Left Ventricular Hypertrophy Index Research Articles

#2406 Echocardiographic characteristics of autosomal dominant polycystic kidney disease

Abstract Background and Aims Cardiovascular complications in patients with autosomal dominant polycystic kidney disease (ADPKD) are one of the most frequently investigated extrarenal manifestations. The results are many times contradictory. This is caused by a limited size of studied populations and high inter- and intrafamilial heterogeneity of ADPKD. Expanding knowledge of populations of patients from different regions and cohorts is crucial for improving the understanding and treatment of cardiovascular morbidity and mortality. This study aims to explore the prevalence of cardiovascular abnormalities in echocardiography and to analyze their relationships with clinical characteristics across different stages of CKD progression in patients with ADPKD. Method Sixty-eight patients were included in the study. All patients underwent transthoracic echocardiography with the use of GE Vingmed Ultrasound (GE Norway Health Tech, Oslo, Norway). Information about demography, prior medical history and taking antihypertension drugs was recorded. The results of creatinine, lipids and haemoglobin were collected. To diagnose the rapid progression of CKD, creatinine was sampled twice, in a one-year interval. Results Using different indicators of left ventricular hypertrophy (LVH), we found it in above 40% of ADPKD patients. A single associate of left ventricular mass was eGFR decline after one year of observation. Other highly prevalent findings were asymptomatic left ventricular diastolic dysfunction (ALVDD) (39%), left atrium (LA) enlargement (39%) and mild valvular regurgitations (80%). Ejection fraction, aortic root dimension, tricuspid annular plane systolic excursion (TAPSE) and prevalence of mitral valve prolapse were not importantly increased. Apart from age, the strong determinant of ALVDD diagnosis was the treatment with beta-blockers. Cardiac indices were not different across the eGFR stages. Conclusion LVH, LA enlargement, ALVDD and valvular regurgitations are characteristics of cardiac phenotype in ADPKD. Cardiac indices were not different across different stages of CKD pointing towards the diagnosis of ADPKD being main drive of their occurrence.

Impact of enzyme replacement therapy and migalastat on left atrial strain and cardiomyopathy in patients with Fabry disease.

Cardiomyopathy in Fabry disease (FD) is a major determinant of morbidity and mortality. This study investigates the effects of FD-specific treatment using enzyme replacement therapy (ERT) and chaperone therapy on left atrial (LA) function using two-dimensional speckle tracking echocardiography (2DSTE). In this prospective observational single-center study, 20 FD patients [10 (50%) females] treated with migalastat, 48 FD patients [24 (50%) females] treated with ERT (agalsidase-alfa and agalsidase-beta), and 30 untreated FD patients (all females) as controls were analyzed. The mean follow-up time ranged from 26 to 81 months. 2DSTE was performed for left ventricle strain, right ventricle strain, and LA strain (LAS). FD-specific treated patients presented with increased left ventricular mass index (LVMi) and higher frequency of left ventricular hypertrophy at baseline, whereas untreated control patients showed normal baseline values. FD-specific treated (including migalastat and ERT) patients showed stabilization of LAS over time (p > 0.05). LVMi was also stable in treated FD patients during observation (p > 0.05). In patients with FD, treated with either ERT or chaperone therapy, LAS values measured by echocardiographic speckle tracking were stable over time, pointing toward disease stabilization.

Abstract 072: Risk Factors for Developing Ischemic Strokes While Taking Non‐Vitamin K Antagonist Oral Anticoagulants

Introduction Over the past decade, non‐vitamin K antagonist oral anticoagulants (NOACs) have replaced warfarin as the initial strategy for stroke prevention in non‐valvular atrial fibrillation. However, ischemic strokes occurring in patients taking NOACs are becoming increasingly more frequent. In this study, we aimed to determine the clinical, echocardiographic, and neuroimaging markers associated with developing ischemic strokes in patients taking NOACs for atrial fibrillation. Methods Among atrial fibrillation patients on NOACs with and without ischemic stroke, brain MRIs were reviewed for the presence of neuroimaging markers of small vessel disease. Transthoracic echocardiography reports were reviewed to obtain left atrial volumes, presence of left ventricular hypertrophy, ejection fractions, and presence of wall motion abnormalities. Clinical and radiologic variables with significant differences between groups were entered into a multivariable regression model to determine predictors of ischemic stroke. In the ischemic stroke group, a Cox regression analysis was constructed to determine predictors of ischemic stroke recurrence during follow‐up. Results 112 patients with ischemic stroke and 94 controls (free of ischemic stroke) were included in the study. The mean age (77±9 years vs. 74±11 years, p = 0.13) and proportion of patients with CHA2DS2‐VASc>2 were similar between controls and ischemic stroke patients (82% vs. 83%, p = 0.86). The variables that were significantly different between groups included apixaban use, dabigatran use, prior cerebrovascular events, hemoglobin A1c (HbA1c), left ventricular hypertrophy, left atrial volume index, and severe white matter hyperintensities. After multivariable adjustment, prior cerebrovascular events (aOR 23.86, 95% CI [6.02–94.48]), HbA1c levels (aOR 2.36, 95% CI [1.39–3.99]), left ventricular hypertrophy (aOR 2.73, 95% CI [1.11–6.71]) and left atrial volume index (aOR 1.05, 95% CI [1.01–1.08]) increased the risk of stroke, whereas apixaban use appeared to decrease the risk (aOR 0.38, 95% CI [0.16–0.92]). Among patients with ischemic stroke, there were 103 survivors, 82 (80%) of which had follow‐up data. The median follow‐up duration for these patients was 2.6 (0.5–4.7) years. Of these 82 patients, 11 (13%) experienced an ischemic stroke during the follow‐up period. Malignancy was associated with ischemic stroke recurrence (aHR 4.90, 95% CI [1.35–18.42]) after adjustment for age and chronic renal failure. Conclusion Prior cerebrovascular events, diabetes, left ventricular hypertrophy, and left atrial size are associated with the development of ischemic stroke among NOAC users. Future studies should aim to investigate nonpharmacological stroke prevention strategies in patients with the vascular risk factors and echocardiographic risk markers identified in the present study.

LBBB and heart failure-Relationships among QRS amplitude, duration, height, LV mass, and sex.

Height, left ventricular (LV) size, and sex were proposed as additional criteria for patient selection for cardiac resynchronization therapy (CRT) but their connections with the QRS complex in left bundle branch block (LBBB) are little investigated. We evaluated these. Among patients with "true" LBBB, QRS duration (QRSd) and amplitude, and LV hypertrophy indices, were correlated with patient's height and LV mass, and compared between sexes. In this study cohort (n = 220; 60 ± 12 years; left ventricular ejection fraction [LVEF] 21 ± 7%; mostly New York Heart Association II-III, QRSd 165 ± 19 ms; 57% female; 70% responders [LVEF increased ≥5%]), LV mass was increased in all patients. QRS amplitude did not correlate with LV mass or height in any individual lead or with Sokolow-Lyon or Cornell-Lyon indices. QRSd did not correlate with height. In contrast, QRSd correlated strongly with LV mass (r = .51). CRT response rate was greater in women versus men (84% vs. 58%, p < .001) despite shorter QRSd [7% shorter (p < .0001)]. QRSd normalized for height resulted in a 2.7% and for LV mass 24% greater index in women. True LBBB criteria do not exclude HF patients with increased LV mass. QRS amplitudes do not correlate with height or LV mass. Height does not affect QRSd. However, QRSd correlates with LV size. QRSd normalized for LV mass results in 24% greater value in women in the direction of sex-specific responses. LV mass may be a significant nonelectrical modifier of QRSd for CRT.

Antidiabetic and Cardioprotective effect of Terminalia phillyreifolia (Van Heurck and Mull. Arg.) Gere and Boatwr. bark extract in Experimental animals

Objective: Objective of the current study was to evaluate the effect of methanolic extract of Terminalia phillyreifolia (Van Heurck and Müll. Arg.) Gere and Boatwr. (TP) bark in Type 2 diabetes mellitus and cardiovascular complications. Methods: Diabetes mellitus was induced in Wistar rats by administration of fructose and streptozotocin (40mg/kg, i.p.). TP bark extract was administered to diabetic animals at doses of 100mg/kg and 300mg/kg for 12 weeks. Glibenclamide (5mg/kg/day, p.o.) was administered as standard treatment. Various biochemical and functional parameters were evaluated at appropriate time intervals. Results: Methanolic extract of TP bark produced statistically significant (p&lt; 0.05) hypoglycemic and antioxidant effect. Treatment with extract resulted in significant reduction in plasma glucose, HbA1C, lipid levels and oxidative stress parameters. TP treated rats demonstrated significantly lower insulin resistance and improved β cell function as compared to untreated diabetic rats. TP treatment resulted in improvement in cardiac and left ventricular hypertrophy as reflected by lower cardiac and left ventricular hypertrophy index. It could successfully improve the levels of cardiac enzyme markers such as LDH and CK-MB levels in a dose dependent manner. TP treatment could also efficiently prevent abnormalities of haemodynamic parameters such as mean blood pressure and heart rate. Conclusion: The results suggest that methanolic extract of TP bark exerted hypoglycemic effect in diabetic rats, comparable to that of standard. TP bark extract treatment was also able to inhibit development of cardiomyopathy in diabetic animals.

Abstract 094: Sex-specific Effects Of Sleep Apnea And Medication-treated Depression On Left Ventricular Mass Index And 3D Left Ventricular Global Longitudinal Strain In The CARDIA Study

Background: Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. CVD risk increases with age; however, sex differences are known to significantly affect progression and survival. We designed this study to assess CVD-related risks associated with depression, sleep apnea, and depression comorbid with sleep apnea, in a biracial cohort of middle-aged men and women. We assessed outcomes such as left ventricular mass index (LVMI)-an index of left ventricular hypertrophy, and 3D left ventricular global longitudinal strain (3D LVGLS), an index of global myocardial function. Methods: Data were obtained from the Coronary Artery Risk Development in Young Adults (CARDIA) Study from black and white men and women (n=2778) who attended visit 9 (year 30 of follow-up) echocardiography scan. Demographics and diagnoses of depression and sleep apnea were obtained from visit 8 (year 25 of follow-up). Binary logistic regression was used to asses factors associated with high blood pressure (BP &gt; 130/80 mmHg) and heart failure with reduced ejection fraction (HFrEF). Linear regression analyses were used to assess the strength of the following predictors: race, age, depression diagnosis and medication use for depression on LVMI and 3D LVGLS. Results: In men, depression alone and comorbid with sleep apnea were associated with higher risk of BP &gt;130/80mmHg (OR = 1.47, p = 0.036 and OR = 2.739, p = 0.006, respectively). In both men and women (median age 55), black race was significantly associated with LVMI (p = 0.008 and p &lt;0.001, respectively). Additional predictors of LVMI found in women were age (p = 0.019) and current medication use for depression (p = 0.006). Black race and current use of medications for depression were significantly associated with 3D LVGLS in both men (p &lt;0.001 and p = 0.029, respectively) and women (p &lt; 0.001 and p = 0.007, respectively). Conclusion: Our results suggest that in middle-aged women, but not men, medication-treated depression is a significant predictor of LVMI. The sex differences were not observed for 3D LVGLS. These results suggest that the severity of depression (i.e. necessitating medication use) may be an important predictor of CVD, especially in women. However, a direct effect of these medications on CVD may occur.

Central blood pressure obtained by cuff-based oscillometry as a determinant of left ventricular hypertrophy in hypertensive patients.

Limited and conflicting data have been reported on the prognostic relevance of central blood pressure (CBP) compared with brachial blood pressure (BP) in the anticipation of hypertension-mediated organ damage and the majority of data derived using applanation tonometry with its known complexities. The objective of the present study was to investigate the diagnostic factors of left ventricular hypertrophy (LVH) with a special highlight on the utility of non-invasive oscillometric CBP measurement and derived hemodynamic indices compared to brachial BP as indicators of LVH. This cross-sectional study included 300 hypertensive patients (mean age 55.3 years, 61.3% female, 51.7% obese) with a mean duration of hypertension was 5.8 years. They underwent measurement of brachial BP, using a mercury sphygmomanometer, and CBP, using a Mobil-O-Graph, alongside the determination of left ventricular (LV) mass by two-dimensional transthoracic echocardiography. LVH and LV geometric patterns were defined by LV mass index/height 2.7 and relative wall thickness. Bivariate then multivariate analysis showed that age, BMI, central systolic BP (SBP), and pulse wave velocity (PWV) were significant determinants of LVH and optimally controlled brachial BP was a significant negative determinant for LVH. Central SBP had an acceptable diagnostic performance to determine LVH in patients with hypertension (AUC = 0.722, 95% confidence interval: 0.618-0.824, SE = 0.21, P -value <0.001). Using one-way ANOVA, a comparison of means among age groups showed that the steady increase in central SBP and PWV with aging was greater among LVH patients than non-LVH patients. Estimated central SBP using Mobil-O-Graph showed a significantly higher correlation to LVH than brachial SBP values. The consistent increase in central SBP and PWV with aging was greater among LVH patients than non-LVH patients.

Left ventricular hypertrophy and left atrial size are associated with ischemic strokes among non-vitamin K antagonist oral anticoagulant users.

Ischemic strokes (IS) occurring in patients taking non-vitamin K antagonist oral anticoagulants (NOACs) are becoming increasingly more frequent. We aimed to determine the clinical, echocardiographic, and neuroimaging markers associated with developing IS in patients taking NOACs for atrial fibrillation. From a quaternary care center, clinical/radiologic data were collected from consecutive NOAC users with IS and age-matched controls without IS. Brain MRIs were reviewed for markers of cerebral small vessel disease. Variables with significant differences between groups were entered into a multivariable regression model to determine predictors of IS. Among IS patients, a Cox regression analysis was constructed to determine predictors of IS recurrence during follow-up. 112 patients with IS and 94 controls were included in the study. Variables significantly different between groups included apixaban use, dabigatran use, prior cerebrovascular events, hemoglobin A1c (HbA1c), left ventricular hypertrophy, left atrial volume index, and severe white matter hyperintensities. After multivariable adjustment, prior cerebrovascular events (aOR 23.86, 95% CI [6.02-94.48]), HbA1c levels (aOR 2.36, 95% CI [1.39-3.99]), left ventricular hypertrophy (aOR 2.73, 95% CI [1.11-6.71]) and left atrial volume index (aOR 1.05, 95% CI [1.01-1.08]) increased the risk of stroke, whereas apixaban use appeared to decrease the risk (aOR 0.38, 95% CI [0.16-0.92]). Malignancy was associated with IS recurrence (aHR 4.90, 95% CI [1.35-18.42]) after adjustment for age and chronic renal failure. Prior cerebrovascular events, diabetes, left ventricular hypertrophy, and increased left atrial size are risk factors for developing an IS among NOAC users.

Inactive Matrix Gla Protein in Relation to Renal and Cardiac Functions and Cardiac Valvular Calcification Among Type 2 Diabetes Patients.

Matrix Gla protein (MGP) is a robust innate suppressor of the detrimental process of vascular calcification in the human body. The interrelationship between circulating MGP levels and renal and cardiac dysfunction, besides echocardiographic calcification score (ECS) was investigated in a sample of type 2 diabetes (T2D) patients. The study included 130 subjects. They were 95 patients with T2D and 35 age- and sex-matched healthy controls. Patients were further subdivided into 52 T2D patients without DKD (eGFR ⩾ 60 ml/minute/1.73 m²) and 43 T2D persons with DKD (eGFR > 60 ml/minute/1.73 m²). Serum MGP levels, determined by ELISA, renal function tests, lipid profile, and echocardiography were studied in all participants. Significantly elevated circulating inactive MGP level was noted in individuals having T2D compared to controls. It correlated negatively with eGFR and left ventricular (LV) diastolic and systolic functions and positively with indices of LV hypertrophy. ECS was significantly increased in both T2D groups compared to controls and in DKD group compared to the diabetic group without DKD. A significant positive correlation was observed between inactive MGP and ECS. Serum inactive MGP may contribute to the development of DKD and to the associated process of cardiac valvular calcification. It may be a beneficial diagnostic marker for early prediction of cardiac calcification and preclinical LV systolic and diastolic dysfunction in T2D patients, especially in those complicated with DKD.

ECG for Detection of Left Ventricular Hypertrophy in patients with Chronic Kidney Disease

Background: Left ventricular hypertrophy is the most common cardiac event associated with chronic kidney disease. Aim: To detect LVH by electrocardiography in patients with CKD. Study design: Observational study. Methodology: It was an observational study with total of 62 CKD patients enrolled through convenience sampling. Their blood 3ml was drawn aseptically for estimation of serum creatinine. All enrolled subjects underwent electrocardiographic examination. Patients with low GFR (&lt;60ml/min/1.73m2) and high serum creatinine concentration (&gt;1.5mg/dl) were included. Data was evaluated by using SPSS vr 24. The results were presented as counts, means and standard deviation as appropriate. Results: Left ventricular hypertrophy was present in 50% of enrolled patients as depicted by ECG recording. The calculated sensitivity and specificity of ECG for LVH were 75% and 100% respectively. Almost 38.7% patients were 56-65 years of age. There were 33.9% patients in the age of 35-45 years and 27.4% was in the age of 46-55 years. The median (IQR) age was 54.50 (41.75-60) years. In our study population, median (IQR) of height was 152cm (150-156). The mean weight was 65.85 kg with standard deviation of 8.42 kg i.e., 65.85 ±8.42kg. Mean body mass index was 27.85. Practical Implication: Current project helped health providers to diagnose cardiac event at an early stage among patients of kidney fail¬ure on ECG findings thus the adverse outcomes could be prevented or delayed. Conclusion: ECG abnormalities are common in hospitalized CKD patients in local population. All hospitalized CKD patients should undergo ECG to screen for cardiovascular disease. It was thus concluded that ECG can be used as a sensitive diagnostic tool in combination with different ECG indices to detect LVH. Key words: Electrocardiography, Chronic Kidney Disease, Left Ventricular Hypertrophy and Sokolow-Lyon Voltage Index

Investigation of the relationship between serum adropin levels, oxidative stress biomarkers, and blood pressure in DOCA-salt hypertensive rats

Background/Aim: Adropin is involved in the pathophysiology and development of cardiovascular diseases, such as hypertension. The aim of this study was to investigate the effects of adropin in serum, potential use as a biochemical biomarker of oxidative stress, and effects on blood pressure in deoxycorticosterone acetate (DOCA) salt hypertensive rats.&#x0D; Methods: Eighteen male Sprague-Dawley rats were divided into two groups: (1) Control (C) and (2) Hypertensive (H). Systolic and diastolic blood pressures (SBP and DBP, respectively), and mean blood pressure (MBP) were measured using the tail-cuff method. At the end of the study, serum endothelin-1 (ET-1), adropin, nitric oxide (NO), total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) were also analyzed.&#x0D; Results: Significant increases in SBP, DBP, MBP, cardiac hypertrophy index (CHI), and left ventricular hypertrophy index (LVCI) in the H group compared with the C group were found. Serum levels of ET-1, TOS, and OSI were significantly higher in the H group and serum levels of NO, adropin, and TAS were lower than in the C group. A negative correlation between serum adropin levels and the variables SBP, DBP, MBP, TOS, OSI, CHI, and LVHI was found. Adropin levels were positively correlated positively with serum NO levels in both groups.&#x0D; Conclusion: Serum adropin levels decreased in hypertensive DOCA-salt rats. Lower serum adropin levels were found to be significantly associated with hypertension and may play a role in this disease. However, further comprehensive and diverse studies are needed.

Abstract 13679: Arterial Stiffness and Carotid Intima-Media Thickness Progression Preceding Worsening Left Ventricular Hypertrophy and Diastolic Dysfunction in Youth: A Temporal Causal Longitudinal Study

Introduction: Left ventricular hypertrophy (LVH) is a marker of cardiovascular events and is driven by ventriculo-vascular interactions with stiffening arteries. But longitudinal relations of left ventricle with aorta is uncharacterized in youth. Hypothesis: Aortic stiffening, measured as change in carotid-femoral pulse wave velocity (cfPWV), and arterial thickening measured as change in carotid intima-media thickness (cIMT) each independently predicts and precedes changes in LVH indices even after adjustment for BP. Methods: From the Avon Longitudinal Study of Parents and Children, UK birth cohort, 1856 adolescents (1011 females) were assessed at mean age 17.7 years and followed for 7 years. Vicorder measured cfPWV and ultrasound measured cIMT were grouped in tertiles as low (reference), moderate, and high. Echocardiography measured cardiac abnormalities are left ventricular mass indexed for height 2.7 (LVMI 2.7 ) ≥51g/m 2.7 as LVH; relative wall thickness ≥44 as hiRWT; LV diastolic function E/A as ≥1.5 (LVDD); and LV filling pressure E/e’ ≥8 as hiLVFP. Data were analysed with generalized logit mixed-effect model and cross-lagged structural equation path model adjusting for cardiometabolic and lifestyle factors. Results: Over follow-up, LVH prevalence increased from 3.6% to 7.2% and LVDD from 11.1 to 16.3%. High cfPWV progression was associated with worsening LVH [Odds ratio 1.23 (1.13 - 1.35); p&lt;0.001] and worsening hiLVFP [1.14 (1.13 - 1.14); p&lt;0.0001]. Likewise, high cIMT progression was associated with worsening LVH [1.27 (1.26 - 1.27); p&lt;0.0001] and worsening hiLVFP [1.17 (1.07 - 1.28); p&lt;0.001]. Neither cfPWV nor cIMT progression was associated with worsening hiRWT nor LVDD. In cross-lagged models, higher baseline cfPWV was associated with future LVMI 2.7 (β=0.06, SE, 5.14, p=0.035), RWT, LVDF, and LVFP. However, baseline LVMI 2.7 , RWT, LVDF, and LVFP were not associated with follow-up cfPWV. Baseline cIMT was not associated with follow-up cardiac indices and vice versa . Conclusions: Youth aortic stiffness progression temporally preceded and may causally associate with worsening LVH and hiLVFP but not hiRWT. Mechanistic delineation of coupling in ventriculo-vascular remodeling and consequent physiologic dysfunction is warranted.

Association of obesity phenotypes with left ventricular mass index and left ventricular hypertrophy in children and adolescents.

It has been argued that metabolically healthy obesity (MHO) does not increase the risk of cardiovascular disease. The aim of this study is to evaluate whether, in a population of obese children/adolescents, the metabolically unhealthy obesity (MUO) phenotype is associated with higher left ventricular mass index and/or higher prevalence of left ventricular hypertrophy than the MHO phenotype. We also tested whether the addition of an insulin resistance index (HOMA-index >90th percentile by sex and age) and the presence of hyperuricemia (serum uric acid >90th percentile by sex and age) to the definition of MUO better identified obese children with early cardiac damage. Left ventricular hypertrophy was defined as the presence of left ventricular mass index greater than or equal to the age- and sex-specific 95th percentile.The study population included 459 obese children (males 53.2%, mean age 10.6 [standard deviation, 2.6] years), of whom 268 (58.4%) were MUO. The left ventricular mass index was higher in MUO children than in MHO children (37.8 vs 36.3 g/m2.7, p=0.015), whereas the percentage of MUO children presenting left ventricular hypertrophy was only slightly higher in MUO children (31.1 vs 40%, p=0.06). Multiple linear regression analyses showed that the variables significantly associated with higher left ventricular mass index were male gender (p<0.01), Body Mass Index z-score (p<0.001) and Waist-to-Height-ratio (p<0.001). Multiple logistic regression analyses showed that the presence of left ventricular hypertrophy was only significantly associated with higher Body Mass Index z-score (p<0.05) and Waist-to-Height-ratio (p<0.05). In spite of the higher left ventricular mass index of MUO as compared to MHO children, the MUO phenotype was not a significant predictor of either higher left ventricular mass index or higher left ventricular hypertrophy prevalence. The MUO phenotype had a low predictive ability on the presence of left ventricular hypertrophy. The area under the receiver operating characteristic curve was 0.57 (sensitivity 0.64, 1-specificity 0.55). The addition of insulin resistance and hyperuricemia to the definition of MUO did not change the results observed with the standard definition of MUO at multivariable analysis.The MUO phenotype appears to be of little usefulness in identifying the early presence of cardiac damage in a large population of obese children and adolescents. Excess weight and abdominal obesity are confirmed as an important determinant of early organ damage in obese children.

Effects Of Prenatal Exercise On Cardiac Morphology And Function In SHR Offspring

Intrauterine environment during pregnancy has important effects on the cardiovascular development of the offspring, which could persist into adulthood. However, it is largely unknown whether maternal exercise during pregnancy has a beneficial effect on cardiac structure and function in the offspring of spontaneously hypertensive rats (SHR). PURPOSE: To investigate the effects of prenatal exercise on cardiac morphology and function in 3-month-old male offspring of SHR. METHODS: Pregnant SHR and Wistar-Kyoto rats (WKY) were separated into a sedentary group (p-WKY-SED, p-SHR-SED) and an exercise group (p-WKY-EX, p-SHR-EX) at random. Exercise group were subjected to swimming (60 min/day, 6 day/week, gestation day 1-19). Physical characteristics, myocardial cell morphology, myocardial collagen volume fraction (CVF%) and cardiac function of male offspring were evaluated at 3 months (3 M). RESULTS: 1) Prenatal exercise significantly decreased the diastolic blood pressure (DBP) and mean arterial pressure (MAP) in the offspring of SHR (DBP: 153.5 ± 2.12 vs. 146.7 ± 1.38 mmHg, p < 0.01; MAP: 169.3 ± 2.60 vs. 161.9 ± 3.82 mmHg, p < 0.01). 2) Prenatal exercise significantly decreased the left ventricular hypertrophy index at 3 M in the offspring of SHR (0.74 ± 0.01 vs. 0.70 ± 0.02, p < 0.05). 3) Loosely arranged cardiomyocytes and significant increase in CVF% in the pathological state of hypertension (6.13 ± 0.70 vs. 20.33 ± 1.36 p < 0.01). Prenatal exercise improved cardiomyocyte morphology and decreased CVF% in the offspring of SHR (20.33 ± 1.36 vs. 14.91 ± 0.72 p < 0.05). 4) Echocardiographic results showed that the p-SHR-SED group had a lower left ventricular ejection fraction (LVEF%) (82.33 ± 4.14 vs. 74.14 ± 1.92 p < 0.05), lower cardiac output (CO) (137 ± 6 vs. 100 ± 5 ml/min, p < 0.05) and significantly lower left ventricular short-axis contraction rate (LVFS%) (52.93 ± 1.56 vs. 42.81 ± 1.05, p < 0.01) compared to the p-WKY-SED group, while the exercise group showed no significant differences compared to their respective sedentary control groups (p > 0.05). CONCLUSION: Prenatal exercise significantly reduces DBP and MAP in 3 M male offspring of SHR and improves cardiac morphology in the pathological state, but do not significantly improve cardiac function.Supported by the National Natural Science Foundation of China 32071174.

Effect and correlation of patent vascular access flow on left ventricular hypertrophy in kidney transplant patients.

BackgroundPatency of vascular accesses (VA) is associated with left ventricular hypertrophy (LVH) in kidney transplant recipients (KTR). This level of VA flow (VAF) as related to LVH was assessed and an upward level of VA flow recommended for VA closure determined. This recommendation has not been previously reported.Methods123 KTR cohort patients were enrolled between August 2016 and December 2017 and their LVH and LV mass index (LVMI) by echocardiography and VAF by Doppler ultrasound were evaluated at baseline and for a 24-month follow-up period. Associations between VAF and LVH were adjusted for other factors.ResultsPatients with patent VA (55.3%) had significantly greater LVH (47.1 vs. 29.1%, an adjusted odds ratio 2.44, p = 0.03) and LVMI (112.15 ± 34.4 vs. 97.55 ± 23.55 g/m2, p = 0.009) when compared with the non-VA group. A positive correlation between VAF rate and LVM was noted (r = 0.40, p < 0.001). Subgroup analysis revealed the VAF ≥ 900 ml/min had risks of LVH 3.61, and 2.86 times compared with the non-VA group and the VAF < 900 ml/min group. After a 24-month follow up, there was no significantly individual change in LVMI in patients with or without VA except 6 patients who lost their VA patency during follow-up time had a significant reduction of LVMI (120.17 ± 52.13 to 80.89 ± 22.72 g/m2, p = 0.046).ConclusionsPatency of VA in post-KT patients was associated with LVH. There was a significant reduction of LMVI after loss of VA patency. Patients with stable kidney graft function should be considered for VA closure especially if VAF is ≥ 900 ml/min.

Clinical significance of epicardial fat assessment in hypertensive patients with non-alcoholic fatty liver disease

Objective. To study the relationship between the thickness of epicardial adipose tissue (EAT) and indicators of the structural and functional heart characteristics and cardiovascular risk in hypertensive patients with nonalcoholic fatty liver disease (NAFLD).Design and methods. A comparative cross-sectional study was conducted involved 120 patients, aged 45 to 65 years, with hypertension (HTN) of I–II stages, degrees 1–2, with NAFLD (Fatty Liver Index (FLI &gt; 60)) and without NAFLD. A clinical examination was carried out: history, physical examination, measurement of “office” blood pressure and heart rate, anthropometric parameters (height, weight, body mass index). The indicators of carbohydrate and lipid metabolism, chronic low-intensity inflammation (C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α)) were determined, insulin resistance indices were calculated. The structural and functional state of the liver and heart was assessed by ultrasound, and the thickness of the EAT was determined. The SCORE scale was used to assess the 10-year fatal risk.Results. Indicators characterizing chronic low-intensity systemic inflammation (CRP, TNF-α) and insulin resistance (HOMA-IR metabolic index (MI), triglycerides (TG) / high-density lipoproteins (HDL)) were higher in patients with HTN and NAFLD than in patients with isolated HTN. Echocardiography showed that patients with comorbid pathology had greater EAT thickness (p &lt; 0,001) and more profound left ventricular myocardial hypertrophy (thickness of the left ventricular posterior wall (LVPW) (p = 0,019), interventricular septum (IVS) (p = 0,012), left ventricular myocardial mass (LVMM) (p = 0,029)). In the group of patients with HTN and NAFLD, the correlation analysis showed direct moderate-strong relationships between EAT thickness and TPWLV (r = 0,345, p &lt; 0,001), IVS (r = 0,344, p &lt; 0,001), LVMM (r = 0,372, p &lt; 0,001), index LVMM (r = 0,221, p = 0,015), FLI (r = 0,722, p &lt; 0,001), TNF-α (r = 0,495, p &lt; 0,001), HOMA-IR (r = 0,38, p &lt; 0,001), MI (r = 0,374, p &lt; 0.001), TG/HDL (r = 0,354, p &lt; 0,001), CRP (r = 0,30, p = 0,002), TG (r = 0,305, p = 0,001), very low density lipoprotein cholesterol (r = 0,306, p = 0,001) and medium strength inverse relationship with HDL (r = 0,30, p = 0,008). A multiple regression analysis was performed to assess the relationship between EAT thickness and the severity of chronic systemic inflammation and insulin resistance in patients with HTN and NAFLD: with an increase in TNF-α by 1 pg/ml and TG/HDL by 1, an increase in EAT thickness by 0,15 and 0,68 mm, respectively, should be expected. An increase in EAT thickness by 1 mm was accompanied by an increase in LVMM by 12,8 g. Logistic regression analysis showed a direct relation between EAT thickness and the probability of cardiovascular 10-year risk increase by 5,0% or more.Conclusions. This study showed that in patients with HTN and NAFLD, the EAT thickness was significantly higher, which strongly correlates with indicators of left ventricular hypertrophy, the severity of liver steatosis (FLI), chronic low-intensity systemic inflammation, and insulin resistance. With an increase in TNF-α and TG/HDL, an increase in the EAT thickness should be expected. EAT thickness was significantly associated with an increase in LVMM and increased chance of high and very high risk of cardiovascular complications in patients with HTN and NAFLD.

Association between atherogenic index of plasma and left ventricular hypertrophy in patients with chronic heart failure with mid-range ejection fraction

Aim: The aim of the present study was to investigate whether an association between lipid indices- atherogenic index of plasma (AIP), Castelli Risk Index I (CRI-I), Castelli Risk Index II (CRI-II) and triglyceride index (TGL-index) and the development of left ventricular hypertrophy exists in patients with heart failure with mid-range ejection fraction (HFmrEF). Material and methods: The study involved 56 patients with HFmrEF and normal lipid profile, median age 64 (47-84) and 22 healthy subjects, median age 58 (51-69). The patients were divided in two subgroups: subjects with left ventricular hypertrophy (n=32); (HFmrEF+LVH) and subjects without left ventricular hypertrophy (n=24); (HFmrEF-LVH). The lipid profile was measured by laboratory, while lipid indices were calculated, using the established formulas. Results: There was not statistically significant difference between the lipid indices in patients with heart failure with mid-range ejection fraction compared to healthy controls (p&amp;gt;0.05). HFmrEF+LVH patients showed statistically significantly higher values of atherogenic index of plasma than HFrEF-LVH patients: 0.16 (0.05/0.37) vs. 0.04 (0.01/0.11); (KW=5.80; p=0.02). TC/HDL, LDL/HDL and TG/HDL values were not significantly higher in HFmrHEF+LVH than HFmrEF-LVH patients: 4.8 (3.98/5.75) vs. 4.49 (3.58/5.63); 2.91 (2.1/4.0) vs. 2.9 (2.5/4.25) and 1.36 (1.11/2.08) vs. 1.13 (0.9/1.53), respectively (p&amp;gt;0.05). No significant gender differences between lipid indices were found. Atherogenic index of plasma showed correlation with LVH (r=0.45; p=0.01) and interventricular septum thickness (r=0.55; p=0.002). Conclusion: Our findings show an association between atherogenic index of plasma and LVH in patients with HFmrEF with normal lipid profile. Further studies are warranted to confirm whether determination of AIP may be used for monitoring development and progression of left ventricular hypertrophy in heart failure with mid-range ejection fraction.

Electrocardiographic features of patients with hypertrophic cardiomyopathy

Introduction. Hypertrophic cardiomyopathy is a disorder of the myocardium characterized by asymmetric or symmetric left ventricular hypertrophy. It is often an inherited disorder with an autosomal dominant pattern. The aim of this study was to evaluate the electrocardiographic characteristics of patients with hypertrophic cardiomyopathy, as well as to assess the accuracy of current electrocardiographic criteria for left ventricular hypertrophy used as indicators of hypertrophic cardiomyopathy. Material and Methods. This retrospective study was conducted using hospital medical records of 42 patients with the diagnosis of hypertrophic cardiomyopathy. Detailed electrocardiography analysis, apart from all the usual parameters, included the calculation of indices used to diagnose left ventricular hypertrophy including Sokolow augmented vector left, Cornell voltage, Cornell product, and Sokolow-Lyon index. Results. Sinus rhythm was present in 95.2% of patients, while atrial fibrillation was found in 4.8%. The majority of patients presented with left axis deviation. A slight positive correlation was found between the Sokolow augmented vector left index and posterolateral wall thickness (r = 0.475; p &lt; 0.05), and also between the Cornell voltage index and posterolateral wall thickness (r = 0.368; p &lt; 0.05). A borderline positive correlation was found between the Cornell product index and posterolateral wall thickness (r = 0.290; p = 0.063). Interventricular septum thickness showed no significant correlation with any of the electrocardiographic indices of left ventricular hypertrophy. Conclusion. In patients with hypertrophic cardiomyopathy, the Sokolow augmented vector left and Cornell voltage indices were the best indicators of posterolateral wall hypertrophy, whereas none of the examined indices correlated well with the interventricular septum thickness.

Interaction of high-intensity endurance exercise and nandrolone on cardiac remodeling: role of adipo-cardiac axis.

Given the cardiac pathological remodeling following to anabolic androgenic steroids (AASs) consumption, we examined the effect of chronic administration of nandrolone decanoate with high-intensity endurance exercise on the left ventricular hypertrophy index, levels of hydroxyproline, tumor necrosis factor-alpha (TNF-α), adiponectin (APN) and its receptors (AdipoR1 and AdipoR2) expression in rats' hearts. The male Wistar rats randomly divided to six groups included the control (CTL), exercise (Ex), nandrolone (Nan), vehicle (Arach), trained vehicle (Ex+Arach), and trained nandrolone (Ex+Nan) groups that were treated for eight weeks. Nandrolone consumption significantly enhanced the hypertrophy index (p<0.05) and exercise intensified this effect. It also increased the level of cardiac hydroxyproline (p<0.001), however exercise completely masked this effect. The values of TNF-α protein and AdipoR1 protein significantly increased in trained nandrolone-treated (Ex+Nan) group in comparison with CTL group (p<0.05), however, did not show significant alteration in Nan or Ex groups. High-intensity endurance exercise significantly enhanced the AdipoR2 protein (p<0.05), but, co-administration of nandrolone with exercise prevented this effect. The mRNA expression of AdipoR1 significantly reduced in the animals that received nandrolone for eight weeks and exercise recovered this effect (p<0.001). Despite an additive effect of high-intensity endurance exercise plus nandrolone on TNF-α level, their effects on hydroxyproline and APN receptors expression is incompatible in heart of rat. It is suggests a part of beneficial regulatory role of endurance exercise against nandrolone induced heart remodeling may apply through modulation of APN system.

Abstract 10695: Early Overnutrition in Rats Induces Premature Cardiac Alterations Independently of Blood Pressure: Leptin-TRH Pathway Involvement

Animal models are an interesting tool to evaluate future consequences of early nutritional insults. We described in adult mice that: leptin induces cardiac cTRH, leading to cardiac damage regardless of blood pressure in hyperleptinemic Agouti. Conversely, cTRH in the ob/ob lacking leptin is similar to control and even do not have Left Ventricular Hypertrophy (LVH). Moreover, leptin restitution induces cTRH and later LVH. Also, in C57BL/6 a 3-week subanorexigenic leptin dose induced cTRH and sequent LVH. All this suggests that heart damage in obesity depends on the novel leptin-cTRH pathway. Plus, Leptin directly induces TRH in cell culture (Aisicovich 2019, AHA) To further investigate the impact of early dietary interventions in childhood, we studied rat litter size reduction, a model with a reported increase in body weight, fat, leptin, insulin and cholesterol levels (Stefanidis A, 2012) We hypothesize that leptin rise increases cTRH leading to cardiac damage, independently of hypertension. On postnatal day 4, Wistar rat litters of 11 pups at birth were adjusted to 4 male pups (overnourished ON) or 11 (control C). At weaning, we individualized rats with free access to water and standard diet up to 7 weeks old. The rise in body weight, food consumption, and fat in ON vs C (p&lt;0.02 n=10 ANOVA) confirmed the model. There weren’t any blood pressure differences between groups, still LVH index increased (heart weight/tibia length) (p&lt; 0.01 n=6) in ON vs C. As expected, in ON the higher leptin increased cTRH mRNA (p&lt; 0.01 n=6) as protein [WB (p=0.05 n=3) IHQ (p&lt;0.04 n=6)] vs C. According to cTRH actions, hypertrophic and fibrotic markers TGF-B and Collagens 1 and 3 mRNA increased (p&lt;0.01, n=6) confirmed by IHQ and Sirius red staining (p&lt; 0.01 n=6) Also, echocardiogram showed increases in LV end-diastolic (0.26±0.08 vs 0.61±0.07 ml p &lt;0.01) and end-systolic (0.02±0.02 vs 0.11±0.01 ml p &lt;0.01) volumes, and decreases in LV ejection fraction (94.5±2.2 vs 83.3±1.9 % p &lt;0.01) and SF (54.4±2.6 vs 45.0±2.3 % p &lt;0.02) This could be restored by cTRH inhibition as demonstrated in the cardiac infarct model (Schuman ML, 2021) Our results point out that early overnutrition induces evident cardiac damage already at 7 weeks, independently of blood pressure and mostly driven by the leptin-TRH pathway.