0.07, p<0.001). CONCLUSION: High MVi levels are associated with AR, and ΔMVi was independently predictor of AR. This may be associated with MMP-2 release due to increased inflammatory response.

FUNDAMENTO: As matrizes metaloproteinases (MMPs) podem afetar o volume extracelular (VEC) e seus compartimentos, e isso pode oferecer informações mais detalhadas sobre o mecanismo de remodelação adversa (RA) do ventrículo esquerdo (VE) após o infarto agudo do miocárdio (IM). OBJETIVOS: Investigar o papel que as alterações (Δ) nos compartimentos de VEC (volume matriz (MVi) e volume celular (CVi)) desempenham no desenvolvimento de RA após o IM, e sua relação com as expressões de MMP-2. MÉTODOS: Um total de noventa e dois pacientes com primeiro IM passaram por exames de imagens por ressonância magnética cardiovascular 3 Tesla realizados 2 semanas (linha de base) e 6 meses após o IM. Medimos o mapeamento T1 com sequências MOLLI. O VEC foi obtido após o realce pelo gadolínio. O VEC e a massa do VE foram usados para calcular o MVi e o CVi. A RA foi definida como um aumento de ≥ 12% no volume diastólico final do VE em 6 meses. As MMPs foram medidas usando-se um sistema de imunoensaio multiplex em grânulos no primeiro dia (linha de base) e 2 semanas após o IM. Um P valor <0,05 foi aceito como estatisticamente significativo. RESULTADOS: Os níveis de linha de base de MVi média e VEC médio foram mais altos no grupo com RA em comparação com o grupo sem RA (42,9±6,4 vs. 39,3±8,2 %, p= 0,037; 65,2±13,7 vs. 56,7±14,7 mL/m2, p=0,010; respectivamente). Os níveis de CVi eram semelhantes entre os grupos. Foi encontrada uma correlação positiva entre os níveis de linha de base de MMP-2 e os níveis de linha de base de VEC (r=0,535, p<0,001) e MVi (r=0,549, p<0,001). O aumento dos níveis de ΔMVi foi um preditor independente da RA (RC=1,03, p=0,010). O ΔMVi teve um desempenho diagnóstico superior quando comparado ao ΔVEC na previsão do (ΔAUC: 0,215±0,07, p<0,001). CONCLUSÃO: Níveis altos de MVi estão associados à RA, e o ΔMVi foi um preditor independente de RA. Isso pode estar associado à liberação de MMP-2 devido ao aumento da resposta inflamatória.

A Relação entre Compartimentos de Volume Extracelular e Matriz Metaloproteinase 2 na Remodelação do Ventrículo Esquerdo após o Infarto do Miocárdio / The Relationship between Extracellular Volume Compartments and Matrix Metalloproteinases-2 in Left Ventricular Remodeling after Myocardial Infarction

Resumo Fundamento: As matrizes metaloproteinases (MMPs) podem afetar o volume extracelular (VEC) e seus compartimentos, e isso pode oferecer informações mais detalhadas sobre o mecanismo de remodelação adversa (RA) do ventrículo esquerdo (VE) após o infarto agudo do miocárdio (IM). Objetivos: Investigar o papel que as alterações (Δ) nos compartimentos de VEC (volume matriz (MVi) e volume celular (CVi)) desempenham no desenvolvimento de RA após o IM, e sua relação com as expressões de MMP-2. Métodos: Um total de noventa e dois pacientes com primeiro IM passaram por exames de imagens por ressonância magnética cardiovascular 3 Tesla realizados 2 semanas (linha de base) e 6 meses após o IM. Medimos o mapeamento T1 com sequências MOLLI. O VEC foi obtido após o realce pelo gadolínio. O VEC e a massa do VE foram usados para calcular o MVi e o CVi. A RA foi definida como um aumento de ≥ 12% no volume diastólico final do VE em 6 meses. As MMPs foram medidas usando-se um sistema de imunoensaio multiplex em grânulos no primeiro dia (linha de base) e 2 semanas após o IM. Um P valor <0,05 foi aceito como estatisticamente significativo. Resultados: Os níveis de linha de base de MVi média e VEC médio foram mais altos no grupo com RA em comparação com o grupo sem RA (42,9±6,4 vs. 39,3±8,2 %, p= 0,037; 65,2±13,7 vs. 56,7±14,7 mL/m2, p=0,010; respectivamente). Os níveis de CVi eram semelhantes entre os grupos. Foi encontrada uma correlação positiva entre os níveis de linha de base de MMP-2 e os níveis de linha de base de VEC (r=0,535, p<0,001) e MVi (r=0,549, p<0,001). O aumento dos níveis de ΔMVi foi um preditor independente da RA (RC=1,03, p=0,010). O ΔMVi teve um desempenho diagnóstico superior quando comparado ao ΔVEC na previsão do (ΔAUC: 0,215±0,07, p<0,001). Conclusão: Níveis altos de MVi estão associados à RA, e o ΔMVi foi um preditor independente de RA. Isso pode estar associado à liberação de MMP-2 devido ao aumento da resposta inflamatória.

Abstract Background: Matrix metalloproteinases (MMPs) can affect myocardial extracellular volume (ECV) and its compartments, and this can provide more detailed information about the mechanism of adverse left ventricular (LV) remodeling (AR) after acute myocardial infarction (MI). Objectives: To investigate the role of changes (Δ) in ECV compartments (matrix volume (MVi) and cell volume (CVi)) in the development of AR after MI, and their relationship with MMP-2 expressions. Methods: Ninety-two first MI patients who underwent 3 Tesla cardiovascular magnetic resonance imaging performed 2 weeks (baseline) and 6 months post-MI. We measured T1 mapping with MOLLI sequences. ECV was performed post-gadolinium enhancement. ECV and LV mass were used to calculate MVi and CVi. AR was defined as an increase of ≥ 12% in LV end-diastolic volume in 6 months. MMPs were measured using a bead-based multiplex immunoassay system at first day (baseline) and 2 weeks post-MI. P <0.05 was accepted as statistically significant. Results: Mean ECV and mean MVi baseline levels were higher in AR group compared to without AR group (42.9±6.4 vs 39.3±8.2%, p= 0.037; 65.2±13.7 vs 56.7±14.7 mL/m2, p=0.010; respectively). CVi levels was similar between groups. A positive correlation was found between baseline levels of MMP-2 and baseline levels of ECV (r=0.535, p<0.001) and MVi (r=0.549, p<0.001). Increased ΔMVi levels was independently predictor of AR (OR=1.03, p=0.010). ΔMVi had superior diagnostic performance compared to ΔECV in predicting AR (ΔAUC: 0.215±0.07, p<0.001). Conclusion: High MVi levels are associated with AR, and ΔMVi was independently predictor of AR. This may be associated with MMP-2 release due to increased inflammatory response.

Low sCD163/TWEAK Ratio at First Day After Acute Myocardial Infarction Associated with Adverse Cardiac Remodeling in Non-Elderly Patients.

Aim    In this study, we aimed to investigate the role of sCD163 / tumor necrosis factor-like weak apoptosis-inducing (TWEAK) ratio in cardiac remodeling in non-elderly patients diagnosed with first acute myocardial infarction (MI).Material and Methods    Forty-four patients (age ranges: 40-64 years) diagnosed with first-time acute ST-elevation MI in the emergency department were evaluated with cardiac magnetic resonance (CMR) imaging. Adverse remodeling (AR) was defined the increases of left ventricular end-diastolic volume by ≥12 % by CMR at 6­month post-MI TWEAK and sCD163 were measured at the first day (baseline), 2 weeks and 6 weeks post-MI.Results    The average age of patients included in the study was 53.6±5.1 years. AR was detected in 18 patients at the 6 months post-MI. At the first day post-MI, median sCD163 concentration (116 069 vs 86 394 pg / mL, p=0.040) and median TWEAK concentration (759.4 vs 220.1 pg / mL, p<0.001) were higher in AR group compared to group without AR (the non-AR group), median sCD163 / TWEAK ratio (101.4 vs. 406.8; p<0.001) was lower. At the first day post-MI, concentrations of TWEAK and sCD163 showed a positive correlation in AR group and group without AR s. At 2 weeks post-MI, positive correlation continued in the non-AR group, but no significant correlation was found in the AR group. At the first day post-MI, sCD163 / TWEAK ratio was higher diagnostic performance compared to TWEAK and sCD163.Conclusion    In the early phase post-MI, the relationship between sCD163 - TWEAK may have an important role in AR pathogenesis. A lower sCD163 / TWEAK ratio on the first day after MI was associated with an increase in left ventricular end-diastolic volume after 6 months of follow-up.

Is there a relationship between heart rate recovery and blood pressure in white coat hypertension?

Aim    Increasing evidence suggests that autonomic dysfunction may be involved in the etiology of white coat hypertension (WCH). The aim of this study was to evaluate cardiac autonomic function by using heart rate recovery (HRR) indices in patients with WCH classified according to their circadian rhythm type of blood pressure (BP).Material and methods    This cross-sectional study included 120 participants over the age of 18 yrs, including 50 patients diagnosed with WCH and 70 healthy controls with normal in- and out-of-office BP and without any known disease. Circadian rhythm types, i.e., dippers and non-dippers, were identified using ambulatory BP monitoring. The HRR indices were calculated by subtracting the 1st-minute (HRR1), 2nd-minute (HRR2), and 3rd-minute (HRR3) heart rates from the maximal heart rate recorded during stress testing.Results    The lesser decline in nighttime BP (6.4±2.14 and 13.3±2.2 mmHg, respectively; p<0.001) and the smaller mean HRR1 (25.5±3.0 and 30.3±3.1 beats / min, respectively; p<0.001) were evident in WCH non-dippers compared to WCH dippers. Linear regression analysis showed that HRR1 (ß±SE=0.43±0.11; p<0.001) and diastolic BP at maximum exercise (ß±SE=0.14±0.07; p=0.040) are independent risk factors for the blunted decline in nighttime BP.Conclusion    Delayed recovery of heart rate after an exercise stress test is associated with non-dipper type of circadian rhythm of BP. This was more pronounced in WCH patients, and these patients are at risk of autonomic dysfunction.

Association of changes in the infarct and remote zone myocardial tissue with cardiac remodeling after myocardial infarction: a T1 and T2 mapping study.

Tissue structure in the infarct and remote zone myocardium post-acute myocardial infarction (MI) may offer prognostic information concerning left ventricular remodeling. We aimed to identify or establish a relationship between adverse remodeling (AR) and changes (Δ) in T1, T2 mapping and extracellular volume (ECV) in post MI periods. Fifty-four MI patients underwent 3 Tesla CMR performed 2 weeks (acute phase) and 6 months post-MI. We measured T1 mapping with MOLLI sequences and T2 mapping with TrueFISP sequences. Hematocrit was quantified in scanning time. ECV was performed post-gadolinium enhancement. AR was defined as an increase of ≥ 10% in left ventricular end-diastolic volume in 6 months. In the acute phase post-MI, high T2 relaxation times of the infarct and remote zone myocardium were associated with AR (OR 1.15, p = 0.023 and OR 1.54, p = 0.002, respectively). There was a decrease in T2 relaxation times of the remote zone myocardium at 6 months in patients with AR (42.0 ± 4.0 vs. 39.0 ± 3.5 ms, p < 0.001), while insignificant difference was found in patients without AR. Increased ΔECV (%) and decreased remote ΔT2 values were associated with AR (OR 1.04, p = 0.043 and OR 0.77, p = 0.007, respectively). The diagnostic performance analysis in predicting AR showed that acute-phase remote T2 was similar to that of remote ΔT2 (p = 0.875) but was superior to that of ΔECV (%) (ΔAUC: 0.19 ± 0.09, p = 0.038). In both acute phase and change of 6 months post-MI, the T2 relaxation times in remote myocardium are independently associated with AR, and this suggests higher inflammation in the remote myocardium in the AR group than the other group, even though no significant pathophysiological difference was observed in the healing of the infarct zone between both groups.

The role of temporal changes of pro-inflammatory cytokines in the development of adverse cardiac remodeling after ST-elevation myocardial infarction.

Introduction: Increasing evidence supports the view that pro-inflammatory cytokines play a role in fibrosis after myocardial infarction (MI). It has been suggested that interleukin (IL)-12p40, a pro-inflammatory cytokine, can induce interferon γ (IFN-γ) and matrix metalloproteinase (MMP). However, the role of IL-12p40 in adverse cardiac remodeling (AR) after ST-elevation MI (STEMI) is unclear. Aim: To examine the role of temporal changes of pro-inflammatory cytokines in the development of post-STEMI AR. Material and methods: A total of 43 patients with STEMI for the first time ever were prospectively analyzed. In cardiac magnetic resonance imaging at 6 months after STEMI, a decrease of left ventricular end-diastolic volume by ≥ 12% was defined as reverse cardiac remodeling (RR), and a 12% increase was defined as AR. Cytokine concentrations were measured on the first day (baseline) and 2 weeks after STEMI. Results: Mean IL-12p40 (59.1 ±14.5 vs. 46.7 ±9.1 pq/ml, p = 0.001), median IFN-γ (20.4 vs. 16.2 pq/ml, p = 0.048) and median MMP-2 (33866 vs. 20691 pq/ml, p = 0.011) baseline concentrations were higher in AR than RR. In patients with AR, IL-12p40 level was lower at 2 weeks than baseline (p < 0.001). There was a positive correlation between the baseline concentrations of IL-12p40, IFN-γ, MMP-2, C-reactive protein and infarct size (p < 0.05). Increased IL-12p40 and MMP-2 baseline levels were independently associated with AR (OR = 1.14, p = 0.010; OR = 1.08, p = 0.035). Conclusions: In the initial phase of MI, greater release of pro-inflammatory cytokines was associated with increased MMP-2 levels. Elevated expression of IL-12 and MMP-2 had an independent association with AR. This may be related to the excessive inflammatory response in the initial phase of MI.

A Novel Risk Assessment Model Using Urinary System Contrast Blush Grading to Predict Contrast-Induced Acute Kidney Injury in Low-Risk Profile Patients.

Contrast-induced acute kidney injury (CI-AKI) can occur after coronary interventions despite protective measures. We evaluated the effect of urinary system contrast blush grading for predicting post-procedure CI-AKI in 486 patients with chronic coronary artery disease. Patient characteristics and blood samples were collected. Urinary system contrast blush grade was recorded during the coronary angiography and interventions. Post-procedure third to fourth day blood samples were collected for diagnosis of CI-AKI. The median age of the patients was 61 years (53-70, interquartile range), and 194 (39.9%) participants were female. Contrast-induced acute kidney injury occurred in 78 (16%) patients. By comparing full and reduced models with the likelihood ratio test, it was observed that in the reduced model, factors such as age, diabetes mellitus, body weight-adapted contrast media (CM), hemoglobin, and urinary system blush were associated with CI-AKI presence. The probability of CI-AKI presence increased slightly from grade 0 to 1 blush, but it increased sharply grade from 1 to 2 blush. According to our results, an increase in body weight-adapted CM and urinary blush grading were the main predictors of CI-AKI. These findings suggest that when body weight-adapted CM ratio exceeds 3.5 mL/kg and urinary contrast blush reaches grade 2, the patients should be followed up more carefully for the development of CI-AKI.

Assessment of epicardial adipose tissue thickness and total calcium score in sarcoidosis patients.

OBJECTIVE: Increased thickness of epicardial adipose tissue (EAT) and the total coronary artery calcium score (TCACS) are independent predictors of atherosclerosis. The aim of this study was to investigate whether EAT thickness, measured using thoracic computed tomography, and TCACS were greater in patients with sarcoidosis. METHODS: This was a retrospective study. The details of participants who presented at the cardiology and pulmonology outpatient clinics between January 2011 and December 2018 with dyspnea, chest pain, or palpitations from the hospital data system were reviewed. Patients with transthoracic echocardiography and thorax computed tomography (CT) (CT) records were identified, and those who were diagnosed with sarcoidosis, had no other health problems, and did not take any medication were included in the study. RESULTS: A total of 45 controls and 78 sarcoidosis patients were enrolled. The mean age of the controls was 46.15±13.1 years, while it was 46.26±12.37 years in the sarcoidosis group, which represented no significant difference between the groups (p>0.05). When the groups were compared in terms of a fasting blood test, erythrocyte sedimentation rate (ESR), TCACS, EAT thickness, levels of C-reactive protein (CRP), total cholesterol, low-density lipoprotein (LDL), and triglycerides, it was observed that CRP and EAT thickness were higher in the sarcoidosis group. CONCLUSION: The results of this study indicated that the thickness of EAT calculated using thorax CT was greater in sarcoidosis patients; however, the TCACS was similar in both groups. In addition, there was a positive correlation between EAT thickness and the level of total cholesterol, LDL, triglycerides, CRP, and the sedimentation rate. These findings suggest that atherosclerosis may start earlier in those with sarcoidosis than in the healthy population.

Relative Fat Mass Index can be solution for obesity paradox in coronary artery disease severity prediction calculated by SYNTAX Score.

BACKGROUND: The relation between body mass index (BMI) and coronary artery disease (CAD) extension remains controversial. A new score was developed to estimate body fat percentage (BFP) known as Relative Fat Mass (RFM) Index. This study aimed to evaluate the value of RFM Index in predicting the severity of the CAD, compared with other anthropometric measurements. METHODS: A total of 325 patients with chronic CAD were investigated. RFM, BFP, BMI and other anthropometric characteristics of patients were measured before angiography. CAD severity was determined by SYNergy between percutaneous coronary intervention with TAXus and cardiac surgery trial (SYNTAX) Score. The association between SYNTAX Score and variables was evaluated using linear regression models. In order to compare the model performance, R-squared (R2), Akaike's information criterion, Bayesian information criterion and root mean square error were used. RESULTS: Univariate linear regression outcome variable, SYNTAX was used to determine whether there was any relationship between variables. Independent variables were included in the multivariable linear logistic regression models. The analysis showed that in model 1, RFM (ß coefficient: 2.31 (0.90 to 3.71), p=0.001)), diabetes mellitus (ß coefficient: 3.72 (1.67 to 3.76), p=0.004)), haemoglobin (ß coefficient: -2.12 (-3.70 to -0.53), p=0.03) and age (ß coefficient: 1.83 (0.29 to 3.37), p=0.02)) were statistically significant. The adjusted R2 values in model 1 were higher than model 2 (BFP) and model 3 (BMI) (0.155, 0.137 and 0.130, respectively), and χ2 values of RFM were higher than BFP and BMI (10.5, 3.4 and 1.0, respectively). CONCLUSION: RFM Index is a more reliable and compatible marker of obesity in showing the severity of CAD compared to BMI.

Higher levels of TWEAK and matrix metalloproteinase-3 during the acute phase of myocardial infarction are associated with adverse left ventricular remodeling.

INTRODUCTION: It is known that the levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK/TNFSF12) increase after myocardial infarction (MI) and that it interacts with sCD163. It has also been argued that TWEAK can induce matrix metalloproteinases (MMPs) in macrophages. AIM: To investigate the roles of TWEAK, sCD163, and MMPs in left ventricular (LV) adverse remodeling (AR) in the early post-MI period. MATERIAL AND METHODS: Forty-six patients with ST-elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention were enrolled in the study. Post-MI LV functions and volumes were assessed by cardiac magnetic resonance imaging at 2 weeks and 6 months. Cytokines and MMPs were measured using a bead-based multiplex immunoassay system at 1 day (baseline) and 2 weeks post-MI. AR was defined as an increase in LV end-diastolic volume of ≥ 10% at the 6-month follow up. RESULTS: The TWEAK, MMP-2, and MMP-3 baseline levels were higher in the patients with AR than those without AR. At 2 weeks post-MI, these expression levels were similar in patients with and without AR, but sCD163 expression was increased in patients without AR. The TWEAK and MMP levels were positively correlated in the early period post-MI. At first day post-MI, higher levels of TWEAK and MMP-3 were predictors of AR (OR = 1.03, p = 0.006; OR = 1.08, p = 0.015; respectively). CONCLUSIONS: TWEAK can induce MMPs in the early period post-MI, and these higher levels contribute to development of AR. Increased sCD163 levels at 2 weeks post-MI seem to be associated with the healing process through neutralizing the excessive inflammatory effects of TWEAK.

Evaluation of Arterial Stiffness Using Pulse Wave Velocity and Augmentation Index in Patients with Chronic Venous Insufficiency.

BACKGROUND AND OBJECTIVES: Chronic venous insufficiency (CVI) is a common pathology of the circulatory system and is associated with a high morbidity for the patients and causes high costs for the healthcare systems. Arterial stiffness has been shown to be a predictor of cardiovascular events and mortality. The relationship between CVI and arterial stiffness using pulse wave velocity (PWV) and augmentation index (Aix) was evaluated in this study. METHODS: Sixty-two patients with the stage of C3-C5 chronic venous disease (CVD) and 48 healthy subjects were enrolled in the study. To assess arterial stiffness, all cases were evaluated with I.E.M. Mobil-O-Graph brand ambulatory blood pressure monitor device. PWV and Aix were used to assess arterial stiffness in this study. RESULTS: The mean age was 61.9±11.05 years and 54 % of the patient population was females. PWV and Aix were significantly higher in CVI patients than controls (8.92±1.65 vs. 8.03±1.43, p=0.001; 25.51±8.14 vs. 20.15±9.49, p=0.003, respectively) and also positive linear correlation was observed between CVI and all measured arterial stiffness parameters (r=0.675 for CVI and PWV, r=0.659 for CVI and Aix, respectively). A PWV value of > 9.2 has 88.9 % sensitivity and 71.4 % specificity to predict the presence of CVI. CONCLUSIONS: PWV and Aix are the most commonly used, easy, reproducible, reliable methods in the clinic to assess arterial stiffness. Logistic regression analysis showed that PWV and Aix were the independent predictors of CVI. PWV has the sensitivity of 88.9 % and specificity of 71.4 % to detect the presence of CVI.