Development Of Left Ventricular Diastolic Dysfunction Research Articles

The association between rheumatoid arthritis and left ventricular diastolic dysfunction: pathogenesis, predictors and managements.

Left ventricular diastolic dysfunction (LVDD) plays a central role in the pathophysiology of heart failure with preserved ejection fraction (HFpEF), a major manifestation of heart failure (HF). Low-grade inflammatory reaction is the key mechanism leading to LVDD. Rheumatoid arthritis (RA) is a systemic inflammatory disease and affects 0.5-1.0% of the adult population. Several epidemiologic studies find that the risk of LVDD is increased in RA than in the general population. Since inflammation plays an important role in the pathogenesis of LVDD and RA is a disease characterised by chronic systemic inflammation. RA may be involved in the occurrence and development of LVDD. This review summarises the pathogenesis, predictors, and management of LVDD in patients with RA.

Evaluating Diastolic Dysfunction as an Indicator of Cirrhotic Cardiomyopathy in Decompensated Chronic Liver Disease.

The clinical syndrome of cirrhotic cardiomyopathy (CCM) occurs quite frequently in decompensated chronic liver disease (DCLD) patients without any prior incidence. The compromised life expectancy under such conditions was the key that prompted us to conduct this study. This study was planned to study the prevalence of diastolic dysfunction in chronic liver disease patients, to understand the diagnostic criteria of left ventricular diastolic dysfunction(LVDD) in cirrhotic patients, and to evaluate its occurrence as an early indicator of CCM. A hospital-based, cross-sectional study was conducted on 158 patients, admitted to the Department of Medicine, Rajendra Institute of Medical Sciences, Ranchi, India, who conformed to our criteria for inclusion and exclusion.The study period was for 18 months. The subjects were clinically and radiologically diagnosed with chronic liver disease. Regression analysis for variables was performed to score the effects of potential variables with outcomes for diastolic dysfunction (DD) prediction. Out of 158 patients, 116 belonged to the age group of 31-60 years, pronouncing age to be a significant factor for LVDD. Fifty-threesubjects had serum bilirubin levels >2mg/dL and we found serum bilirubin levels to bear a significant correlation with LVDD by exhibiting a p-value <0.0001. Both the Child-Turcotte-Pugh score class (p-value=0.0180) and QTc (p-value <0.0001) bear significant correlation with the development of LVDD, which is also evident from their area under the curve (AUC) values of 0.64 in the receiver operating characteristic (ROC) curve. Our study concludes that LVDD is an early indicator for assessing the severity of liver cirrhosis in DCLD. The correlation of DCLD with prolonged QTc could predispose patients with DCLD to ventricular arrhythmias. Hence, such patients should undergo serum bilirubin tests, and electrocardiographic checks at regular intervals for early detection, to increase their overall survival rates.

The association between higher cardiac troponin levels and the development of left ventricular diastolic dysfunction in septic patients with diabetes mellitus.

This study was designed to retrospectively analyze the relationship between the levels of cardiac troponin T (cTnT) and cardiac troponin I (cTnI) and the development of left ventricular diastolic dysfunction (LVDD) in septic patients with diabetes mellitus. Furthermore, the predictive value of cTnT and cTnI in the LVDDdevelopment in those patients was investigated. The clinical information of 159 septic patients with diabetes mellitus treated in the intensive care unit of Affiliated Hospital of Chengde Medical University from June 2016 to January 2023 were retrospectively analyzed. These patients were separated into LVDD group (LVFP > 15mmHg) and non-LVDD group (LVFP ≤ 15mmHg) based on left ventricular filling pressure (LVFP). The differences in clinical data, echocardiographic parameters, as well as cTnT and cTnI levels between the LVDD and non-LVDD groups were compared. The relationship between the cTnT and cTnI levels and the echocardiographic parameters was studied using Pearson correlation analysis. Logistic regression analysis wasconducted to explore the factors that influenced the LVDDdevelopment in septic patients with diabetes. Receiver operator characteristic (ROC) curves were created to evaluate the predictive value of cTnT and cTnI levels for the LVDD developmentin septic patients with diabetes. Totally 159 septic patients with diabetes were included in this study, with 97 patients in the LVDD group and 62 in the non-LVDD group. Compared with the non-LVDD group, patients in the LVDD group had much lower left ventricular (LV) early diastolic peak inflow velocity (E), LV advanced diastolic peak inflow velocity (A), E/A, and early diastolic mitral annular velocity (Em) while significantly higher E/Em. The LVDD group showed much higher levels of cTnI and cTnT than the non-LVDD group (P < 0.05). Significant positive correlation between log10cTnI level and E/Em ratio (r = 0.425, P < 0.001)was revealed by the Pearson correlation analysis. Multivariate analysis showed that E/A, E/Em, cTnI and cTnT were independent risk factorsfor the LVDD developmentin septic patients with diabetes (P < 0.05). As for ROC curve results, the area under the curve (AUC) of cTnT to predict the development of LVDD in septic patients with diabetes was 0.849 (95% CI 0.788-0.910, P < 0.001); the AUC of cTnI was 0.742 (95% CI 0.666-0.817, P < 0.001). Both cTnT and cTnI are independent risk factors and have predictive value for the LVDD development in septic patients with diabetes mellitus.

The role of epicardial obesity in the development of left ventricular diastolic dysfunction

To study the effect of epicardial adipose tissue on risk of left ventricular (LV) diastolic dysfunction (DD) in patients with visceral obesity. Obesity leads to the development of LV DD and is a major cause of heart failure with preserved LV ejection fraction (HFpEF). However, the contribution of epicardial adipose tissue to DD is understudied. This study included 101 men with general obesity (body weight index, 32.9±3.6 kg /m2). Based on severity of epicardial obesity (EO), two groups were formed: group 1, patients with an epicardial adipose tissue thickness (EATt) &gt;7 mm (n=70), and group 2, patients with EATt &lt;7 mm (n=31). Arterial hypertension, diabetes mellitus, coronary atherosclerosis, and disorders of LV diastolic function according to echocardiography (EchoCG) were the exclusion criteria. Diastolic function and LV mechanics were evaluated by speckle-tracking EchoCG for all patients at the start of the study and again at 4.7±0.3 years. At baseline, none of the patients of either group had significant differences in EchoCG characteristics of LV diastolic function (left atrial volume index, LV early diastolic longitudinal lengthening velocity, peak tricuspid regurgitation velocity, and the ratio of diastolic transmitral flow velocity to mean mitral annular velocity (E / e'). However, there were significant increases in the LV untwisting velocity to -122.11 [-142.0; -116.0 degrees /s -1] degrees/s and the time to LV peak untwisting velocity to 472.3 ms. Repeated EchoCG showed an increase in left atrial volume index in group 1 to 35.04 [33.0; 39.7] ml /m2. Repeated evaluation of the LV mechanics revealed increases in the times to LV peak untwisting and twisting and decreases in the LV twisting and untwisting velocities. The logistic regression analysis showed that EATt was a risk factor for LV DD in obesity. Furthermore, the ROC analysis determined the optimal EATt cut-off threshold of ≥9 mm as a predictor for LV DD development. EO facilitates the development of LV DD and, thus, represents a major cause for HFpEF. An EATt value of ≥9 mm can be considered as a risk factor for LV DD development in patients with EO.

Echocardiographic assessment of left cardiac structure and function in antiretroviral therapy (ART)-naïve people living with HIV/AIDS.

Patients with human immunodeficiency virus (HIV) are at a significantly higher risk of cardiovascular disease (CVD) compared to HIV-negative people. Left heart dysfunction is the most common cardiac complication in people living with HIV/acquired immune deficiency syndrome (PLWHA), and diastolic dysfunction is an important predictor of cardiovascular events. The aims of this study were (1) to detect changes in left cardiac structure and function in antiretroviral therapy (ART)-naive PLWHA using echocardiography; and (2) to investigate the risk factors for the development of left ventricular diastolic dysfunction (LVDD) in ART-naive PLWHA. We retrospectively included 105 ART-naïve PLWHA and included 90 healthy subjects as controls to compare the differences in left heart structure and function between the two groups. Univariate and multifactorial logistic regression were employed to explore the risk factors of the development of LVDD in ART-naive PLWHA. The left ventricular end-diastolic internal diameter (LVEDD), left ventricular mass index (LVMI), and left atrial volume index (LAVI) were significantly greater in PLWHA than in controls (p < .05). The E/A ratio, lateral e' velocity, and mitral deceleration time were significantly lower in PLWHA than in controls (p < .05). Average E/e' ratio was significantly higher in PLWHA than in controls (p < .05). Left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were not significantly different between PLWHA and controls (p > .05). Multifactorial logistic regression analysis showed that age, body mass index (BMI), and CD4+ count <200 cells/μL were independent risk factors for LVDD in ART-naive PLWHA (OR = 1.781, 1.228, 3.683, p < .05). Left ventricular systolic function did not differ between PLWHA and controls, and left ventricular diastolic function was lower in PLWHA than in controls. Age, BMI, and CD4+ count were independent factors affecting LVDD in ART-naive PLWHA.

Increased protein phosphatase 5 expression in inflammation-induced left ventricular dysfunction in rats

Titin phosphorylation contributes to left ventricular (LV) diastolic dysfunction. The independent effects of inflammation on the molecular pathways that regulate titin phosphorylation are unclear. We investigated the effects of collagen-induced inflammation and subsequent tumor necrosis factor-α (TNF-α) inhibition on mRNA expression of genes involved in regulating titin phosphorylation in 70 Sprague-Dawley rats. LV diastolic function was assessed with echocardiography. Circulating inflammatory markers were quantified by enzyme-linked immunosorbent assay and relative LV gene expression was assessed by Taqman® polymerase chain reaction. Differences in normally distributed variables between the groups were determined by two-way analysis of variance (ANOVA), followed by Tukey post-hoc tests. For non-normally distributed variables, group differences were determined by Kruskal-Wallis tests. Collagen inoculation increased LV relative mRNA expression of vascular cell adhesion molecule 1 (VCAM1), pentraxin 3 (PTX3), and inducible nitric oxide synthase (iNOS) compared to controls, indicating local microvascular inflammation. Collagen inoculation decreased soluble guanylate cyclase alpha-2 (sGCα2) and soluble guanylate cyclase beta-2 (sGCβ2) expression, suggesting downregulation of nitric oxide-soluble guanylate cyclase-cyclic guanosine monophosphate (NO-sGC-cGMP) signaling. Inhibiting TNF-α prevented collagen-induced changes in VCAM1, iNOS, sGCα2 and sGCβ2 expression. Collagen inoculation increased protein phosphatase 5 (PP5) expression. Like LV diastolic dysfunction, increased PP5 expression was not prevented by TNF-α inhibition. Inflammation-induced LV diastolic dysfunction may be mediated by a TNF-α-independent increase in PP5 expression and dephosphorylation of the N2-Bus stretch element of titin, rather than by TNF-α-induced downregulation of NO-sGC-cGMP pathway-dependent titin phosphorylation. The steady rise in number of patients with inflammation-induced diastolic dysfunction, coupled with low success rates of current therapies warrants a better understanding of the systemic signals and molecular pathways responsible for decreased titin phosphorylation in development of LV diastolic dysfunction. The therapeutic potential of inhibiting PP5 upregulation in LV diastolic dysfunction requires investigation.

Serum Uric Acid Is Associated with the Progression of Left Ventricular Diastolic Dysfunction in Apparently Healthy Subjects.

Background Left ventricular (LV) diastolic dysfunction (LVDD) is the defining feature of heart failure with preserved ejection fraction (HFpEF) and predicts subsequent incident heart failure (HF) and all-cause mortality. Mounting evidence reveals that cardiometabolic risk factors play critical roles in the development of LVDD. In this study, we sought to investigate the relation between serum uric acid (SUA) level and the progression of LVDD in apparently healthy patients. Methods A total of 1082 apparently healthy subjects without diagnosed cardiovascular disease and LVDD were consecutively enrolled. SUA levels were measured, and repeat echocardiography and tissue Doppler imaging (TDI) were performed at baseline and during 1-year follow-up. Results By dividing the study population based on quartiles of SUA, we found subjects in higher quartiles had greater increases in TDI-derived early diastolic velocity (e′) and E (peak LV filling velocity)/e′ ratios during 1-year follow-up. After multivariate adjustment, high SUA persisted to be an independent predictor for the subsequent worsening of LVDD (odds ratio: 1.351 [95% CI 1.125~1.625], per 100 μmol/L SUA). Subgroup analysis suggested that the association between SUA and LVDD development was more pronounced in subjects without other cardiometabolic risk factors involved. Factor analysis demonstrated that high SUA was the major cardiometabolic attribute in patients with LVDD progression. Conclusion Our findings suggest that high SUA is an independent cardiometabolic risk factor for the progression of LVDD in apparently healthy subjects.

Mean and Variability of Lipid Measurements and Risk for Development of Subclinical Left Ventricular Diastolic Dysfunction.

BackgroundSubclinical left ventricular diastolic dysfunction (LVDD) is an emerging consequence of increased insulin resistance, and dyslipidemia is one of the few correctable risk factors of LVDD. This study evaluated the role of mean and visit-to-visit variability of lipid measurements in risk of LVDD in a healthy population.MethodsThis was a 3.7-year (interquartile range, 2.1 to 4.9) longitudinal cohort study including 2,817 adults (median age 55 years) with left ventricular ejection fraction >50% who underwent an annual or biannual health screening between January 2008 and July 2016. The mean, standard deviation (SD), coefficient of variation (CV), variability independent of the mean (VIM), and average real variability of total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein B (apoB), non-HDL-C, and triglycerides were obtained from three to six measurements during the 5 years preceding the first echocardiogram.ResultsAmong the 2,817 patients, 560 (19.9%) developed LVDD. The mean of no component of lipid measurements was associated with risk of LVDD. CV (hazard ratio [HR], 1.35; 95% confidence interval [CI], 1.10 to 1.67), SD (HR, 1.27; 95% CI, 1.03 to 1.57), and VIM (HR, 1.26; 95% CI, 1.03 to 1.55) of LDL-C and all the variability parameters of apoB were significantly associated with development of LVDD. The association between CV-LDL and risk of LVDD did not have significant interaction with sex, increasing/decreasing trend at baseline, or use of stain and/or lipid-modifying agents.ConclusionThe variability of LDL-C and apoB, rather than their mean, was associated with risk for LVDD.

Association between cortisol and left ventricular diastolic dysfunction in patients with diabetes mellitus.

Aims/IntroductionDiabetes mellitus is a major risk factor for the development of cardiovascular diseases. Heart failure with preserved ejection fraction is characterized by left ventricular diastolic dysfunction (LVDD). It has been reported that excess cortisol found in patients with Cushing's syndrome was associated with the development of LVDD. However, the relationship between cortisol concentration and LVDD in patients with diabetes mellitus has not been addressed.Materials and MethodsWe enrolled 109 patients with diabetes mellitus and 104 patients without diabetes mellitus who had undergone echocardiographic examination at Kyushu University Hospital, Fukuoka, Japan, between November 2016 and March 2019. Left ventricular function was evaluated and the ratio of early diastolic velocity from transmitral inflow to early diastolic velocity (E/eʹ) was used as an index of diastolic function. Plasma cortisol concentrations, glycemic control, lipid profiles, treatment with antidiabetic drugs and other clinical characteristics were evaluated, and their associations with E/eʹ were determined using univariate and multivariate analyses.ResultsMultivariate linear regression analysis showed that log E/eʹ was positively correlated with age (P = 0.017), log systolic blood pressure (P = 0.004) and cortisol (P = 0.037), and negatively correlated with estimated glomerular filtration rate (P = 0.016) and the use of sodium–glucose cotransporter 2 inhibitors (P = 0.042) in patients with diabetes mellitus. Multivariate analysis showed that cortisol was positively correlated with age (P = 0.016) and glycated hemoglobin (P = 0.011). There was no association between E/eʹ and cortisol in patients without diabetes mellitus.ConclusionsIncreased cortisol levels might increase the risk of developing LVDD in diabetes mellitus patients.

Association of microalbuminuria with left ventricular dysfunction in type 2 diabetes mellitus

BackgroundThe prevalence of diabetes mellitus is on rising trend in developing countries like India. In type 2 diabetes patients, albuminuria has been shown to predict development of dysfunction in other organ systems such as kidneys, nervous system, and retina and increase risk of cardiovascular (CV) morbidity and mortality. In this study, we plan to assess association of microalbuminuria with left ventricular dysfunction in type 2 diabetes mellitus.ResultsThis cross-sectional study was conducted among 100 type 2 diabetes mellitus patients attending a tertiary care hospital in Gujarat, Western India. Based on urine albumin excretion status, they were divided in two groups of 50 each—normoalbuminuric and microalbuminuric patients. The mean FBS, PPBS, and HbA1c level was significantly lower in normoalbuminuric group compared to microalbuminuric group. There was an increase in cholesterol, triglyceride, VLDL, and LDL levels and decrease in HDL levels in microalbuminuric group as compared to normoalbuminuric group. Multivariate logistic regression analysis revealed that increase in age and a decrease in E/A ratio in patients with microalbuminuria was significantly associated with left ventricular diastolic dysfunction (LVDD).ConclusionThe presence of microalbuminuria is associated with increased likelihood of LVDD in type 2 diabetes patients. Increase in age and decrease in E/A ratio show direct and independent association with LVDD in normotensive diabetic patients with microalbuminuria. Therefore, diabetes patients who have microalbuminuria should be regularly (or more frequently) evaluated for development of LVDD using Echocardiography. This can allow early identification of myocardial diastolic dysfunction.

Cortisol Levels Is Associated With Left Ventricular Diastolic Dysfunction in Diabetic Patients

Abstract Introduction: Diabetes mellitus (DM) is a major cause of cardiovascular disease including heart failure with preserved ejection fraction (HFpEF), which is characterized by left ventricular diastolic dysfunction (LVDD). It is reported that Cushing’s syndrome is also associated with LVDD. The relationship between plasma cortisol concentration and LVDD, however, has not been investigated in patients with DM. Methods: In this study, 109 patients with DM and 104 patients with non-DM without overt heart failure were enrolled. Left ventricular function were assessed using echocardiography. The ratio of early diastolic velocity (E) from transmitral inflow to early diastolic velocity (e’) of tissue Doppler at mitral annulus (E/e’) was used as an index of diastolic function. Parameters of plasma cortisol concentration, glycemic control, lipid profile, treatment with anti-diabetic drugs and other clinical characteristics were evaluated, and their association with E/e’ determined. Patients taking steroids, undergoing dialysis treatment and with overt heart failure were excluded. Results: Univariate analysis showed that E/e’ was significantly correlated with age (p&amp;lt;0.001), duration of diabetes (p=0.039), systolic blood pressure (SBP) (p&amp;lt;0.001), eGFR (p=0.002), sodium glucose cotransporter 2 (SGLT2) inhibitor use (p&amp;lt;0.001) and cortisol (p=0.009) in patients with DM. Multivariate linear regression analysis showed that log E/e’ was positively correlated with age (p=0.018), log SBP (p= 0.005), eGFR (p=0.015), cortisol (p=0.028) and that log E/e’ was inversely with inhibitor use (p=0.018). There was no association between E/e’ and cortisol in patients with non-DM. Conclusions: Cortisol may be important in the development of LVDD in patients with DM.

Factors Predicting Cardiac Dysfunction in Patients with Liver Cirrhosis.

BACKGROUND Left ventricular diastolic dysfunction (LVDD) is the earliest cardiac dysfunction noted in patients with liver cirrhosis, which increases the morbidity and mortality in such patients. There are sparse studies from India evaluating the predictive factors of LVDD in patients with cirrhosis. Hence we undertook this prospective study with an aim to evaluate the factors predicting the development of LVDD in liver cirrhosis. METHODS 104 patients with cirrhosis were enrolled in this prospective study. A detailed cardiac evaluation was done by 2 D echocardiography with tissue Doppler imaging by an experienced senior cardiologist. The severity of liver disease was defined by Model For End-Stage Liver Disease (MELD) and Child-Pugh score. RESULTS The prevalence of LVDD was 46% in our study. Multivariate logistic regression analysis revealed that serum albumin, MELD score, and presence of ascites (OR = 0.1, 95%CI 0.03-0.3, p < 0.001; Or = 1.12, 95%CI 1.03-1.22, p < 0.001; OR = 4.19, 95%CI 1.38-12.65, p < 0.01, respectively) were independent predictors of LVDD in patients with cirrhosis. Diastolic dysfunction was unrelated to age, sex, and etiology of cirrhosis. The patients with cirrhosis and LVDD had significantly higher child Pugh score, MELD score, and lower serum albumin than patients without LVDD. The echocardiographic parameters like E/e' ratio, Deceleration time (DT), and Left atrial volume index (LAVI) were significantly different in cirrhotic patients with higher MELD and child Pugh score than lower. CONCLUSION The present study showed a significant correlation of diastolic dysfunction with the severity of the liver disease. Low serum albumin, high MELD score, and presence of ascites significantly predict the development of LVDD in patients with cirrhosis.

Serum Uric Acid may be Associated with Left Ventricular Diastolic Dysfunction in Military Individuals.

We investigated the correlation and association between serum uric acid (SUA) and left ventricular diastolic dysfunction (LVDD) criteria in military individuals. We prospectively enrolled military individuals who visited our hospital for evaluation of electrocardiographic abnormalities detected at an annual health exam between January 1, 2018 and December 31, 2019. Hyperuricemia was defined as an SUA level ≥7 mg/dL in men and ≥6 mg/dL in women. The definitions of LVDD criteria and LV hypertrophy were according to contemporary echocardiographic guidelines. The study included 268 individuals (89% male), with a mean age of 32.9 ± 7.6 years and SUA of 6.1 ± 1.3 mg/dL. The hyperuricemic (n = 74) and normouricemic (n = 194) groups had no significant differences in lifestyle choices and baseline characteristics. Serum uric acid correlated weakly with heart size parameters (r = 0.354, P < .001 for left atrial diameter and r = 0.146, P = .017 for left ventricular mass index (LVMI) and average E/e' >14 (r = 0.204, P = .001). The hyperuricemic group had higher LVMI (87.6 g/m2 vs. 81.8 g/m2, P = .022), septal e' velocity <7 cm/s (14.9% vs. 5.2%, P = .019), lateral e' velocity <10 cm/s (27.0% vs. 11.3%, P = .003), and average E/e' >14 (4.1% vs. 0%, P = .020) values than the normouricemic group. In multivariate logistic regression analyses, SUA was significantly associated with septal e' velocity <7 cm/s (adjusted HR: 2.398; 95% CI, 1.427-4.030; P = .001). Elevated SUA was significantly associated with the presence of LVDD criteria, namely, septal e' velocity <7, in military individuals. Maintaining SUA levels within normal limits may prevent the development of LVDD.

ApoA-I mimetic does not improve left ventricular diastolic dysfunction in rabbits without aortic valve stenosis

BackgroundWe previously demonstrated that high-density lipoprotein (HDL) infusions may improve left ventricular diastolic dysfunction (LVDD) in an aortic valve stenosis (AVS) model. Whether the benefit was direct or mediated by the observed reduction in AVS severity is not clear. Here, we aimed to test the direct effect of an ApoA-I mimetic on LVDD in the absence of AVS. MethodsRabbits were exposed to three different protocols to develop LVDD. First, rabbits were exposed to 0.5% cholesterol-rich diet for an average of 17 weeks. Second, rabbits were subjected to surgical ascending aortic constriction (AAC), to mimic the effect of fixed reduced aortic valve area, and studied after 10 weeks. The third model combined both cholesterol-enriched diet (for 12 weeks) and surgical AAC. The control group consisted of age-matched rabbits under normal diet. After development of LVDD, rabbits were randomized to receive infusions of saline or apoA-I mimetic (25 mg/kg) 3 times per week for 4 weeks. Detailed cardiac structure and function measurements were assessed at baseline and weekly during treatment period. Histological and molecular analyses were performed on LV samples. ResultsIn the three models, echocardiographic results showed development of LVDD over time, with preserved LV systolic and aortic valve functions versus controls. ApoA-I mimetic infusions did not significantly improve echocardiographic parameters nor molecular markers of cardiac inflammation, oxidative stress and fibrosis. ConclusionApoA-I mimetic therapy did not directly improve LVDD. These results indicate that previously observed changes of LVDD were caused by AVS improvement induced by this treatment.

Relationships between kidney dysfunction and left ventricular diastolic dysfunction: a hospital-based retrospective study.

Preclinical left ventricular diastolic dysfunction (LVDD) is a high-risk state for heart failure. Kidney dysfunction is a known risk factor for heart failure, but its association with asymptomatic LVDD is not well-known. A hospital-based retrospective cohort study was conducted on patients who underwent echocardiogram between 2006 and 2016 to assess the association between baseline kidney function and LVDD on echocardiogram. E/e' ratio was defined as the ratio of peak velocity of early diastolic left ventricular inflow (E) to mitral annular velocity (e'). The primary outcome was time to development of LVDD, which was defined as E/e' ratio > 14. The changes in the E/e' ratio and other echocardiographic parameters were assessed using a mixed effects model. Among 1167 patients, the mean age was 61 years, and the mean baseline E/e' ratio and ejection fraction were 9.6 and 69%, respectively. During a median follow-up of 3.2 years, 231 (19.8%) people developed LVDD. According to eGFR (mL/min/1.73m2), the risk for LVDD based on hazard ratio [95% confidence interval (95% CI)] was 1.20 (0.82, 1.75) for 60 to < 90, 1.42 (0.87, 2.31) for 45 to < 60, and 2.57 (1.61, 4.09) for < 45 (P trend < 0.001). The adjusted risks (95% CI) for annual change in E/e' ratio was 0.09 (0.03, 0.14) overall and 0.28 (0.11, 0.45) in the lowest eGFR group; the trend in changes in annual E/e' ratio by baseline eGFR was significant (P trend = 0.01). Relatively low kidney function was related with the risks for LVDD. Long-term cohort studies are warranted to confirm the association between LVDD and symptomatic heart failure in patients with kidney dysfunction.

Mean and visit-to-visit variability of glycemia and left ventricular diastolic dysfunction: A longitudinal analysis of 3025 adults with serial echocardiography

ObjectiveWe aimed to determine the mean glucose thresholds to increase the risk of left ventricular diastolic dysfunction (LVDD) and whether visit-to-visit variability of fasting plasma glucose (FPG) and glycated hemoglobin (A1C) could independently increase the risk in a cohort with serial echocardiography. MethodsThis was a 3.5-year (range, 0.5–8.3) retrospective longitudinal cohort study of 3025 adults (age, 55.15 ± 7.6 years; without diabetes, n = 2755) with LV ejection fraction > 50% by serial echocardiography between 2006 and 2016. Mean, standard of deviation (SD) and coefficient of variation (CV) of FPG and A1C obtained from three consecutive measurements preceding the first echocardiography. The definition of LVDD in this study was primarily based on early peak mitral inflow velocity and early diastolic mitral annulus motion velocity. ResultsLVDD developed in 611/3025 subjects (20.2%). Cox proportional hazard models showed increased adjusted hazard ratios (HRs) for incident LVDD in the highest quartile of FPG-mean (HR 1.76, 95% confidence interval [CI]; 1.36–2.30), FPG-SD (HR 1.63, 95% CI; 1.27–2.09), FPG-CV (HR 1.47, 95% CI; 1.15–1.89), and A1C-mean (HR 1.83, 95% CI; 1.41–2.38) versus the lowest quartile, which was consistent even in subjects without diabetes. Mean glucose thresholds for the increased risk were below the lower limits for pre-diabetes. ConclusionsIn terms of mean glycemia, LVDD may be initiated in the earliest diabetic continuum, and such changes could be measurable within several years. Visit-to-visit variability of FPG, but not that of A1C, predicted accelerated development of LVDD.

The associations of circulating microRNA-133a with parameters of hypertension heart disease in patients with arterial hypertension and obesity

Abstract Introduction Blood pressure (BP) elevation leads to chronical increasing left ventricular (LV) overload, LV hypertrophy (LVH), impaired LV relaxation, development of LV diastolic dysfunction (DD), left atrial (LA) enlargement, which result in development of hypertension heart disease (HDD), increased risk of atrial fibrillation and heart failure. MicroRNA-133a is one the epigenetics factor, which has cardioprotective properties, but its role in the development of HHD in hypertension patients with obesity is not well understood. Purpose The aim of the study was to investigate the circulating microRNA-133a levels in patients with hypertension and obesity and to define its associations with components of HHD. Methods The study involved 82 patients with arterial hypertension grades 2–3 and obesity (44 men and 38 women) aged 43 to 70. All patients were separate in two groups: 45 patients with HHD (main group) and 37 patients without HHD (comparison group). The control group consisted of 21 practically healthy individuals of comparable gender and age. The HHD was defined as LVH in hypertension patients with/without LV DD. The LVH was determined according to the 2018 ESC/ESH guidelines. The LV DD was determined according to the 2016 ASE/EACVI recommendations. Obesity was diagnosed at body mass index ≥30 kg/m2. Circulating plasma microRNA-133a levels were obtained by polymerase chain reaction using the CFX96 Touch System, “TaqMan microRNA Assay” and “TaqMan® Universal PCR Master Mix” reagent kits. Results The levels of microRNA-133a in main group were significantly lower than in comparison group and control group (0.133 [0.099; 0.184] vs 0.238 [0.155; 0.410], p&amp;lt;0.05 and 0.382 [0.198; 0.474]), p&amp;lt;0.05). In the main group 23 patients had LV DD and 25 patients had normal LV diastolic function. In patients with LV DD the levels of circulating plasma microRNA-133a were significantly lower than in patients with normal LV diastolic function (0.094 [0.067; 0.147] vs 0.152 [0.092; 0.189]), p&amp;lt;0.05). In the main group there was a statistically significant negative correlation between microRNA-133a levels and LV mass index (R=−0.37, p&amp;lt;0.01) and no significant correlation with ejection fraction, LA size or E/e' (averaged) ratio (p&amp;gt;0.05). In patients of the comparison group there were not significant associations of microRNA-133a levels with LV parameters (p&amp;gt;0.05). Conclusion The results of the study indicate a significant role of decreased circulating plasma microRNA-133a levels in patients with arterial hypertension and obesity in the pathogenesis and development of HHD and such its components as LVH and LV DD. Funding Acknowledgement Type of funding source: None

Structural and functional myocardial abnormalities and arrhythmias in patients with type 1 diabetes complicated with ketoacidosis

Aim.To study the structural and functional cardiac changes and arrhythmias in patients with type 1 diabetes (T1D) complicated with ketoacidosis.Material and methods.We analyzed 24-hour Holter monitoring data in 112 patients with T1D complicated with diabetic ketoacidosis (DKA). To assess the left ventricular (LV) diastolic function, all patients underwent echocardiography.Results.In patients with T1D complicated with DKA, the following cardiac arrhythmias were recorded: supraventricular arrhythmias — 60,7%, premature ventricular contractions — 26,2%, premature ventricular and supraventricular contractions — 13,1%. In 30% of patients with T1D complicated with DKA, premature ventricular contractions were classified as class 4A, in 10% — class 4B. With severe DKA, 5% of patients had short runs of unstable ventricular tachycardia. As the severity of ketosis increases, myocardial remodeling and LV diastolic dysfunction are recorded, as well as the spectral and temporal parameters of heart rate variability decrease.Conclusion.In patients with T1D complicated with DKA, structural and functional LV abnormalities, the development of LV diastolic dysfunction and cardiac arrhythmias are more often recorded. The most pronounced changes were found in the group of patients with T1D with moderate and severe DKA.

Abstract P476: Consumption Of Animal And Plant Food And Likelihood Of Left Ventricular Diastolic Dysfunction: A Prospective Study Among Black And White Adults Of The Bogalusa Heart Study

Introduction: Left ventricular diastolic dysfunction (LVDD) is one key subclinical precursor of heart failure with preserved ejection fraction (HFpEF). Whether dietary correlates serve as independent predictors of LVDD in adults without HFpEF is unknown. Hypothesis: We hypothesized that dietary habits in young adulthood would prospectively influence the likelihood of LVDD in middle age. Methods: The analysis included 456 individuals of the Bogalusa Heart Study (26.5% black, 62.7% female, baseline age=36.1 + 4.4 years) with an ejection fraction &gt; 55%. Diet was measured at baseline via food frequency questionnaires. LVDD was defined at follow-up (median=12.9 years) through echocardiographic measurement of the E/A ratio, E/e’ ratio, isovolumic relaxation time, and deceleration time. Logistic regression estimated the odds of LVDD according to protein source, adjusting for cardiovascular disease risk factors and total energy intake. Results: There were 72 cases of LVDD. Using the lowest tertile as reference, persons in the middle tertile of total protein (OR=3.31, 95% CI: 1.47, 7.46; p=8.5x10 -3 ) and animal protein (OR=2.93, 95% CI: 1.35, 6.37; p=0.03) intake had the highest likelihoods of LVDD. We observed 54% and 57% lower odds of LVDD for persons in the highest vs. lowest tertile of vegetable (OR=0.46, 95% CI: 0.22, 0.95; p=8.0x10 -4 ) and legume consumption (OR=0.43, 95% CI: 0.20, 0.92; p=0.02), respectively. Total protein, animal protein, processed meat, and eggs indicated a significant quadratic trend towards increased odds of LVDD, while legumes and vegetables indicated a significant quadratic trend toward decreased odds of LVDD ( Table ). There were no significant relationships of LVDD with other animal or plant foods. Conclusions: Animal and plant food consumption result in an increased and decreased likelihood of LVDD, respectively. Adherence to plant-based diets in young adulthood may protect against the development of LVDD, and thus future HFpEF, later in life.

Incidence and predictors of new onset left ventricular diastolic dysfunction in asymptomatic patients with rheumatoid arthritis without overt cardiac disease.

Rheumatoid arthritis (RA) is associated with higher risk of heart failure. Several studies report that left ventricular (LV) diastolic dysfunction (LVDD), a silent precursor of heart failure, is widely present in RA patients. Very little is known about the factors related to the development of LVDD in this disease. In this study we assessed the incidence and the predictors of new-onset LVDD in RA patients. Two-hundred-ninety-five adults with RA without overt cardiac disease were prospectively analyzed from March 2014 to March 2015 by Doppler echocardiography. Among the 295 subjects evaluated, 217 (73.6%) had normal LV diastolic function and represented the final study population. At 1-year follow-up, 53 of 217 patients (24%) developed LVDD, which was of degree I (mild dysfunction) in all of them. By multivariate logistic regression analysis, lower E/A ratio of transmitral flow (ratio between the peak velocity of early diastolic "E" wave and late diastolic "A" wave of transmitral flow) was independently associated with new-onset LVDD [OR 0.17 (CI 0.09-0.57)], together with older age and higher systolic blood pressure. In a clinical predictive model derived from multivariate analysis, the new-onset LVDD rate event ranged from 0% (patients without any factor) to 75% (patients in whom the three predictors coexisted). A significant portion of patients with RA without overt cardiac disease develop LVDD at 1-year follow-up. This condition can be predicted by a simple clinical model which could improve the clinical management and the prognostic stratification of patients with RA.