Echocardiographic Assessment Of Left Ventricular Mass Research Articles

Abstract 5930: The Effect of Spironolactone on Myocardial Structure and Function Measured by Echocardiography in Patients with Early Stage Chronic Kidney Disease

Introduction Early stage chronic kidney disease (CKD) is associated both with a high rate of adverse cardiovascular events and abnormal myocardial structure and function. Activation of the renin-angiotensin-aldosterone system is common in CKD and may result in adverse inflammatory, fibrotic and hypertrophic effects upon the heart and vasculature. Treatment with ACE inhibitors and ARBs frequently fails to suppress aldosterone production. We hypothesized that addition of the aldosterone antagonist spironolactone to ACE Inhibitors and ARB’s might reduce left ventricular (LV) mass and improve systolic and diastolic function measured by echocardiography. Methods One hundred and seventeen patients with stage 2 and 3 CKD, controlled hypertension (<130/85mmHg) and no history of cardiovascular disease or diabetes were recruited in to a double blind placebo controlled trial. After an active 4 week run in of spironolactone 25mg daily, patients were randomized to continue this treatment or receive placebo for a further 36 weeks. Echocardiographic assessment of LV mass, systolic and diastolic LV function was performed before run in and after 40 weeks of treatment. Results Compared to placebo, spironolactone reduced LV mass (mean (SD) −10g ± 10 vs.+3g ± 13, p<0.01). There was an improvement in LV Tei Index (−0.08 ± 0.1 vs. −0.001 ± 0.1, p<0.01) and mean basal long axis annular systolic velocities (Sm +1.4cm/s ± 1.9 vs. +0.1cm/s ± 1.1, p<0.01) but no difference in ejection fraction (+3% ± 5 vs.+2% ± 7). Transmitral E/A filing ratio (E/A +0.3 ± 0.3 vs −0.02 ± 0.2, p<0.05), basal annular early myocardial diastolic velocities (Ea +0.5cm/s ± 2.1 vs. −0.3cm/s ± 2.1, p<0.05), E/Ea ratio (−0.7 ± 1.9 vs. 0.1 ± 2.0, p<0.05), and colour flow propogation velocities (+8.7 ± 16.3 vs. −0.1 ± 16.6, p<0.05) were all improved. Systolic blood pressure was reduced with spironolactone but was not an independent predictor of change in any echocardiographic parameters. Conclusion Treatment with spironolactone reduced LV mass and improved both systolic and diastolic LV function. These data suggest that aldosterone plays an important role in cardiovascular disease in CKD and provides support for a clinical outcome trial investigating the use of aldosterone inhibitors to reduce cardiovascular risk.

Echocardiographic Assessment of Left Ventricular Mass in Neonatal and Adult Mice: Accuracy of Different Echocardiographic Methods

Echocardiography is an established method to estimate left-ventricular mass (LVM) in mice. Accuracy is determined by cardiac size and morphology and influenced by mathematical models. We investigated accuracy of three common algorithms in three early developmental stages. High-resolution echocardiography was performed in 35 C57/BL6-mice. Therefore, two-dimensional-guided M-mode echocardiography and parasternal short- and long-axis views in B-mode were obtained. LVM was assessed in vivo applying Penn (P), Area Length (AL), and Truncated Ellipsoid (TE) algorithms and validated with histomorphometry. Regression analysis of all mice showed fair estimation of LVM assessed with M-mode-based Penn algorithm (y = 0.6*x - 0.12, r: 0.71). In contrast two-dimensional assessment of LVM revealed close linear relationship with histomorphometry (y(AL)= 1.21*x - 12.1, r: 0.88, y(TE)= 1.38*x - 2.88, r: 0.86). Bias was lowest for LVM-AL at diastole underestimating 3.2%. In concordance with the summarized data, LVM-P revealed lower regression coefficients and significant underestimation in all three subgroups. Small hearts (<50 mg, n = 12) correlated best with LVM-AL at systole. Hearts of adolescent (50-75 mg, n = 13) and adult (75-100 mg, n = 10) mice revealed close linear relationship with LVM-AL and LVM-TE at diastole. Echocardiographic assessment of LVM is feasible in hearts weighting less than 50 mg and can be estimated best in systole. Hearts weighting more than 50 mg are estimated most accurately by means of LVM-AL at diastole.

Relation of Increase in Adiposity to Increase in Left Ventricular Mass from Childhood to Young Adulthood

This study evaluated the influence of adiposity on the progression of left ventricular (LV) mass from childhood to adulthood and the relation of LV mass to insulin resistance in young adulthood. One hundred thirty-two healthy children recruited into a longitudinal study at a mean age of 13 years and reevaluated at 27 years, at which time insulin resistance studies were also performed, were studied. Echocardiographic assessment of LV mass was made and indexed for height. Body mass index (BMI) at 13 years was highly correlated with BMI at 27 years, as was LV mass index at 13 and 27 years. The cross-sectional correlation of LV mass index and BMI at 13 years (r = 0.38, p < 0.0001) had strengthened considerably by 27 years (r = 0.55, p < 0.0001). A BMI increase > or = 5.5 kg/m2 from 13 to 27 years was associated with a significantly greater increase in the LV mass index (p < 0.0001) than a BMI change < 5.5 kg/m2, and this relation was similar in children who were thin and heavy at baseline. In young adulthood, the relation of LV mass index to lean mass was weaker than that of LV mass index to fat mass. The association of LV mass with insulin resistance was dependent on adiposity. In conclusion, adiposity and LV mass are related in childhood, and this association tracks and becomes stronger in young adulthood. Moreover, the increase in LV mass from childhood to young adulthood is related to the degree of increase in BMI, independent of BMI at 13 years, suggesting that an excessive increase in LV mass could be limited by controlling gain in body fat during adolescence.

The genetic determination of left ventricular mass in healthy adults.

The extent to which left ventricular (LV) mass, an independent cardiovascular risk factor, is determined by genetic factors is unclear. The aim of this study was to assess the heritability of LV mass and its association with three potential candidate genes. A population-based adult twin study model was utilized. Echocardiographic assessment of LV mass was performed in 110 twin pairs (mean age 55.9+/-10.9 years). An estimate of genetic determination, heritability, was calculated for the main echocardiographic parameters. The cohort were genotyped for the G-protein beta-3, aldosterone synthase, and beta-1 adrenoceptor genes. The intra-class correlation coefficients for LV mass were 0.69 for monozygotic (r-MZ) twins and 0.32 for dizygotic (r-DZ) twins, P=0.008 (heritability estimate of 0.69). This pattern persisted following correction for known confounding factors. Within-pair differences in the monozygotic, discordant and concordant dizygotic twins showed no differences for the three genes with respect to left ventricular wall thickness or mass. There was a non-significant trend towards a relationship between LV mass and the beta-1 adrenoceptor genotype. Within a normal population left ventricular mass has a significant genetic determination. Further investigation of potential candidate genes is required.

Echocardiographic assessment of LV mass in rabbits: models of pressure and volume overload hypertrophy.

We describe a method for the noninvasive measurement of left ventricular mass in small animals using two-dimensionally guided M-mode echocardiography. We compared echocardiographic cross-sectional area (CSA) and cubed-based volumetric indexes of left ventricular (LV) mass with postmortem wet weight in renovascular hypertension-induced pressure overload (group I) and acute aortic insufficiency-induced volume overload (group II) models of ventricular hypertrophy. CSA and cubed echocardiographic indexes correlated well with wet weight from a combination of group I and II animals and their controls (r = 0.89, P < 0.001 for both groups). Separate analyses of groups I and II also demonstrated significant relationships between mass indexes and wet weight using CSA and cubed formulas, respectively, in both pressure (r = 0.57, P = 0.01 and r = 0.71, P < 0.001) and volume (r = 0.90 and r = 0.89, P < 0.001) overload models. Echocardiographically predicted LV mass derived from cubed and CSA regression formulas was 89 and 56% sensitive for pressure overload hypertrophy in group I and 100% sensitive (both cubed and CSA methods) for volume overload hypertrophy in group II. Cubed and CSA mass regression formulas were 60 and 80% specific for hypertrophy in group I and 100 and 90% specific in group II. Normalization of predicted LV mass for body weight added little to the overall technique accuracy with measured sensitivities of 83 and 75% and specificities of 92 and 77%, respectively, for cubed and CSA methods. Two-dimensionally guided M-mode echocardiography provides a reasonably accurate method of LV mass determination in rabbits with pressure- or volume-overloaded ventricles.