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Background and aims Elevated serum calcium and phosphorus have been associated with increased risk of cardiovascular disorders. We evaluated whether abnormal calcium and high serum phosphorus are associated cross-sectionally with echocardiographic measures of left ventricular (LV) structure and function, as doing so may provide insight into the etiology of cardiac disorders. Methods and results Included in the analysis were 5213 Atherosclerosis Risk in Communities Study (ARIC) participants who in 2011–2013 had echocardiography and serum calcium and phosphorus measurements. We evaluated the association of serum calcium (corrected for albumin) and phosphorus quintiles with measures of LV structure and function, after adjusting for other cardiovascular risk factors. Participants were on average 75.3 years old; 59.1% were female and 19.8% were African American. Mean (±SD) concentrations of calcium and phosphorus were 9.33 ± 0.38 and 3.46 ± 0.45 mg/dL, respectively. Higher calcium was associated with lower LV end-diastolic diameter (LVEDD) but greater prevalence of concentric remodeling (p-trend: 0.005 and 0.004 respectively). We observed association between high phosphorus and high septal E/e’ (p-trend: 0.02). Likewise, higher serum phosphorus was associated with higher left atrial volume index (p-trend: 0.001) and LV hypertrophy prevalence (p-trend: 0.04). Conclusions In conclusion, higher calcium was associated with more concentric remodeling but lower LVEDD, suggesting complex associations between calcium and cardiac function. Serum phosphorus was related to worse indices of LV diastolic function and LV hypertrophy, but not to LV systolic function. However, the magnitudes of association were modest, so clinical implications of these findings may be limited.

Heart failure (HF) is a leading cause of morbidity. Strategies for preventing HF are paramount. Prevalent valvular calcification (VC) is associated with HF risk but less is known about progression of mitral annular (MAC) and aortic valve calcification (AVC). VC progression (interval change of >0

Obesity and low muscle mass may coexist as age-related changes in body composition. We aimed to investigate the effect of visceral adiposity and skeletal muscle mass on left ventricular (LV) structure and function in the general population.A total of 1941 participants without known cardiovascular disease were enrolled from the Korean Genome and Epidemiology Study. Visceral fat area (VFA) was assessed by computed tomography. Appendicular skeletal muscle mass (ASM) was estimated by dual-energy X-ray absorptiometry and was used as a percentage of body weight (ASM/Wt). LV structure and function were assessed by tissue Doppler imaging (TDI) echocardiography.Across VFA tertiles, ASM increased, but ASM/Wt decreased (all P0.001). In multivariate models adjusted for conventional cardiovascular risk factors, LV mass index and LV diastolic parameters, such as left atrial dimension, TDI Ea velocity, and E/Ea ratio, were significantly impaired as VFA increased. On the other hand, an increase in ASM/Wt was associated with a decrease in LV mass index and improvement of LV diastolic parameters. With regard to LV mass index and TDI Ea velocity, VFA and ASM/Wt showed synergistic effects (all P interaction0.05). When both VFA and ASM/Wt were simultaneously included in the same model, both remained independent predictors of LV mass index and TDI Ea velocity.More visceral fat and less muscle mass are independently and synergistically associated with an increase in LV mass index and impairment of LV diastolic parameters. Further research is needed to explore the complex mechanisms underlying these associations.

Ultrasound targeted microbubbles destruction (UTMD) mediated the angiopoietin 1 (Ang1) gene transfecting can improve angiogenesis, it may be also reverse left ventricular structure and sympathetic remodeling in myocardial infarction (MI) canines. 30 canines were randomly divided into 3 groups (each

Central blood pressure (BP) is a predictor of target organ damage. No previous population study addressed the question to what extent central compared with peripheral is related to left ventricular (LV) structure and function. In 577 Flemish recruited from the general population (47.8% women; mean

Background Transforming growth factor β (TGF-β) may be a crucial regulator of cardiac remodeling. We investigated the association between the TGF-β gene polymorphisms and left ventricular structure. Methods A total of 658 hypertensive subjects were genotyped for the TGF-β1 T869C and TGF-β3 (rs3917187 and rs4252338) polymorphisms. Results TGF-β3 rs3917187 AA homozygotes had, while accounting for covariates, greater left ventricular end-systolic (LVESD, P = 0.004) and end-diastolic dimension (LVEDD, P = 0.007) than G allele carriers. Moreover, left ventricular mass index (LVMI) in AA genotype was 123.0 ± 3.1 g/m 2 significantly higher than that in AG (114.6 ± 1.6 g/m 2 ) and GG (115.4 ± 2.1 g/m 2 , P = 0.03) genotypes. In multivariate regression analysis, TGF-β3 rs3917187 genotype as an independent predictor had statistically significant effects on LVESD ( β = 0.164, P = 0.002), LVEDD ( β = 0.172, P = 0.003) and LVMI ( β = 0.136, P = 0.016), respectively. In further analyses, we observed a significant interaction between the rs3917187 and alcohol intake in relation to LVESD ( P int = 0.04) and left ventricular fractional shortening (LVFSH, P int = 0.012). However, no relationship could be found between left ventricular parameters and the T869C or the rs4252338. Conclusion The present results demonstrated that the TGF-β3 rs3917187 polymorphism was associated with left ventricular structure, and had an interactive influence with alcohol on LVESD and LVFSH in hypertensive subjects.

We examined the association of serum leptin with future cardiac structure and function. Multicenter longitudinal study of black, white, Hispanic and Asian men and women. 948 participants were included in this study. Cardiac MRI(CMR) was completed 6 years after serum leptin was measured. Leptin

Twelve heart transplant recipients selected for conversion from cyclosporine to tacrolimus because of adverse effects of cyclosporine therapy underwent echocardiography at baseline and 6 months after conversion. Left ventricular mass decreased by 24% and left ventricular geometry returned toward normal at 6 months after conversion, without significant changes in blood pressure.

OBJECTIVESThis study was designed to assess the relation of electrocardiographic (ECG) strain to increased left ventricular (LV) mass, independent of its relation to coronary heart disease (CHD).BACKGROUNDThe classic ECG strain pattern, ST depression and T-wave inversion, is a marker for left ventricular hypertrophy (LVH) and adverse prognosis. However, the independence of the relation of strain to increased LV mass from its relation to CHD has not been extensively examined.METHODSElectrocardiograms and echocardiograms were examined at study baseline in 886 hypertensive patients with ECG LVH by Cornell voltage-duration product and/or Sokolow-Lyon voltage enrolled in the Losartan Intervention For End point (LIFE) echocardiographic substudy. Strain was defined as a downsloping convex ST segment with inverted asymmetrical T-wave opposite to the QRS axis in leads V5and/or V6.RESULTSStrain occurred in 15% of patients, more commonly in patients with than without evident CHD (29%, 51/175 vs. 11%, 81/711, p < 0.001). When differences in gender, race, diabetes, systolic pressure, serum creatinine and high density lipoprotein cholesterol were controlled, strain on baseline ECG was associated with greater indexed LV mass in patients with (152 ± 33 vs. 131 ± 32 g/m2, p < 0.001) or without CHD (131 ± 24 vs. 119 ± 22 g/m2, p < 0.001). In logistic regression analyses, strain was associated with an increased risk of anatomic LVH in patients with CHD (relative risk 5.14, 95% confidence interval [CI] 1.16 to 22.85, p = 0.0315), without evident CHD (relative risk 2.91, 95% CI 1.50 to 5.65, p = 0.0016), and in the overall population when CHD was taken into account (relative risk 2.98, 95% CI 1.65 to 5.38, p = 0.0003).CONCLUSIONSWhen clinical evidence of CHD is accounted for, ECG strain is likely to indicate the presence of anatomic LVH. Greater LV mass and higher prevalence of LVH in patients with strain offer insights into the known association of the strain pattern with adverse outcomes.

OBJECTIVESOur study goal was to analyze whether gene variants of angiotensin II type 2-receptor (AT2-R) modulate the effects of angiotensin II on the left ventricle (LV).BACKGROUNDExperimental data suggest that angiotensin II modifies ventricular growth responses via angiotensin II type 1-receptors (AT1-R) and AT2-R.METHODSIn 120 white, young male subjects with normal or mildly elevated blood pressure, we assessed plasma angiotensin II and aldosterone concentrations (RIA), 24-h urinary sodium excretion, 24-h ambulatory blood pressure and LV structure (two-dimensional guided M-mode echocardiography). The intronic +1675 G/A polymorphism of the X-chromosomal located AT2-R gene was investigated by single-strand conformational polymorphism analysis and DNA-sequencing.RESULTSHypertensive subjects with the A-allele had a greater LV posterior (11.0 ± 1.3 vs. 9.9 ± 1.3 mm, p < 0.001), septal (11.8 ± 1.4 vs. 10.1 ± 1.2 mm, p < 0.001) and relative wall thickness (0.44 ± 0.06 vs. 0.39 ± 0.06, p < 0.01) as well as LV mass index (138 ± 23 vs. 120 ± 13 g/m2, p < 0.001) than those with the G-allele. Confounding factors (i.e., body mass index and surface area, plasma angiotensin II, sodium excretion, systolic and diastolic ambulatory blood pressure) were similar between the two genotypes. In normotensive subjects, relative wall thickness (0.36 ± 0.05 vs. 0.35 ± 0.05) and LV mass index (115 ± 21 vs. 112 ± 17 g/m2) were nearly identical across the two genotypes, with similar confounding variables.CONCLUSIONSOur data indicate that the X-chromosomal located +1675 G/A-polymorphism of the AT2-R gene is associated with LV structure in young male humans with early structural changes of the heart due to arterial hypertension.

OBJECTIVES The study was done to evaluate reliability of echocardiographic left ventricular (LV) mass. BACKGROUND Echocardiographic estimation of LV mass is affected by several sources of variability. METHODS We assessed intrapatient reliability of LV mass measurements in 183 hypertensive patients (68% men, 65 ± 9 years) enrolled in the Prospective Randomized Enalapril Study Evaluating Regression of Ventricular Enlargement (PRESERVE) trial after a screening echocardiogram (ECHO) showed LV hypertrophy. A second ECHO was repeated at randomization (45 ± 25 days later). Two-dimensional (2D)-guided M-mode or 2D linear measurements of LV cavity and wall dimensions were verified by one experienced reader. RESULTS Mean LV mass was similar at first and second ECHO (243 ± 53 vs. 241 ± 54 g) and showed high reliability as estimated by intraclass correlation coefficient (RHO) = 0.93. Within-patient 5th, 10th, 90th and 95th percentiles of between-study difference in LV mass were −32 g, −28 g, +25 g and +35 g. Mean LV mass fell less from the first to the second ECHO than expected from a formula to predict regression to the mean (2 ± 19 vs. 17 ± 12 g, p < 0.001). Reliability was also high for LV internal diameter (RHO = 0.87), septal (RHO = 0.85) and posterior wall thickness (RHO = 0.83). Substantial or moderate reliability was observed for measures of LV systolic function and diastolic filling (RHO from 0.71 to 0.57). CONCLUSIONS Left ventricular mass had high reliability and little regression to the mean; between-study LV mass change of ±35 g or ±17 g had ≥95% or ≥80% likelihood of being true change.

Abnormalities in left ventricular (LV) structure and function have been shown in patients with diastolic hypertension and recently in subjects with isolated systolic hypertension. The purpose of this study was to determine whether abnormalities of cardiac structure or function are present in elderly subjects with borderline isolated systolic hypertension (defined as systolic blood pressure [BP] between 140 and 159 mm Hg, and diastolic BP90 mm Hg). Ninety-one subjects (mean age 77 years) from the original Framingham Heart Study with untreated borderline isolated systolic hypertension, who were free of cardiovascular disease, were compared with 139 normotensive (BP140/90 mm Hg) subjects (mean age 76 years). Measurements included M-mode values for LV structure, and 6 Doppler indexes of LV diastolic filling. Subjects with borderline isolated systolic hypertension and the control group differed in mean systolic (147 vs 125 mm Hg) and diastolic (76 vs 70 mm Hg) BP. Borderline systolic hypertension was the most frequent form of untreated hypertension in this elderly group. The sum of LV wall thicknesses (septum+posterior wall) was significantly higher in borderline hypertensive subjects than in normotensive ones (20.5 vs 19.7 mm; p = 0.002). No difference was detected in LV internal dimension or systolic function. After adjustment for age and other clinical variables, comparisons between the groups revealed significant differences in indexes of Doppler diastolic filling. Peak velocity of early filling, and the ratio of early to late peak velocities were lower in the hypertensive group (40 vs 44 cm/s [p = 0.03] and 0.69 vs 0.76 [p = 0.01], respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

The use of early coronary angiography to assess the benefits of coronary patency on left ventricular size and function fails to account for subsequent reocclusion or spontaneous reperfusion. To investigate the relationship between late vessel patency and changes in left ventricular structure and function after thrombolysis, echocardiography was performed within 48 hours and at 6 to 12 weeks in 30 patients treated with intravenous thrombolysis. Left ventricular endocardial surface area index (ESAj; cm2/m2) and extent of abnormal wall motion were quantitated in those with a patent (n = 20) and those with an occluded (n = 10) infarct-related artery on coronary angiography performed 8 +/- 6 days after thrombolysis. Mean ESAi increased from (53 +/- 7 to 61 +/- 10 cm2/m2; p less than 0.02) in the occluded group during the follow-up period but remained unchanged (60 +/- 11 to 62 +/- 11 cm2/m2; p = NS) in the patient group. Mean percentage of abnormal wall motion decreased in the patent group (27 +/- 16% to 18 +/- 16%; p less than 0.01), whereas no significant change was noted in the occluded group (20 +/- 13% to 23 +/- 17%; p = NS). Thus coronary patency at days after thrombolysis is associated with both improvement in regional left ventricular function and attenuated left ventricular dilatation.

To better characterize the cardiac structural and functional changes that are associated with aging, Doppler-echocardiography was performed on 23 young (mean age, 25 years) and 30 old (mean age, 70 years) healthy normotensive subjects. Left ventricular cavity dimensions and wall thickness were determined and left ventricular mass index was calculated from M-mode echocardiograms. Stroke volume was calculated from Doppler-measured aortic flow. Diastolic filling was evaluated by pulsed Doppler echocardiography of mitral inflow. Posterior wall thickness (1.0 vs 0.8 cm, p less than 0.05) and relative wall thickness (0.42 vs 0.35, p less than .05) were significantly greater in the elderly subjects compared with the younger subjects. Left ventricular mass index increased on average 0.25 gm/m2/yr but was not significantly increased in the elderly compared with the younger subjects (89 vs 77 gm/m2). Shortening fraction and stroke volume did not differ between the two groups. Diastolic filling was dramatically altered with aging, and the elderly subjects demonstrated a doubling of percent atrial contribution (37% vs 19%, p less than 0.0001) and halving of peak early-to-peak atrial velocity ratio (0.85 vs 1.77, p less than .01).

2010;55;A27.E259 J. Am. Coll. Cardiol. Sarah Lagedrost, Ted Plappert, Martin St John Sutton, and David Lynch STRUCTURE AND FUNCTION IN FRIEDREICH'S ATAXIA INFLUENCE OF GENETIC FACTORS ON LEFT VENTRICULAR This information is current as of April 13, 2010 http://content.onlinejacc.org located on the World Wide Web at: The online version of this article, along with updated information and services, is

Cross-sectional and longitudinal studies are reviewed that address the effects of training on several measures of central circulatory function, including gas exchange, cardiac output, left ventricular structure, and left ventricular function. Responses to training in healthy individuals, athletes, and patients with ischemic cardiovascular disease are compared.

M-mode and two-dimensional echocardiography now provide an armamentarium of noninvasive techniques that permit assessment of left ventricular pump function, quantitation of afterload, a load-independent assessment of contractile state, and quantitation of pressure overload hypertrophy. Combined application of these methods to problems in the assessment of hypertensive heart disease can clarify both disease mechanisms and therapeutic effects by identifying the contributions of changes in myocardial mass, alterations in contractile state and variations in afterload to a given phenomenon.

The utility of echocardiography in a clinical office practice was assessed by prospectively studying 93 patients. Each patient was examined by a cardiologist and a diagnosis and management plan was outlined. An M-mode and 2D echocardiogram was then obtained and interpreted by a second cardiologist without knowledge of the clinical findings. Patients were then categorized as follows: group 1, clinical and echo diagnosis agree, management unchanged (67 patients); group 2, clinical and echo diagnosis agree, management changed (two patients); group 3, clinical and echo diagnosis disagree, management unchanged (16 patients); and group 4, clinical and echo diagnosis disagree, management changed (eight patients). Echocardiography significantly altered management of 11 percent of patients, provided additional important information in 48 percent, and confirmed the clinical impression in 74 percent of patients. It was particularly helpful in determining left ventricular structure and function, valvular anatomy, and in the diagnosis of clinically unsuspected idiopathic hypertrophic subaortic stenosis.

It has been suggested that the heart plays an active role in the pathogenesis of arterial hypertension. If this is true, there must be early cardiac involvement in young normotensive subjects who develop hypertension later in life and differences in cardiac morphology or function may exist between young normotensive subjects with different risks of developing hypertension. M-mode echocardiography was performed in 51 normotensive male adolescents with at least one hypertensive parent (SHT). These subjects were compared with 55 normotensive sons of normotensive parents (SNT) and with 25 adolescents with borderline hypertension (BH). Control groups were matched for sex and age. The following morphologic parameters were significantly greater in the SHT group than in the SNT group: interventricular septum (0.54 +/- 0.08 vs 0.49 +/- 0.09 cm/m2; p less than 0.01) and posterior wall (0.54 +/- 0.11 vs 0.50 +/- 0.08 cm/m2; p less than 0.05) thickness, left ventricular mass (125.0 +/- 29.1 vs 109.2 +/- 25.4 gm/m2; p less than 0.005), and cross-sectional area (9.9 +/- 1.8 vs 8.9 +/- 1.6 cm2/m2; p less than 0.005). No significant differences between SHT and BH subjects were observed. Excursion of left ventricular posterior wall was significantly higher in the BH group. No differences were observed between SHT and SNT subjects. These data show that the same kinds of changes in cardiac morphology are present in normotensive subjects with a family history of hypertension and in subjects with borderline hypertension, suggesting that cardiac involvement may precede elevation of blood pressure.