Risk Of Left Ventricular Hypertrophy Research Articles

#1784 The potential impact of chronic subclinical hypervolemia on left ventricular hypertrophy in children on dialysis: a prospective longitudinal study

Abstract Background and Aims Hypervolemia poses a significant challenge in pediatric patients undergoing dialysis, potentially leading to severe complications such as left ventricular hypertrophy (LVH) and cardiac dysfunction. Accurately assessing fluid status in growing children on dialysis could be particularly difficult, and although several non-invasive methods are emerging, each individual measurement has its own strengths and diagnostic limitations in terms of sensitivity and specificity. To date, only a few studies in children have compared the use of different methods simultaneously to detect fluid status, and none of these have evaluated the potential cardiovascular impact of a prolonged subclinical hypervolemia. The latter can be defined as a condition of euvolemia at clinical assessment but hypervolemia at technical evaluation. We evaluated the role of three methods—lung ultrasound (LUS), bioimpedance spectroscopy (BIS), and ultrasound assessment of inferior vena cava collapsibility index (IVC-CI)—in detecting subclinical hypervolemia and examined the cardiac implications. Method In this prospective observational longitudinal study, we included 23 children (<18 years) who were receiving chronic hemodialysis or peritoneal dialysis at the regional pediatric nephrology center of Meyer University Children's Hospital IRCSS, Florence, Italy, between 01/06/2018 and 01/11/2020. We excluded patients with clinical signs of fluid overload. Each patient underwent a multiparametric evaluation of their fluid status (physical examination, LUS, IVC-CI, BIS) every 2 months, and an echocardiography every six months starting from a baseline evaluation. The LVH was defined as a left ventricular mass index (LVMI) of ≥ 95th percentile or a left ventricular wall-thickness z-score > 2 z-score. We divided the patients into two groups and arbitrarily assigned them to the subclinical hypervolemia (SH) group if they had at least two out of three parameters of fluid overload at different methods (≥5 B-lines at LUS, overhydration normalized to extracellular water “OH/ECW” > 7% at BIS, and/or IVC-CI < 40%) in the absence of clinical signs of fluid overload. The others were included in the euvolemic (EU) group. The overload rate by weight (clinical OH), prescribed by the physician clinically, was calculated as the proportional increase from the dry weight (kg of fluid overload / dry weight in kg × 100). Results The two analyzed groups did not differ regarding gender, age and BSA (Table). The clinical OH was significantly higher in the SH population than in the EU group (2.2 ± 1.84 vs 1.30 ± 2.16%, p < 0.01). In the correlation analysis, we found that clinical OH positively correlated with the number of B-lines by LUS (R = 0.2923, p < 0.001) and OH/ECW by BIS (R = 0.4144, p < 0.001), while there was a negative correlation with IVC-CI (R = −0.2597, p = 0.019). However, each method taken individually (LUS, BIS, and IVC-CI) appeared to be inaccurate in predicting fluid status in several individual cases. Although the frequency of hypertension did not differ between the SH and EU groups, uncontrolled hypertension, treatment-resistant hypertension, and hospital admission for hypertensive crises were more frequent in the SH group, with the latter being statistically significant (67% vs 0%, p < 0.01). Furthermore, in the entire cohort, we observed a significant linear correlation between LVMI values and the average values of pre-HD systolic blood pressure recorded in the prior six months (R2 = 0.16, p = 0.002). It is worth noting that the presence of LVH at the last follow-up was significantly more prevalent in the SH group (75% vs 27%, p = 0.04). Conclusion Chronic subclinical hypervolemia, detected with a multi-method evaluation (including LUS, BIS, and IVC-CI), was significantly correlated with clinical OH and associated with a higher risk of LVH. To mitigate the intrinsic limitations of each technique, adopting two or more methods simultaneously can bypass and minimize the risk of evaluative error in assessing fluid status, and help reduce cardiovascular risk.

The effect of intensive blood pressure lowering on left ventricular hypertrophy in patients with hypertension: a systematic review and meta-analysis of randomized controlled trials

Background We conducted a comprehensive systematic review to examine the efficacy of intensive blood pressure lowering on the risk of left ventricular hypertrophy (LVH). Methods We searched PubMed, Scopus, Web of Science, Cochrane Central, and EMBASE for all relevant randomized controlled trials. The primary outcome was the incidence of left ventricular hypertrophy. We used the risk ratio (RR) and hazard ratio (HR) with a 95% confidence interval as our effect sizes. Results Four studies, comprising 20,747 patients, were included. Intensive blood pressure lowering was linked with a diminished LVH incidence (RR: 0.66, 95% CI [0.56–0.77]). We also found that intensive blood pressure lowering increased the risk of LVH regression in patients with baseline LVH (RR: 1.21, 95% CI [1.11–1.32]). Finally, intensive blood pressure lowering was linked with a reduced risk of cardiovascular disease (HR: 0.71, 95% CI [0.60–0.85]). No significant heterogeneity was seen in either outcome. Conclusion Our study suggests that intensive blood pressure lowering effectively reduces the risk of LVH and cardiovascular disease. An interactive version of our analysis can be accessed here: https://databoard.shinyapps.io/lvh_hypertophy/

Abstract P493: A Multivariate Analysis of Genetic Risk Scores for Heart Failure and Left Ventricular Mass Derived From Multi-Ancestry Populations and Left Ventricular Mass Amongst African Americans: The Jackson Heart Study

Background: Increased left ventricular (LV) mass is an outcome of LV remodeling that can result in development of left ventricular hypertrophy (LVH), a maladaptive disorder that increases the risk of heart failure. Elevated LV mass is a sensitive predictor of adverse cardiovascular events. African Americans experience a disproportionate burden of heart failure risk and development of LVH. The influence of genetics on this health disparity is unclear and a topic of interest. Genome-wide association studies (GWAS) have uncovered many variants associated with numerous adverse cardiovascular outcomes, such as heart failure and LV phenotypes. However, the relevance of these studies for African Americans may be limited as these analyses have been conducted in multi-ancestry populations with limited representation of African heritage. The question of whether these genetic risk variants can be used to predict LV phenotypes in an independent African American population remains unanswered. Hypothesis: Variant loci that have been associated with heart failure and LV mass in multi-ancestry populations will be associated with LV mass amongst African Americans in the Jackson Heart Study (JHS). Methods: Thirty-nine (39) SNPs associated with heart failure and ten (10) SNPs associated with LV mass were identified from two published studies in which participants of African ancestry or Black individuals comprised less than 15% and 2%, respectively. Using the published effect size estimates, genetic risk scores (GRSs) for heart failure and LV mass were computed for 2,175 African American participants (mean age 55, 63% female) in the JHS with complete data and consent for genetic research. We assessed the linear association of heart failure and LV mass GRSs with LV mass indexed to height (LVM h ) and indexed to body surface area (LVM bsa ). A multivariate general linear model was fit to both LVM h and LVM bsa containing both GRS predictors and accounting for age, sex, BMI (mean 31.5), diabetes (22%), and hypertension (52%). No multicollinearity was noted among these explanatory variables using variance inflation factors. Due to non-constant error variance, a log transformation was conducted on both LV mass response variables. Type III MANOVA Pillai tests were run to assess the effects of the GRSs on the log LVM bsa and log LVM h values. Conclusion: When accounting for age, BMI, sex, diabetes, and hypertension, we found that neither the heart failure GRS (p-val = 0.4012) nor the LV mass GRS (p-val = 0.8332) had an effect on both log LVM bsa and log LVM h . There is insufficient evidence to suggest that heart failure and LV mass variants derived from predominantly European multi-ancestry populations are linearly associated with log LV mass amongst African Americans in the Jackson Heart Study. Our work highlights the need for greater recruitment and targeted studies of populations with African ancestry for GWAS of LV phenotypes.

Cardio-Ankle Vascular Index as a Marker of Left Ventricular Hypertrophy in Treated Hypertensives: Findings From the Pamela Study.

Findings regarding the association between Cardio-Ankle Vascular Index (CAVI) and cardiac hypertension-mediated organ damage (HMOD), such as left ventricular hypertrophy (LVH) assessed by echocardiography, in elderly hypertensive patients are scanty. We sought to investigate this issue in the hypertensive fraction of the general population treated with anti-hypertensive drugs enrolled in the Pressioni Monitorate E Loro Associazioni (PAMELA) study. The study included 239 out of 562 participants who attended the second and third surveys of the PAMELA study performed after 10 and 25 years from the initial evaluation. Data collection included medical history, anthropometric parameters, office, home, ambulatory blood pressure (BP), blood examinations, echocardiography, and CAVI measurements. In the whole study sample (age 69 ± 9 years, 54% males), CAVI was positively correlated with age, office, home, ambulatory systolic BP, LV mass (LVM) index, and negatively associated with body mass index (BMI). In multivariate analysis, CAVI was associated with the LVM index (P < 0.05) independently of major confounders. The participants with LVH exhibited significantly higher CAVI (10.6 ± 2.8 vs. 9.2 ± 1.8 m/s P < 0.001), larger left atrial diameter, and lower LV ejection fraction values than their counterparts without it. The CAVI value of 9.4 m/s was the best cut-off for prediction of LVH in the whole sample. Our study provides new evidence of an independent association between CAVI and LVH in treated elderly hypertensive patients and suggests that the use of this metric of arterial stiffness could not only be used to evaluate vascular damage but also to stratify the risk of LVH.

Patient-Specific Haemodynamic Analysis of Virtual Grafting Strategies in Type-B Aortic Dissection: Impact of Compliance Mismatch.

Compliance mismatch between the aortic wall and Dacron Grafts is a clinical problem concerning aortic haemodynamics and morphological degeneration. The aortic stiffness introduced by grafts can lead to an increased left ventricular (LV) afterload. This study quantifies the impact of compliance mismatch by virtually testing different Type-B aortic dissection (TBAD) surgical grafting strategies in patient-specific, compliant computational fluid dynamics (CFD) simulations. A post-operative case of TBAD was segmented from computed tomography angiography data. Three virtual surgeries were generated using different grafts; two additional cases with compliant grafts were assessed. Compliant CFD simulations were performed using a patient-specific inlet flow rate and three-element Windkessel outlet boundary conditions informed by 2D-Flow MRI data. The wall compliance was calibrated using Cine-MRI images. Pressure, wall shear stress (WSS) indices and energy loss (EL) were computed. Increased aortic stiffness and longer grafts increased aortic pressure and EL. Implementing a compliant graft matching the aortic compliance of the patient reduced the pulse pressure by 11% and EL by 4%. The endothelial cell activation potential (ECAP) differed the most within the aneurysm, where the maximum percentage difference between the reference case and the mid (MDA) and complete (CDA) descending aorta replacements increased by 16% and 20%, respectively. This study suggests that by minimising graft length and matching its compliance to the native aorta whilst aligning with surgical requirements, the risk of LV hypertrophy may be reduced. This provides evidence that compliance-matching grafts may enhance patient outcomes.

The relationship between fetuin-A level and the clinical features of patients with coronary artery disease associated with iron deficiency

The aim of the study: to assess the relationship between the level of fetuin-A and features of clinical hemogram, ferrokinetic parameters, vegetative and structural-functional changes of the myocardium in patients with coronary artery disease (CAD) associated with different stages of iron deficiency (ID). Materials and methods. The study involved 90 patients with CAD: stable angina pectoris II–III FC (35 men and 55 women, age – 69 (61; 72)). All patients were divided into 4 clinical groups depending on the parameters of iron metabolism and hemogram: I (n = 16) – patients with absolute ID, II (n = 15) – with latent ID, III (n = 14) – with functional ID; IV (n = 45) – patients CAD without iron metabolism disorders. The physiological concentration of fetuin-A was determined in 15 conditionally healthy people. The results of echocardioscopy, Holter ECG monitoring and their relationship with the level of fetuin-A were analyzed. Results. In patients with CAD associated with various stages of ID, there is a decrease in the concentration of fetuin-A in direct proportion to the degree of progression of sideropenia was established. It was established that there is a relationship between the level of fetuin-A and the concentration of ferritin and transferrin saturation for patients with absolute ID as well as the number of erythrocytes in patients with functional ID. It was established that there is a relationship between the level of fetuin-A and PWd (rs = -0.60, p &lt; 0.05) for patients with absolute ID; for patients with latent ID – with the E/A ratio (rs = +0.66, p &lt; 0.05). In patients with absolute ID and latent ID a number of correlations between fetuin-A level and heart rate variability indicators in active and passive periods was established. The presence of a low level of fetuin-A in patients with CAD and ID increased the risk of left ventricular hypertrophy by 1.5 times, left ventricular diastolic dysfunction by 1.6 times, autonomic dysfunction by 2.14 times in the active period and 1.95 times in the passive period. Conclusions. In patients with CAD, there is a progressive decrease in the fetuin-A level depending on the degree of ID, which contributes to the deepening of disorders of iron metabolism and clinical hemogram, negatively affects the structural and functional state of the myocardium and heart rate variability, increases the risk of developing myocardial hypertrophy, left ventricular diastolic dysfunction and vegetative imbalance.

Early Famine Exposure Results in Left Ventricular Remodeled, Diastolic Dysfunction and Systolic Function Preserved in Adults

Introduction: Malnutrition during a critical window of development in a fetus or infant can result in abnormal cardiac remodeling and function. It is uncertain whether the contribution of these effects continues to impact the cardiac remodeling and function of adults over the course of several decades of growth. Our study examined the impact of early Chinese famine exposure on cardiac remodeling, left ventricular (LV) diastolic function, and LV systolic function in adults. Methods: Participants at high risk of cardiovascular disease from the China Patient-Centered Evaluative Assessment of Cardiac Events Million Persons Project (PEACE MPP) were enrolled. The famine in China lasted from 1959 to 1962. A total of three groups were formed based on the participants’ birth dates: pre-famine group, famine exposure group, and post-famine group. Logistic regression and linear mixed models were used to explore the association between famine exposure and cardiac remodeling, LV diastolic function and LV systolic function in adults. Results: The study included 2,758 participants, the mean age was 57.05 years, 62.8% were female, 26.4% had LV hypertrophy (LVH), 59.6% had LV diastolic dysfunction (LVDD), and 10.5% had reduced global longitudinal strain (GLS). Compared to post-famine exposure, participants had independently increased risk of LVH in the famine exposure group (OR: 2.02, 95% CI: 1.60–2.56) and pre-famine exposure (OR: 1.36, 95% CI: 1.06–1.76). Compared to post-famine exposure, the risk of LVDD remarkably increased in the famine exposure group (OR: 3.04, 95% CI: 2.49–3.71) and pre-famine exposure group (OR: 1.87, 95% CI: 1.52–2.31). Famine exposure had no significant impact on GLS but was associated with a significant increase in LV ejection fraction (LVEF) and LV end-diastolic diameter (LVEDD). Significant interactions were observed between the effects of famine exposure and other clinical/sociodemographic variables (gender, systolic blood pressure [SBP] ≥140 mm Hg or not, high school or above or not, and annual income <50,000 RMB or not) on these outcomes. Conclusion: Exposure to famine, particularly during fetal and infant stages, increases the risk of LVH and LVDD in adults. However, the LV systolic function remains preserved. These impacts are more pronounced in females, individuals with SBP ≥140 mm Hg, those with low income, or those with high educational status.

The correlation between serum fibroblast growth factor-23 levels and left ventricular hypertrophy in chronic kidney disease patients

Introduction: Hyperphosphatemia in chronic kidney disease (CKD) patients can stimulate the production of the fibroblast growth factor-23 (FGF-23) phosphatonin hormone, which is associated with cardiac remodeling resulting in left ventricular hypertrophy (LVH). Objectives: To determine the correlation between FGF-23 level and LVH incidence in CKD patients and establish the associated risk factors. Materials and Methods: This cross-sectional study involved 74 CKD patients who were classified as stage 3 (n=18), stage 4 (n=17), stage 3 (n=18), dialysis stage 5 (n=20), or non-dialysis stage 5 (n=19). The FGF-23 levels of the patients were measured using the ELISA (enzyme-linked immunosorbent assay) kit method, whereas a cardiologist verified LVH using an echocardiographic examination based on the LVH criteria of &gt;95 g/m2 for females and &gt;115 g/m2 for males. Results: A significant difference was observed in the mean FGF-23 values between the LVH and non-LVH patients (443.27±437.047 RU/mL and 172.68±185.56 RU/mL, respectively; P&lt;0.05). The receiver operating characteristics revealed that patients with FGF-23 levels &gt;123.95 RU/mL had a 3.6 times greater risk of LVH compared to those with values ≤123.95 RU/mL. The LVH risk factors of gender and age, as well as hypertension, diabetes mellitus, and obesity diagnoses were not associated with LVH incidence in CKD patients. Conclusion: A significant association was found between FGF-23 level and LVH incidence in CKD patients, in which an FGF-23 level &gt;123.95 RU/mL corresponded to a 3.6 times greater risk of LVH than those with FGF-23 levels below this value.

Association of lipoprotein(a) with left ventricular hypertrophy assessed by electrocardiogram in adults: a large cross-sectional study.

Increasing evidence supports a causal relationship between lipoprotein(a) [Lp(a)] and atherosclerotic cardiovascular disease, yet its association with left ventricular hypertrophy (LVH) assessed by electrocardiogram (ECG) remains unknown. The aim of this study was to explore the relationship between Lp(a) and LVH assessed by ECG in general population. In this cross-sectional study, we screened 4,052 adults from the participants of the third National Health and Nutrition Examination Survey for analysis. Lp(a) was regarded as an exposure variable. LVH defined by the left ventricular mass index estimated from ECG was considered as an outcome variable. Multivariate logistic regression and restricted cubic spline (RCS) were used to assess the relationship between Lp(a) and LVH. Individuals with LVH had higher Lp(a) compared to individuals without LVH (P< 0.001). In the fully adjusted model, Lp(a) was strongly associated with LVH when as a continuous variable (per 1-unit increment, OR: 1.366, 95% CI: 1.043-1.789, P = 0.024), and higher Lp(a) remained independently associated with a higher risk of LVH when participants were divided into four groups according to quartiles of Lp(a) (Q4 vs Q1, OR: 1.508, 95% CI: 1.185-1.918, P = 0.001). And in subgroup analysis, this association remained significant among participants< 60 years, ≥ 60 years, male, with body mass index< 30 kg/m2, with hypertension and without diabetes (P< 0.05). In addition, we did not observe a nonlinear and threshold effect of Lp(a) with LVH in the RCS analysis (P for nonlinearity = 0.113). Lp(a) was closely associated with LVH assessed by ECG in general population.

Association between Sleep Duration and Left Ventricular Hypertrophy for Patients with Type 2 Diabetes Mellitus.

In this study, we aimed to estimate the impact of sleep duration on left ventricular hypertrophy (LVH) in type 2 diabetes mellitus (T2DM). Consecutive patients with T2DM undergoing transthoracic echocardiography (TTE) in our center from October 2017 to February 2021 were analyzed. The association of the risk of LVH in T2DM patients was evaluated using univariable and multivariable logistic regression analyses. This study finally included 2689 adult patients (mean age 51.8 ± 12.5 years, 56.2% men, mean sleep duration 7.6 ± 1.4 hours per day). Of all patients, 655 (24.4%) patients were diagnosed with LVH and 2034 did not have LVH. All patients were adults and were diagnosed with T2DM. In the univariate and multivariate regression analyses, gender, sleep duration, body mass index (BMI), waist, hemoglobin (Hb), blood creatinine (Cr), and high-density lipoprotein cholesterol (HDL-c) were associated with LVH. In the restricted cubic spline (RCS) model, the cut-off points of sleep duration given refer to the group of patients with T2DM and LVH were 8 hours per day. With the cut-off points, the multivariable analysis demonstrated that, for diabetic patients, LVH was significantly correlated with a sleep duration of 8 hours per day, hemoglobin, blood urea nitrogen (BUN), and HDL-c. For patients with T2DM, long sleep duration (>8 hours per day), hemoglobin, BUN, and HDL-c were independently associated with LVH. This trial is registered with NCT03811470.

Nighttime blood pressure and glucose control impacts on left ventricular hypertrophy: The Japan Morning Surge Home Blood Pressure (J-HOP) Study.

Several studies investigated the association between nighttime blood pressure (BP) and left ventricular hypertrophy (LVH) in diabetes, but since most of these studies were conducted in diabetes populations only, they did not compare differences in the impact of nighttime BP on LVH in subjects without diabetes. Moreover, data about the impact of glucose control in diabetes on the relationship between nighttime BP and LVH are sparse. We classified 1277 adults (age 64.7 ± 11.8 years) performing ambulatory BP monitoring while enrolled as part of the Japan Morning Surge Home Blood Pressure (J-HOP) study into groups according to the control status of daytime BP (systolic BP [SBP] < 135 mmHg or ≥135 mmHg), nighttime BP (SBP < 120 mmHg or ≥120 mmHg), and diabetes (HbA1c < 7.0% or ≥7.0%). LVH was assessed by echocardiography. LVH according to echocardiographic criteria was identified in 33.7% of the participants. The group with poorly controlled diabetes plus uncontrolled nighttime BP (n = 90) had a 2.1-fold higher risk of LVH compared to the group with controlled nighttime BP and non-diabetes (n = 505) (odds ratio [OR] 2.10, 95% confidence interval [CI]: 1.29-3.44). No association was observed between uncontrolled daytime BP and diabetes for LVH. In the participants with poorly controlled diabetes (n = 146), uncontrolled nighttime BP posed a 3.1-fold higher risk of LVH compared to controlled nighttime BP (OR 3.12, 95%CI: 1.47-6.62). This association was not found in controlled diabetes. Uncontrolled nighttime BP was associated with a risk of LVH, especially among individuals with poorly controlled diabetes.

Influence of hypertension and global or abdominal obesity on left ventricular hypertrophy: A cross-sectional study.

Although hypertension and obesity are both risk factors for left ventricular hypertrophy (LVH), the extent of their impact on LVH in the general population is still unclear, and the predictive value of obesity indicators for LVH remains to be elucidated. In this study, obesity-related indicators, including waist circumference (WC), waist-height ratio (WHTR), and waist-hip ratio (WHR), were used to define abdominal obesity (AO), whereas body mass index (BMI) was used to measure general obesity (GO). The effects of hypertension and obesity on LVH were estimated using logistic regression analysis, as was the relative risk of LVH based on the presence of obesity, hypertension, or both. Subgroup analyses were performed based on sex and age. Of the 9134 participants (≥35 years old), 915 (10.0%) developed LVH. After adjusting for covariates, the odds ratios (95% confidence intervals) for LVH were 3.94 (3.27-4.75) in patients with hypertension, 1.90 (1.60-2.26) in those with GO, and 1.45 (1.25-1.69), 1.69 (1.43-2.00), and 1.54 (1.33-4.75) in individuals with AO defined based on WC, WHTR, and WHR, respectively. Analysis by sex showed similar values in women, but AO based on WC and WHR were not significantly associated with LVH in men. Further, after adjusting for potential confounding factors, concomitant hypertension and obesity had an increased risk of developing LVH in all age ranges, particularly in patients aged 35-45 years (risk increased 14.14-fold, 10.84-fold, 7.97-fold, and 9.95-fold for BMI-based GO and WC-, WHTR-, and WHR-based AO, respectively), and in both men and women but particularly in men (risk increased 7.71-fold, 4.67-fold, 5.83-fold, and 5.58-fold, respectively). In summary, all obesity indicators (BMI, WC, WHTR, and WHR) had predictive value for LVH in women; however, only BMI and WHTR should be considered for men. Furthermore, monitoring for the occurrence and progression of LVH is imperative for rural Chinese patients with concomitant hypertension and obesity, especially men and those aged 35-45 years.

Left Ventricular Hypertrophy Geometry and Vascular Calcification Co-Modify the Risk of Cardiovascular Mortality in Patients with End-Stage Kidney Disease: A Retrospective Cohort Study.

Patients with end-stage kidney disease (ESKD) have an unparalleled risk of left ventricular hypertrophy (LVH) and vascular calcification (VC), both of which introduce excessive cardiovascular risk. However, it remains unclear whether LVH geometry co-modulates cardiovascular outcomes with VC in this population. A retrospective cohort study was conducted. Patients with ESKD requiring chronic hemodialysis were identified from Shin Kong Wu Ho-Su Memorial Hospital between October and December 2018, with echocardiographic LVH geometry and aortic arch calcification (AoAC) determined. They were divided into four groups according to AoAC severity and eccentric or concentric LVH. We used Kaplan-Meier analysis and Cox proportional hazard regression to analyze their cardiovascular and all-cause mortality after multivariate adjustment. Overall, 223 patients with ESKD with LVH were analyzed, among whom 29.1%, 23.3%, 25.1%, and 22.4% had non-to-mild AoAC with eccentric and concentric LVH and moderate-to-severe AoAC with eccentric and concentric LVH, respectively. After 3.5 years of follow-up, patients with ESKD with moderate-to-severe AoAC and concentric LVH had a significantly higher risk of cardiovascular mortality than those with non-to-mild AoAC and eccentric LVH (hazard ratio 3.35, p=0.002). However, those with moderate-to-severe AoAC but eccentric LVH did not have higher cardiovascular mortality. Similarly, patients with ESKD with moderate-to-severe AoAC and concentric LVH had a significantly higher all-cause mortality than those with non-to-mild AoAC and eccentric LVH, whereas the other two groups did not have higher risk. LVH geometry could help stratify the risk of patients with ESKD when they had severe VC, and co-existing severe VC and concentric LVH aggravated cardiovascular risk.

Association between clustering of cardiovascular risk factors and left ventricular geometric remodeling in Chinese children.

Several cardiovascular (CV) risk factors are reported to be associated with abnormal cardiac structure in children and adults. However, no study has assessed the association between clustering of multiple CV risk factors and left ventricular geometric (LVG) remodeling. We examined the association between clustering of CV risk factors and LVG remodeling among Chinese children. This cross-sectional study included 1,406 children aged 6-11 years. Clustering of CV risk factors was quantified as the sum of the number of five CV risk factors (abdominal obesity, elevated blood pressure, high fasting blood glucose, high triglycerides and low high-density lipoprotein cholesterol). Based on left ventricular mass index and relative wall thickness (RWT), left ventricular hypertrophy (LVH), high RWT and LVG remodeling [concentric remodeling (CR), eccentric hypertrophy (EH) and concentric hypertrophy (CH)] were defined. Compared to participants without CV risk factor, those with 1, 2 and ≥3 risk factors were at increased risk of LVH [ORs (95% CIs): 3.49 (2.19-5.56), 5.53 (3.20-9.55), and 19.19 (9.67-38.08), respectively]; corresponding values for high RWT were 2.47 (1.63-3.74), 3.76 (2.25-6.27), and 5.47 (2.65-11.28). Similar associations between clustering of CV risk factors and LVG remodeling were found [CR: 1.71 (1.06-2.76), 2.83 (1.54-5.18), and 3.82 (1.37-10.62); EH: 2.42 (1.42-4.11), 4.23 (2.24-7.96), and 16.86 (7.70-36.92); CH: 14.92 (4.41-50.47), 23.15 (6.32-84.83), and 71.19 (17.09-296.56)]. CV risk factors in isolation and combination were associated with an increased risk of LVH, high RWT and LVG remodeling among children, emphasizing the need to consider multiple risk factors when assessing the risk of cardiac outcomes.

Association of depression with hypertensive left ventricular hypertrophy in age, sex, and education level-specific differences.

Previous studies have shown that hypertension and depression are associated with worse cardiovascular outcomes and reduced quality of life. Left ventricular hypertrophy (LVH) is strongly linked to increased mortality and cardiovascular disease, and depression may be one of the key factors contributing to hypertensive LVH. The authors consecutively enrolled 353 patients with uncomplicated hypertension between November 2017 and May 2021. All participants completed the Hamilton Depression Scale (HAM-D) to assess their depression status, with depression defined as a HAM-D score of 20 or higher. Linear regression analysis revealed a positive association between HAM-D and LVMI (adjusted β, 1.51, 95% CI, 1.19-1.83, p<.001). Logistic regression models showed that individuals with hypertension and depression had a higher risk of LVH than those with hypertension alone (adjusted OR, 2.51, 95% CI, 1.14-5.52, p=.022). The association between depression and LVH significantly interacted with age, sex, education levels, but not BMI and household income. Following age, sex, and education levels stratification, an independent association of depression and LVH was observed only in age<60 years (age<60 years: OR, 7.36, 95% CI, 2.25-24.13, p<.001), male (male: OR, 16.16, 95% CI, 3.80-68.73, p<.001), and higher education levels (high school and above: OR, 11.09, 95% CI, 2.91-42.22, p<.001). Our findings suggest that depression is a significant risk factor for LVH in hypertensive patients, particularly in those who are under 60 years of age, male, and have higher education levels.

24-LB: Diabetic Microvascular Disease Is Associated with Left Ventricular Hypertrophy in Patients with Type 2 Diabetes Mellitus

Background: Left ventricular hypertrophy (LVH) is an important feature in patients with diabetes mellitus and increased the risk of cardiac events. The pathophysiology of LVH in diabetes mellitus remains unclear and is not fully explained by hyperglycemia and hypertension. Microvascular diseases, the most common and specific complications of diabetes mellitus, which may be involved in LVH. Therefore, we aimed to explore the association between diabetic microvascular diseases and LVH in patients with type 2 diabetes mellitus (T2DM). Material and methods: In the cross-sectional study, we enrolled 2912 patients with T2DM, including 360 patients with LVH. Demographic data, medical history, anthropometric indices, laboratory examination, diabetic microvascular diseases and cardiac ultrasound index were collected. Correlation analysis and regression analysis were performed to analyze the relationship between diabetic microvascular diseases and LVH in whole population and in gender subgroup. Result: Patients with LVH were older and had larger BMI, waist circumference and hip circumference. And a higher proportion of males had LVH compared with females. Patients with LVH had a larger proportion of hypertension, coronary heart disease, diabetic retinopathy (DR), and diabetic kidney disease (DKD). After adjusting potential confounding factors, patients with one or two microvascular diseases especially DR and DKD, had more possibility of LVH (OR = 1.287 and OR = 2.118 respectively). In gender subgroup analysis, microvascular diseases obviously increased the risk of LVH, especially in males. Moreover, the risk of LVH gradually increased with the number of diabetic microvascular diseases. Conclusions: Diabetic microvascular diseases, especially DR and DKD, were positively and independently associated with LVH in T2DM. In addition, the risk of LVH obviously increased with the number of microvascular diseases in male. Disclosure J. Ke: None. X. Feng: None. L. Zhu: None. Y. Xu: None. S. Liu: None. L. Yang: None. D. Zhao: None.

Amino acid homeostasis is a target of metformin therapy

ObjectiveUnexplained changes in regulation of branched chain amino acids (BCAA) during diabetes therapy with metformin have been known for years. Here we have investigated mechanisms underlying this effect. MethodsWe used cellular approaches, including single gene/protein measurements, as well as systems-level proteomics. Findings were then cross-validated with electronic health records and other data from human material. ResultsIn cell studies, we observed diminished uptake/incorporation of amino acids following metformin treatment of liver cells and cardiac myocytes. Supplementation of media with amino acids attenuated known effects of the drug, including on glucose production, providing a possible explanation for discrepancies between effective doses in vivo and in vitro observed in most studies. Data-Independent Acquisition proteomics identified that SNAT2, which mediates tertiary control of BCAA uptake, was the most strongly suppressed amino acid transporter in liver cells following metformin treatment. Other transporters were affected to a lesser extent. In humans, metformin attenuated increased risk of left ventricular hypertrophy due to the AA allele of KLF15, which is an inducer of BCAA catabolism. In plasma from a double-blind placebo-controlled trial in nondiabetic heart failure (trial registration: NCT00473876), metformin caused selective accumulation of plasma BCAA and glutamine, consistent with the effects in cells. ConclusionsMetformin restricts tertiary control of BCAA cellular uptake. We conclude that modulation of amino acid homeostasis contributes to therapeutic actions of the drug.

Hepatic and Systemic Inflammation for Left Ventricular Mass in Physically Fit Adults: CHIEF Heart Study.

Both low-grade systemic and hepatic inflammation could result in increased left ventricular mass (LVM) in the general population. However, the associations, which might be modified by exercise, have not been clarified in physically active young adults. The study included 2,004 military males aged 18-43 years in eastern Taiwan. Systemic and hepatic inflammation was defined by the upper tertiles of blood white blood cell (WBC) counts (7.51-11.00 x 103/μL) and serum alanine aminotransferase (ALT: 30-120 U/L), respectively. LVM indexed for the body height ≥49 g/m2.7 was defined as left ventricular hypertrophy (LVH) based on echocardiography. Multiple logistic regression analysis adjusting for age, smoking, alcohol intake, physical fitness, and metabolic syndrome was utilized to determine the associations. As compared to the lower WBC/lower ALT group, there tended to have an increased risk of LVH with the higher WBC/lower ALT group, the lower WBC/higher ALT group, and the higher WBC/higher ALT group [odds ratios: 0.89 (95% confidence intervals (CI): 0.41-1.94), 1.90 (95% CI: 0.86-4.22) and 2.48 (95% CI: 1.04-5.92); p-value for trend = 0.01]. Our study suggested that in physically active males, those with hepatic inflammation rather than low-grade systemic inflammation had a higher risk of LVH. Hepatic injury might be relevant to LVH as an early sign of end-organ damage regardless of physical fitness in young adults.

Establishment of an Individual-Specific Nomogram for Predicting the Risk of Left Ventricular Hypertrophy in Chinese Postmenopausal Hypertensive Women.

Background and Objectives: The physiological phenomenon peculiar to women, namely menopause, makes the occurrence of left ventricular hypertrophy (LVH) in postmenopausal hypertensive women more characteristic. Less is known about the risk of developing LVH in Chinese postmenopausal hypertensive women. Thus, the present study was intended to design a nomogram for predicting the risk of developing LVH in Chinese postmenopausal hypertensive women. Materials and Methods: Postmenopausal hypertensive women aged between 49 and 68 years were divided into either the training set (n = 550) or the validation set (n = 284) in a 2:1 ratio. Patients in the validation set were followed up for one year. A stepwise multivariable logistic regression model was used to assess the predictors of LVH in postmenopausal women with hypertension. The best-fit nomogram was executed using R software. The calibration and decision curve were employed to verify the predictive accuracy of the nomogram. The results were evaluated in the validation set. Results: Menopause age (OR = 0.929, 95% CI 0.866-0.998, p = 0.044), BMI (OR = 1.067, 95% CI 1.019-1.116, p = 0.005), morning systolic blood pressure (SBP: OR = 1.050, 95% CI 1.032-1.069, p = 0.000), morning diastolic BP (DBP OR = 1.055, 95% CI 1.028-1.083, p = 0.003), angiotensin II receptor blocker (ARB) utilization rate (OR = 0.219, 95% CI 0.131-0.365, p = 0.000), LDL-C (OR = 1.460, 95% CI 1.090-1.954, p = 0.011) and cardio-ankle vascular index (CAVI) (OR = 1.415, 95% CI 1.139-1.757, p = 0.028) were associated with LVH in postmenopausal hypertension patients. The nomogram model was then developed using these variables. The internal validation trial showed that the nomogram model described herein had good performance in discriminating a C-index of 0.881 (95% CI: 0.837-0.924) and high quality of calibration plots. External validation of LVH-predictive nomogram results showed that the area under the ROC curve was 0.903 (95%CI 0.900-0.907). Conclusions: Our results indicate that the risk prediction nomogram model based on menopausal age, BMI, morning SBP, morning DBP, ARB utilization rate, LDL-C and CAVI has good accuracy and may provide useful references for the medical staff in the intuitive and individualized risk assessment in clinical practice.

Prevalence of masked hypertension and its association with left ventricular hypertrophy in children and young adults with chronic kidney disease: a systematic review and meta-analysis.

There are limited studies using ambulatory blood pressure monitoring (ABPM) to assess blood pressure (BP) status in young patients with chronic kidney disease (CKD) on dialysis or after kidney transplantation. The aim of this meta-analysis is to estimate the prevalence of both white-coat hypertension (WCH) and masked hypertension, along with the prevalence of left ventricular hypertrophy (LVH), in children and young adults with CKD on dialysis or after kidney transplantation. We performed a systematic review and meta-analysis of observational studies assessing the prevalence of BP phenotypes using ABPM, in children and young adults with CKD stages 2-5d. Records were identified by search in databases (Medline, Web of Science, CENTRAL) and sources of grey literature, until 31 December 2021. A random-effects meta-analysis of proportions (double arcsine transformation) was conducted. Ten studies were included in the systematic review, reporting data from 1140 individuals (children and young adults with CKD with a mean age of 13.79 ± 4.35 years). Masked hypertension and WCH were diagnosed in 301 and 76 patients, respectively. It was estimated an overall pooled masked hypertension prevalence of 27% [95% confidence interval (95% CI) 18-36, I2 = 87%] and an overall pooled WCH prevalence of 6% (95% CI 3-9, I2 = 78%). Among kidney transplant recipients, masked hypertension had a prevalence of 29% (95% CI 14-47, I2 = 86%). The prevalence of LVH was found 28% (95% CI 0.19-0.39) in a total of 238 CKD patients with ambulatory hypertension. In 172 CKD patients with masked hypertension, LVH was present in 49, with the estimated prevalence being 23% (95% CI 0.15-0.32). Masked hypertension has a significant prevalence in children and young adults with CKD. Masked hypertension carries an adverse prognosis, with an increased risk of LVH, warranting clinical attention when assessing cardiovascular risk in this population. Therefore, ABPM and echocardiography is of high importance when assessing BP status in children with CKD. 10.17605/OSF.IO/UKXAF.