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Changes in 2D echocardiography (2DE) speckle tracking imaging (STI) derived left ventricular (LV) strain (S) and strain rate (SR) precedes diminution of LV ejection fraction (LVEF) in adult valvular aortic stenosis (AS). We prospectively examined whether 2DE-STI derived multidirectional LV S and SR correlate with AS severity in children using LV mass index (MI) as the principal outcome variable. 52 children (10.4 ± 7.3 years) with isolated congenital AS were included; 13 mild (2.5 m/s < V max < 3.0 m/s), 25 moderate (3.0 m/s < V max < 4.0 m/s), and 14 severe (V max > 4.0 m/s). 2DE including Doppler and STI longitudinal strain (LS), strain rate (LSR), circumferential strain (CS), and strain rate (CSR) were measured. Univariate and multivariable linear regressions identified correlations between LVMI and strain indices. Three clinical and 2DE variables, and four strain indices were independently associated with LVMI. LVMI correlated positively with systolic blood pressure and aortic regurgitation, and negatively with LVEF. LVMI correlated positively with LSR (four-chamber) and CSR (basal), and negatively with segmental CS in the inferior (basal) and anteroseptal (distal) segments. LVMI showed significant inverse association with LS (P =.05), LSR (P <.001), CS (P <.005), and CSR (P <.0001), independent of AS severity. Independent of clinical and 2DE findings including contemporaneous Doppler estimates of AS gradient, both longitudinal and circumferential strain indices correlate with LVMI as a measure of cumulative hemodynamic burden. This association implies subclinical LV dysfunction. • LV strain indices correlate with AS severity in children using LV mass index. • LVMI correlated positively with systolic blood pressure and aortic regurgitation. • Longitudinal and circumferential strain indices correlate with LVMI. • Myocardial strain indices notably correlated with of cumulative hemodynamic burden. [ABSTRACT FROM AUTHOR]

Purpose We investigated the relationship of left ventricular (LV) diastolic dysfunction and LV mass index (LVMI) against pulmonary hypertension (PH) in systemic autoimmune disease (SAD). Methods A total of 84 SAD patients (68 females; 53 ± 17 years; systemic lupus erythematosus, 27%; scleroderma, 17%; vasculitis, 16%; mixed connective tissue disease, 13% and polymyositis/dermatomyositis complex, 10%) without significant pericardial effusion (PE) on TTE (Vivid E9, GE) were analyzed. On TTE, PH was defined as peak tricuspid regurgitation velocity (TRV) of ≥ 2.9 m/s based upon 2015 ESC guideline. Left atrial volume index (LAVI) and E/E′ were measured as indicators of LV diastolic dysfunction. LVMI was also measured. Results Seven patients (8%) had PH. PH patients had greater LAVI (p < 0.001), E/E′ (p = 0.004), LVMI (p = 0.009) than non-PH patients. LAVI (R = 0.458), E/E′ (R = 0.337), and LVMI (R = 0.313) significantly and positively correlated with TRV (all p < 0.05). Multiple regression analysis was performed to explore determinants of TRV. Age, female sex, and brain natriuretic peptide (BNP) were included in all the models. Three multiple regression models were generated using 1) LAVI, 2) E/E′, and 3) LVMI and included LAVI, E/E′, LVMI, and BNP as significant variables influencing TRV. Multi logistic regression analysis for predicting TRV of ≥ 2.9 m/s showed that LAVI, and E/E′ were significant predictors (Odds ratio, 1.296, and 1.370, respectively). Conclusion In SAD patients without PE, LV diastolic dysfunction and increment of LVMI was closely associated with PH based upon TRV. LAVI and E/E′ were independent predictors for PH. Measuring LAVI and E/E′ may be a key to determine the mechanism of PH in these patients. [ABSTRACT FROM AUTHOR]

Aims To examine whether increasing fasting plasma glucose (FPG) levels were associated with worsening left ventricular (LV) diastolic function, independently of LV mass index (LVMI) in elderly, otherwise healthy subjects. Methods and results We tested cross-sectional associations between echocardiographically determined averaged E/é ratio/diastolic function, LVMI, cardiovascular risk factors, and FPG categorized as normal (NFG), impaired (IFG), and new-onset diabetes mellitus (DM), in 483 men and 208 women aged 56–79 years without overt cardiovascular disease, who received no cardiovascular, anti-diabetic, or lipid-lowering drugs and had a preserved LV ejection fraction > 50%. Median E/é was significantly higher among subjects with diabetes than those without (8 vs. 7; p = 0.03), as was the prevalence of grade 2 or 3 diastolic dysfunction (25% vs. 16%; p = 0.02). E/é and diastolic function were significantly associated with LVMI (p ⩽ 0.002), but not FPG category, on multivariable analysis. However, interaction analyses revealed that increasing LVMI was primarily associated with worsening diastolic function (higher E/é) in subjects with FPG > 6 mmol/L (β = 0.005 for IFG and DM vs. 0.001 for NFG; p = 0.02), whereas increasing systolic blood pressure was primarily associated with worsening diastolic function (higher E/é) in subjects with FPG ⩽ 6.9 mmol/L (β = 0.005 for NFG and 0.003 for IFG vs. − 0.001 for DM; p = 0.001). [ABSTRACT FROM AUTHOR]

Background/objectives: There are few studies investigating the long-term association between childhood blood pressure (BP) and adult cardiovascular remodeling. We seek to examine the effect of elevated childhood BP on cardiovascular remodeling in early or middle adulthood. Methods: We used the “Beijing BP Cohort Study”, where 1259 subjects aged 6–18 years old were followed over 24 years from childhood (1987) to early or middle adulthood (2011). Anthropometric measures and BP were obtained at baseline and follow-up examinations. Carotid–femoral pulse wave velocity (cfPWV), carotid intima-media thickness (cIMT), and left ventricular mass index (LVMI) were measured to assess cardiovascular remodeling in early or middle adulthood. Multiple logistic regression models were used to assess the odds ratio (OR) and 95% confidence interval (CI) for cardiovascular remodeling. Results: 82 out of 384 children with elevated BP (21.4%) had adult hypertension. Compared to those with normal BP, children with elevated BP were at 2.1 times (95% CI: 1.4–3.1) likely to develop hypertension in early or middle adulthood. Compared to those with normal BP, children with elevated BP were at higher OR of developing high cfPWV (OR = 1.8, 95% CI = 1.3–2.4), high cIMT (1.4, 1.0–1.9), or high LVMI (1.4, 1.0–1.9) in early or middle adulthood. The ORs for remodeling (for any measures) were 1.4 (0.9–2.0) in early adulthood for children age 6–11 years, and 1.6 (1.1–2.4) in middle adulthood for those aged 12–18 years. Conclusions: Children with elevated BP from 6 years old have accelerated remodeling on both cardiac and arterial system in early or middle adulthood. [ABSTRACT FROM AUTHOR]

Structural and functional cardiac changes are known in obese adults. We aimed to assess the relationship between body mass index (BMI) and cardiac function in overweight and obese asymptomatic adolescents. Ninety three healthy adolescents, aged 12.6±1.2years, received weight, height, BMI, waist, hips, waist/hips ratio assessment, hematology and biochemistry tests and an echocardiogram. Based on BMI, subjects were divided into: lean (L, n=32), overweight (Ov, n=33) and obese (Ob, n=32). Interventricular septal and LV posterior wall thickness were increased parallel to the BMI (L: 0.84±0.1cm, Ov: 0.88±0.1cm, Ob: 0.96±0.1cm, p<0.001, and L: 0.78±0.1cm, Ov: 0.8±0.1cm, Ob: 0.94±0.1cm, p<0.001, respectively) as were relative wall thickness (RWT) and mass index (LVMI) (L: 0.34±0.05, Ov: 0.34±0.05, Ob: 0.40±0.04, p<0.001, and L: 47.7±8.4g/m2, Ov: 51.9±8.3g/m2, Ob: 65.2±13.3g/m2, p=0<001, respectively). LV early diastolic (E′) lateral and septal velocities (L: 15.3±3.9cm/s, Ov: 13.6±4cm/s, Ob: 10.5±3.4cm/s, p<0.001, and L: 12.2±2.3cm/s, Ov: 11.1±2.4cm/s, Ob: 9.8±3.1cm/s, p=0.003, respectively), and systolic (S′) velocities (L: 9.2±1.4cm/s, Ov: 9.3±2.3cm/s, Ob: 8.04±1.5cm/s, p=0.018, and L: 9.05±2.3cm/s, Ov: 9±2.4cm/s, Ob: 7.6±1.1cm/s, p=0.014, respectively) were all reduced, only in obese adolescents. LV lateral E′ (r=−0.44, p<0.001) and S′ (r=−0.29, p=0.005) correlated with BMI. In asymptomatic adolescents, LV wall is thicker and diastolic function impaired and correlate with BMI. These findings demonstrate early cardiac functional disturbances which might explain the known obesity risk for cardiac disease. [ABSTRACT FROM AUTHOR]

Background: Farnesyltransferase (FT), an essential enzyme at the downstream of mevalonate pathway, was reported to be upregulated in hypertrophic cardiomyocytes of spontaneously hypertensive rats (SHRs) compared with myocardium of Wistar-Kyoto rats (WKYs). This upregulation was accompanied with cardiac remodeling. This study was designed to determine whether FT inhibition can alter cardiac remodeling in SHRs., Methods: Twelve-week-old SHRs were randomized to receive infusion of either NS or FTI-276 (307 μg/kg/d i.v. each n=10). WKY rats served as normal controls (n=6). Echocardiography was performed before and after intervention. SHR hearts were perfused ex vivo for the evaluation of cardiac performance, collagen deposition and biochemical changes (activation of Ras, extracellular-signal regulated kinases/ERK1/2, procollagen type І/Ш, TGF-β1, connective tissue growth factor/CTGF, and bone morphogenetic protein-7/BMP-7 expression)., Results: FTI-276 intervention decreased interventricular septum wall thickness at end- diastole (IVSd) and relative wall thickness (RWT) of SHRs (P<0.05). Three week intervention with FTI-276 attenuated hydroxyproline content (P<0.05), collagen deposition (P<0.01), Ras activation, ERK1/2 phosphorylation (P<0.01) and mRNA expression of procollagen type I, TGF-β1 and CTGF and elevated mRNA expression of BMP-7 (P<0.05) in left ventricle of SHRs., Conclusion: The present study indicated that FT inhibition could attenuate myocardial fibrosis and partly improve cardiac remodeling in SHRs. The beneficial effects might be mediated through suppression of the activation of Ras and ERK1/2 phosphorylation pathway. The enhanced mRNA expression of BMP-7 with inhibition of TGF-β1 and CTGF mRNA expression might be an important mechanism., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)