Left Ventricular Concentric Remodeling Research Articles

Sex differences in clinical profile, left ventricular remodeling and cardiovascular outcomes among diabetic patients with heart failure and reduced ejection fraction: a cardiac-MRI-based study

BackgroundHeart failure with reduced ejection fraction (HFrEF) is associated with a high rate of mortality and morbidity. Evidence has shown that sex differences may be an important contributor to phenotypic heterogeneity in patients with HFrEF. Although diabetes mellitus (DM) frequently coexists with HFrEF and results in a worse prognosis, there remains a need to identify sex-related differences in the characteristics and outcomes of this population. In this study, we aimed to investigate the between-sex differences in clinical profile, left ventricular (LV) remodeling, and cardiovascular risk factors and outcomes in patients with HFrEF concomitant with DM.MethodsA total of 273 patients with HFrEF concomitant with DM who underwent cardiac MRI were included in this study. Clinical characteristics, LV remodeling as assessed by cardiac MRI, and cardiovascular risk factors and outcomes were compared between sexes.ResultsWomen were older, leaner and prone to have anemia and hypoproteinemia but less likely to have ischemic etiology. Cardiac MRI revealed that despite similar LVEFs between the sexes, there was more LV concentric remodeling, less impaired global systolic peak strain in longitudinal and circumferential components and a decreased likelihood of late gadolinium enhancement presence in women than in men. During a median follow-up time of 34.6 months, women exhibited better overall survival than men did (log-rank P = 0.042). Multivariable Cox proportional hazards analysis indicated different risk factors for predicting outcomes between sexes, with hypertension [hazard ratio (HR) = 2.05, 95% confidence interval (CI) 1.05 to 4.85, P = 0.041] and hypoproteinemia (HR = 2.27, 95% CI 1.06 to 4.37, P = 0.039) serving as independent determinants of outcomes in women, whereas ischemic etiology (HR = 1.96, 95% CI 1.11 to 3.48, P = 0.021) and atrial fibrillation (HR = 1.86, 95% CI 1.02 to 3.41, P = 0.044) served as independent determinants of outcomes in men.ConclusionsAmong patients with HFrEF concomitant with DM, women displayed different LV remodeling and risk factors and had better survival than men did. Sex-based phenotypic heterogeneity in patients with HFrEF in the context of DM should be addressed in clinical practice.

Left ventricular concentric remodeling in COPD patients: A cross-sectional observational study

ObjectiveTo investigate the association between left ventricular structure and disease severity in COPD patients. MethodsTwenty-eight COPD patients were stratified according to the disease severity, using the BODE index, into Lower (n=17) and Higher (n=11) groups, composed of patients with lower severity (BODE <5) and higher severity (BODE ≥5), respectively. Left ventricle (LV) was assessed by 2D-echocardiography. BODE index was calculated using body mass index (BMI); forced expiratory volume in the first second (FEV1, %); modified Medical Research Council (mMRC) and distance walked during 6-minute walk test (6MWD). ResultsPatients in the Higher group showed lower oxygen arterial saturation (p=0.02), FEV1 (p<0.01) and 6MWD (p=0.02) and higher value of relative posterior wall thickness (RWT) compared to Lower group (p=0.02). There were significant associations between LV end-systolic diameter (LVESD) and BODE index (r=−0.38, p=0.04), LV end-diastolic diameter (LVEDD) and FEV1 (r=0.44, p=0.02), LVEDD and BMI (r=0.45, p=0.02), LVESD and BMI (r=0.54, p=0.003) and interventricular septal thickness and 6MWD (r=−0.39, p=0.04). ConclusionsMore severe COPD patients, BODE score ≥5, may have higher RWT, featuring a possible higher concentric remodeling of LV in this group. Besides that, a greater disease severity may be related to LV chamber size reduction.

Association of body adiposity with left ventricular concentric remodeling and diastolic dysfunction

AbstractBackgroundObesity is a significant risk factor for heart failure with preserved ejection fraction (HFpEF). In this study, we explore the relationships between body mass index (BMI) and adipose tissue compartments such as visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and epicardial adipose tissue (EAT), with respect to left ventricular (LV) structure and function in subjects with preserved LV systolic function.MethodsBetween January and December 2020, this retrospective study included 749 participants who exhibited preserved LV systolic function and underwent transthoracic echocardiography along with abdominal computed tomography. LV structural and functional variables as well as EAT, VAT, and SAT thickness were evaluated using echocardiography and computed tomography.ResultsSAT decreased, while VAT and EAT progressively increased with age. There were significant correlations between BMI and various adipose tissues, with the strongest correlation observed with SAT (r = .491, p &lt; .001) compared to VAT (r = .371, p &lt; .001) or EAT (r = .135, p &lt; .001). However, EAT demonstrated the most substantial association with decreased LV end‐diastolic dimension, LV end‐systolic dimension, and septal mitral annular velocity and increased relative wall thickness (all p &lt; .05), while VAT and SAT did not show significant associations with LV remodeling and functional parameters after adjusting for clinical variables.ConclusionEAT is the most critical adipose tissue influencing LV geometric and functional changes, compared with VAT or SAT. Thick EAT is associated small LV chamber size, concentric remodeling, and relaxation abnormalities.

Association of Cardiovascular Fibrosis, Remodeling, and Dysfunction With Frailty, Prefrailty, and Functional Performance: The Multi-Ethnic Study of Atherosclerosis.

Cardiovascular disease is associated with higher incidence of frailty. However, the nature of the mechanisms underlying this association remains unclear. The purpose of this study is to identify cardiovascular phenotypes most associated with physical frailty and functional performance in the Multi-Ethnic Study of Atherosclerosis (MESA). As part of the MESA study, 3 045 participants underwent cardiovascular magnetic resonance and computed tomography between 2010 and 2012. Of these, 1 743 completed a Six-Minute Walk test (6MWT) and questionnaires (follow-up exam: 2016-2018) which were used to generate a binary combined frail/prefrail versus robust score according to a modified FRAIL Scale (self-report questionnaire). Multivariable logistic (binary frail outcome) or linear (6MWT) regression assessed the association between frailty and cardiovascular structure and function, aortic stiffness, coronary artery calcium, and myocardial fibrosis (ECV, extracellular volume fraction). Participants were 66 ± 8 years, 52% female at the time of imaging, and 29.4% were classified as frail or prefrail. Older age and female gender were associated with greater odds of being in the frail/prefrail group. Concentric left ventricular remodeling (odds ratio [OR] 1.89, p = .008; Coef. -52.9, p < .001), increased ECV (OR 1.10, p = .002; Coef. -4.0, p = .001), and worsening left atrial strain rate at early diastole (OR 1.56, p ≤ .001; Coef. -22.75, p = .027) were found to be associated with a greater likelihood of being in a frail state and lower 6MWT distance (m). All associations with 6MWT performance were attenuated with adjustments for risk factors whereas ECV and LA strain rate remained independently associated with frailty. These findings suggest a significant overlap in pathways associated with subclinical cardiac dysfunction, cardiovascular fibrosis, and physical frailty.

Cardiomyocyte Specific MLK3 Deletion Opposes LV Dysfunction and Cardiac Fetal Gene Re-Expression

Study Objective: To determine the cardiac myocyte (CM) and blood pressure-independent effects of Mixed lineage kinase 3 (MLK3) in the regulation of left ventricular (LV) function at baseline and in response to pathological stress. Background: MLK3 functions as a direct substrate effector of cGMP-dependent protein kinase 1α (PKG1α). Whole-body MLK3 deletion in mice increases cardiac dysfunction and remodeling after pressure overload and prevents the therapeutic effect of cGMP augmentation on LV function. However, MLK3 deletion also causes hypertension, which may confound these findings. Hypothesis: MLK3 opposes LV dysfunction through a blood pressure-independent function in the cardiac myocyte (CM). Methods: We generated mice harboring LoxP sites flanking the MAP3K11 gene encoding MLK3 (MLK3fl/fl) and crossed them with αMHC-Cre transgenic mice, enabling constitutive postnatal cardiac myocyte-specific MLK3 deletion (CMKO). Male and female 3- and 6-month-old MLK3 CMKO and control MLK3 intact (MLK3fl/fl Cre-) littermates were studied in the basal state. We also performed transaortic constriction (TAC) or sham surgery for 4 weeks on 3-month-old male mice. We assessed LV structure and function by organ mass, echocardiography, pressure volume loop analysis, qPCR, and immunoblot. In basal and TAC studies, we used age-matched αMHC-Cre x MLK3+/+ (non-floxed) mice as additional controls. Results: MLK3 gene excision in CMs was confirmed by PCR. By 6 months of age, MLK3 CMKO mice displayed: progressive reduction in LV ejection fraction; increase in LV internal diameter; and LV hypertrophy, indicating LV dysfunction and pathological remodeling, compared with littermate controls or with αMHC-Cre x MLK3+/+ non-floxed mice. This effect was more prominent in females than in males. LV fetal gene expression did not differ between genotypes at 3 months. At 6 months of age, however, the fetal genes nppa, RCAN, and CTGF were significantly upregulated in both male and female MLK3 CMKO mice, compared with MLK3 intact, indicating pathological remodeling. After 4-week TAC, MLK3 CMKO LVs developed more severe reduction in LV systolic function compared with MLK3 intact littermates as assayed by echocardiographic measures of LV ejection fraction; and invasive hemodynamic indices of preload recruitable stroke work, maximum LV pressure and LV developed pressure. The MLK3 CMKO LVs also demonstrated a more eccentric remodeling phenotype in which LV mass/tibia length, LV end diastolic and end systolic diameters increased more severely in CMKO mice, with corresponding reduced LV wall thicknesses. Finally, lung mass/tibia length was elevated in the MLK3 CMKO TAC mice compared to MLK3 intact TAC littermates, indicating overt heart failure. Conclusion: (1) MLK3 functions as a tonic inhibitor of LV dysfunction and pathological remodeling through a role in the CM, possibly through sex-specific mechanisms. (2) Intact MLK3 is required for normal LV compensation and concentric remodeling in response to pressure overload. These findings have important clinical implications, as drugs which activate PKG1 in heart failure improve outcomes but are limited by excess hypotension. As a myocardial PKG1 substrate which opposes pathological LV remodeling through blood pressure-independent mechanisms, MLK3 may represent a candidate therapeutic target for heart failure. NIH 1R01HL162919. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Features of structural and geometric cardiac remodeling in patients with diabetes mellitus depending on chronic kidney disease stages

Objective. To study the features of structural and geometric cardiac remodeling in patients with diabetes mellitus (DM) depending on the stage of chronic kidney disease (CKD). Materials and methods. We examined 499 patients (127 men and 322 women) with type 1 DM (133 people) and type 2 DM (316 people) aged 62 [52;69] years. The comparison group consisted of 65 randomly selected volunteering individuals (54 women and 11 men) without disorders of carbohydrate metabolism and kidney damage aged 59 [46;66] years. The laboratory examination of the patients included the measurement of serum creatinine, eGFR according to the CKD-EPI equation. An echocardiographic investigation was performed to study structural and geometric heart parameters. Left ventricular hypertrophy (LVH) was diagnosed when the left ventricular myocardial mass index (LVMI) exceeded 115 g/m2 in men and 95 g/m2 in women. Results. LVH was detected in 57.7 % of patients with DM, while in the comparison group – in 35.4 %. The frequency of LVH increased with a decrease in eGFR and was diagnosed in 100 % of cases with CKD 5. In patients with DM, the left ventricular concentric remodeling significantly predominated (29.2%). Multiple linear regression analysis demonstrated the influence of age (ß=0.30, p=0.01) and serum creatinine (ß = 0.15, p &lt; 0.0001) on the LVMI, independent of other factors, which confirms their independent pathogenetic significance. Conclusion. Thus, patients with DM regardless of the CKD stage have structural and functional changes in the LV myocardium. Regardless of the nitrogen-excretion function of the kidneys, the predominant pattern of LV remodeling is concentric. The study of the features of structural and functional restructuring of the left heart in patients with diabetes should be taken into account in determining the cardiovascular prognosis.

Cardiac magnetic resonance patterns of left ventricular remodeling in patients with severe aortic stenosis referred to surgical aortic valve replacement

Left ventricular (LV) hypertrophy is a common finding in patients with severe aortic stenosis (AS). Cardiac magnetic resonance (CMR) is the gold-standard technique to evaluate LV remodeling. Our aim was to assess the prevalence and describe the patterns of LV adaptation in AS patients before and after surgical aortic valve replacement (AVR). Prospective study of 130 consecutive patients (71y [IQR 68–77y], 48% men) with severe AS, referred for surgical AVR. Patterns of LV remodeling were assessed by CMR. Besides normal LV ventricular structure, four other patterns were considered: concentric remodeling, concentric hypertrophy, eccentric hypertrophy, and adverse remodeling. At baseline CMR study: mean LV indexed mass: 81.8 ± 26.7 g/m2; mean end-diastolic LV indexed volume: 85.7 ± 23.1 mL/m2 and median geometric remodeling ratio: 0.96 g/mL [IQR 0.82–1.08 g/mL]. LV hypertrophy occurred in 49% of subjects (concentric 44%; eccentric 5%). Both normal LV structure and concentric remodeling had a prevalence of 25% among the cohort; one patient had an adverse remodeling pattern. Asymmetric LV wall thickening was present in 55% of the patients, with predominant septal involvement. AVR was performed in 119 patients. At 3–6 months after AVR, LV remodeling changed to: normal ventricular geometry in 60%, concentric remodeling in 27%, concentric hypertrophy in 10%, eccentric hypertrophy in 3% and adverse remodeling (one patient). Indexes of AS severity, LV systolic and diastolic function and NT-proBNP were significantly different among the distinct patterns of remodeling. Several distinct patterns of LV remodelling beyond concentric hypertrophy occur in patients with classical severe AS. Asymmetric hypertrophy is a common finding and LV response after AVR is diverse.

Increased aortic pressures and pulsatile afterload components promote concentric left ventricular remodeling in adults with transposition of the great arteries and arterial switch operation

BackgroundFunctional abnormalities of the ascending aorta (AA) have been mainly reported in young patients who underwent arterial switch operation (ASO) for transposition of the great arteries (TGA). ObjectivesTo compare systolic, diastolic brachial and central blood pressures (bSBP, bDBP, cSBP, cDBP), aortic biomechanical parameters, and left ventricular (LV) afterload criteria in adult ASO patients with healthy controls and to assess their relationships with LV remodeling and aortic size. Materials and methodsForty-one prospectively enrolled patients (16.8 to 35.8 years) and 41 age- and sex-matched healthy volunteers underwent cardiac MRI to assess LV remodeling with simultaneous brachial BP estimation. After MRI, carotid-femoral tonometry was performed to measure pulse wave velocity (cfPWV), cSBP and cDBP for further calculation of pulse pressure (cPP), AA distensibility (AAD), and AA and LV elastance (AAE, LVE). ResultsbSBP, bDBP, cSBP,cDBP and cPP were all significantly higher in ASO group than in controls: cSBP (116.5 ± 13.8 vs 106.1 ± 12.0, p < 0.001), cDBP (72.5 ± 6.9 vs 67.1 ± 9.4, p = 0.002), cPP (44.0 ± 12.1 vs 39.1 ± 8.9, p = 0.003) and not related to aortic size. AAD were decreased in ASO patients vs controls (4.70 ± 2.72 vs 6.69 ± 2.16, p < 0.001).LV mass was correlated with bSBP, cSBP, cPP (ρ = 0.48; p < 0.001), while concentric LV remodeling was correlated with AAE (ρ = 0.60, p < 0.001) and LVE (ρ = 0.32, p = 0.04), but not with distensibility. ConclusionEven without reaching arterial hypertension, aortic sBP and PP are increased in the adult TGA population after ASO, altering the pulsatile components of afterload and contributing to LV concentric remodeling.

Physical exercise is essential for increasing ventricular contractility in hypertensive rats treated with losartan.

The treatment of hypertensive patients with losartan is very common. Despite the reduction in blood pressure, its effects on cardiac contractility and sympathetic autonomic drive are still controversial. In turn, aerobic physical training (APT) also presents an important therapeutic option, providing significant improvements in cardiovascular autonomic control, however little is known about its effects on cardiac contractility, especially when associated with losartan. Therefore, we investigated in spontaneously hypertensive rats (SHR) the effects of losartan and APT on cardiac hemodynamics and functionality, with emphasis on autonomic tonic balance and cardiac contractility. Sixty-four SHR (18 weeks old) were divided into four groups (N = 16): vehicle; vehicle submitted to APT through swimming for 12 weeks; treated with losartan (5 mg·kg-1·d-1) for 12 weeks; and treated with losartan associated with APT. The groups were submitted to cardiac morphological and functional analysis by echocardiography; double blockade of cardiac autonomic receptors with atropine and propranolol; and coronary bed reactivity and left ventricular contractility analyses by the Langendorff technique. APT improved functional parameters and autonomic balance by reducing sympathetic drive and/or increasing vagal drive. In contrast, it promoted a concentric remodeling of the left ventricle (LV). Treatment with losartan reduced sympathetic autonomic drive and cardiac morphological parameters, but there were no significant gains in cardiac functionality and contractility. When combined, the concentric remodeling of the LV to APT was abolished and gains in cardiac functionality and contractility were observed. Our findings suggest that the effects of losartan and APT are complementary and should be applied together in the treatment of hypertension. In spontaneously hypertensive rats, the combination of aerobic physical training with losartan treatment was crucial to greater blood pressure reductions and an increase in left ventricular contractility. Furthermore, losartan treatment prevented the concentric left ventricular remodeling caused by aerobic physical training.

Cardiac reverse remodeling in a mouse model with many phenotypical features of heart failure with preserved ejection fraction: effects of modifying lifestyle.

Multiple factors cause heart failure with preserved ejection fraction (HFpEF) and involve various systems. HFpEF prevalence is rapidly rising, and its prognosis remains poor after the first hospitalization. Adopting a more active lifestyle has been shown to provide beneficial clinical outcomes for patients with HFpEF. Using a two-hit HfpEF murine model, we studied cardiac reverse remodeling (RR) after stopping the causing stress and introducing voluntary exercise (VE). We checked in 2-mo-old male and female C57Bl6/J mice the heart's response to angiotensin II (ANG II; 1.5 mg/kg/day for 28 days) fed or not with a high-fat diet (HFD). Then, ANG II and/or the HFD were stopped, and VE was started for an additional 4 wk. ANG II and ANG II + HFD (metabolic-hypertensive stress, MHS) caused cardiac hypertrophy (CH) and myocardial fibrosis, left ventricular (LV) concentric remodeling, atrial enlargement, and reduced exercise capacity. HFD alone induced CH and LV concentric remodeling in female mice only. CH and LV concentric remodeling were reversed 4 wk after stopping ANG II, starting VE, and a low-fat diet. Left atrial enlargement and exercise capacity were improved but differed from controls. We performed bulk LV RNA sequencing and observed that MHS upregulated 58% of the differentially expressed genes (DEGs) compared with controls. In the RR group, compared with MHS animals, 60% of the DEGs were downregulated. In an HfpEF mouse model, we show that correcting hypertension, diet, and introducing exercise can lead to extensive cardiac reverse remodeling.NEW & NOTEWORTHY Using a two-hit murine model of heart failure with preserved ejection fraction (HfpEF), combining elevated blood pressure, obesity, and exercise intolerance in male and female animals, we showed that correction of hypertension, normalization of the diet, and introduction of voluntary exercise could help reverse the remodeling of the left ventricle and double exercise capacity. We also identify genes that escape normalization after myocardial recovery and differences between males' and females' responses to stress and recovery.

Association of 20-Year Longitudinal Depressive Symptoms With Left Ventricular Geometry Outcomes in the Coronary Artery Risk Development in Young Adults Study: A Role for Androgens?

Depression is a risk factor for coronary heart disease and left ventricular hypertrophy (LVH) is a potent predictor of coronary heart disease events. Whether depression is associated with LVH has received limited investigation. This study assessed cross-sectional and 20-year longitudinal associations of depressive symptoms with LVH outcomes after accounting for important known confounders. From 5115 participants enrolled in 1985-1986 in the Coronary Artery Risk Development in Young Adults Study, 2533 had serial measures of depressive symptoms and subsequent echocardiography to measure normal LV geometry, concentric remodeling, and LVH. The primary exposure variable was trajectories of the Center for Epidemiologic Studies Depression (CES-D) scale score from 1990-1991 to 2010-2011. Multivariable polytomous logistic regression was used to assess associations of trajectories with a composite LV geometry outcome created using echocardiogram data measured in 2010-2011 and 2015-2016. Sex-specific conflicting results led to exploratory models that examined potential importance of testosterone and sex hormone-binding globulin. Overall CES-D and Somatic subscale trajectories had significant associations with LVH for female participants only. Odds ratios for the subthreshold (mean CES-D ≈ 14) and stable (mean CES-D ≈ 19) groups were 1.49 (95% confidence interval = 1.05-2.13) and 1.88 (95% confidence interval = 1.16-3.04), respectively. For female participants, sex hormone-binding globulin was inversely associated with LVH, and for male participants, bioavailable testosterone was positively associated with concentric geometry. Findings from cross-sectional and longitudinal regression models for female participants, but not male ones, and particularly for Somatic subscale trajectories suggested a plausible link among depression, androgens, and LVH. The role of androgens to the depression-LVH relation requires additional investigation in future studies.

Kiosk 1R-TA-01 - Association of Visceral Adipose Tissue with Left Ventricular Concentric Remodeling and Left Atrial Dysfunction in Patients with Known or Suspected Coronary Artery Disease

Kiosk 1R-TA-01 - Association of Visceral Adipose Tissue with Left Ventricular Concentric Remodeling and Left Atrial Dysfunction in Patients with Known or Suspected Coronary Artery Disease

Association of left ventricular structural remodeling types with fibronectin deficiency in patients with multivessel coronary artery disease

Aim. To evaluate the serum fibronectin level in patients with multivessel coronary artery disease, and to identify the relationship of fibronectin level with atrial fibrillation (AF) developed in the hospital after coronary artery bypass grafting (CABG) and types of left ventricular (LV) structural remodeling.Material and methods. This prospective observational study of 80 patients after elective CABG at the Cardiac Surgery Department № 1 of the N.V. Sklifosovsky Research Institute for Emergency Medicine from October 2020 to May 2022. The groups were divided depending on the development of AF after CABG surgery (19 patients with AF developed in the hospital after CABG (up to 10 days), 61 patients — control group). All patients underwent a general clinical examination and transthoracic echocardiography, with estimation of left ventricular remodeling type. Serum fibronectin level was determined by enzyme immunoassay using the Fibronectin agent (Technozym, Austria).Results. The median fibronectin values in the group with AF was 110,10 [86,86; 134,00] mcg/ml versus 120,90 [92,01; 161,50] µg/ml of the comparison group (p=0,19). The following LV patterns were observed: normal LV geometry (NLVG) — in 1 patient (5,26%), concentric LV remodeling (CLVR) — in 3 patients (15,79%), concentric LV hypertrophy (CLVH) — in 10 patients (52,63%), eccentric LV hypertrophy (ELVH) — in 5 patients (26,32%). In the group without AF, 25 patients (40,98%) were diagnosed with NLVG, 26 patients (42,62%) — CLVR, 6,56% (n=4) — CLVR, while ELVH was diagnosed in 6 patients (9,84%). Differences in geometry types between groups were significant (p&lt;0,0001). Multivariate analysis adjusted for gender, age, cardiopulmonary bypass time, the predictive value remained for CLVH — odds ratio 15,83 (95% confidence interval, 4,082-1,442,00; p=0,0001) and ELVH — odds ratio 5,17 (95% confidence interval, 1,365-19,573; p=0,015). A further study showed that fibronectin &lt;116,496 µg/ml with a sensitivity of 78% and specificity of 53% is associated with CLVH (p=0,006) in patients of both groups.Conclusion. Fibronectin &lt;116,496 µg/ml is associated with CLVH in patients with multivessel coronary artery disease (sensitivity 78%, specificity 53%; p=0,006).

Predictors of Atrial Fibrillation Developing in Hospital Stage After Coronary Artery Bypass Surgery

Aim To identify independent predictors associated with in-hospital atrial fibrillation (AF) following coronary artery bypass grafting (CABG).Material and methods The study included 80 patients (88.75 % men) who had elective CABG surgery at the Sklifosovsky Research Institute of Emergency Medicine. Based on the development of AF during the hospital stage of treatment (up to 10 days after CABG surgery), patients were divided into two groups. The group with AF consisted of 19 patients, and the group without AF consisted of 61 patients. All patients underwent electrocardiography (ECG), transthoracic echocardiography (EchoCG) with calculation of the left ventricular (LV) geometry type, and assessment of operational indexes. During surgery, biopsy of a part of the right atrial (RA) appendage was taken from 61 patients to verify the severity of myocardial fibrosis on a four-score scale where 0 is no interstitial fibrosis, 1 is slight fibrosis, 2 is moderate fibrosis, and 3 is severe fibrosis.Results All included patients had a low risk of developing postoperative complications according to the EuroSCORE II scale. According to EchoCG data, patients with AF had significantly higher ratios of left ventricular myocardial mass to body surface area (LVMM / BSA) (p = 0.0006) and of left atrial volume to body surface area (LA volume / BSA), p = 0.008). The distribution of patients by type of LV geometry was as follows: in the group with AF, 52.63 % (n=10) of patients were diagnosed with concentric LV hypertrophy (LVH) whereas in the group without AF, the majority of patients (83.60 %, n=51) had normal LV geometry and concentric LV remodeling (LVR) (p&lt;0.0001). According to the results of histological study, patients of the AF group more frequently had moderate and severe interstitial fibrosis in the AF appendage (p = 0.003). After multivariate regression and ROC analysis, the predictive value remained for concentric LVH (p=0.002), LVMM / BSA ratio ≥97 g / m2 (p=0.006), LA volume / BSA ratio ≥ 34.4 ml / m2 (p=0.04), and for RA appendage interstitial fibrosis score ≥2 (p=0.004). Based on the identified predictors, a regression model was developed to predict the development of AF at the hospital stage after CABG (p&lt;0.0001). The sensitivity and specificity of the model were 86.67 % and 78.26 %, respectively.Conclusion In patients at low perioperative risk, the LVMM / BSA ratio ≥97 g / m2, the LA volume ratio / BSA ≥34.4 ml / m2, a RA appendage interstitial fibrosis score ≥2, and the presence of LVH were independent predictors of the development of AF at the hospital stage after CABG operation.Conclusion In patients at low perioperative risk, a LVMM / BSA ratio ≥97 g / m2, a LA volume / BSA ratio ≥34.4 ml / m2, a RA appendage interstitial fibrosis score ≥2, and the presence of LVH were independent predictors of the development of AF at the hospital stage after CABG.

Short-term echocardiographic follow-up after hospitalization for COVID-19: a focus on early post-acute changes

BackgroundImpaired physical functional status is one of the typical long-term sequelae of COVID-19 infection that significantly affects the quality of life and work capacity. Minor changes in cardiac structure and function that are unable to cause the manifestation of overt heart failure may remain undetected in COVID-19 convalescents, at the same time potentially contributing to the persistence of symptoms and development of long COVID syndrome.PurposeTo study the typical features and short-term dynamics of cardiac remodeling and possible signs of cardiac dysfunction following hospitalization for COVID-19.MethodsThis is a combined cross-sectional and longitudinal cohort study in which 176 hospitalized patients (93 female and 83 male, mean age 53.4 ± 13.6 years) with COVID-19 infection underwent comprehensive transthoracic echocardiography pre-discharge (22.6 ± 7.1 days from the onset of symptoms) with repeated evaluation after 1 month. The control group included 88 age-, sex-, height- and weight-matched healthy individuals, with a subset of those (n = 53) matched to the subset of non-hypertensive study participants (n = 106).ResultsConcentric left ventricular geometry was revealed in 59% of participants, including 43% of non-hypertensive subjects; predominantly Grade I diastolic dysfunction was found in 35 and 25% of patients, respectively. Other findings were naturally following from described phenotype of the left venticle and included a mild increase in the absolute and relative wall thickness (0.45 ± 0.07 vs. 0.39 ± 0.04, p &amp;lt; 0.001), worsening of diastolic indices (e’ velocity 9.2 ± 2.2 vs. 11.3 ± 2.6 cm/s, p &amp;lt; 0.001, E/e’ ratio 7.5 ± 1.8 vs. 6.8 ± 1.7, p = 0.002) and global longitudinal strain (17.5 ± 2.4 vs. 18.6 ± 2.2, p &amp;lt; 0.001). No significant improvement was found on re-evaluation at 1 month.ConclusionsHospitalized patients recovering from COVID-19 were characterized by a high prevalence of left ventricular concentric remodeling, predominantly Grade I diastolic dysfunction, and a mild decrease in the longitudinal systolic function. These changes were less frequent but still prevalent in the non-hypertensive subgroup and largely persisted throughout the 1-month follow-up.

Blood volume contributes to the mechanical synchrony of the myocardium during moderate and high intensity exercise in women.

Whether blood volume (BV) primarily determines the synchronous nature of the myocardium remains unknown. This study determined the impact of standard blood withdrawal on left ventricular mechanical dyssynchrony (LVMD) in women. Transthoracic speckle-tracking echocardiography and central hemodynamic measurements were performed at rest and during moderate- to high-intensity exercise in healthy women (n = 24, age = 53.6 ± 16.3year). LVMD was determined via the time to peak standard deviation (TPSD) of longitudinal and transverse strain and strain rates (LSR, TSR). Measurements were repeated within a week period immediately after a 10% reduction of BV. With intact BV, all individuals presented cardiac structure and function variables within normative values of the study population. Blood withdrawal decreased BV (5.3 ± 0.7 L) by 0.5 ± 0.1L. Resting left ventricular (LV) end-diastolic volume (-8%, P = 0.040) and passive filling (-16%, P = 0.001) were reduced after blood withdrawal. No effect of blood withdrawal was observed for any measure of LVMD at rest (P ≥ 0.225). During exercise at a fixed submaximal workload (100W), LVMD of myocardial longitudinal strain (LS TPSD) was increased after blood withdrawal (36%, P = 0.047). At peak effort, blood withdrawal led to increased LVMD of myocardial transverse strain rate (TSR TPSD) (31%, P = 0.002). The effect of blood withdrawal on TSR TPSD at peak effort was associated with LV concentric remodeling (r = 0.59, P = 0.003). Marked impairments in the mechanical synchrony of the myocardium are elicited by moderate blood withdrawal in healthy women during moderate and high intensity exercise.

Association of fatty liver with left ventricular concentric remodeling: Insights from the Corinthia study

Abstract Introduction Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver disease, affecting approximately 25% of the population worldwide. In the majority of patients with NAFLD, other metabolic disorders, such as obesity, diabetes mellitus, dyslipidemia, and metabolic syndrome, are usually present. Purpose To study how NAFLD and steatosis are associated with left ventricular (LV) concentric remodeling and LV hypertrophy (LVH). Methods In this cross-sectional study we examined 1649 participants (997 women) of the Corinthia region, with a mean age of 64±12 years. Several demographic and clinical characteristics were recorded. Echocardiography was performed to all subjects. LV mass was calculated with the method of Devereux et al. LV mass was subsequently indexed for body surface area (BSA), and LVH was defined as left ventricular mass indexed for BSA ≥ 115 g/m2 in men and ≥ 95 g/m2 in women. Hepatic steatosis index (HSI) with the formula (8 × (ALT/AST) + BMI + (2, if diabetes mellitus) + (2, if female)) was used as a predictor of NAFLD. HSI values &amp;gt;36 was used to rule in steatosis. Results From the study population, 1353 were included in the steatosis category. Between the steatosis and non-steatosis group, there was a significant difference in age, gender, BMI and BSA and in several cardiovascular risk factors, including hypertension (Table 1). Interestingly, LV mass 155±38 gr vs. 142±31 gr, p&amp;lt;0.001) and LV mass index (82±17 gr/m2 vs. 79±14 gr/m2, p=0.01) were increased in the steatosis compared to non-steatosis group. LVH prevalence was higher in the steatosis compared to non-steatosis group (11% vs. 2%, p&amp;lt;0.001). Since significant confounders may interfere in the association of steatosis with LVH, we proceeded to a logistic regression analysis that confirmed the independent predictive value of steatosis to LVH (Table 2). Conclusion These findings highlight the interaction of cardiometabolic risks factors, liver steatosis and NAFLD with left ventricular remodeling and left ventricular hypertrophy independently of other known cardiovascular risk factors.

Abstract 14700: Associations of Left Ventricular Structure With Cumulative Systolic Blood Pressure Load: A Report From Women’s Ischemia Syndrome Evaluation - Coronary Vascular Dysfunction Study

Background: Recent studies have identified cumulative systolic blood pressure load to be associated with increased risk of adverse cardiovascular disease (CVD) outcomes. Similarly, associations between left ventricular (LV) structure and CVD events have long been recognized. Purpose: The purpose of this study was to assess the association between cumulative systolic blood pressure (CuSBP) load and LV structure in women with suspected ischemia with no obstructive coronary arteries (INOCA). Methods: Women enrolled in the Women’s Ischemia Syndrome Evaluation - Coronary Vascular Dysfunction (WISE-CVD) study (NCT00832702) underwent cardiac magnetic resonance imaging (CMRI) for LV structure and those (n= 225) who had at least 2 blood pressure (BP) measures recorded at a single site before their baseline CMRI were included in this analysis. Cumulative systolic BP (CuSBP) was defined as systolic BP (SBP) ≥ 130 divided by all SBP readings and each mean value multiplied by the years. LV remodeling index was defined as the ratio between LV mass and LV end diastolic volume (LVEDV). Results: The mean age was 55±10 years, body mass index (BMI) 26.3 ± 5.5 kg/m 2 , 36% had a history of hypertension, number of BP medications was mean 2.7 ± 1.6 [median 2 (range 0, 8)], and SBP and DBP were 126 ± 15 and 66 ± 10 mmHg respectively. Age, BMI and history of hypertension were significantly associated with higher CuSBP load. In univariate analyses, LV end diastolic volume and LV end systolic volume decreased, and LV remodeling index increased across CuSBP quartiles while LV mass index did not significantly differ among the quartiles (Figure 1) . In multivariable regression analysis, the association between CuSBP and LV mass index and LV remodeling index remained significant. Conclusions: Among women with suspected INOCA, higher CuSBP load was associated with greater LV mass index and concentric LV remodeling independent of age. Changes in LV volumes may represent age-related changes in LV structure.

The Negative Impact of Insulin Resistance/Hyperinsulinemia on Chronic Heart Failure and the Potential Benefits of Its Screening and Treatment.

This opinion article highlights the potential alterations caused by insulin resistance and hyperinsulinemia on the cardiovascular system and their negative impact on heart failure (HF), and describes the potential benefits of an early screening with consequent prompt treatment. HF is the final event of several different cardiovascular diseases. Its incidence has been increasing over the last decades because of increased survival from ischemic heart disease thanks to improvements in its treatment (including myocardial revascularization interventions) and the increase in life span. In particular, incidence of HF with preserved ejection fraction (HFpEF) is significantly increasing, and patients with HFpEF often are also affected by diabetes mellitus and insulin resistance (IR), with a prevalence > 45%. Concentric left ventricular (LV) remodeling and diastolic dysfunction are the main structural abnormalities that characterize HFpEF. It is well documented in the literature that IR with chronic hyperinsulinemia, besides causing type 2 diabetes mellitus, can cause numerous cardiovascular alterations, including endothelial dysfunction and increased wall thicknesses of the left ventricle with concentric remodeling and diastolic dysfunction. Therefore, it is conceivable that IR might play a major role in the pathophysiology and the progressive worsening of HF. To date, several substances have been shown to reduce IR/hyperinsulinemia and have beneficial clinical effects in patients with HF, including SGLT2 inhibitors, metformin, and berberine. For this reason, an early screening of IR could be advisable in subjects at risk and in patients with heart failure, to promptly intervene with appropriate therapy. Future studies aimed at comparing the efficacy of the substances used both alone and in association are needed.

High Rates of Undiagnosed Target Organ Damage Among Adults with Elevated Blood Pressure or Diabetes Mellitus in a Community-Based Survey in Lesotho

IntroductionPrevalence of elevated blood pressure (BP) and diabetes mellitus (DM) is increasing in sub-Saharan Africa. Data on target organ damage such as retinopathy, left ventricular hypertrophy (LVH), renal impairment and peripheral neuropathy (PN) among persons with elevated BP and/or DM in sub-Saharan Africa remain scarce.AimTo determine at community-level the prevalence of retinopathy, LVH, renal impairment, and PN among adults with elevated BP and/or DM, and assess the association of elevated BP and/or DM with target organ damage in Lesotho.MethodsDuring a household-based survey, a sub-sample of adults with elevated BP (≥ 140/90 mmHg) and/or DM (glycosylated hemoglobin ≥ 6.5%), as well as comparators (BP < 140/90 mmHg, HbA1c < 6.5%) were screened for retinopathy, LVH, renal impairment, and PN. We used multivariable logistic regression for inferential analysis.ResultsOut of 6108 participants screened during the survey, 420 with elevated BP only, 80 with DM only, 61 with elevated BP and DM, and 360 comparators were assessed for target organ damage. Among those with elevated BP, and among those with DM with or without elevated BP, prevalence of retinopathy was 34.6% (89/257) and 14.4% (15/104); renal impairment was 45.0% (156/347) and 42.4% (56/132), respectively. Among those with elevated BP, 2.3% (7/300) and 65.7% (224/341) had LVH and left ventricular concentric remodeling, respectively. PN, only assessed among those with DM, was present in 32.6% (42/129). Elevated BP was associated with increased odds of retinopathy (aOR, 19.13; 95% CI, 8.52–42.94; P < 0.001) and renal impairment (aOR, 1.80; 95% CI, 1.27–2.55; P = 0.001). Presence of both elevated BP and DM was associated with an increased odds of retinopathy (aOR, 16.30; 95%CI, 5.69–46.68; P < 0.001), renal impairment (aOR, 2.55; 95% CI, 1.35–4.81; P = 0.004), and PN (aOR, 2.13; 95% CI, 1.04–4.38; P = 0.040).ConclusionWe found a high prevalence of undiagnosed target organ damage among adults with elevated BP and/or DM during community-based screening. These findings emphasize the importance of regular prevention and screening activities in this setting.