bluuebunny/crossref_metadata_2025_split huggingface dataset:
ADDITIVE DAMAGE IN THE CONTRACTILITY OF INTRAMURAL CORONARY ARTERIOLES IN A RAT MODEL OF ANDROPAUSAL HYPERTENSION
Authors: Várbíró Szabolcs , Jósvai Attila , Hetthéssy Judit , Mátrai Máté , Monori-Kiss Anna , Makk Jennifer , Vezér Márton , Székács Béla , Nádasy György , Török Marianna 
Published: June 2022

Objective:
Hypertension accelerates vascular aging, and changes associated with vascular aging play a role in hypertension. Andropause also contributes to age – related vascular damage and increases cardiovascular risk. Our aim is to investigate the combined effect of hypertension and androgen deficiency on the contractility of intramural coronary resistance arteries.

Design and method:
Male Sprague-Dawley rats were distributed into 4 groups: control (Co, n = 10); orchidectomized (OCT, n = 13), angiotensin II infused (AII, n = 10) and AII infused plus orchidectomized (AII+OCT, n = 8). Early hypertension was established using osmotic minipumps containing angiotensin II (100 ng / min / kg), while testosterone deficiency achieved via orchidectomy. After 4 weeks, spontaneous, thromboxane- and bradykinin-induced tones of intramural coronary resistance arterioles were investigated by in vitro pressure microarteriography.

Results:
Inner radius was reduced in the AII+OCT group compared to all other groups. Spontaneous tone was significantly higher in AII and AII+OCT groups than in Co and OCT groups. U46619-induced vasoconstriction was significantly smaller in OCT and AII+OCT groups compared to Co and AII rats. Bradykinin-induced relaxation was also significantly reduced in orchidectomized rats (OCT and AII+OCT groups) to a greater extent than in Co and AII animals.

Conclusions:
Spontaneous vascular tone is increased in AII hypertension. As a result of orchidectomy, adaptation range of the blood vessels narrows both regarding vasoconstriction and vasodilation. Therefore, the reactivity of the coronary arterioles deteriorates due to testosterone deficiency. In case of parallel manifestation of hypertension and testosterone deficiency, these two effects add up, which may increase age-related cardiovascular risk significantly in men.
GONADOECTOMY REDUCED THE DEGREE OF DEVELOPMENT OF RENOVASCULAR HYPERTENSION IN FEMALE RATS CAUSED BY STOP OF HIGH-SALT DIET
Authors: Artemieva Marina , Biriukova Natalia , Kuropatkina Tatiana , Medvedeva Natalia 
Published: June 2022

Objective:
Excessive dietary salt intake is associated with an increased risk for hypertension. However, more research on measurement, storage and kinetics of sodium on blood pressure and sex hormones is required for dietary salt restrictions.
The aim was to study the influence of gonadoectomy and stop of the high-salt diet on the development of renovascular hypertension (RVH) in female rats.

Design and method:
Was used the model of RVH 1 kidney 1 clip (1K1C) on female Wistar rats. All manipulations with animals were carried out according to the Council Directive 86/609/EEC principles. Gonadoectomized and normal rats of 8 weeks old (eight groups) were used. |There were two control groups: one with gonads © and one without (OvE). 4 groups out of remaining 6 groups of rats, had a high salt diet (4%). All rats from 6 groups the Goldblatt’s (1K1C) surgery was subjected. We had two groups with RVH with normal diet (0,25 % NaCl - RVH and OvE-RVH; two groups with high salt diet - RVH-HS and OvE-RVH-HS; and two groups with high salt diet, which was stop in two weeks after the Goldblatt’s (1K1C) surgery: RVH-ChHS and OvE-RVH-ChHS. In all animals the systemic blood pressure (mBP), diastolic (dBP), systolic (sBP) pressure, left ventricular pressure (LVP) and heart rate was directly measured. Left ventricular hypertrophy (LVH) was calculated as (LVweight)/(rat b.w.)*100%.

Results:
In all RVH groups, with and without gonads, the systemic arterial hypertension was developed. The most level of RVH was in RVH-ChHS rats: mBP - 145,7 ± 9,5 mmHg, dBP - 123,5 ± 10,4 mmHg, LVH - 0,214 ± 0,013 %. Ovariectomy leads to significant (p < 0,05) decrease in the degree of development of RVH. In OvE-RVH-ChHS was mBP 122,2 ± 6,3 mmHg, dBP 94,0 ± 6,0 mmHg and LVH 0,182 ± 0,009 %.

Conclusions:
Changing the diet from high salt to normal during the development of renovascular hypertension in female rats leads to an increase in the degree of disease. This effect was not observed in gonadoectomized female rats.
PATHOGENICITY AND LONG-TERM OUTCOMES OF LIDDLE SYNDROME CAUSED BY A NONSENSE MUTATION OF SCNN1G IN A CHINESE FAMILY
Authors: Zhang Di , Qu Yi , Lu Yi-Ting , Yang Kun-Qi , Fan Peng , Liu Ya-Xin , Gao Ling-Gen , Zhou Xian-Liang 
Published: June 2022

Objective:
Liddle syndrome (LS) is a common monogenic hypertension with continuous activation of epithelial sodium channels (ENaCs) encoded by SCNN1A, SCNN1B, and SCNN1G. This study aimed to identify the pathogenicity of a nonsense mutation in SCNN1G in a Chinese family with LS and the outcomes of tailored treatment with amiloride.

Design and method:
Clinical data were collected from six family members and this mutation site was reported by our team at 2015. To explore the pathogenicity of candidate variants, we constructed mutant and wild-type models in vitro and measured amiloride-sensitive current in Chinese Hamster Ovary cells using patch clamp technique. Participants were followed up for 6 years to monitor their target organ damage after tailored treatment with amiloride.

Results:
Four family members presented with severe hypertension and hypokalemia, and two had stroke. This nonsense variant resulted in a termination codon at codon 572, truncating the Pro-Pro-Pro-X-Tyr motif. The mutant epithelial sodium channels displayed higher amiloride-sensitive currents than the wild-type channels (P < 0.05). Tailored treatment with amiloride achieved ideal blood pressure control in the patients, and no adverse events occurred during follow-up.

Conclusions:
We found the pathogenicity of a nonsense SCNN1G mutation (p.Glu571*) with enhanced amiloride-sensitive currents in a LS family. Tailored treatment with amiloride may be an effective strategy for the long-term control of blood pressure and the prevention of cardiovascular events in these patients.
ARE METABOLIC DISORDERS IN HYPERTENSIVE PATIENTS ASSOCIATED WITH GNB3 (RS5443) GENETIC POLYMORPHISMS?
Authors: Sydorchuk Andrii , Voronyuk Ksenia , Sydorchuk Larysa , Repchuk Yulia , Semianiv Marianna , Sydorchuk Ruslan 
Published: June 2022

Objective:
Primary/essential hypertension (PH) is the most common cause of left ventricular hypertrophy (LVH) and is often associated with metabolic disorders. The aim of the study was to analyse dependence of metabolic parameters on the guanine nucleotide binding protein (G-protein) 3 subunit gene polymorphism (GN3, rs5443) in hypertensive patients.

Design and method:
A cross-sectional study involved 72 PH patients of high and very high cardiovascular risk (29.16% men and 70.84% women); the average age 59.87 ± 7.98 y. The control group included 48 healthy individuals (aged 49.13 ± 6.28 y) and sex distribution (62.5% women and 37.5% men). GN3 (C825T) polymorphism was investigated by Real Time PCR. LVH was assessed by EchoKG. Metabolic disorders were studied by lipids panel (Total cholesterol (TC), Triglycerides (TG), Low-, and High- density lipoprotein cholesterol (LDL-C, HDL-C) levels) and Glucose blood value. The atherogenic index (AI) was calculated by the formula: (TC – HDL-C)/ HDL-C.

Results:
In CC-genotype carriers of the GN3 gene metabolic parameters were as follows: TC 5.50 ± 0.79 mmol/L, TG 2.10 ± 0.8 mmol/L, HDL-C 1.22 ± 0.22 mmol/L, LDL-C 4.03 ± 0.76 mmol/L, AI 3.66 ± 0.84 U, Glucose 7.7 ± 2.34 mmol/L. In PH patients with TC-genotype the concentration of TC was 5.82 ± 1.15 mmol/L (pCC>0.05), TG 1.73 ± 0.55 mmol/L (pCC> 0.05), HDL-C 1.30 ± 0.21mmol/L (pCC> 0.05); LDL-C 4.39 ± 1.07 mmol/L (pCC> 0.05), AI 3.61 ± 0.95 (pCC> 0.05), Glucose 7.37 ± 2.34 mmol/L (pCC> 0.05). In TT-genotype carriers the concentration of TC was 6.6 ± 0.64 mmol/L (it was higher than in C-allelle carriers by 20.0% (pCC> 0.05) and 13.79% (pTC = 0.016) as much), TG – 2.6 ± 1.27 mmol/L, that was higher than in C-allelle patients by 23.81% (pCC> 0.05) and 52.94% (pTC = 0.038), respectively. The other parameters did not differed significantly between genotypes’ carriers and in mutation homozygous T-allele carriers were as follows: HDL-C 1.3 ± 0.05 mmol/L (pCC, TC> 0.05), LDL-C 4.7 ± 0.69 mmol/L (pCC, TC> 0.05), AI 4.0 ± 0.69 (pCC, TC> 0.05), Glucose 6.20 ± 1.2 mmol/L (pCC,TC> 0.05).

Conclusions:
Therefore, the metabolic disorders in hypertensive patients do not depend on the GN3 (rs5443) gene polymorphism.
SALT SENSITIVITY IS MODULATED BY LANOSTEROL SYNTHASE RS2254524 POLYMORPHISM
Authors: Faienza Sipontina , Citterio Lorena , Messaggio Elisabetta , Zagato Laura , Manunta Paolo 
Published: June 2022

Objective:
The blood pressure (BP) response to different salt intake is associated with hypertension (HT). Elevated levels of the steroid hormone Endogenous Ouabain (EO) have been also associated with HT and salt sensitivity.
We characterized the missense variation rs2254524 (V642: CC variant; L642: AA variant) of the Lanosterol Synthase (LSS), a key enzyme in steroid biosynthesis, because AA patients on a low salt diet showed a greater reduction in BP compared to the LSS CC and only CC patients had an increase in plasma EO after the low salt protocol. Hence, we hypothesized that LSS could affect salt-sensitive HT by regulation of EO biosynthesis.

Design and method:
We generated a knock-in mouse model carrying the variation ubiquitously. Male mice were fed with Normal Salt (NSD; 0.5% NaCl), High Salt (HSD; 4% NaCl) or Low Salt Diet (LSD; 0.03 % Na) for 15 days.
BP was measured by the tail-cuff system, on 5 consequent days in conscious trained mice.

Results:
LSS AA mice were viable, healthy, and undistinguishable phenotypically from LSS CC.
The LSS mRNA and protein levels were reduced in the adrenal gland of LSS AA mice at 3 months.
At baseline, the LSS did not affect kidney function, while at 9 and 12 months the Systolic BP (SBP) in LSS CC mice showed a progressive increase with age; this increase was not observed in LSS AA mice.
At 3 months, we observed an increase in SBP in both genotypes upon HSD compared to those on an NSD, however only the AA mice showed a significant SBP reduction after an LSD (Fig.1).
The same response of BP upon HSD has also been observed in AA e CC mice at 12 months but only AA mice showed statistically significant cardiac hypertrophy (Fig. 2), a common feature of hypertensives.

Conclusions:
The new LSS mouse model resembles what was observed in hypertensive patients and provides a good model to prove our hypothesis. In the perspective of clinical practice, these findings allow the identification of patients whose SBP can seriously benefit from a low salt diet as a lifestyle modification.
PROTEOMIC PROFILE OF CYSTEINE OXIDATION IN VASCULAR SMOOTH MUSCLE CELLS IN HUMAN HYPERTENSION
Authors: Camargo Livia , Samji Sheon , Lilla Sergio , Zanivan Sara , Bulleid Neil , Hartley Richard , Delles Christian , Leiper James , Fuller Will , Montezano Augusto , Touyz Rhian 
Published: June 2022

Objective:
Phenotypic switching of vascular smooth muscle cells (VSMCs) is a fundamental process in vascular dysfunction and remodeling associated with hypertension. Mechanisms underlying this process involve reactive oxygen species (ROS) and redox-dependent signaling pathways. However, the proteomic signature and effects of ROS on VSMC proteome in human hypertension are unknown. Using high fidelity proteomic analysis, we characterized the proteome of VSMC in human hypertension.

Design and method:
VSMC from resistance arteries from normotensive (NT) and hypertensive (HT) subjects were studied. Protein expression and cell migration were assessed by immunoblotting and wound healing assay respectively. VSMC proteins were labelled with isobaric tandem mass tags and identified by liquid chromatography tandem mass spectrometry. The oxidative proteome was assessed using stable isotope-labelled iodoacetamide to target cysteine thiols.

Results:
VSMCs from HT subjects exhibit reduced expression of alpha-SMA (0.05+0.01 vs NT:0.20 + 0.03, p < 0.05), increased expression of the proliferation marker, PCNA (0.162 + 0.3 vs NT:051 + 0.004, p < 0.05) and increased migration (54.68 + 2.86 vs NT:23.37 + 8.36, p < 0.05). The proteomic analysis identified 207 proteins upregulated in HT subjects (fold change> 1.5, p < 0.05). Gene ontology enrichment of upregulated proteins in HT showed that most proteins belong to extracellular space and plasma membrane compartments and were involved in biological processes such as extracellular matrix organization, immune response, proteolysis and cell proliferation. Extracellular matrix (ECM) proteins COL1A1, COL9A1, COL10A1, FBN1, FBLN1 were increased in cells from HT (fold change> 1.5, p < 0.05), suggesting a switch to a fibroblast-like phenotype in hypertension. Expression of proteins related to the interferon and IL-1beta pathways (IFIT1, IFIT2, IFIT3, MX1, MX2, ABCA1, ABCA2, IL1RAP, CD36, ICAM1) were also increased in cells from HT subjects (fold change> 1.5, p < 0.05). Considering the importance of oxidative stress in hypertension, we assessed the VSMC oxidative proteome. Results identified 130 significant cysteine-containing peptides, 88 showed increased oxidation in HT (fold change> 1.5, p < 0.05). Among the highly oxidized proteins in HT were ECM proteins, COL11A1, COL16A1, FBLN1 and FBLN2 (fold change> 1.5, p < 0.05).

Conclusions:
Our study provides new insights into the proteomic changes related to vascular phenotype in hypertension and highlights differentially oxidised candidate targets that may drive phenotypic switching associated with vascular injury and remodeling in hypertension.
ASSOCIATION OF NDUFC2 POLYMORPHIC VARIANTS WITH LEFT VENTRICULAR HYPERTROPHY IN HUMAN HYPERTENSION
Authors: Gallo Giovanna , Forte Maurizio , Tocci Giuliano , Cotugno Maria , Marchitti Simona , Stanzione Rosita , Bianchi Franca , Palmerio Silvia , Sciarretta Sebastiano , Volpe Massimo , Rubattu Speranza 
Published: June 2022

Objective:
Previous experimental studies showed that a dysfunction of the NADH dehydrogenase (ubiquinone), the mitochondrial Complex I (CI), is associated with the development of left ventricular hypertrophy (LVH). A deficiency of Ndufc2 (a subunit of CI) impairs CI activity and causes severe mitochondrial dysfunction. The NDUFC2/rs11237379 polymorphic variant is associated with reduced gene expression and impaired mitochondrial function, contributing to increased susceptibility to vascular diseases.
We examined the association of NDUFC2/rs11237379 and another NDUFC2 polymorphic variant (rs641836) with the development of LVH in hypertensive patients.

Design and method:
Two-hundred-fourty-six hypertensive subjects (147 male, 59.7%) with a mean age of 59 ± 15 years were studied. Seventy-nine individuals (32%) presented LVH.

Results:
The association analysis for both SNPs showed that hypertensive patients carrying the TT genotype at the NDUFC2/rs11237379 had a significant increase of echocardiographically assessed septal thickness (p = 0.001), posterior wall thickness (p = 0.003), relative wall thickness (RWT) (p = 0.01), LV mass/ body surface area (BSA) (p = 0.012) and LV mass/height2.(p = 0.0033) compared to subjects carrying either CC or CT genotypes. To better dissect the genetic effect, a covariate ANOVA was performed for each cardiac variable, considering age, gender, body mass index (BMI), office blood pressure (BP), antihypertensive treatment with a combination of 2 or more drugs and the number of BP-lowering agents as covariates. The adjustment for covariates revealed significant differences for septal thickness (p = 0.07), posterior wall thickness (p = 0.008), RWT (p = 0.021), LV mass/BSA (p = 0.03). With regard to NDUFC2/rs641836, hypertensive subjects carrying the mutant A allele had a significant increase of septal thickness (p = 0.001), posterior wall thickness (p = 0.001), RWT (p = 0.005), LV mass (p = 0.001), LV mass/BSA(p = 0.001), LV mass/height2.7(p = 0.002) compared to wild-type homozygotes. After adjustment for covariates, the results were significant for septal thickness (p = 0.017), posterior wall thickness (p = 0.011), LV mass (p = 0.003), LV mass/BSA (p = 0.002) and LV mass/height2.7(p = 0.010).

Conclusions:
Our results demonstrate for the first time a significant association of NDUFC2 variants with LVH in hypertensives and highlight a novel role of CI dependent mitochondrial dysfunction on increased susceptibility to cardiac damage in human hypertension. This study paves the way of a new pathophysiological mechanism of LVH which may lead to new clinical strategies.
EFFICACY AND SAFETY OF SACUBITRIL/VALSARTAN (LCZ696) IN HYPERTENSION CONTROL AND ADVERSE CARDIOVASCULAR EVENT REDUCTION AMONG ASIANS: A SYSTEMATIC REVIEW AND META-ANALYSIS
Authors: Cruz Patrick Vera , Ang Wisdom , Calatrava Jose 
Published: June 2022

Objective:
To evaluate the benefits and harms of Sacubitril/Valsartan (LCZ696) for controlling hypertension and reducing the risk of adverse cardiovascular events (MACE) in Asians by synthesising data from randomised controlled trials.

Design and method:
This is a systematic review and meta-analysis. We searched PubMed, ScienceDirect, Cochrane databases, trial registries HERDINPlus, ClinicalTrials.gov, and forward and backward citations to identify applicable articles. All randomised controlled trials with data of Asian patients comparing the effect of Sacubitril/Valsartan (LCZ696) against an active control for cardiovascular mortality, heart failure hospitalisation, blood pressure control, and adverse events were included without language or date restrictions. We did separate fixed-effects meta-analysis for major adverse cardiovascular events (MACE), hypertension control, serious and non-serious adverse events. Evidences were synthesised as pooled hazards ratio(HR) for MACE, pooled odds ratio for blood pressure control, and safety outcomes. The quality of evidence was assessed with the Cochrane risk of bias tool.

Results:
Ten of 2249 articles were included involving 6,120 patients. With high certainty of evidence, pooled data showed that Asians with mild to moderate hypertension had better hypertension control with LCZ696 against olmesartan (OR 1.63; CI 1.38, 1.92; p < 0.00001; I2 = 7%) (Figure1). However, the risk for MACE was not significantly reduced for Asians with reduced ejection fraction (HR 0.89; CI 0.73, 1.08; p = 0.22; I2 = 0%) or acute myocardial infarction (HR 0.90; CI 0.65,1.24; p 0.50; I2 = 0%) given LCZ696 (Figure2). The overall safety of LCZ696 was comparable to conventional ACEi/ARB but subgroup analysis revealed greater pooled odds ratios for hypotension (OR 1.59; 95% CI 1.19, 2.13; p = 0.002; I2 0%) and dizziness (OR 3.54; 95% CI 1.61, 7.81; p = 0.002; I2 0%) with LCZ696 and reduced pooled odds for cough occurrence(OR 0.70; 95% CI0.56, 0.87; p = 0.002; I2 0%) (Figure 3&4).

Conclusions:
Among Asians, LCZ696 is strongly associated with better hypertension control against olmesartan. However, its efficacy in reducing MACE is not as robust. Finally, the overall safety profile of sacubitril/valsartan is comparable to conventional ACEi/ARBs but it is associated with hypotension and dizziness with a lower risk for cough.
HEALTH-RELATED QUALITY OF LIFE AND ASSOCIATED FACTORS AMONG HYPERTENSIVE PATIENTS
Authors: Cong Duy Tran , Ngoc Hoa Chau 
Published: June 2022

Objective:
To survey the health-related quality of life (HRQOL) and its associated factors among hypertensive patients.

Design and method:
A cross-sectional study was carried out from October 2013 to March 2014 to investigate treated hypertensive patients at the Cardiovascular Clinic, Cho Ray Hospital, Viet Nam. Participants who had been diagnosed with hypertension and taking antihypertensive medications, aged 18 or older, able to read or understand Vietnamese were recruited into this study. All participants were interviewed, examined, and tested to collect data including socio-demographic information, cardiovascular risk factors, co-morbidities, and target organ damages (TODs). HRQOL was assessed by the SF-36 questionnaire. The Vietnamese version of SF-36 was translated, validated in Vietnam. The instrument consists of 36 items that are scored to measure eight domains of health such as physical functioning, role physical, bodily pain, and general health, vitality, social functioning, role emotional, and mental health. Scores range from 0 (poorest health) to 100 (optimal health). All statistical analyses were performed using SPSS 22.0 version.

Results:
There were 300 hypertensive patients attending our study for 6 months. The mean age of patients was 64.0 ± 12.5. The most frequent age group was 65 years or older. The common cardiovascular risk factors were dyslipidemia (69.7%), diabetes (25.7%), and smoking (25.7%). The most often TODs were carotid atherosclerosis (41.7%), retinopathy (36.3%), left ventricular hypertrophy (27.7%), microalbuminuria (24.3%), and coronary artery disease (21.3%). The male-female ratio was 1.2. The mean scores of 4 physical health domains including physical functioning, role physical, bodily pain, and general health were 68.3; 57.2; 57.1, and 37.2, respectively. The mean scores of 4 mental health domains including vitality, social functioning, role emotional, and mental health were 55.5; 57.5; 58.7, and 48.8, respectively. In multivariate analysis, factors associated with HRQOL among hypertensive patients were age, occupation, health insurance, marital status, education level, diabetes mellitus, heart failure, coronary heart disease, stroke, transient ischemic attack, and lower extremity artery disease.

Conclusions:
Hypertensives had low HRQOL scores in all domains. Factors affecting their HRQOL should be taken into account when treating these patients.
THE RELATIONSHIP OF ARTERIAL AND MYOCARDIAL STIFFNESS WITH LEFT VENTRICLE DIASTOLIC DYSFUNCTION IN PATIENTS WITH ARTERIAL HYPERTENSION
Authors: Abdullaeva Guzal , Kevorkov Amayak , Yusupova Khafiza , Khamidullaeva Gulnoz , Sadullaeva Mohinur , Safarov Jamshid 
Published: June 2022

Objective:
to study the relationship of left ventricular diastolic dysfunction (LVDD) with the degree of myocardial and arterial stiffness arterial hypertension (AH) patients.

Design and method:
Study included 219 patients with I-III stages of hypertension (ESC/ESH 2018) of both sexes. The average age of the patients was 55.8 ± 11.0 years, duration of AH was 55.8 ± 11.0 years. All patients were divided into two groups: 1 - patients with LVDD, n = 113 (51.6%) and 2 - without LVDD, n = 106 (48.4%). Echocardiographic assessment was performed in M-and B-modes. The systemic and regional stiffness of arterial bed was performed applanation tonometry using the SphygmoCor. The Intima-Media thickness (IMT) of common carotid artery was measured by duplex scanning. Statistical processing was carried out using the Statistica 10.0 program. Results are presented as M ± SD and Me [Q1; Q3].

Results:
Initial parameters of ultrasound examination of carotid arteries showed the evidence of IMT on the left and right in patients with LVDD. Left IMT in patients with LVDD was 1.0 [0.9; 1.2] mm versus 1.0 [0.8;1.1] mm in group without LVDD (p < 0.05); right IMT was 1.0 [0.9; 1.2] mm versus 1.0 [0.8;1.1] mm, respectively (p < 0.02). Analysis of the initial parameters of central hemodynamics and vascular stiffness, revealed some features. The Barberg index was lower in group of patients with LVDD than in patients without LVDD: 142.1 ± 26.3 versus 148.5 ± 28.5, respectively (p < 0.05). Arterial stiffness was higher in the group of patients with LVDD than in group of patients without LVDD. The pulse wave velocity (PWV) in the group 1 with LVDD was 10.8 ± 2.7 m/s, and in the 2 group without LVDD - 9.9 ± 2.8 m/s (p < 0.02). A direct correlation was found for LVDD with the severity of vascular remodeling, in particular with indices of right IMT (R = 0.153, p = 0.025), with left IMT (R = 0.141, p = 0.040) and with the PWV (R = 0.169, p = 0.015).

Conclusions:
Our study showed an association of the severity of arterial and myocardial stiffness with LVDD.