Left Ventricular Structural Changes Research Articles

Left Ventricular Geometrical Changes in Severely Obese Adolescents: Prevalence, Determinants, and Clinical Implications

Left ventricular hypertrophy (LVH) is independently associated with a higher risk of cardiovascular morbidity and mortality in adults. Adiposity is a risk factor for LVH, independent of blood pressure. Potential causes of this nonhemodynamic pathogenesis identified in adults include adverse body fat distribution, insulin resistance, dyslipidemia, and obstructive sleep apnea syndrome (OSA). In severely obese adolescents, the determinants of obesity-induced changes in left ventricular structure are poorly characterized. Cardiac ultrasonographic, demographic, anthropometric, and comorbidity-related data were prospectively collected in adolescents with severe obesity refractory to conservative treatment who presented for surgical therapy. Differences between adolescents with LVH and without LVH were evaluated using independent samples t, chi-square, or Fisher’s exact test. Multivariable linear regression analysis was performed to evaluate associations with left ventricular structural changes, corrected for body mass index (BMI) z score. Forty-three patients entered analysis, of whom 24 (55.8%) showed LVH. The most common geometrical change was eccentric LVH (eLVH), occurring in 21 subjects (48.8%). Demographic and anthropometric variables did not differ between patients with and without LVH. Independent of BMI z score, left ventricular mass index was significantly associated with apnea–hypopnea index (AHI) (regression parameter B = 0.8; 95% CI 0.3 to 1.2). Interventricular septum thickness (IVST) was significantly associated with HOMA-IR values (B = 0.1; 95% CI 0.04 to 0.2), HDL-cholesterol (B = − 1.2; 95% CI − 2.2 to 0.1), and triglyceride levels (B = 0.5; 95% CI 0.001 to 0.9). LVH, especially eLVH, is highly prevalent amongst severely obese adolescents. Adverse changes in cardiac structure, increased IVST in particular, are independently associated with several nonhemodynamic comorbidities that are common in this population, namely OSA, insulin resistance, and dyslipidemia.

Treatment of Left Ventricular Circulation Disorder: Application of Echocardiography Information Data Monitoring.

BackgroundCardiac hypertrophy induced by pressure overload is one of the important causes of heart failure and sudden cardiac death. At present, there are few studies on the outcome of left ventricular hypertrophy and left ventricular function after complete pressure load removal.ObjectiveThis study aims to better simulate the changes of left ventricular structure and function during the process of left ventricular pressure overload and deloading, and to explore the application of echocardiography in it.MethodsIn this study, healthy male (BALB/C) mice were used as research objects to establish an ascending aorta constriction model, to carry out echocardiographic and hemodynamic examinations, to establish an ascending aorta deconstriction model in mice, and to carry out echocardiographic and hemodynamic examinations.ResultsCompared with the sham operation group, the left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD), interventricular septal (IVS), and left ventricular posterior wall (LVPW) in the constriction operation group were significantly increased (P=.02, P=.02, P=.02, and P=.02, respectively). LVESD, LVEDD, IVS, and LVPW in the early and late constriction groups were significantly decreased, and the degree of decrease in the early group was greater than that in the late group; compared with the sham operation group, left ventricular diastolic pressure in the constriction operation group increased significantly at 9 and 15 weeks after operation (P=.03). Left ventricular systolic pressure at 15 weeks after operation decreased to a certain extent but was higher than that of the sham operation group (P=.02). The maximal rate of the increase of left ventricular pressure at 3 weeks, 9 weeks, and 15 weeks after operation decreased significantly (P=.03, P=.02, and P=.02, respectively).ConclusionsIn this study, the ascending aorta coarctation model and descending aorta coarctation model were successfully established, which verifies the value of echocardiography information data monitoring in the treatment of left ventricular circulation disorders and the evaluation of surgical treatment.

Impact of Long-Term Burden of Body Mass Index and Blood Pressure From Childhood on Adult Left Ventricular Structure and Function.

BackgroundData are limited regarding the relationship between the life‐course burden of risk factors and adult cardiac function. This study sought to examine the impact of long‐term burden of body mass index (BMI) and blood pressure (BP) levels on changes in adult left ventricular (LV) structure and function in a community‐based cohort.Methods and ResultsThe longitudinal study cohort consisted of 1108 adult patients (726 White; 41.9% men; mean age, 48.2 years in the last survey) who had been examined 4 to 16 times for BMI and BP and echocardiographic LV structure and function in adulthood, with a mean follow‐up period of 38.8 years. The area under the curve was used as a measure of long‐term burden of BMI and BP. Adult LV mass index was significantly associated with childhood and adulthood BMI and systolic BP (SBP), and their area under the curve values (β=0.07–0.37; P<0.05 for all). Adult LV ejection fraction was negatively associated with childhood BMI (β=−0.08), adult BMI (β=−0.07) and BMI area under the curve (β=−0.07) (P<0.05 for all); the effects of SBP measures were not significant. Adult E/A ratio was negatively associated with adulthood SBP (β=−0.13; P<0.01) and total area under the curve of SBP (β=−0.13; P<0.01). E/e′ ratio was positively associated with BMI and SBP measures. The effects of diastolic BP measures were substantially similar to those of SBP measures. Participants with LV hypertrophy, eccentric hypertrophy, and concentric hypertrophy had significantly lower LV ejection fraction and higher E/e′ ratio.ConclusionsThese observations provide strong evidence that early‐life adiposity and BP levels and their life‐course cumulative burdens are associated with subclinical changes in adult LV structure and function in the general population.

Anthropometric and Biochemical Markers as Possible Indicators of Left Ventricular Abnormal Geometric Pattern and Function Impairment in Obese Normotensive Children.

Εmerging data indicate that various effects of obesity on the cardiovascular system can be evident during childhood. The aim of this study was to detect early changes in left ventricular structure and function in obese normotensive children and explore possible associations of these changes with anthropometric and biochemical parameters. Normotensive 8–11-year-old obese and normal weight children were included in the study. They all underwent anthropometric measurements, laboratory tests, and echocardiography study by conventional and tissue Doppler to assess geometric pattern and function of left ventricle. Statistically significant differences in most anthropometric and metabolic parameters were noticed between groups. Obese children showed higher left ventricular mass index (LVMI) (40.05 ± 9.44 vs. 28.31 ± 6.22), lower E/A ratio (1.76 ± 0.33 vs. 2.08 ± 0.56), and higher E/e’ (6.04 ± 1.13 vs. 5.43 ± 0.96) compared to lean peers. Waist-to-height ratio and hs-CRP correlated significantly with E/A in the obese group. Left ventricular hypertrophy was present in 47.2% of obese children and eccentric was the prominent type. Waist-to-height ratio and serum cortisol levels in plasma increased the odds of having any type of abnormal ventricular geometric pattern. Echocardiographic evaluation of left ventricle and diastolic function could be considered for obese normotensive children based on waist-to-height ratio, hs-CRP, and serum cortisol.

A randomized controlled trial of dapagliflozin on left ventricular hypertrophy in people with type two diabetes: the DAPA-LVH trial.

AimWe tested the hypothesis that dapagliflozin may regress left ventricular hypertrophy (LVH) in people with type 2 diabetes (T2D).Methods and resultsWe randomly assigned 66 people (mean age 67 ± 7 years, 38 males) with T2D, LVH, and controlled blood pressure (BP) to receive dapagliflozin 10 mg once daily or placebo for 12 months. Primary endpoint was change in absolute left ventricular mass (LVM), assessed by cardiac magnetic resonance imaging. In the intention-to-treat analysis, dapagliflozin significantly reduced LVM compared with placebo with an absolute mean change of −2.82g [95% confidence interval (CI): −5.13 to −0.51, P = 0.018]. Additional sensitivity analysis adjusting for baseline LVM, baseline BP, weight, and systolic BP change showed the LVM change to remain statistically significant (mean change −2.92g; 95% CI: −5.45 to −0.38, P = 0.025). Dapagliflozin significantly reduced pre-specified secondary endpoints including ambulatory 24-h systolic BP (P = 0.012), nocturnal systolic BP (P = 0.017), body weight (P < 0.001), visceral adipose tissue (VAT) (P < 0.001), subcutaneous adipose tissue (SCAT) (P = 0.001), insulin resistance, Homeostatic Model Assessment of Insulin Resistance (P = 0.017), and high-sensitivity C-reactive protein (hsCRP) (P = 0.049).ConclusionDapagliflozin treatment significantly reduced LVM in people with T2D and LVH. This reduction in LVM was accompanied by reductions in systolic BP, body weight, visceral and SCAT, insulin resistance, and hsCRP. The regression of LVM suggests dapagliflozin can initiate reverse remodelling and changes in left ventricular structure that may partly contribute to the cardio-protective effects of dapagliflozin.ClinicalTrials.gov IdentifierNCT02956811

Diastology: 2020-A practical guide.

Left ventricular (LV) diastolic function can be most conveniently assessed by echocardiography which provides reliable assessments of LV structure and function. Most patients with structural heart disease have variable degrees of myocardial dysfunction. LV structural changes as pathologic hypertrophy and systolic functional abnormalities as depressed LV long-axis systolic function are associated with diastolic dysfunction. The recognition of structural abnormalities and abnormal LV long-axis function as indices of diastolic dysfunction is an important difference between 2016 and 2009 guidelines. In addition, there are other Doppler findings indicative of diastolic dysfunction and abnormally elevated LV filling pressures. In the absence of clinical, 2D echocardiographic, and specific Doppler indices of diastolic dysfunction, mitral annulus early diastolic velocity (e'), left atrium (LA) maximum volume index, peak velocity of tricuspid regurgitation jet by continuous-wave Doppler, and ratio of mitral inflow early diastolic velocity to e' velocity can be used to draw inferences about LV diastolic function. In the presence of diastolic dysfunction, mean LA pressure and grade of diastolic dysfunction should be determined. When LA pressure at rest is normal, it is reasonable to proceed to diastolic stress testing in an attempt to identify patients with dyspnea due to heart failure. There are specific algorithms recommended in patients with atrial fibrillation, moderate or severe mitral annular calcification, and noncardiac pulmonary hypertension.

Relation Between Aortic Stiffness Index and Distensibility with Age in Hypertensive Patients.

BackgroundSystolic and diastolic blood pressure is associated with physiologic changes of aortic wall and left ventricular structure. We aimed to evaluate aortic stiffness index and distensibility, global longitudinal strain (GLS), post systolic index (PSI) in hypertensive patients and compare these parameters with normotensive subjects.Patients and MethodsEighty-two patients (42 hypertensive compared with 40 normotensive subjects) with preserved left ventricular ejection fraction and without significant coronary artery disease were enrolled in the study. Systolic and diastolic blood pressure was measured by automated BP measurement system. Aortic stiffness index and distensibility, GLS and PSI were measured by transthoracic echocardiography and compared in both study groups.ResultsAortic stiffness index (0.097 vs 0.069) and E/e´ (8.16 vs 6.56) were significantly higher in hypertensive patients, respectively (p<0.05). Aortic distensibility (cm2/dyn) (0.28 vs 0.42) and e´ (cm/s) (8.25 vs 9.52) were significantly lower in hypertensive patients than normotensive subjects (p<0.05). PSI and GLS were not significantly different between both study groups. Aortic stiffness index and distensibility had significant correlation with age in normotensive subjects while this correlation was not statistically significant in hypertensive patients.ConclusionHypertension is associated with diastolic dysfunction and abnormal aortic wall compliance. Age-related aortic wall changes can present early in hypertensive patients.

Patients with elevated blood pressure or stage 1 hypertension have structural heart disease.

The 2017 American College of Cardiology (ACC) and the American Heart Association (AHA) recommendations lower the hypertension threshold to 130/80 mmHg and recommends treatment for high-risk patients. Our aim is to determine whether the new blood pressure categories are associated with left ventricular (LV) structural changes and whether echocardiograms can provide risk stratification and help treatment initiation. We conducted a cross-sectional study and performed screening echocardiograms to consecutive primary care patients. We calculated the Framingham score to identify patients with a low or intermediate score who had structural heart disease.We classified everyone as having normal, elevated blood pressure, stage 1 or stage 2 hypertension according to the 2017 ACC/AHA guidelines. We defined structural heart disease as having LV hypertrophy and an abnormal LV mass index. We included 16 650 patients who underwent a screening echocardiogram and had recorded blood pressure. Out of the 16 650 patients, 1465 patients had a normal blood pressure, 1382 had elevated blood pressure, 1333 had stage 1 hypertension, and the remainder had stage 2 hypertension. The adjusted odds ratios of having structural heart disease for elevated blood pressure and stage 1 hypertension were 1.30; 95% CI, 1.112-1.64; P < 0.01 and 1.69; 95% CI, 1.25-2.30; P < 0.01, respectively. We identified 542 patients with stage 1 hypertension who had a low or intermediate Framingham score and 19% (95% CI, 16-23%) had structural heart disease. A quarter of patients identified as having elevated blood pressure or stage 1 hypertension have structural heart disease. Screening echocardiograms may help to risk stratify those patients deemed ineligible for treatment.

Reductions in Cardiac Structure and Function 24 Months After Spinal Cord Injury

Smaller heart structures and reduced cardiac function are documented in cross‐sectional comparisons of individuals with spinal cord injury (SCI) and age/weight matched able bodied controls. The smaller heart structures and reduced function may result from progressive cardiac atrophy similar to that observed with diminished physical activity, extended periods of bed rest, and space flight. It is unknown if there is progressive cardiac atrophy in the months following SCI. Additionally, slightly larger hearts and greater retention of function are found in individuals with thoracic compared to cervical injuries, suggesting that the level of spinal injury may differentially affect reductions in heart structure and function after SCI. Therefore, the purpose of this research was to 1) quantify cardiac structure and function of individuals within the first 24 months after injury, 2) identify the relationship between cardiac structure and function and time since injury, and 3) examine injury level’s effect on heart structure/function and time since injury. A cross‐sectional assessment of cardiac structure and function was made using transthoracic echocardiography (Vivid‐Q; GE Healthcare) on twenty‐nine (4F) volunteers who were 3‐ to 24‐months post‐injury. Myocardial structure and function were assessed using 2D, speckle‐tracking, and tissue Doppler in accordance with contemporary clinical echocardiographic guidelines. Heart rate and blood pressures were assessed simultaneously using a combination of a standard lead II electrocardiogram (ECG) and brachial oscillometric blood pressure monitor (Dash 5000 patient monitor, GE). The relationship between cardiac structure/function and time since injury were analyzed using linear regression. Neurological and sensory level of injury were entered into the model as covariates to determine whether or not the relationships differed with time since injury. Time since injury was most strongly associated with a reduction in left ventricular end‐diastolic volume (Δ= −2.07±0.70 ml·mo−1, r2=0.266, p=0.007), end‐systolic volume (Δ= −1.05±0.38 ml·mo−1, r2=0.237, p=0.012), and left ventricular mass (Δ= −3.0 ± 1.2 g·mo−1, r2=0.192, p=0.018). These changes in left ventricular structure were paralleled by a reduced stroke volume (Δ= −1.03±0.50 ml·mo−1, r2=0.154 p=0.048) and cardiac output (Δ= −0.12±0.04 L·min−1·mo−1, r2=0.322, p=0.002). There were no significant associations of blood pressures, wall thickness, or measures of diastolic function with time since injury (p&gt;0.050). The reductions in left ventricular structure and systolic function were not differentially affected by neurological or sensory level of injury (p= 0.412–0.973). These results suggest there are gradual reductions in left ventricular structure and systolic function over the 24 months following spinal cord injury which are not affected by the neurological or sensory level of injury. Although there is loss of left ventricular structure and function, blood pressure appears maintained suggesting peripheral compensatory adjustments. This information indicates that cardiac rehabilitation interventions should occur relatively soon after spinal cord injury to mitigate cardiac atrophy.Support or Funding InformationFunded by NIH Grant (R01‐HL‐117037) and The Spaulding Research Institute Leadership Catalyst

Chronic Nicotine Inhalation Promotes Differential Remodeling of the Right and Left Ventricles in Mice

IntroductionCigarette smoking continues to decline in the United States, but a rise in e‐cigarette use poses a threat to human health. E‐cigarettes, oft marketed as a healthier alternative to traditional forms of tobacco consumption, still contain nicotine. Cigarette smoking is a major risk factor in a vast array of pathological conditions including cancer and cardiovascular disease. Despite knowledge regarding the risks of cigarettes, the effects of inhaled nicotine have been poorly characterized. In this study, we sought to investigate the effects of inhaled nicotine on cardiac function and remodeling.MethodsMale C57BL6/J mice were exposed to air (control) or nicotine vapor (daily, 12 hours on/12 hours off) for 8 weeks. Nicotine exposure was assessed by weekly measurement of serum cotinine levels, which showed an average of 599±54 ng/ml in nicotine‐exposed mice. A subset of mice were implanted with an Angiotensin‐II (AngII) osmotic minipump (450 ng/kg/min) for 4 weeks. Cardiac structure and function were assessed using echocardiography and cardiac catheterization, followed by tissue collection for analysis.ResultsNicotine exposure produced a significant increase in right ventricular systolic pressure (RVSP; 39.6±4.2 mmHg, n=7) compared to air‐exposed controls (22.3±1.7 mmHg, n=8, p&lt;0.01). Nicotine‐associated RVSP elevation was similar to AngII infusion (38.0±2.0 mmHg, n=7). RVSP changes were associated with RV hypertrophy (free wall thickness of 0.50±0.02 mm in nicotine exposure versus 0.42±0.03 mm in air‐exposed control, n=8–9, p&lt;0.05) and increased angiotensin converting enzyme expression (3.87‐fold increase in nicotine exposure versus air‐exposed control, n=5, p&lt;0.05).Nicotine exposure alone produced no significant changes in left ventricular (LV) structure or angiotensin converting enzyme expression. Interestingly, co‐administeration of nicotine and AngII resulted in blunting of AngII‐mediated LV hypertrophy (posterior wall thickness; 0.83±0.03 mm versus 0.93±0.02 mm for AngII alone, n=19–23, p&lt;0.01). Furthermore, we have found preliminary evidence of blunted LV hypertrophic signaling in nicotine‐exposed, AngII‐infused mice which exhibited reduced phosphorylated mTOR/mTOR compared to AngII alone (n=5, p=0.076).DiscussionTaken together, these findings led us to conclude that chronic nicotine inhalation promotes differential remodeling of the right and left heart. Nicotine inhalation alone promotes hypertrophic remodeling of the RV, but produces no significant changes in the LV. Nicotine inhalation does, however, abrogate AngII‐induced hypertrophic LV remodeling. Ongoing experiments within our laboratory are exploring the mechanisms underlying this differential remodeling and anti‐hypertrophic effect.Support or Funding InformationNational Institutes of Health R01HL135635 (JG/EL/XY).

The role of inflammation in driving left ventricular remodeling in a pre-HFpEF model

The incidence of HFpEF continues to increase and ∼2/3 of the patient population are post-menopausal women. Unfortunately, most studies focus on the use of male animal models of remodeling. In this study, however, using female rats to set a model of pre-HFpEF, we provide insights to possible mechanisms that contribute to HFpEF development in humans that will lead us to a better understanding of the underlying pathophysiology of HFpEF.

Myocardial structural and functional changes in patients with liver cirrhosis awaiting liver transplantation: a comprehensive cardiovascular magnetic resonance and echocardiographic study

BackgroundCardiac dysfunction is increasingly recognized in patients with liver cirrhosis. Nevertheless, the presence or absence of structural alterations such as diffuse myocardial fibrosis remains unclear. We aimed to investigate myocardial structural changes in cirrhosis, and explore left ventricular (LV) structural and functional changes induced by liver transplantation.MethodsThis study included 33 cirrhosis patients listed for transplantation and 20 healthy controls. Patients underwent speckle-tracking echocardiography and cardiovascular magnetic resonance (CMR) with extracellular volume fraction (ECV) quantification at baseline (n = 33) and 1 year after transplantation (n = 19).ResultsCMR-based LV ejection fraction (CMRLV-EF) and echocardiographic LV global longitudinal strain (LV-GLS) demonstrated hyper-contractile LV in cirrhosis patients (CMRLV-EF: 67.8 ± 6.9% in cirrhosis vs 63.4 ± 6.4% in healthy controls, P = 0.027; echocardiographic GLS: − 24.2 ± 2.7% in cirrhosis vs − 18.6 ± 2.2% in healthy controls, P < 0.001). No significant differences in LV size, wall thickness, mass index, and diastolic function between cirrhosis patients and healthy controls were seen (all P > 0.1). Only one of the cirrhosis patients showed late gadolinium enhancement. However, cirrhosis patients showed a higher ECV (31.6 ± 5.1% vs 25.4 ± 1.9%, P < 0.001) than healthy controls. ECV showed a positive correlation with Child-Pugh score (r = 0.564, P = 0.001). Electrocardiogram-based corrected QT interval was prolonged in cirrhosis (P < 0.001). One-year post-transplantation, echocardiographic LV-GLS (from − 24.9 ± 2.4% to − 20.6 ± 3.4%, P < 0.001) and ECV (from 30.9 ± 4.5% to 25.4 ± 2.6%, P = 0.001) moved to the normal ranges. Corrected QT interval decreased after transplantation (from 475 ± 41 to 429 ± 30 msec, P = 0.001).ConclusionsMyocardial extracellular volume expansion with augmented resting LV systolic function was characteristic of cirrhotic cardiomyopathy, which normalizes 1-year post-transplantation. Thus, myocardial extracellular expansion represents a structural component of myocardial changes in cirrhosis.

Left ventricular structural and functional changes in Friedreich ataxia - Relationship with body size, sex, age and genetic severity.

IntroductionAlthough a concentric pattern of left ventricular (LV) geometry appears to be common in Friedreich ataxia (FRDA), there is no accepted method for diagnosing LV abnormalities in FRDA, sex and body size have often not been taken into consideration, and it has not been clear whether children and adults should be classified using the same criteria. The aim of this study was to better define the LV geometric changes in FRDA with respect to sex, body size and subject age, and to investigate the relationship of LV changes with genetic severity, as assessed by GAA repeat length within the shorter allele of the FXN gene (GAA1).MethodsEchocardiography was performed in 216 subjects (68 children, 148 adults), measurements were made at end-diastole of LV internal diameter (LVEDID), septal wall thickness (SWT), LV length (LVEDL) and LV volume (LVEDV), and calculations were made of relative wall thickness (RWT), LV mass and LV ejection fraction (LVEF).ResultsThe most common LV abnormalities in both adults and children with FRDA were increases in RWT and age-normalized RWT. In adults with a normal LVEF, all LV variables other than RWT were larger in males independent of body surface area (BSA), and all LV variables other than SWT and RWT were positively correlated with BSA. After adjustment for sex and BSA, GAA1 was a positive correlate of SWT and RWT (but not of LV mass), and was an inverse correlate of LVEDID, LVEDL and LVEDV. In children with a normal LVEF, SWT, LV mass and LVEDL were larger in males than females after adjusting for BSA, and in combination with sex, BSA was a positive correlate of all the LV variables except SWT and RWT. In children there were no correlations of GAA1 with any of the LV variables.ConclusionIn FRDA, increases in RWT and age-normalized RWT are the most frequent LV structural abnormalities, sex and body size are important determinants of most other LV structural variables in both children and adults, and increased genetic severity is associated with a smaller left ventricle and increased LV wall thickness in adults, but not associated with LV size or wall thickness in children.

Changes in Left Ventricular Function and Structure in Young Healthy Obese Women

Changes in Left Ventricular Function and Structure in Young Healthy Obese Women

Subclinical leaflet thrombosis is associated with impaired reverse remodelling after transcatheter aortic valve implantation.

Cardiac CT is increasingly applied for planning and follow-up of transcatheter aortic valve implantation (TAVI). However, there are no data available on reverse remodelling after TAVI assessed by CT. Therefore, we aimed to evaluate the predictors and the prognostic value of left ventricular (LV) reverse remodelling following TAVI using CT angiography. We investigated 117 patients with severe, symptomatic aortic stenosis (AS) who underwent CT scanning before and after TAVI procedure with a mean follow-up time of 2.6 years after TAVI. We found a significant reduction in LV mass (LVM) and LVM indexed to body surface area comparing pre- vs. post-TAVI images: 180.5 ± 53.0 vs. 137.1 ± 44.8 g and 99.7 ± 25.4 vs. 75.4 ± 19.9 g/m2, respectively, both P < 0.001. Subclinical leaflet thrombosis (SLT) was detected in 25.6% (30/117) patients. More than 20% reduction in LVM was defined as reverse remodelling and was detected in 62.4% (73/117) of the patients. SLT, change in mean pressure gradient on echocardiography and prior myocardial infarction was independently associated with LV reverse remodelling after adjusting for age, gender, and traditional risk factors (hypertension, body mass index, diabetes mellitus, and hyperlipidaemia): OR = 0.27, P = 0.022 for SLT and OR = 0.22, P = 0.006 for prior myocardial infarction, OR = 1.51, P = 0.004 for 10 mmHg change in mean pressure gradient. Reverse remodelling was independently associated with favourable outcomes (HR = 0.23; P = 0.019). TAVI resulted in a significant LVM regression on CT. The presence of SLT showed an inverse association with LV reverse remodelling and thus it may hinder the beneficial LV structural changes. Reverse remodelling was associated with improved long-term prognosis.

Effects of dexrazoxane on doxorubicin-related cardiotoxicity and second malignant neoplasms in children with osteosarcoma: a report from the Children\u2019s Oncology Group

BackgroundDexrazoxane protects from lower-cumulative-dose doxorubicin cardiotoxicity, but the effect of dexrazoxane in children with sarcoma treated with higher-cumulative-dose doxorubicin is unknown.MethodsWe evaluated children with osteosarcoma (OS) on two Children’s Oncology Group trials with higher dose doxorubicin (375–600 mg/m2) preceded by dexrazoxane (10:1 dexrazoxane:doxorubicin dosing). They were evaluated after the minimum expected treatment time (METT), defined as 28 weeks. Cardiotoxicity was identified by echocardiography and serum N-terminal pro-brain natriuretic peptide (NT-proBNP). Second malignant neoplasm (SMN) data was collected.ResultsAll children had normal left ventricular (LV) systolic function as measured by LV fractional shortening and no heart failure. The end-diastolic septal thickness Z-scores (P < 0.01) and LV mass Z-scores (P < 0.01) were significantly smaller than normal for body-surface area in both sexes. The average LV mass Z-scores were significantly smaller for girls (P < 0.01) and marginally smaller for boys (P = 0.06). Girls had significantly smaller LV end-diastolic dimension Z-scores normalized to BSA (P < 0.01) compared to healthy controls and had significant increases in NT-proBNP. Four children developed SMNs as first events, a rate similar to historical controls.ConclusionsDexrazoxane prevented LV dysfunction and heart failure in children with OS receiving higher dose doxorubicin. However, LV structural changes were not fully prevented, especially in girls. As a result, hearts become abnormally small for body size, resulting in higher LV stress. Dexrazoxane did not increase the risk of SMN. Dexrazoxane should be used in this population, particularly for girls, to mitigate anthracycline-induced cardiotoxicity.Trial registrationsClinicalTrials.gov: NCT00003937 (P9754) registered 1 Nov 1999, and NCT00023998 (AOST0121) registered 13 Sept 2001.

A Pilot Study of Third-Generation Dual-Source Computed Tomography for the Assessment of Global Dynamic Changes in Left Ventricular Structure and Function in a Porcine Model of Acute Myocardial Infarction.

BackgroundFirst-generation and second-generation dual-source computed tomography (DSCT) are useful for analyzing left ventricle (LV) structure and function. This pilot study aimed to investigate the feasibility and role of third-generation DSCT for the evaluation of dynamic changes in LV structural and functional characteristics in a Diannan small-ear pig model of acute myocardial infarction (AMI).Material/MethodsThe model of AMI was established by balloon occlusion of the distal third of the left anterior descending (LAD) coronary artery in 14 Diannan small-eared pigs. Third-generation DSCT was performed to observe dynamic changes in LV structure and function before and after AMI was induced, with a follow-up period of 30 days.ResultsThe mean structural measurements at baseline included interventricular septum thickness (8.50±0.90 mm), LV anterior wall thickness (8.40±1.30 mm), LV posterior wall thickness (7.80±1.20 mm), LV end-diastolic dimension (LVEDD) (45.00±4.90 mm), and LV end-systolic dimension (LVESD) (25.90±4.10 mm). The mean functional measurements at baseline included the LV end-diastolic volume (LVEDV) (74.62±13.54 ml), LV end-systolic volume (LVESV) (23.06±7.46 ml), LV ejection fraction (LVEF) (69.29±6.83%), LV mass (86.35±14.02 g), stroke volume (SV) (51.56±9.77 ml), and cardiac output (CO) (4.22±2.14 l/min). Trends of time-dependent changes were observed for LVESV, LVEF, SV, and CO, but not for LVEDV or LV mass.ConclusionsThird-generation DSCT was validated as a tool for assessing dynamic changes in LV global function in a porcine model of AMI.

P5316Birthweight, childhood growth patterns and left ventricular structure at midlife: Northern Finland 1966 Birth Cohort Study

Abstract Background Higher cardiac left ventricular (LV) mass (LVM) has independently been associated with cardiovascular risk and mortality. Changes in LV structure have been observed in children with obesity. However, information about the long-term influence of early growth on LV structure is limited. Purpose To explore the associations between early growth patterns, specifically birth weight, age and body mass index (BMI) at infant BMI peak and at childhood BMI rebound, and LV structure at midlife. Methods At the age of 46, a sample of the participants of the Northern Finland Birth Cohort 1966 took part in follow-up examinations. A randomly selected subpopulation was enrolled to echocardiographic examinations (n=1124). BMI at various ages in childhood was calculated from frequent anthropometric measurements collected from child welfare clinical records. Age and BMI at BMI peak (n=541, mean age 9.0 months) and at BMI rebound (n=657, mean age 5.8 years) were derived from random effect models. Results Birth weight (n=1124), BMI at BMI peak and at BMI rebound were directly associated with LVM (beta [standardized]: 0.171, 0.186 and 0.223, respectively, p&lt;0.001 for all) and LVM index (LVMI) (beta: 0.146, 0.120 and 0.120, respectively, p&lt;0.01 for all) at midlife. All the associations, except that between BMI at BMI peak and LVMI, remained significant after adjustments for gender, adult blood pressure, heart rate, antihypertensive medications, heart diseases and diabetes (p&lt;0.05 for all). Significant interaction between gender and age at BMI rebound was observed in LVMI. Age at BMI rebound was inversely associated with LVMI in both genders, the association being stronger in males (beta: −0.212, p&lt;0.001) compared to females (beta: −0.117, p=0.025) and independent of potential confounders. There were direct univariate associations of birth weight and BMI at BMI peak and rebound with LV relative wall thickness (p=0.009–0.019), which were largely explained by potential confounders. However, the association of birth weight with LV relative wall thickness retained its significance even after relevant adjustments (beta: 0.097, p=0.001). After additional adjustments for adult BMI, only associations of birth weight and BMI at BMI peak with LVM remained significant, which, however, did not remain significant after additional adjustment for adult height. Conclusions This study shows that birth weight and early growth patterns are associated with LV structure at midlife, which is largely explained by adult BMI. Therefore, the relationship between early growth patterns to LV structure in the adulthood may be largely explained by their strong tracking to obesity and related cardiovascular risk factors at midlife and to some extent by normal somatic growth.

Subclinical alterations in left ventricular structure and function according to obesity and metabolic health status.

BackgroundObesity and metabolic syndrome (MetS) are associated with high risk of cardiac dysfunction and heart failure. We assessed the effect of obesity and metabolic health status on left ventricular (LV) structure and function in subjects without overt heart disease.MethodsIn 789 subjects (58.8±13.0 years, 50.7% males) without overt heart disease, LV morphology and function were compared among 6 groups stratified by body mass index (BMI) (normal weight, overweight and obese) and metabolic health status (meeting ≤1 criterion of MetS excluding waist circumference defined as metabolically healthy; otherwise, metabolically unhealthy).ResultsLV ejection fraction (LVEF) was not different among the 6 groups (P>0.05). However, high BMI and poor metabolic health were associated with poorer global longitudinal strain (GLS), higher LV mass index (LVMI) and higher E/e′ (P<0.001). Poor metabolic health status was associated with greater adverse changes in LV structure and function than obesity, and among MetS components, high systolic blood pressure (SBP) showed the greatest impact. Higher SBP, BMI and triglycerides were independently associated with worse GLS, and higher SBP was also associated with worse LVMI and E/e´. GLS, LVMI and E/e´ worsened in proportion to the number of MetS criteria or continuous MetS scores. Adverse myocardial changes associated with obesity were significant in the metabolically healthy group, but not in the metabolically unhealthy group.ConclusionsObesity and poor metabolic health status were associated with subclinical decrement in LV systolic and diastolic function, and higher LV mass, but not with LVEF, in subjects without overt heart disease.

Age related structural and functional changes in left ventricular performance in healthy subjects: a 2D echocardiographic study

Left ventricular (LV) adaptation to aging is currently poorly understood. We aimed to characterize age related changes in LV structure and function by studying a large group of healthy subjects across a wide age range. Prospectively enrolled healthy volunteers (n = 778, 327 females; age 18 to 100years, mean age 49.8 ± 18.1years), were divided into 4 age groups: 18 to 34years (n = 165); 35 to 49years (n = 242), 50 to 79years (n = 334) and ≥ 80years (n = 40). All subjects underwent clinical examination, as well as comprehensive transthoracic echocardiogram [TTE]. Body mass index, systolic blood pressure (BP), and left atrial volume (p < 0.0001) increased with age while diastolic BP (p < 0.0001) decreased over time. LV mass/body surface area (BSA) and relative wall thickness increased with age (p < 0.0001) coincident with worsening parameters of diastolic function (E/A and E/Em, p < 0.0001). The ejection fraction and Sm did not change significantly. Stroke volume, ejection time index, flow rate and stroke work significantly increased with age (p < 0.01). The arterial elastance (Ea), a measure of ventricular afterload, and ventricular elastance (Ees), an index of LV systolic stiffness did not change with age nor did their ratio (Ees/Ea) the latter being an expression of ventricular-arterial coupling. Age, gender and LVM were the main independent variables associated with LV systolic function. In conclusion, LV adaptation to aging in a healthy cohort is characterized by concentric LV remodeling, increased contractility and preserved ventricular-arterial coupling.