Aortic Stiffness Index Research Articles

P5496Effect of the time delay of PDA closure on aortic stiffness index and its relation with cardiac function

P5496Effect of the time delay of PDA closure on aortic stiffness index and its relation with cardiac function

Are aortic coarctation and rheumatoid arthritis different models of aortic stiffness? Data from an echocardiographic study

BackgroundPatients who underwent a successful repair of the aortic coarctation (CoA) show high risk for cardiovascular (CV) events. Mechanical and structural abnormalities in the ascending aorta (Ao) might have a role in the prognosis of CoA patients. We analyzed the elastic properties of Ao measured as aortic stiffness index (AoSI) in CoA patients in the long-term period and we compared AoSI with a cohort of 38 patients with rheumatoid arthritis (RA) and 38 non-RA matched controls.MethodsData from 19 CoA patients were analyzed 28 ± 13 years after surgery. Abnormally high AoSI was diagnosed if AoSI > 6.07% (95th percentile of the AoSI detected in our reference healthy population). AoSI was assessed at the level of the aortic root by two-dimensional guided M-mode evaluation.ResultsCoA patients showed more than two-fold higher AoSI compared to RA and controls (9.8 ± 12.6 vs 4.8 ± 2.5% and 3.1 ± 2.0%, respectively; all p < 0.05 and in 5 of 19 patients with CoA (26%) AoSI was exceptionally high. The 5 patients with abnormally high AoSI were older with higher BP, LV mass and prevalence of LV diastolic dysfunction. Multiple linear regression analysis revealed that AoSI was independently related to the presence of LV hypertrophy and higher LV relative wall thickness.ConclusionsCoA patients have higher AoSI levels than RA patients and non-RA matched controls. AoSI levels are abnormally high in a small sub-group of CoA patients who show a very high-risk clinical profile for adverse CV events.

The predictive role of aortic propagation velocity for coronary artery disease

BackgroundIt is well recognized that cardio- vascular risk factors lead to histological and functional changes in aorta, and aortic stiffness is the best predictor of cardiovascular morbidity and mortality. In this study we evaluated the relation of a less evaluated echocardiographic parameter of aortic stiffness, aortic propagation velocity (APV) with the presence and severity of CAD.MethodsThis cross sectional study was conducted from May 2015 to March 2016 in Imam Reza hospital, Mashhad, Iran. Seventy patients who were referred for elective coronary artery angiography were enrolled. Patients were divided into two sub-groups based on angiographic findings: patients with CAD (38 patients, 54.3%) and non-CAD (32 patients, 45.7%). Transthoracic echocardiography was performed using the conventional 2D and color M-Mode imaging. Aortic propagation velocity (APV), aortic strain (AS) and distensibility (AD) were measured. The presence and Severity of CAD (assessing by syntax score) and their relation with aortic stiffness indices were assessed.ResultsAortic strain (6.23 ± 1.93% versus 11.66 ± 4.86%, P < 0.0001), distensibility (2.46 ± 0.91 vs 5.57 ± 2.25 cm 2 dyn-110-3, P < 0.0001) and APV (48.63 ± 10.31 cm/sec vs 77.75 ± 9.97 cm/s, P < 0.0001) were significantly decreased in CAD group compared with non-CAD group. In our study, APV showed significant inverse relationship with CAD. Based on our results, APV less than 56 cm/sec could be used to predict CAD with sensitivity and specificity of 96.9 and 78.9% respectively. We also found an inverse correlation between APV and severity of CAD.ConclusionAortic strain, AD and APV (a less evaluated echocardiographic index) showed significant inverse correlation with presence and severity of CAD.

Ascending aorta in tetralogy of Fallot: Beyond echocardiographic dimensions.

Late after tetralogy of Fallot (TOF) repair some patients exhibit aortic dilatation and stiffness. Noninvasive assessment of aortic stiffness could contribute to understand this aortopathy and may be important in risk stratification for major aortic event. We included prospectively 82 adults after TOF repair and 41 age- and sex-matched normal controls. Aortic diameters were measured by two-dimensional transthoracic echocardiography and the aortic z-score was estimated. Aortic deformation was assessed by M-mode strain and global peak circumferential ascending aortic strain (CAAS), derived from two-dimensional speckle tracking echocardiography (2D-STE). Corrected CAAS was calculated as CAAS/pulse pressure. Ascending aorta (AAo) distensibility and stiffness index were calculated. TOF patients (age 29.7±8.4years; follow-up since TOF repair 23.0±6.8years) had smaller body surface area but a larger aorta compared to controls. TOF patients had lower AAo distensibility (2.2 [0.0-21.0] vs 5.6 [0.0-12.5] cm2 dyne-1 10-6 , P<.01), higher aortic stiffness index (9.5 [2.7-98.4] vs 7.1 [2.3-20.4], P=.02) and lower CAAS (6.0±3.9 vs 8.1±4.4%, P=.01) compared to controls. CAAS showed a better correlation with AAo z-score (r=-.25, P=.03) compared to M-mode strain. Systemic arterial compliance, arterial stiffness and corrected CAAS (β=-0.23, P=.02) were independently associated with AAo diameter. TOF patients have a larger and stiffer AAo compared to controls. CAAS derived from 2D-STE allows a routine noninvasive method for assessing AAo stiffness, with advantages over M-mode strain, and may be used as predictor of major aortic or cardiovascular events.

AORTIC VISCOELASTIC PROPERTIES AND ALTERED ELECTROMECHANICAL CARDIO-AORTIC CONNECTION IN PATIENTS WITH CARDIAC AMYLOIDOSIS

Objective: Cardiac amyloidosis (CA) is an infiltrative disorder caused by deposition of amyloid fibrils in the myocardial extracellular matrix. Although there is a wide scientific literature regarding amyloid heart disease, no data about aortic viscoelastic properties in these patients are available. This studio has the aims to start filling this gap.Design and method: 113 outpatients attending the Pavia Amyloid Center either with suspected or already diagnosed amyloidosis were enrolled; 58 of them were affected by cardiac amyloidosis. Arterial applanation tonometry (PulsePen, DiaTecne, Milan, Italy) was performed in carotid and femoral arteries to calculate carotid-to-femoral pulse wave velocity (PWV) as index of aortic stiffness. Carotid pressure wave was calibrated with oscillometric brachial blood pressure (BP) to obtain central BP, pulse pressure amplification (PPA) and augmentation index (AIx). Tonometric data were related to biochemical parameters, clinical data and treatment. Populations with and without cardiac involvement (NCA) were compared. Results: Carotid-femoral PWV was not significantly higher in CA subjects compared to NCA (p = 0.462). PPA was significantly reduced in subjects with CA (26.9 ± 10.6% in NCA, 19.8 ± 12.4% in CA, p = 0.0014). Multivariate Regression Analysis highlighted that the presence of cardiac involvement is the main element in determining a reduction in PPA. CA subjects had lower both peripheral pressure values and central ones. There were no significant differences in central pulse pressure (42.6 ± 12.3 in NCA vs 39.5 ± 12.6 mmHg in CA, p = 0.187), and AIx. The morphological analysis of the central pulse wave in its components (direct and reflected wave) did not show significant differences in the parameters studied, with the exception of Ti, detecting an early wave overlap in CA. Conclusions: Although there were no significant differences in aortic stiffness evaluated by PWV in subjects with CA, a reduced PPA was found. An altered electromechanical cardio-aortic connection, with preserved aortic properties, may be an explanation for this finding. In other words, amyloid cardiopathy strongly impairs cardiac function without significantly alteration in aortic function. Significantly reduced central and peripheral pressure values could be caused by the inability of the diseased heart to develop a post load compared to that of subjects without cardiac involvement.

Smooth Muscle Cullin‐3 Deficiency Causes Vascular Dysfunction, Arterial Stiffness and Severe Hypertension

Cullin‐3 (CUL3) mutations resulting in exon 9 skipping (CUL3D9) cause human hypertension. We recently showed that selective expression of CUL3D9 protein in smooth muscle caused mild hypertension. Herein, we hypothesized that complete genetic deletion of CUL3 in smooth muscle would cause severe hypertension. Mice carrying a conditional allele of CUL3 were bred with mice expressing a tamoxifen‐inducible CRE‐recombinase driven by a smooth muscle myosin heavy chain promoter. Mice were administered tamoxifen i.p. (75 mg/kg) for 5 consecutive days to generate smooth muscle CUL3 knockout mice (S‐CUL3KO). CUL3 protein was undetectable whereas Cullin‐1 and Cullin‐5 proteins were preserved in aorta. CUL3 protein was also preserved in heart and kidney. We assessed vascular function in the cerebral basilar artery and aorta using pressurized and wire myograph, respectively. Pulse wave velocity (PWV) as index of aortic stiffness was measured by Doppler ultrasound, and blood pressure (BP) was measured by radiotelemetry. Aorta from S‐CUL3KO mice exhibited extremely impaired vasorelaxation to acetylcholine (ACh) compared to controls (at 100 μM: 1±3% vs 77±5%, p&lt;0.0001), and to the nitric oxide donor sodium nitroprusside (SNP) (at 100 μM: 15±4% vs 96±1%, p&lt;0.001). Cerebral basilar artery from S‐CUL3KO mice also exhibited equivalent impairment to ACh‐ and SNP‐mediated vasorelaxation. Although RhoA/Rho‐kinase signaling was significantly elevated in aorta from S‐CUL3KO mice, pre‐incubation with a specific Rho‐kinase inhibitor, Y27632 did not restore vasorelaxation suggesting importance of an alternative pathway in response to CUL3 deletion. Conversely, S‐CUL3KO aorta exhibited only modestly impaired relaxation to a cGMP analogue (8‐pCPT‐cGMP, at 100 μM: 70±3% vs 98±2% controls) and to the heme‐independent soluble guanylate cyclase activator (BAY 58–2667, at 10 μM: 94±2% vs 101±1% controls) with a preservation of maximal relaxation. Aorta from S‐CUL3KO mice and CUL3‐deficient primary aortic smooth muscle cells (AoSMC) exhibited a significant two‐fold reduction in the expression of guanylate cyclase β1 and α1 subunits. As consequence, CUL3‐deficient primary AoSMC exhibited impaired cGMP production following stimulation with SNP (baseline cGMP pmol/mg protein: 0.9±0.1 vs 1.3±0.4 controls, SNP‐induced cGMP pmol/mg protein: 3.4±0.5 vs 8.7±1.6 controls). Interestingly, systolic BP (SBP) progressively increased in S‐CUL3KO mice upon tamoxifen‐induced CUL3 deletion (2 weeks SBP mmHg: 145±1 vs 115±2, p&lt;0.001; 4 weeks SBP: 169±1 vs 115±3, p&lt;0.001, n=6/genotype). Pulse wave velocity was also significantly increased in S‐CUL3KO mice (3.7±0.1 m/s vs 2.2±0.1, P&lt;0.001), suggesting increased arterial stiffness. We conclude that smooth muscle CUL3 is a major BP determinant, and identifying novel CUL3 substrates in smooth muscle would be beneficial in the search for new anti‐hypertensive targets.Support or Funding InformationThis project is funded by R01 HL125603 and R01 HL131689 to Dr. Curt Sigmund.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Effects of ivabradine on endothelial function, aortic properties and ventricular-arterial coupling in chronic systolic heart failure patients.

Heart rate (HR) is an important prognostic factor in patients affected by chronic heart failure (CHF); ivabradine has been demonstrated to significantly reduce nonfatal myocardial infarction and hospitalization rate for acute heart failure and to improve left ventricular (LV) reverse remodeling, quality of life, exercise capacity, and arterial elastance (Ea) in these patients. We aimed at evaluating the short-term effects of ivabradine on ventricular-arterial coupling (VAC), aortic stiffness, and endothelial function in stable patients with CHF. We evaluated 30 consecutive CHF patients (LVEF≤ 35%, NYHA class II) with sinus rhythm and HR ≥ 70bpm on optimized pharmacological therapy. All of them underwent both transthoracic echocardiogram to assess aortic elastic properties (aortic distensibility, AD; aortic stiffness index, ASI; systolic aortic strain, SAS) and VAC, and peripheral arterial tonometry to measure endothelial function. Therapy with ivabradine 5mg bid was added and each patient was evaluated with the same examinations after 4months. At the baseline, 73% of patients had impaired VAC and 63% endothelial dysfunction. After 4months, there was a significant improvement in the VAC value (ΔVAC -0.10±0.18, P=.021), mainly linked to Ea (ΔEa -0.40±0.23mm Hg/mL; P=.003). All the parameters of aortic elasticity underwent significant improvement (ΔAD 1.82±1.43cm² × dyn- ¹, P=.004; ΔASI -4.73±6.07, P=.033; ΔSAS -7.98±4.37%, P=.003). Lastly, we also noted a significant improvement of endothelial function (Δ RHI 0.35±0.35; P<.001). At follow-up 40% of patients had impaired VAC (P=.018) and 33% endothelial dysfunction (P=.038). In patients with CHF adding ivabradine on top to the standard optimized medical therapy, when indicated, seems to improve endothelial function, aortic properties, and VAC.

Left Atrium Volume Index and Aortic Stiffness as Predicting Factors for Severity of Coronary Artery Disease

AbstractBackground: Recently, it has been demonstrated that left atrial distension and aortic stiffness have a predictive value for cardiovascular outcomes especially in high-risk, elderly, and hypertensive adults.Aim of Study: Evaluation of predictive value of Left Atrium Volume Index (LAVI) and aortic stiffness for severity of angiographic pattern of Coronary Artery Disease (CAD).Methods: A prospective observational cohort single-center study conducted from May 2016 to May 2017, at Cardiovas-cular Medicine Department, Tanta University Hospitals in Gharbia Governorate, Egypt. The study enrolled 100 consec-utive adult patients of both genders who were diagnosed with chronic stable coronary artery disease and were candidates for invasive coronary angiography. Each patient was subjected to echocardiographic assessment for Left Atrium Volume Index (LAVI) and Aortic Stiffness Index (ASI) followed by invasive coronary angiography for assessment of severity of coronary artery disease by Gensini score. Patients were classified into 3 groups by Gensini score: Group I (gensini score equal zero), Group II (Gensini score more than 0 and less than 20) and Group III (Gensini score equal or more than 20).Results: The prevalence of severe CAD was higher among patients with high LAVI (p-value 0.002) and ASI (p-value 0.05). The significant positive relation between LAVI and Gensini score was mainly between Groups II, III (non-severe and severe coronary artery disease). ASI was more sensitive than LAVI for detection of the severity of CAD as ASI showed statistically significant positive strong correlation with the coronary angiographic score (p=0.001) while LAVI showed no significant correlation with the coronary angiographic score (p=0.061). The LAVI carried sensitivity of 67% and specificity of 49.5% in predicting CAD with cutoff value >19.5. While The ASI carried sensitivity of 66.7% and spe-cificity of 21% in predicting CAD with cutoff value >2.88.Conclusion: It was demonstrated that there is significant elevation at aortic stiffness index and left atrium volume index within the group of patient with the higher Gensini score. So ASI and LAVI could be used as promising factors for evalu-ation of the severity of coronary artery disease.

Enlarged Size and Impaired Elastic Properties of the Ascending Aorta are Associated with Endothelial Dysfunction and Elevated Plasma Matrix Metalloproteinase-2 Level in Patients with Bicuspid Aortic Valve

The aim of this study was to test whether enlarged size and impaired elastic properties of the ascending aorta are associated with impaired endothelial function and increases in plasma matrix metalloproteinase (MMP)-2 concentrations in patients with bicuspid aortic valve (BAV) without significant valvular dysfunction. The size and the elasticity of the ascending aorta and the flow-mediated vasodilation (FMD) in the brachial artery in response to hyperemia were evaluated with 2-D echocardiography and high-frequency linear ultrasound in 42 patients with BAV without significant valvular dysfunction and 30 age- and sex-matched healthy controls. In the BAV group, diastolic ascending aortic diameter (AoD) (32.1 ± 8.1 mm vs. 25.3 ± 3.6 mm, p < 0.001) and aortic stiffness index (8.0 ± 5.3 vs. 4.0 ± 1.8, p < 0.001) were significantly higher, and aortic strain (7.4 ± 3.6% vs. 11.1 ± 3.0%, p < 0.001) and aortic distensibility (7.4 ± 4.1 × 10−6cm2/dyn vs. 11.1 ± 4.3 × 10−6cm2/dyn, p < 0.001) were significantly lower than those in the control group. The BAV group also had lower FMD (6.5 ± 2.2% vs. 11.9 ± 2.7%, p < 0.001) and higher plasma MMP-2 levels (226.7 ± 55.0 ng/mL vs. 177.0 ± 45.3 ng/mL, p < 0.001) compared with the control group. In the BAV group, AoD, aortic strain, aortic stiffness index and aortic distensibility significantly correlated with FMD and MMP-2 (all p < 0.05). The multivariable linear regression analysis further indicated that FMD and MMP-2 were independently associated with AoD (β = −1.1, p = 0.005, and β = 0.09, p < 0.001, respectively). These findings suggest that enlarged size and impaired elastic properties of the ascending aorta are associated with endothelial dysfunction and elevated plasma MMP-2 level in patients with BAV without significant valvular dysfunction. FMD and plasma MMP-2 level are the significant and independent predictors of dilation of the ascending aorta in patients with BAV.

Prognostic significance of arterial stiffness and osteoprotegerin in patients with stable coronary artery disease.

Arterial stiffness and vascular calcification significantly contribute to coronary atherosclerosis progression. The prognostic value of increased arterial stiffness and vascular calcification in subjects with stable coronary artery disease (CAD) after percutaneous coronary intervention(PCI) is currently under question. We randomly enrolled 262 patients with stable CAD 1month after successful PCI. Carotid-femoral pulse wave velocity (PWV) was measured as a well-established index of central aortic stiffness. Osteoprotegerin (OPG) plasma levels were measured as a biomarker of vascular calcification. Patients were followed up prospectively up to 52months. The primary endpoint was the composite of death from cardiovascular causes, myocardial infarction, stroke or hospitalization for cardiovascular causes. During the follow-up period, 48 patients presented the primary composite endpoint. Subjects who presented the primary endpoint, compared to subjects free of cardiovascular events, had significantly increased PWV (9.45±2.19m/s vs 8.73±2.07m/s, P=.04) and OPG levels (4.21±2.19pmol/L vs 3.18±1.74pmol/L, P=.003). Survival analysis indicated that PWV predicted adverse cardiac events MACE (Hazard ratio=1.29 95%CI: 1.07-1.57, P=.008) independently from confounders such as age, sex, smoking habits, ejection fraction, extent of coronary artery disease, hypertension and diabetes mellitus. Interestingly, for every increase in pulse wave velocity by 1m/s, there is an anticipated increase in the risk of major adverse cardiovascular event (MACE) by 29%. These findings extend the current knowledge concerning the role of arterial stiffness as powerful biomarkers in cardiovascular disease. Measurement of PWV might have a role in ascertaining prognosis and managing treatment in patients with stable CAD after PCI.

Analysis of Aortic Remodeling and Stiffness in Patients with Obstructive Sleep Apnea Syndrome: Preliminary Results.

to analyse aortic remodelling in OSA. Thirty consecutive OSA patients (22 males and 8 females, aged 58.5 ± 13.2years) were studied. All patients underwent a morning blood gas analysis, a full cardiorespiratory evaluation, including nocturnal polygraphy and echocardiography, that assessed aortic root diameter (ARD) and aortic stiffness index (ASI). Patients were grouped as follows: Group 1, non-severe OSA (Apnea-Hypopnea Index; AHI <30, 14 patients); Group 2, severe OSA (AHI ≥30, 16 patients). No difference was found between the groups in ARD as absolute value (Group 1, 33.64 ± 0.91mm; Group 2, 33.64 ± 1.02, p = ns) and as normalized value for the body surface area- ARDi (Group 1, 16.72 ± 0.63mm/m2; Group 2, 16.09 ± 0.44, p = ns). Moreover, no difference was found in the ASI (Group 1, 14.04 ± 2.26; Group 2, 13.41 ± 2.22, p=ns). Considering all OSA patients, AHI showed an inverse correlation with ARDi (p=0.018) and ASI (p=0.0449). Moreover, the ASI showed a direct correlation with ARDi (p=0.01) and morning PaO2 (p=0.0349) as well as an inverse correlation with the oxygen desaturation index (ODI, p=0.031) and total time with apnea and hypopnea (p=0.039). No difference was found between severe and non-severe OSA in ARD. Surprisingly, the data show that the severity of OSA correlates inversely with the ASI and ARDi. The relation between PaO2 and stiffness might be explained by a feedback mechanism that tries to overcome the reduction of aortic elasticity due to night desaturation. These findings need to be investigated in further studies with a larger study population.

Impaired Cardiac Functions and Aortic Elastic Properties in Patients with Severe Vitamin D Deficiency.

Background:The study explored the effect of severe Vitamin D deficiency on cardiac functions and aortic elastic properties determined by echocardiography.Patients and Methods:It included 56 patients with Vitamin D deficiency (Group 1; 16 men, 40 women; mean age 43.1 ± 11.4 years) and 42 healthy individuals with normal Vitamin D levels (Group 2; 11 men, 31 women; mean age 40.0 ± 7.5 years). Calcium, parathormone, alkaline phosphatase, and Vitamin D levels were measured from blood samples, and all participants underwent echocardiographic examination.Results:Left ventricular diastolic functions were determined by both conventional and tissue Doppler methods and were found to be impaired in Group 1 compared to Group 2. Aortic distensibility was significantly reduced in Group 1 compared to Group 2, whereas aortic stiffness index was significantly increased. Left atrial active emptying volume and fraction (LAAEV and LAAEF) were significantly higher in Group 1 than in Group 2. There were significant negative correlations between Vitamin D level and LAAEV, LAAEF, and septal E/E′ ratio and significant positive correlations between Vitamin D level and septal, lateral, anterior, and right ventricular annular E′ velocities.Conclusion:In severe Vitamin D deficiency, echocardiographically assessed diastolic functions appeared particularly impaired, and ventricular myocardial velocities and aortic elastic parameters were also adversely affected. In addition, LA mechanical functions were impaired, probably secondary to disturbed diastolic functions.

Aortic stiffness index and diurnal variability (dipper/non-dipper) in hypertensive patients

Aortic stiffness index and diurnal variability (dipper/non-dipper) in hypertensive patients

End-Stage Renal Disease Impairs the Multidirectional Movements of the Common Carotid Artery: Assessment Using Dimensional Speckle-Tracking Carotid Strain Ultrasonography.

BACKGROUNDArterial stiffening is a major contributing factor in the development of cardiovascular disease in patients with end-stage renal disease (ESRD). However, there is no gold standard for evaluating arterial stiffness. This study aimed to evaluate the newly developed speckle-tracking carotid strain imaging method in assessing arterial stiffness in patients with ESRD.METHODSIn total, 85 patients with normal renal function (controls) and 36 with ESRD were enrolled in this single-center study. Carotid B-mode ultrasonography was performed for all patients. Arterial stiffness indices and strain parameters of the common carotid arteries were analyzed. Values were compared between the groups, and multivariate linear regression analysis was performed to assess the impact of ESRD on carotid strain.RESULTSThere were no differences in the intima-media thickness, β stiffness index, and arterial compliance, but arterial distensibility was lower, and the elastic modulus and pulse wave velocity β (PWV) were higher among patients with ESRD (all p < 0.05), whether assessed in the longitudinal or transverse plane. Both longitudinal and transverse strain rates were reduced in patients with ESRD (all p < 0.05). In multivariate analyses, ESRD independently reduced both transverse radial strain and strain rate (all p < 0.05), and the transverse circumferential strain and strain rate (p < 0.05). However, all conventional aortic stiffness indices and longitudinal strain parameters were not associated with ESRD.CONCLUSIONSSpeckle-tracking carotid strain ultrasonography was successfully performed in both normal subjects and patients with ESRD. Multidirectional carotid strain analyses may provide more value than conventional aortic stiffness indices for risk stratification in patients with ESRD.

Increased arterial stiffness in rheumatoid arthritis and Its relation to disease activity: A cross sectional study.

BackgroundRheumatoid arthritis (RA) is associated with elevated plasma level of inflammatory markers. Chronic inflammation is known to predispose to endothelial dysfunction and increased arterial stiffness, which is an important marker of subclinical atherosclerosis and increased cardiovascular risk.ObjectiveThe aim is to test for the relationship between disease activity and arterial stiffness in RA patients.MethodsThe study included 90 RA patients, at different grades of disease activity and 45 healthy subjects, as a control group. Patients were subjected to full history taking and clinical examination, laboratory investigations including serum lipid profile and high sensitivity CRP (hs-CRP) measurements and plain x-rays of hands and feet. Modified Larsen method was used as radiographic scoring method. Disease activity score (DAS 28) was used for assessment of disease activity. Transthoracic echocardiography was performed to detect aortic stiffness parameters. Duplex ultrasound imaging of both common carotid arteries was performed to measure carotid stiffness parameters.ResultsThe mean age of RA patients was 39.86 ± 9.39 years and most of them (83.3%) were females. RA patients had higher carotid stiffness index compared to control group patients (8.57 ± 4.83 vs 4.08 ± 1.13, p < .001). Very poor correlation was found between DAS-28 and aortic (r = 0.1, p = .28) as well as carotid (r = 0.05, p = .7) stiffness indices. No statistically significant correlation was found between hs-CRP and aortic stiffness index (r = 0.64, p = .55). Disease duration was significantly correlated to intima-media thickness (p < .01) as well as with other carotid stiffness parameters. Age also show a statistically significant positive correlation with carotid stiffness parameters.ConclusionRA is associated with increased arterial stiffness, a well-recognized marker of cardiovascular risk. This is attributed to the inflammatory nature of the disease. It seems that the most important factors determining stiffness are patients' age and duration of illness.

Dapagliflozin acutely restores endothelial dysfunction, reduces aortic stiffness and renal resistive index in type 2 diabetic patients: A pilot study

ObjectiveSodium-glucose co-transporter-2 inhibitors reduce blood pressure and renal and cardiovascular events in patients with type 2 diabetes through not fully elucidated mechanisms. Aim of this study was to investigate whether dapagliflozin is able to acutely modify systemic and renal vascular function.MethodsNeuro-hormonal and vascular variables, together with 24h-urinary sodium, glucose, isoprostanes, diuresis and free-water clearance, were assessed before and after a 2- day treatment with dapagliflozin 10 mg/die in 16 type 2 diabetic patients. Brachial artery endothelium-dependent and independent vasodilation (by flow-mediated dilation) and pulse wave velocity were assessed. Renal resistive index was obtained at rest and after glyc-eril trinitrate administration.ResultsDapagliflozin decreased systolic blood pressure and urinary isoprostanes and induced an increase in 24h-diuresis, 24h-urinary glucose and serum magnesium; 24h-urinary Na and fasting blood glucose were unchanged; serum magnesium slightly increased. Flow-mediated dilation was significantly increased (2.8 ± 2.2 to 4.0 ± 2.1%, p < 0.05), and pulse-wave-velocity was reduced (10.1 ± 1.6 to 8.9 ± 1.6 m/s, p < 0.05), even after correction for mean blood pressure. Renal resistive index was reduced (0.62 ± 0.04 to 0.59 ± 0.05, p < 0.05), as well as its response to nitrates.ConclusionsAn acute treatment with Dapagliflozin significantly improves systemic endothelial function, arterial stiffness and renal resistive index; this effect is independent of changes in blood pressure and occurs in the presence of stable natriuresis, suggesting a fast, direct beneficial effect on the vasculature, possibly mediated by oxidative stress reduction.

Aortic stiffness is increased in patients with hypereosinophilic syndrome being in early necrotic phase.

Persistent eosinophilia and eosinophil-mediated single- or multiple-organ damage are typical features of hypereosinophilic syndrome (HES). Theoretically, eosinophilic infiltration of the ascending aortic wall could not be excluded in HES, therefore the present study aimed to test whether HES is associated with abnormalities in aortic elastic properties. The present study comprised 10 HES patients (mean age: 57.6±10.1 years, 5 males) without known cardiovascular disease, their results were compared to 19 age-, gender- and risk factor-matched controls (59.2±4.2 years, 15 males). Complete two-dimensional Doppler echocardiography with measurement of echocardiographic aortic elastic properties was performed in all HES cases and controls. Although neither systolic (30.6±3.4 vs. 30.1±3.6 mm, P=ns), nor diastolic (28.7±3.6 vs. 27.8±3.2 mm, P=ns) aortic diameter differed significantly between HES patients and matched controls, significantly increased aortic stiffness index (11.19±5.65 vs. 7.04±2.97, P<0.05) could be demonstrated in HES patients. Increased aortic stiffness could be demonstrated in HES patients in their early necrotic phase.

Impact of kidney transplantation on aortic stiffness index β0

Purpose/ Background/ ObjectivesWe have shown that aortic stiffness improves as early as 3 months post-kidney transplantation (KTx). Aortic stiffness index β0, a blood pressure independent parameter, has been proposed to be a better indicator of vascular wall property. This study was designed to examine 1) the early versus late changes in aortic stiffness index β0 and 2) to define the characteristics of patients with favourable and unfavourable trajectories of aortic stiffness index β0 after KTx.MethodsIn 79 patients who underwent KTx, aortic stiffness was assessed before, 3, 6 and 24 months after KTx. Aortic stiffness was determined by carotid-femoral pulse wave velocity (cf-PWV), while aortic stiffness index β0 was obtained using a formulae proposed by Spronck and colleagues. Cytokines profile was measured in plasma by ELISA.ResultsThere was a reduction of β0 3 months after KTx (29.0 ± 2.0 to 25.8 ± 1.2, P = 0.033). Then, aortic stiffness index β0 gradually increased at 6 (28.0 ± 1.4, P = 0.005 vs 3 months) and 24 months (28.3 ± 1.3, P = 0.003 vs 3 months). Unfavourable progression of β0 was not related to renal function, age, comorbidities or kidney donor characteristics. However, the unfavourable progression of β0 was associated with higher levels of interleukin-6 (P = 0.029).ConclusionsThe improvement of aortic stiffness index β0 3 months after KTx suggests that KTx leads to an early improvement of the intrinsic mechanical properties of aorta.However, this improvement is followed by a late progression of β0, which is associated with increased pro-inflammatory cytokine, suggesting that activation of immune system may be involved in arterial wall remodeling in kidney transplant recipients.

Dapagliflozin acutely improves endothelial dysfunction, reduces aortic stiffness and renal resistive index in type 2 diabetic patients: a pilot study

BackgroundSodium-glucose cotransporter-2 inhibitors reduce blood pressure (BP) and renal and cardiovascular events in patients with type 2 diabetes through not fully elucidated mechanisms. Aim of this study was to investigate whether dapagliflozin is able to acutely modify systemic and renal vascular function, as well as putative mechanisms.MethodsNeuro-hormonal and vascular variables, together with 24 h diuresis, urinary sodium, glucose, isoprostanes and free-water clearance were assessed before and after a 2-day treatment with dapagliflozin 10 mg QD in sixteen type 2 diabetic patients; data were compared with those obtained in ten patients treated with hydrochlorothiazide 12.5 mg QD. Brachial artery endothelium-dependent and independent vasodilation (by flow-mediated dilation) and pulse wave velocity were assessed. Renal resistive index was obtained at rest and after glyceryl trinitrate administration. Differences were analysed by repeated measures ANOVA, considering treatment as between factor and time as within factor; Bonferroni post hoc comparison test was also used.ResultsDapagliflozin decreased systolic BP and induced an increase in 24 h diuresis to a similar extent of hydrochlorothiazide; 24 h urinary glucose and serum magnesium were also increased. 24 h urinary sodium and fasting blood glucose were unchanged. Oxidative stress was reduced, as by a decline in urinary isoprostanes. Flow-mediated dilation was significantly increased (2.8 ± 2.2 to 4.0 ± 2.1%, p < 0.05), and pulse-wave-velocity was reduced (10.1 ± 1.6 to 8.9 ± 1.6 m/s, p < 0.05), even after correction for mean BP. Renal resistive index was reduced (0.62 ± 0.04 to 0.59 ± 0.05, p < 0.05). These vascular modifications were not observed in hydrochlorothiazide-treated individuals.ConclusionsAn acute treatment with dapagliflozin significantly improves systemic endothelial function, arterial stiffness and renal resistive index; this effect is independent of changes in BP and occurs in the presence of stable natriuresis, suggesting a fast, direct beneficial effect on the vasculature, possibly mediated by oxidative stress reduction.

PP.06.21] VOLUME-COMPRESSIVE OSCILLOMETRY IN NONINVASIVE ASSESSMENT OF HEMODYNAMIC PARAMETERS IN HYPERTENSIVE PATIENTS

Objective: To evaluate hemodynamic parameters in patients with arterial hypertension (AH) before and during antihypertensive treatment using volume-compressive oscillometry (VCO) - new cuff-based device. The main advantages of VCO comparing to other oscillometry technic of BP registration is formation and recording the curve automatically in synchronism with the cuff inflation and recording the artery response by changing the cuff volume throughout the all period of cuff compression. VCO diagram could considered as indicator of aortic stiffness. Design and method: 45 untreated patients hospitalized with AH without acute coronary syndrome, severe valve problems, secondary hypertension, advanced chronic heart failure were enrolled. Mean age 55 ± 11.8 yrs, 51% male, mean BMI - 28.9 ± 6.7 kg/m2. Antihypertensive treatment included combination of amlodipine 5 mg/fosinopril 10 mg per day. The pulse wave velocity (PWV), brachial blood pressure (BP), cardiac index, stroke index and systemic vascular resistance were measured twice (at admission and discharging) by VCO (EDTV, Russia). Results: The mean systolic BP by VCO at admission was 147.7 ± 14.8 mmHg (by Korotkoff method 161 ± 9.8 mm Hg), diastolic 83.1 ± 14.1 mmHg (by Korotkoff method 99 ± 11.3 mmHg) and mean pulse pressure 64 ± 9.5 mmHg. Mean heart rate was 70.4 ± 14.5 bpm. Mean cardiac index was 3.08 ± 0.44 l/(min*m2), stroke index - 45.7 ± 11.7 ml/m2 and systemic vascular resistance (SVR) was 1373 ± 236 dyn*s/cm5. Mean PWV in these population was 7.6 ± 1.1 m/sec. After treatment with mean duration of hospitalization 6.3 ± 2.5 days, systolic and diastolic BP by VCO were reduced to 123.3 ± 10.8 mmHg and 57.5 ± 13.3 mmHg respectively (p < 0.05). Mean pulse pressure increased to 65.9 ± 11.8 mm Hg nonsignificantly. Mean stroke index increased to 49.7 ± 16.7 ml/m2 and SVR decreased to 1169 ± 374 dyn*s/cm5. We found no significant changes in cardiac index, heart rate and PWV. Conclusions: Systolic and diastolic BP by VCO is significantly lower comparing to Korotkoff method. Next studies are needed to determine the feasibility of VCO in noninvasive assessment of central hemodynamics.