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Purpose: Chronic plaque psoriasis is associated with the presence of non-alcoholic fatty liver disease (NAFLD), but the magnitude of this association remains currently uncertain. We aimed to investigate the magnitude of the association between psoriasis and the risk of prevalent and incident NAFLD, and to assess whether psoriasis severity and/or psoriatic arthritis are associated with a greater risk of NAFLD. Methods: A systematic review and meta-analysis of observational studies evaluating the association between psoriasis and NAFLD, as diagnosed by imaging or International Classification of Diseases codes was performed. Literature search on PubMed, Scopus and Web of Science on May 3, 2021 was undertaken. Studies using liver biopsy were not available. For the meta-analysis, the random-effects modelling was adopted. Results: We identified 15 observational (case–control and cross-sectional) studies for a total of 249,933 patients with psoriasis (49% with NAFLD) and 1,491,402 controls (36% with NAFLD). Psoriasis was associated with prevalent NAFLD (n= 11 studies; pooled random-effects odds ratio [OR] 1.96, 95% CI 1.70–2.26; I2= 97%, p< 0.01). Psoriatic patients with NAFLD had a higher mean psoriasis area and severity index (PASI) than their counterparts without NAFLD (n= 8 studies, pooled weighted mean difference: 3.93, 95% CI 2.01–5.84; I2= 88%, p< 0.01). The risk of NAFLD was marginally higher in patients with psoriatic arthritis than in those with psoriasis alone (n= 5 studies, pooled random-effects OR 1.83, 95% CI 0.98–3.43; I2= 64%, p= 0.03). Sensitivity analyses did not alter these findings. Funnel plot did not show any significant publication bias. A major limitation of the study was the high degree of heterogeneity across studies. Conclusion: Psoriasis is associated with prevalent NAFLD and this risk parallels the severity of psoriasis.

Aim: Type 2 diabetes (T2D) is a risk factor for metabolic dysfunction-associated fatty liver disease (MAFLD), which is becoming the commonest cause of chronic liver disease worldwide. We estimated MAFLD prevalence among patients with T2D using the hepatic steatosis index (HSI) and validated it against liver ultrasound. We also examined whether glucose-lowering medications (GLM) beneficially affected HSI. Methods: We collected data from 46 diabetes clinics (n= 281,381 T2D patients), extracted data to calculate HSI and validated it against ultrasound-detected hepatic steatosis. We then examined changes in HSI among patients with a follow-up visit within 1 year after initiating newer GLMs. Results: MAFLD (defined by HSI > 36, i.e., a high probability of steatosis) was present in 76.3% of the 78,895 included patients, while only 2.7% had HSI < 30 (low probability of steatosis). After age- and sex-adjusting, higher HSI was associated with higher prevalence of chronic kidney disease (odds ratio 1.35; 95%CI 1.22–1.51) and macroangiopathy (odds ratio 1.18; 95%CI 1.07–1.30). Among 2,179 subjects in the validation cohort, the prevalence of MAFLD was 67.8% and was greater in those with high HSI. Performance of HSI for ultrasound-detected MAFLD was moderate (AUROC 0.70), yet steatosis prevalence was > threefold higher among subjects with HSI > 36 than among those with HSI < 30. Notably, HSI declined significantly ~ 6 months after initiation of dapagliflozin or incretin-based therapies, but not gliclazide. Conclusion: About three quarters of patients with T2D have HSI values suggestive of MAFLD, a condition associated with macroangiopathy and nephropathy. Treatment with dapagliflozin or incretin therapies might improve MAFLD in T2D.

Increased arterial stiffness is an early sign of endothelial dysfunction. Nevertheless, measures of the elastic properties of the aortic root in patients with type 1 diabetes are still lacking. The aim of this study was to compare aortic root stiffness index in type 1 diabetes and healthy controls. Ninety-three patients with type 1 diabetes without cardiovascular diseases were recruited and compared to 33 healthy controls. Aortic root elastic properties were estimated by measuring the systolic and diastolic diameters on M-mode acquisition. None of the subjects showed alterations of either systolic or diastolic echocardiographic parameters. Patients with type 1 diabetes had a very low prevalence of chronic complications and their metabolic control was good. Significantly increased aortic stiffness index was found in type 1 diabetes compared to controls, and the same different pattern was found in men and women. The presence of type 1 diabetes and increased pulse pressure was significantly associated with aortic stiffness index in a multivariate linear analysis. This study strongly suggests that patients with type 1 diabetes develop aortic root stiffness in the absence of cardiovascular diseases. This alteration may be part of a more generalized arterial dysfunction in type 1 diabetes.

Several studies have reported an association between hyperuricemia and increased risk of permanent atrial fibrillation (AF) in patients with and without type 2 diabetes mellitus (T2DM). Currently, no published data are available on the relationship between hyperuricemia and risk of paroxysmal AF. We retrospectively evaluated 245 T2DM outpatients without pre-existing AF, cancer, cirrhosis and end-stage renal disease, who underwent a 24-h ECG-Holter monitoring for various clinical indications. Hyperuricemia was defined as a serum uric acid level >7 mg/dl for men and >6 mg/dl for women or allopurinol use. The diagnosis of paroxysmal AF was confirmed in affected individuals on the basis of 24-h ECG-Holter monitoring by experienced cardiologists. Hyperuricemia was observed in 59 (24.1%) patients, whereas paroxysmal AF was found in 11 (4.5%) patients. The prevalence of paroxysmal AF was higher in patients with hyperuricemia than in those without hyperuricemia (10.2 vs. 2.7%, p= 0.026). Logistic regression analysis showed that hyperuricemia was associated with an increased risk of prevalent paroxysmal AF. This association remained significant even after adjustment for age, metabolic syndrome and chronic kidney disease (adjusted-odds ratio 4.01, 95% CI 1.08–14.9; p= 0.039). Similar results were found when we used serum uric acid levels as a continuous measure. This study shows for the first time that hyperuricemia is independently associated with an approximately fourfold increased risk of prevalent paroxysmal AF in patients with T2DM. These findings may partly explain the increased risk of permanent atrial fibrillation and cardiovascular death observed among patients with hyperuricemia.

Hyperuricemia/gout and atrial fibrillation (AF) are two pathological conditions that are highly prevalent in type 2 diabetes and share multiple cardiovascular risk factors. However, the relationship between elevated levels of serum uric acid and risk of AF in type 2 diabetes is currently poorly known. We studied a hospital-based sample of 842 (male/female = 463/379) patients with type 2 diabetes discharged from our Division of Endocrinology during 2007–2011. Hyperuricemia was defined as a serum uric acid level >7 mg/dl for men and >6 mg/dl for women or allopurinol use. The diagnosis of AF was confirmed in affected participants on the basis of ECGs and medical history by experienced cardiologists. Overall, 243 (28.9 %) patients had hyperuricemia and 91 (10.8 %) patients had persistent or permanent AF. Compared with those with normal serum uric acid levels, patients with hyperuricemia had a remarkably greater prevalence of AF (20.6 vs. 7.1 %; p< 0.001). Hyperuricemia was significantly associated with an increased risk of prevalent AF (odds ratio 3.41, 95 % CI 2.19–5.32; p< 0.001). Adjustments for age, sex, smoking, hemoglobin A1c, hypertension status, chronic kidney disease, chronic obstructive pulmonary disease and previous histories of hyperthyroidism, ischemic heart disease and valvular heart diseases did not weaken this association (adjusted-odds ratio 6.27, 95 % CI 1.82–21.5; p< 0.01). These results indicate that hyperuricemia is associated with an increased prevalence of AF in hospitalized patients with type 2 diabetes, independently of multiple risk factors and potential confounders.

Liver diseases are associated with decreased bone mineral density (BMD) and evidence suggests that nonalcoholic fatty liver disease (NAFLD) affects several extra-hepatic organs, interacting with the regulation of multiple endocrine and metabolic pathways. This review focuses on the rapidly expanding body of evidence that supports a strong association between NAFLD and the risk of decreased BMD, expression of low bone mass (osteoporosis), or reduced mineralization (osteomalacia). We identified studies by searching PubMed for original articles published in English through March 2015 using the keywords “nonalcoholic fatty liver disease” or “fatty liver” combined with “bone mineral density”, “osteoporosis”, or “osteomalacia”. Recent cross-sectional and case–control studies involving both adults and children have consistently shown that patients with NAFLD exhibit a greater prevalence of decreased BMD compared with age-, sex-, and body mass index-matched healthy controls. Accumulating clinical and experimental evidence suggests that NAFLD may contribute to the pathophysiology of low BMD, possibly through the direct contribution of NAFLD to whole-body and hepatic insulin resistance and/or the systemic release of multiple pro-inflammatory, pro-coagulant, and pro-fibrogenic mediators. Although more research is needed before firm conclusions can be drawn, it appears that there is a non-chance, statistical association between NAFLD and low BMD. This finding argues for more careful monitoring and evaluation of BMD among patients with NAFLD. The potential contribution of NAFLD itselfto the development and progression of decreased BMD warrants further study.

Backgrounds and aims: We assessed the associations between pancreatic fat accumulation and other fat compartments, including liver fat and visceral adipose tissue as well as insulin resistance and other metabolic abnormalities in obese individuals. Subjects and methods: We studied 42 Caucasian adults with obesity [20 men and 22 women; mean body mass index (BMI) 35.2±4 kg/m2], who had no history of liver diseases or excessive alcohol consumption, in which subcutaneous, visceral, liver, and pancreatic fat contents were quantified by an in-opposed-phase magnetic resonance imaging (MRI) technique. Results: Compared with patients in the lower tertile (&lt;5.6%, no.=15), those in the upper tertile of liver fat content had more visceral adipose tissue, greater insulin resistance and had higher values of BMI, blood pressure, triglycerides and lower HDL-cholesterol and adiponectin. Notably, pancreatic fat accumulation also significantly increased across tertiles of liver fat content. In univariate analysis, the strongest correlates of pancreatic fat were visceral and liver fat contents (r=0.80 and r=0.54, p&lt;0.001–0.0001, respectively). Pancreatic fat accumulation was also moderately associated with insulin resistance and other metabolic syndrome features. However, when adjusted for age, gender and visceral adipose tissue, the associations of pancreatic fat accumulation with liver fat and other metabolic abnormalities were no longer significant. Conclusions: There are significant associations between pancreatic fat accumulation and liver fat content as well as insulin resistance and other metabolic abnormalities in obese, but otherwise healthy, individuals. However, these associations are largely mediated by the amount of visceral adipose tissue.

Background and aims:Non-alcoholic fatty liver disease (NAFLD) is associated with an increased prevalence of cardiovascular disease (CVD) in both non-diabetic and Type 2 diabetic individuals. We sought to examine whether NAFLD is associated with prevalent CVD in patients with Type 1 diabetes. Subjects and methods:We studied 343 (156 men; mean age ∼45 yr) consecutive Type 1 diabetic patients with and without NAFLD, which was diagnosed by ultrasonography. The presence of CVD was diagnosed by patient history, chart review, electrocardiogram, and echo-Doppler scanning of carotid and lower limb arteries. Results:Compared with those without steatosis, patients with ultrasound-diagnosed NAFLD (no.=182) had a remarkably greater age-and sex-adjusted prevalence of coronary (15.4 vs1.2%, p<0.0001), cerebrovascular (41.7 vs9.3%, p<0.0001) and peripheral (29.7 vs6.2%, p<0.0001) vascular disease. A multivariable logistic regression analysis revealed that NAFLD was associated with an ∼8-fold higher odds of CVD (composite endpoint), independently of age, sex, body mass index, family history of CVD, smoking status, physical activity, alcohol consumption, diabetes duration, glycated hemoglobin, systolic blood pressure, plasma lipids, estimated glomerular filtration rate, albuminuria, and use of anti-hypertensive, lipid-lowering and anti-platelet medications (adjusted odds ratio 7.6, 95% confidence intervals 3.6–24.0, p<0.001). Conclusions:Our results demonstrate that NAFLD is associated with an increased prevalence of asymptomatic/symptomatic CVD in patients with Type 1 diabetes, independently of several established risk factors, including the components of metabolic syndrome.

Background:Non-alcoholic fatty liver disease (NAFLD) and left ventricular hypertrophy (LVH) are highly prevalent in Type 2 diabetes and both conditions are associated with an increased risk of incident cardiovascular disease. The aim of this study is to evaluate whether there is an association between NAFLD and echocardiographically detected LVH in Type 2 diabetes. Methods:We studied 116 consecutive patients with hypertension and Type 2 diabetes after excluding those with pre-existing history of cardiovascular disease, advanced kidney disease, excessive alcohol consumption and other known causes of chronic liver disease (e.g., virus, medications, autoimmunity, iron overload). NAFLD was diagnosed by means of ultrasonography, whereas LVH was diagnosed by means of conventional trans-thoracic echocardiography in all patients. Results:The prevalence of LVH was markedly higher among diabetic patients with NAFLD than among those without this disease (82% vs 18%; p=0.01). Multivariate logistic regression analysis revealed that NAFLD was associated with LVH independently of age, sex, body mass index, systolic blood pressure, glycated hemoglobin, duration of diabetes, and parameters of kidney function. Conclusions:Our findings suggest that hypertensive Type 2 diabetic patients with NAFLD have a remarkably higher frequency of LVH than do hypertensive diabetic patients without steatosis, and that NAFLD is associated with LVH independently of classical cardiovascular risk factors and other potential confounders.

The role of serum uric acid (UA) as a marker or risk factor of cardiovascular disease (CVD) is still controversial. The strong association of serum UA with established risk factors such as hypertension, Type 2 diabetes, dyslipidemia, and chronic kidney disease makes it difficult to establish a direct causal role of serum UA in the development and progression of CVD. The main aims of this review are: 1) to briefly summarize the most relevant studies concerning the association of serum UA with hypertension, chronic kidney disease, CVD events, and death both in patients without diabetes and in those with Type 2 diabetes; and 2) to briefly discuss the putative underlying mechanisms that link serum UA to adverse CVD outcomes. A search was conducted to identify relevant studies in the major electronic databases (MEDLINE and EMBASE, from January 1990 to December 2010) using Medical Subjects Headings and keywords. Collectively, by reviewing the published data in the literature, it emerges that serum UA may exert a number of potentially adverse cardiovascular effects. Nevertheless, the prognostic role of elevated serum UA level as a causal risk factor of adverse CVD outcomes remains still controversial, especially in patients with Type 2 diabetes. At this time, the treatment of asymptomatic hyperuricemia for the primary prevention of CVD is not recommended.

Non-alcoholic fatty liver disease (NAFLD) is estimated to afflict ∼20–30% of the general population, and over 70% of the patients with Type 2 diabetes. Given the expected rise in the prevalence of obesity and diabetes, NAFLD will be, if not already there, an epidemic. The consequences of NAFLD are numerous, and range from progression to chronic liver disease with its associated morbidity and mortality, to worsening insulin resistance and Type 2 diabetes, to being a contributor to both cardiovascular disease (CVD) and chronic kidney disease (CKD). NAFLD is, therefore, a complex problem with implications far beyond the liver. This review focuses on the rapidly expanding body of clinical evidence suggesting that NAFLD is associated with an increased prevalence and incidence of both CVD and CKD in patients with diabetes. This association appears to be independent of obesity, hypertension, and other potential confounding factors. However, given the heterogeneity and small number of observational studies, further research is urgently required to corroborate the prognostic role of NAFLD in the development and progression of CVD and CKD among patients with diabetes, and to further elucidate the complex and intertwined mechanisms that link NAFLD with these adverse outcomes.

Background and aim: Non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS) are both associated with insulin resistance. We assessed whether NAFLD is associated with impaired insulin sensitivity in PCOS women independently of age and total adiposity. Subjects and methods: We enrolled 14 young PCOS women with NAFLD, 14 women with PCOS alone and 14 healthy controls, who were matched for age, body mass index, and total body fat (by bio-impedance analyzer). NAFLD was diagnosed by the surrogate measure of abnormal serum alanine aminotransferase (ALT) concentrations (defined as ALT>19 U/l) after excluding other secondary causes of liver disease (alcohol, virus, and medications). Insulin sensitivity was measured by euglycemic hyperinsulinemic clamp. Results: Insulin sensitivity was markedly decreased (p<0.001) in PCOS women with abnormal ALT levels, whereas it was similar between PCOS women with normal ALT levels and matched healthy controls (8.3±2.5 vs12.1 ±1.7 vs13.2±1.8 mg/min × kg of fat-free mass, respectively). PCOS women with abnormal ALT levels also had higher plasma triglycerides and lower HDL-cholesterol concentrations than those with PCOS alone. There was a strong inverse association between serum ALT levels and insulin sensitivity in the whole group of PCOS women (r=−0.59, p=0.0013). Conclusions: Abnormal serum ALT levels, as surrogate measure of NAFLD, are closely associated with impaired insulin sensitivity in young PCOS women in a manner that is independent from the contribution of age and total adiposity. Early recognition of NAFLD by radiological imaging tests in this group of young patients is warranted.

Non-alcoholic fatty liver disease (NAFLD) is closely associated with several metabolic syndrome (MetS) features. We assessed whether NAFLD is significantly associated with carotid artery intima-media thickness (IMT), as a marker of subclinical atherosclerosis, and whether such association is independent of classical cardiovascular risk factors and MetS features. We studied 100 diet-controlled Type 2 diabetic patients with ultrasonographically diagnosed NAFLD and 100 diabetic patients without NAFLD who were comparable for age and sex. Main outcome measures were carotid IMT (by ultrasonography), classical risk factors, insulin resistance [as estimated by homeostasis model assessment (HOMA)-IR] and MetS (as defined by the Adult Treatment Panel III criteria). NAFLD patients had a markedly greater carotid IMT (1.24±0.13 vs0.95±0.11 mm; p<0.001) than those without the condition. The MetS and all its clinical traits were more highly prevalent in those with NAFLD (p<0.001). Adjustment for age, sex, smoking history, diabetes duration, glycosylated hemoglobin, LDL cholesterol, liver enzymes and microalbuminuria did not really affect the significant differences in carotid IMT that were observed between the groups. Further adjustment for the MetS also had little impact, but additional adjustment for HOMA-IR score consistently attenuated any statistical significance (p=0.28). In multivariate regression analysis, HO-MA-IR score along with age and MetS (principally raised blood pressure values) were independently related to carotid IMT, whereas NAFLD was not. In conclusion, these results suggest that among diet-controlled Type 2 diabetic individuals the significant increase of carotid IMT in the presence of NAFLD is largely explained by HOMA-estimated insulin resistance.

Serum lipoprotein(a) [Lp(a) ], blood lipids, serum insulin and anthropometric parameters were determined in randomized samples of 38-year-old men living in six European cities: Ede (The Netherlands), Deinze (Belgium), Warsaw (Poland), Lumiar (Portugal), Verona and Naples (respectively in northern and in southern Italy). In total, 406 healthy men were studied. Serum Lp(a), blood lipids and serum insulin were measured in one laboratory. All the anthropometric and metabolic variables considered were statistically different among the participating sites, with the exception of Lp(a) serum levels. In spite of the lack of overall significant inter-center differences (Kruskal-Wallis test), the subjects from the two Italian cities had significantly lower Lp(a) serum levels than the subjects from Belgium and Portugal (Mann-Whitney U test, p < 0.01). In all cities the distribution of serum Lp(a) levels were highly skewed; the percentage of subjects with serum Lp(a) levels higher than 30 mg/dl (i.e., the commonly accepted risk level of cardiovascular disease) was 6% in both Verona and Naples (Italy), 12% in The Netherlands, 16% in Poland, 18% in Belgium and 19% in Portugal (for the last two cities, respectively, p < 0.02 and p < 0.01 vs Italian cities, chi-square test). Neither anthropometric (body mass index, waist/hip circumference ratio) nor metabolic (serum lipids and insulin) parameters showed any significant relationship with serum Lp(a) levels in any of the sites (Spearman's rank correlation).

The associations between fasting plasma insulin concentration and risk factors for cardiovascular diseases were examined in 979 18-year-old men participating in the Verona Young Men Atherosclerosis Risk Factors Study, a cross-sectional population-based study. Body mass index (BMI), waist-to-hip ratio (WHR), plasma triglycerides and uric acid concentrations, and blood pressure values significantly increased, and the high-density lipoprotein (HDL)-total cholesterol ratio decreased, across quartiles of fasting insulin. Total and low-density lipoprotein cholesterol concentrations did not change significantly with the increase in fasting insulin levels. After adjustment for BMI, WHR, smoking, alcohol intake and physical activity, only plasma triglycerides significantly increased across insulin quartiles (F =7.1; P &lt;0.001). However, systolic blood pressure and uric acid were close to statistical significance (P =0.06-0.07). Multiple linear regression analysis confirmed that plasma insulin was independently correlated with plasma triglycerides and, to a lesser extent, with blood pressure and uric acid concentration. This analysis pointed out that BMI was a stronger independent predictor of all cardiovascular disease risk factors than fasting insulin. When subjects were categorized according to the number of metabolic and haemodynamic disorders occurring within the same individual, subjects with multiple disorders (i.e. three or four) had higher plasma insulin levels than those with none or few disorders, even after adjusting for BMI, WHR and behavioural variables (F =4.0; P &lt;0.01). These results indicate that hyperinsulinaemia is already associated with a cluster of cardiovascular disease risk factors in young adulthood, the strongest independent association being with plasma triglycerides.

Introduction: The relationship between the appropriateness of the transthoracic echocardiography (TTE) and its clinical impact is still a matter of debate. Objective: The aim of this study was to assess the degree of adherence to the appropriate use criteria for echocardiography, in a tertiary public hospital in the United Kingdom, as well as the clinical impact of the exam on patient management. Methods: 859 TTE’s performed consecutively during January 2014 were reviewed to assess its appropriateness, and were classified as appropriate, uncertain or inappropriate using the 2011 guidelines. Subsequently, patient’s files were examined to determine the clinical impact of the TTE which was assigned to one of the following three categories: (1) active change in care, (2) continuation of current care, or (3) no change in care. Patients which files were not available were excluded (259). All classifications were evaluated by two independent cardiologists, with no direct relation to the study. Results: Our sample had a mean age of 63 ± 17 years with a gender balance. The majority of the exams were requested at the outpatient (81.4%) clinic, by cardiologists (50.3%) and general practitioners (13.4%). Regarding the main findings, in 7.6% of the studies there were moderate to severe systolic dysfunction; 4.0% showed severe valvular heart disease and 5.1% had significant pulmonary hypertension. Relatively to the appropriateness of the TTE requests, 76.5% were considered appropriate, 7.1% inappropriate and 12.6% uncertain. With respect to the clinical impact of the TTE’s, 42.7% of the exams led to an active change in care, 15.6% to a continuation of the care and 11.5% revealed no change in care. Age (β0.90, P=0.05) and outpatient setting (β4.4, P<0.01) were the most important predictors of an active change of care exam. On the contrary, the appropriateness of the TTE’s requests (β1.1, P=0.56) and the specialist ordering the exams (β0.81, P=0.26) were not independently associated. Conclusion: Our data showed that almost 8 out of 10 TTE were considered appropriate, and 4 out of 10 exams had an active clinical impact.

Background: Preclinical diastolic dysfunction is highly prevalent in the aging population, but mechanisms for progression into heart failure with preserved ejection fraction (HFpEF) are still obscure. Recently, microvascular endothelial inflammation and endothelial dysfunction (ED) were advocated as primum movens in the development of HFpEF. Purpose: We aimed to evaluate whether ED and arterial stiffness relate to diastolic and other structural and functional cardiac parameters. This was studied in patients with chronic kidney disease (CKD), known to be prone to diastolic dysfunction and left ventricular hypertrophy. Methods: Consecutive CKD patients, without concomitant cardiovascular disease, were included. Diastolic parameters were assessed by cardiac ultrasound using E/e´ ratio and left atrial volume index (LAVi). Also, left ventricular mass index (LVMi) and interventricular septum thickness (IVSd) were included. Endothelial function was evaluated by flow-mediated dilation (FMD) of the brachial artery induced by hyperaemia. Arterial stiffness was assessed by measuring carotid-femoral pulsed wave velocity (PWV). Results: After exclusion of patients with normal diastolic function (n=11), 52 patients (age 53.9 ± 12.8 years, 53.2% male) were assessed, of whom 36 underwent a second analysis after 3 months (total measurements 88). Mean creatinin clearance (eGFR) was 42.9 ± 23.2 ml/min/1.73m2. Comorbidities included arterial hypertension (90.4%) and diabetes mellitus (9.6%). Mean Framingham Heart score was 18.9% ± 18.7. Endothelial function was impaired (FMD 4.64% ± 2.61), and patients showed increased arterial stiffness (PWV 8.96 m/s ± 2.18). Ratio of E/e´ was elevated (>12) in 36.4% of measurements. LVMi was raised in 28.4%, and LAVi was elevated in 45.1%. Patients with E/e´>12 had impaired FMD (p=0.005) and elevated PWV (p=0.047). In bivariate correlation analysis, FMD correlated with E/e´ (r=-0.289, p=0.010) and with IVSd (r=-0.315, p=0.005). PWV did not show a relation with any of the diastolic indices (all p>0.05). In a multiple linear regression model, accounting for age, sex, smoking, eGFR, and PWV, FMD remained independently associated to E/e´ (ß=-0.279, p=0.011) and IVSd (ß=-0.232, p=0.026). Conclusions: In CKD patients with preclinical diastolic dysfunction, impaired endothelial function correlates with higher filling pressures and structural cardiac changes. This observation supports the paradigm that ED plays a role in the pathophysiology of diastolic dysfunction, even in an asymptomatic stage.

Purpose: We have previously demonstrated that multi-line transmit (MLT) beam forming can provide high quality full field-of-view (90° sector) B-mode images at very high frame rates, i.e. up to 500 fps. The purpose of this study was to test the feasibility of this technique in imaging the mechanical intraventricular waves such as the one associated with activation of the left ventricle. Methods: A dedicated pulse sequence using MLT was implemented on the ULA-OP research scanner equipped with a 2.0 MHz phased array to obtain 90° sector images at a frame rate of 436 fps. The left ventricle of a healthy volunteer was imaged from the apical 4 chamber view and the RF data was acquired. Subsequently, the strain rate was extracted from the RF data using a normalized cross-correlation method. Results: As expected, during the early filling phase, myocardium lengthening (positive strain rate) was observed propagating from the base of the septum to the apex and back (Figure a). A similar wave was detected in the lateral wall, although a brief shortening (negative strain rate) was detected in the mid-wall which could be the result of reverberations (Figure b). During isovolumetric contraction, the septal wall shortened before the lateral wall (as expected) - moreover - there seemed to be an intra-wall base-apex shortening gradient (Figure c and d). Conclusions: Our preliminary results show that visualization of the cardiac mechanical activation could be feasible using MLT based high frame rate imaging. Further research is required to examine this in depth, which is the topic of on-going work. Figure Curved M-mode of strain rate