Abstract 14866: Hyperglycemia is an Independent Predictor of Left Ventricular Hypertrophy

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Mohan Thanikachalam ◽  
Vijaykumar Harivanzan ◽  
Jahnavi Sunderarajan ◽  
Ragavendra Baliga ◽  
Sadagopan Thanikachalam
Keyword(s):  
Insulin Resistance ◽  
Left Ventricular Hypertrophy ◽  
Odds Ratio ◽  
Aortic Stiffness ◽  
Ventricular Hypertrophy ◽  
Blood Lipids ◽  
Independent Predictor ◽  
Left Ventricular ◽  
Model Assessment ◽  
Lv Mass

Background: Diabetes mellitus (DM) is a risk factor for cardiovascular morbidity and mortality. In the current study we examine the association of hyperglycemic with left ventricular hypertrophy (LVH) independent of major correlates of LVH, such as, age, body size, blood pressure (BP) and aortic stiffness. Methods: We conducted a population-based, cross-sectional survey in 8,080 South Indians over the age of 20 years. The study included anthropometric, socioeconomic, psychosocial, BP, blood lipids, insulin, HbA1C, glucose tolerance test and carotid-femoral pulse wave velocity (PWV) assessments. Insulin resistance (IR) was defined as the 25% of the population with the highest values for homeostasis model assessment of insulin resistance (HOMA-IR). LV mass and relative wall thickness (RWT) were determined using echocardiography. LVH was defined as LV mass index (LVMI) >109 g/m 2 for men and >89 g/m 2 for women. Results: After the exclusion of people with hypertension, 5,841 subjects (mean age 41 years, 59% women) constituted the study sample. The mean LVMI in subjects with normoglycemia (n=3585), pre-DM (impaired fasting and/or post prandial blood sugar; n=1315) and DM (n=888) was 78.5 ± 17.5, 80.7 ± 19.4 and 87.2 ± 20.3, while mean RWT was 0.46 ± 0.09, 0.48 ± 0.09 and 0.51 ± 0.1, respectively (p<0.01). After adjustments for age, sex, BMI, BP, PWV, blood lipids, history of coronary artery disease, socioeconomic and smoking status, and physical activity, when compared to persons with normoglycemia, the odds ratio (95% CI) for LVH in pre-DM and DM men was 1.12 (0.89, 1.42) and 1.37 (1.04, 1.8), respectively; the odds ratio in pre-DM and DM women was 1.07 (0.89, 1.28) and 1.4 (1.08, 1.82), respectively. Among the persons with normoglycemia those with IR the odds ratio for LVH was 1.23 (0.85, 1.78) in men and 1.01 (0.79, 1.30) in women. In the multi-linear regression models HbA1c was independently correlated with LVMI. The correlation coefficients were higher in men (β= 0.07, p <0.001) compared to women (β= 0.037, p = 0.032). Conclusion: Hyperglycemia is an independent predictor of LVH in South Asian population. These findings indicate potential adverse myocardial effects of DM independent of associated risk factors, such as obesity, BP and aortic stiffness.

scholarly journals A randomized controlled trial of dapagliflozin on left ventricular hypertrophy in people with type two diabetes: the DAPA-LVH trial

2020 ◽  
Vol 41 (36) ◽  
pp. 3421-3432 ◽  
Author(s):  
Alexander J M Brown ◽  
Stephen Gandy ◽  
Rory McCrimmon ◽  
John Graeme Houston ◽  
Allan D Struthers ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Controlled Trial ◽  
High Sensitivity ◽  
Left Ventricular ◽  
Model Assessment ◽  
Protective Effects

Abstract Aim We tested the hypothesis that dapagliflozin may regress left ventricular hypertrophy (LVH) in people with type 2 diabetes (T2D). Methods and results We randomly assigned 66 people (mean age 67 ± 7 years, 38 males) with T2D, LVH, and controlled blood pressure (BP) to receive dapagliflozin 10 mg once daily or placebo for 12 months. Primary endpoint was change in absolute left ventricular mass (LVM), assessed by cardiac magnetic resonance imaging. In the intention-to-treat analysis, dapagliflozin significantly reduced LVM compared with placebo with an absolute mean change of −2.82g [95% confidence interval (CI): −5.13 to −0.51, P = 0.018]. Additional sensitivity analysis adjusting for baseline LVM, baseline BP, weight, and systolic BP change showed the LVM change to remain statistically significant (mean change −2.92g; 95% CI: −5.45 to −0.38, P = 0.025). Dapagliflozin significantly reduced pre-specified secondary endpoints including ambulatory 24-h systolic BP (P = 0.012), nocturnal systolic BP (P = 0.017), body weight (P &lt; 0.001), visceral adipose tissue (VAT) (P &lt; 0.001), subcutaneous adipose tissue (SCAT) (P = 0.001), insulin resistance, Homeostatic Model Assessment of Insulin Resistance (P = 0.017), and high-sensitivity C-reactive protein (hsCRP) (P = 0.049). Conclusion Dapagliflozin treatment significantly reduced LVM in people with T2D and LVH. This reduction in LVM was accompanied by reductions in systolic BP, body weight, visceral and SCAT, insulin resistance, and hsCRP. The regression of LVM suggests dapagliflozin can initiate reverse remodelling and changes in left ventricular structure that may partly contribute to the cardio-protective effects of dapagliflozin. ClinicalTrials.gov Identifier NCT02956811

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

2011 ◽  
pp. 119-125
Author(s):  
Thi Thuy Hang Nguyen
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Left Ventricular Mass ◽  
Ventricular Hypertrophy ◽  
Structural Changes ◽  
Left Ventricular ◽  
Control Group ◽  
Concentric Left Ventricular Hypertrophy ◽  
Increased Risk ◽  
Lv Mass ◽  
Left Ventricular Morphology

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

Abstract 3435: Left Ventricular Hypertrophy is Resistant to Inhibition of Expression of the R403Q Alpha-Myosin Heavy Chain Cardiac Hypertrophy-Inducing Mutant Protein

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Leah Cannon ◽  
Tadeusz Marciniec ◽  
Bryony Mearns ◽  
Robert M Graham ◽  
Diane Fatkin
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Interstitial Fibrosis ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Familial Hypertrophic Cardiomyopathy ◽  
Lv Function ◽  
Dependent Manner ◽  
Cardiovascular Morbidity And Mortality ◽  
Lv Mass

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

Candesartan, an angiotensin II receptor blocker, improves left ventricular hypertrophy and insulin resistance

Metabolism ◽  
2004 ◽  
Vol 53 (6) ◽  
pp. 777-781 ◽  
Author(s):  
Futoshi Anan ◽  
Naohiko Takahashi ◽  
Tatsuhiko Ooie ◽  
Masahide Hara ◽  
Hironobu Yoshimatsu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Angiotensin Ii ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor

scholarly journals N-terminal pro brain natriuretic peptide as a cardiac biomarker in Japanese hemodialysis patients

2018 ◽  
Vol 41 (3) ◽  
pp. 135-143 ◽  
Author(s):  
Minako Shimizu ◽  
Shigehiro Doi ◽  
Ayumu Nakashima ◽  
Takayuki Naito ◽  
Takao Masaki
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Odds Ratio ◽  
Ventricular Hypertrophy ◽  
Hemodialysis Patients ◽  
Left Ventricular ◽  
Ultrafiltration Rate ◽  
Natriuretic Peptide Level ◽  
Peptide Level

Purpose: This study examined the clinical significance of N-terminal pro brain natriuretic peptide level as a cardiac marker in Japanese hemodialysis patients. Methods: This was a multicenter cross-sectional study involving 1428 Japanese hemodialysis patients. Ultrasonic cardiography data at post-hemodialysis were obtained from 395 patients. We examined whether serum N-terminal pro brain natriuretic peptide levels were associated with cardiac parameters and assessed cut-off values and investigated factors associated with a reduced ratio of N-terminal pro brain natriuretic peptide levels pre- and post-hemodialysis. Results: Multivariate logistic regression analysis showed that pre- and post-hemodialysis N-terminal pro brain natriuretic peptide levels were associated with left ventricular hypertrophy on electrocardiogram (odds ratio: 3.10; p < 0.001 at pre-hemodialysis and odds ratio: 2.70; p < 0.001 at post-hemodialysis) and left ventricular hypertrophy on ultrasonic cardiography (odds ratio: 3.06; p < 0.001 at pre-hemodialysis and odds ratio: 3.15; p < 0.001 at post-hemodialysis). Post-N-terminal pro brain natriuretic peptide levels were also significantly associated with ejection fraction on urine chorionic gonadotrophin (ultrasonic cardiography; odds ratio: 35.83; p < 0.001). Receiver operating characteristic curves for predicting the presence of left ventricular hypertrophy on electrocardiogram and ultrasonic cardiography showed similar sensitivity (57.7%, 57.3% at pre-hemodialysis and 63.9%, 48.2% at post-hemodialysis) and specificity (66.5%, 72.9% at pre-hemodialysis and 59.2%, 81.9% at post-hemodialysis). Decreased ejection fraction on ultrasonic cardiography showed better sensitivity (78.6%) and specificity (88.7%). The N-terminal pro brain natriuretic peptide reduction ratio during a hemodialysis session correlated with Kt/V, membrane area, membrane type, modality, body weight gain ratio, treatment time, and ultrafiltration rate with multiple linear regression ( R: 0.53; p < 0.001 except for ultrafiltration rate ( p = 0.003)). Conclusion: Both pre- and post-hemodialysis N-terminal pro brain natriuretic peptide are associated with the presence of left ventricular hypertrophy in this population. The post-hemodialysis N-terminal pro brain natriuretic peptide level is a useful marker for systolic dysfunction.

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