EVALUATION OF LEFT VENTRICULAR MASS IN THE PREHYPERTENSIVES BY ELECTROCARDIOGRAPHY AND ECHOCARDIOGRAPHY

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

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Shan Tu ◽  
Zhi-Jie Shen ◽  
Xiao-Yan Wang ◽  
Li-Xiong Zeng ◽  
Zhi-Hui Zhang

This study explored the effects of renal sympathetic denervation (RDN) on hyperlipidity-induced cardiac hypertrophy in beagle dogs. Sixty beagles were randomly assigned to the control group, RDN group, or sham-operated group. The control group was fed with a basal diet, while the other two groups were given a high-fat diet to induce model hypertension. The RDN group underwent an RDN procedure, and the sham-operated group underwent only renal arteriography. At 1, 3, and 6 months after the RDN procedure, the diastolic blood pressure (DBP) and systolic blood pressure (SBP) levels were markedly decreased in the RDN group relative to the sham group ( P < 0.05 ). After 6 months, serum norepinephrine (NE) and angiotensin II (AngII), as well as left ventricular levels, in the RDN group were statistically lower than those in the sham group ( P < 0.05 ). Also, the left ventricular mass (LVM) and left ventricular mass index (LVMI) were significantly decreased, while the E/A peak ratio was drastically elevated ( P < 0.05 ). Pathological examination showed that the degree of left ventricular hypertrophy and fibrosis in the RDN group was statistically decreased relative to those of the sham group and that the collagen volume fraction (CVF) and perivascular circumferential collagen area (PVCA) were also significantly reduced ( P < 0.05 ). Renal sympathetic denervation not only effectively reduced blood pressure levels in hypertensive dogs but also reduced left ventricular hypertrophy and myocardial fibrosis and improved left ventricular diastolic function. The underlying mechanisms may involve a reduction of NE and AngII levels in the circulation and myocardial tissues, which would lead to the delayed occurrence of left ventricular remodeling.


1993 ◽  
Vol 32 (03) ◽  
pp. 214-218
Author(s):  
A. F. Bowyer ◽  
R. A. Thomas ◽  
C. E. Cannon

Abstract:Concentric left ventricular hypertrophy (LVH) frequently occurs in subjects with normal resting systolic and diastolic pressures (SP and DP, respectively). LVH in this normotensive-hypertrophic group (NH) may be due to an abnormally exaggerated pressure response to exercise. The SP and DP responses to exercise were studied in 130 subjects free from coronary artery disease or cardiomyopathy. The NH subjects (n = 35) had normal resting pressure (SP ≤140 and DP ≤85 mmHg) and increased LV wall thickness (T) by echocardiography (T >1.1 cm). A normal control group (NN) (n = 57) and a hypertensive control group (HH) (n = 23) were simultaneously evaluated. The original groups, subgroups censored for age and weight, and matched-pair subgroups demonstrated greater exercise SP for NH than for NN (p <0.005). Moreover, the rate of SP increase with exercise was greater for NH than for NN or HH (p <0.05). Hence, an exaggerated exercise SP response may have been the stimulus for LVH in these NH subjects.


2014 ◽  
Vol 54 (5) ◽  
pp. 305
Author(s):  
Erling David Kaunang ◽  
Jane G. C. Metusala ◽  
Audrey M. I. Wahani

Background Systematic exercise leads to increased left ventricular mass, which may be misleading in a differential diagnosis of heart disease in athletes (physiologic hypertrophy versus pathologic hypertrophy). T he cause of left ventricular hypertrophy is an important risk factor in the morbidity and mortality of cardiovascular diseases.Objective To compare left ventricular mass and left ventricular hypertrophy in male adolescent athletes and non-athletes.Methods We conducted a cross-sectional, analytic study, from September to December 2012 in male adolescents aged 15-18 years. The case group included athletes from the Bina Taruna Football Club Manado, while the control group included non-athlete adolescents. All subjects underwent history-taking, physical examinations and further supporting examinations. Left ventricular mass was measured by cardiovascular echocardiography (Esaote Mylab 4.0) and calculated based on a formula. Left ventricular hypertrophy was defined as left ventricular mass of > 134 g/m2 body surface area.Results Subjects' mean left ventricular masses were 359.69 (SD 188.4; 95%CI 283.58 to 435.81) grams in the athlete group and 173.04 (SD 50.69; 95%CI 152.56 to 103.51) grams in the non· athlete group, a statistically significant difference (P=0.0001). Ventricular hypertrophy was found 76.9% compared to 11.5% in  the non-athlete group (P= 0.0001).Conclusion Left ventricular mass in athletes is bigger than in non-athletes. In addition, left ventricular hypertrophy is more cornmon in male adolescent athletes than in non-athletes.


VASA ◽  
2013 ◽  
Vol 42 (4) ◽  
pp. 284-291 ◽  
Author(s):  
Seong-Woo Choi ◽  
Hye-Yeon Kim ◽  
Hye-Ran Ahn ◽  
Young-Hoon Lee ◽  
Sun-Seog Kweon ◽  
...  

Background: To investigate the association between ankle-brachial index (ABI), left ventricular hypertrophy (LVH) and left ventricular mass index (LVMI) in a general population. Patients and methods: The study population consisted of 8,246 people aged 50 years and older who participated in the baseline survey of the Dong-gu Study conducted in Korea between 2007 and 2010. Trained research technicians measured LV mass using mode M ultrasound echocardiography and ABI using an oscillometric method. Results: After adjustment for risk factors and common carotid artery intima-media thickness (CCA-IMT) and the number of plaques, higher ABIs (1.10 1.19, 1.20 - 1.29, and ≥ 1.30) were significantly and linearly associated with high LVMI (1.10 - 1.19 ABI: β, 3.33; 95 % CI, 1.72 - 4.93; 1.20 - 1.29 ABI: β, 6.51; 95 % CI, 4.02 - 9.00; ≥ 1.30 ABI: β, 14.83; 95 % CI, 6.18 - 23.48). An ABI of 1.10 - 1.19 and 1.20 - 1.29 ABI was significantly associated with LVH (1.10 - 1.19 ABI: OR, 1.35; 95 % CI, 1.19 - 1.53; 1.20 - 1.29 ABI: OR, 1.59; 95 % CI, 1.31 - 1.92) and ABI ≥ 1.30 was marginally associated with LVH (OR, 1.73; 95 % CI, 0.93 - 3.22, p = 0.078). Conclusions: After adjustment for other cardiovascular variables and CCA-IMT and the number of plaques, higher ABIs are associated with LVH and LVMI in Koreans aged 50 years and older.


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


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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