THE IMPACT OF OBESITY ON THE PREVALENCE OF LEFT VENTRICULAR HYPERTROPHY IN RELATION TO THE TYPE OF ADJUSTMENT OF LV MASS IN PATIENTS WITH ARTERIAL HYPERTENSION

2004 ◽  
Vol 22 (Suppl. 2) ◽  
pp. S34
Author(s):  
J.-C. Lubanda ◽  
A. Linhart ◽  
T. Palecek ◽  
Z. Hlubocka ◽  
E. Kejrova ◽  
...  
2011 ◽  
pp. 119-125
Author(s):  
Thi Thuy Hang Nguyen

Objective: Prehypertensive individuals are at increased risk for developing hypertension and their complication. Many studies show that 2/3 prehypertensive individuals develop hypertension after 4 years. ECG and echocardiography are the routine tests used to assess LV mass. The objective of the research to determine the percentage of change in left ventricular morphology in the ECG, echocardiography, which explore the characteristics of left ventricular structural changes by echocardiography in pre-hypertensive subjects. Materials and method: We studied a total of 50 prehypertensive, 30 males (60%) and 20 females (40%), mean age 48.20±8.47years. 50 normotensive volunteers as control participants. These subjects were examined for ECG and echocardiography. Results: In prehypertensive group, with 18% of left ventricular hypertrophy on electrocardiogram, 12% of left ventricular hypertrophy on echocardiography; in the control group, we did not find any subjects with left ventricular hypertrophy. In the group with left ventricular hypertrophy, mostly eccentric left ventricular hypertrophy (83.33%), concentric left ventricular hypertrophy is 16.67%. Restructuring of left ventricular concentric for 15.9% of subjects without left ventricular hypertrophy on echocardiography. Conclusion: There have been changed in left ventricular morphology even in prehypertensive


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Leah Cannon ◽  
Tadeusz Marciniec ◽  
Bryony Mearns ◽  
Robert M Graham ◽  
Diane Fatkin

Left ventricular hypertrophy (LVH) develops as a compensatory response to myocardial dysfunction due to diverse causes, but is nonetheless a major risk factor for premature cardiovascular morbidity and mortality. It is thus unclear if regressing LVH is beneficial or may worsen patient outcome. To evaluate the effects of LVH regression, we developed a transgenic mouse model in which the expression of a familial hypertrophic cardiomyopathy (FHC)-inducing mutation (R403Q alpha-MHC) can be regulated in a temporal and dose-dependent manner. In this model, transgene expression can be shut off by feeding with a tetracycline analogue (doxycycline). Serial echocardiography and histology studies were performed in a cohort of mice expressing the FHC mutant (“gene-on”) and in wildtype (WT) littermates. A second cohort of WT and 403/+ mice was randomised to placebo or doxycycline (“gene off”) from 6 (Dox6) or 20 weeks (Dox20) and evaluated at 40 weeks of age. Compared to WT littermates, “gene on” 403/+ mice showed increased LV mass, LV end-diastolic diameter (LVDD) and left atrial diameter (LAD), and reduced fractional shortening (LVFS), with changes evident from 12 weeks of age. LV sections from 403/+ mice showed typical features of FHC: myofibre disarray and interstitial fibrosis. LV mass, LV function and myocardial histology were unchanged in both male and female placebo- vs Dox6 or Dox20 mice at 40 weeks (Table 1 ). Thus, consistent with the major LV thickening in FHC humans occurring in adolescence, overexpression of R403Q for only 6 weeks is sufficient to trigger the complete LVH phenotypic response. Moreover, switching off the genetic trigger for LVH in 403/+ mice at 6 weeks (prior to overt disease manifestation) or 20 weeks (established disease) does not induce regression of LVH or exacerbate contractile dysfunction. Interventions to induce LVH regression may, therefore, need to be directed at downstream factors in hypertrophic pathways. Table 1. Echo data for male WT and 403/+ mice aged 40 weeks


Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1803
Author(s):  
Paweł Gać ◽  
Karolina Czerwińska ◽  
Małgorzata Poręba ◽  
Adam Prokopowicz ◽  
Helena Martynowicz ◽  
...  

The aim of the study was to assess the relationship between serum selenium and zinc concentrations (Se-S and Zn-S) and the left ventricle geometry in patients suffering from arterial hypertension. A total of 78 people with arterial hypertension (mean age: 53.72 ± 12.74 years) participated in the study. Se-S and Zn-S were determined in all patients. The type of left ventricular remodelling and hypertrophy was determined by the left ventricular mass index (LVMI) and relative wall thickness (RWT) measured by echocardiography. Se-S and Zn-S in the whole group were 89.84 ± 18.75 µg/L and 0.86 ± 0.13 mg/L. Normal left ventricular geometry was found in 28.2% of patients; left ventricular hypertrophy (LVH) in 71.8%, including concentric remodelling in 28.2%, concentric hypertrophy in 29.5%, and eccentric hypertrophy in 14.1%. LVH was statistically significantly more frequent in patients with Se-S < median compared to patients with Se-S ≥ median (87.2% vs. 56.4%, p < 0.05), as well as in patients with Zn-S < median compared to patients with Zn-S ≥ median (83.8% vs. 60.9%, p < 0.05). In hypertensive patients, older age, higher LDL cholesterol, higher fasting glucose, lower Se-S, and lower Zn-S were independently associated with LVH. In conclusion, in hypertensive patients, left ventricular hypertrophy may be associated with low levels of selenium and zinc in the serum.


2020 ◽  
Vol 73 (5) ◽  
pp. 943-946
Author(s):  
Olha M. Chernatska ◽  
Liudmyla N. Prystupa ◽  
Hanna A. Fadieieva ◽  
Alina V. Liashenko ◽  
Yuliia O. Smiianova

The aim is the analysis of hyperuricemia influence on the heart features in patients with arterial hypertension. Materials and methods: We include 75 patients with arterial hypertension which were divided in two groups according to the level of uric acid in the blood, 30 practically healthy people. Patients from the I group (n = 40) had arterial hypertension and coexistent hyperuricemia; ІІ (n = 35) – arterial hypertension. Left ventricular mass index was determined for left ventricular hypertrophy confirmation. We used clinical, anthropometric, biochemical, instrumental, statistical method. Serum uric acid level was observed by the reaction with uricase. Left ventricular mass index was calculated as left ventricular mass to body surface area ratio. The results were analyzed statistically by SPSS 21 and Graphpad. Results: Left ventricular mass index was significantly higher (р = 0,0498) in patients from the І group (109,7 ± 3,21) g/m2 comparable with the ІІ (97,6 ± 5,35) g/m2 and increased in proportion to the biggest level of uric acid (r = 0,31; p = 0,04) in patients with arterial hypertension and hyperuricemia. Conclusions: Concentric and excentric left ventricular hypertrophy, increased left ventricular mass index proportionally to uric acid levels (r = 0,31; p = 0,04) is the confirmation of important role of hyperuricemia in the left ventricular hypertrophy development in patients with arterial hypertension.


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