LV Mass Index (lv + mass_index)

Distribution by Scientific Domains

Selected Abstracts

Right Ventricular Adaptations Along with Left Ventricular Remodeling in Older Athletes

Oner Ozdogan M.D.
Background: Afterload changes and anatomic interaction between the ventricles cause right ventricle (RV) adaptation along with left ventricle (LV) remodeling. This study was designed to evaluate RV adaptations along with LV remodeling and to determine the effect of aging on both ventricles in a population of older athletes. Methods: Echocardiographic characteristics of 48 endurance trained older athletes were examined by tissue Doppler imaging (TDI) and integrated backscatter (IBS). Results: Mean LV mass index was calculated as 107.8±17.0 g/m2. Twenty-two athletes were > 55 years old. Age was found to be a risk factor for diastolic dysfunction regarding lateral TDI velocities (Em < Am) (r = 0.385, P < 0.001). RV long-axis (LAX) diameters were associated with LA volumes and LV masses (r = 0.380, P < 0.01 and r = 0.307, P < 0.05). RV LAX diameters were correlated with RV TDI E-wave (r =,0.285, P < 0.05), RV LAX average, and peak IBS values (r = 0.36, P < 0.05 and r = 0.348, P < 0.05). Conclusions: TDI and IBS are applicable methods to evaluate the relationship between the two ventricles in athletes' heart. Increased RV LAX IBS values indicate increased LV mass and LA volume as a result of RV changes along with LV remodeling. Our data suggest that RV TDI E-wave and average RV IBS values reflect cardiac adaptations of both RV and LV in older athletes. [source]

The effect of low-carbohydrate diet on left ventricular diastolic function in obese children

Cenap Zeybek
Abstract Background:, This study was conducted to evaluate left ventricle (LV) functions using conventional and tissue Doppler imaging in childhood obesity and to identify the effects of diet on LV diastolic functions. Methods:, Conventional and tissue Doppler echocardiographic measurements were compared in 34 obese children and 24 age- and gender-matched lean controls. Fasting plasma glucose, insulin and homeostatic model assessment of insulin resistance levels were also obtained. Thirty-one of the obese children were subjected to a low-carbohydrate diet and their follow-up measurements were obtained after 6 months. Results:, Left atrial diameter, LV mass and LV mass index were higher in obese children than in lean controls. Lateral mitral myocardial early diastolic (Em) and peak Em/myocardial late diastolic (Am) were lower, and mitral E/Em and lateral mitral myocardial isovolumetric relaxation time were higher in obese subjects than in lean controls. Insulin and homeostatic model assessment of insulin resistance levels were higher in obese patients and decreased significantly after diet. After diet therapy, lateral mitral Em and peak Em/Am, were increased, mitral E/Em and myocardial isovolumetric relaxation time were decreased. Conclusions:, Obesity predisposes children to increased preload reserve, left ventricular subclinical diastolic dysfunction and deterioration in diastolic filling. Weight reduction with a low-carbohydrate diet seems to be associated with significant improvement in LV diastolic function and a decrease in diastolic filling, as well as causing reversal in insulin resistance seen in obese children. [source]

Myocardial iron clearance during reversal of siderotic cardiomyopathy with intravenous desferrioxamine: a prospective study using T2* cardiovascular magnetic resonance

Lisa J. Anderson
Summary Heart failure from iron overload causes 71% of deaths in thalassaemia major, yet reversal of siderotic cardiomyopathy has been reported. In order to determine the changes in myocardial iron during treatment, we prospectively followed thalassaemia patients commencing intravenous desferrioxamine for iron-induced cardiomyopathy during a 12-month period. Cardiovascular magnetic resonance assessments were performed at baseline, 3, 6 and 12 months of treatment, and included left ventricular (LV) function and myocardial and liver T2*, which is inversely related to iron concentration. One patient died. The six survivors showed progressive improvements in myocardial T2* (5·1 ± 1·9 to 8·1 ± 2·8 ms, P = 0·003), liver iron (9·6 ± 4·3 to 2·1 ± 1·5 mg/g, P = 0·001), LV ejection fraction (52 ± 7·1% to 63 ± 6·4%, P = 0·03), LV volumes (end diastolic volume index 115 ± 17 to 96 ± 3 ml, P = 0·03; end systolic volume index 55 ± 16 to 36 ± 6 ml, P = 0·01) and LV mass index (106 ± 14 to 95 ± 13, P = 0·01). Iron cleared more slowly from myocardium than liver (5·0 ± 3·3% vs. 39 ± 23% per month, P = 0·02). These prospective data confirm that siderotic heart failure is often reversible with intravenous iron chelation with desferrioxamine. Myocardial T2* improves in concert with LV volumes and function during recovery, but iron clearance from the heart is considerably slower than from the liver. [source]

Transforming growth factor ,1 genotype and change in left ventricular mass during antihypertensive treatment,results from the swedish irbesartan left ventricular hypertrophy investigation versus atenolol (Silvhia)

Pär Hallberg M.D.
Abstract Background: Angiotensin II, via the angiotensin II type 1 (AT1) receptor, may mediate myocardial fibrosis and myocyte hypertrophy seen in hypertensive left ventricular (LV) hypertrophy through production of transforming growth factor ,1(TGF-,1); AT1-receptor antagonists reverse these changes. The TGF-(,1 G + 915C polymorphism is associated with in-terindividual variation in TGF- ,1 production. No study has yet determined the impact of this polymorphism on the response to antihypertensive treatment. Hypothesis: We aimed to determine whether the TGF- ,1 G + 915C polymorphism was related to change in LV mass during antihypertensive treatment with either an AT1 -receptor antagonists or a beta1 -adrenoceptor blocker. The polymorphism was hypothesized to have an impact mainly on the irbesartan group. Methods: We determined the association between the TGF-,1 genotype and regression of LV mass in 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, randomized in a double-blind study to receive treatment for 48 weeks with either the AT1 -receptor antagonist irbesartan or the beta1 -adrenoceptor blocker atenolol. Results: Irbesartan-treated patients who were carriers of the C-allele, which is associated with low expression of TGF-,1, responded with a markedly greater decrease in LV mass index (LVMI) than subjects with the G/G genotype (adjusted mean change in LVMI ,44.7 g/m2 vs. ,22.2 g/m2, p = 0.007), independent of blood pressure reduction. No association between genotype and change in LVMI was observed in the atenolol group. Conclusions: The TGF- ,1 G + 915C polymorphism is related to the change in LVMI in response to antihypertensive treatment with the AT1 -receptor antagonist irbesartan. [source]