scholarly journals Left Ventricular Hypertrophy in Diabetic Cardiomyopathy: A Target for Intervention

2021 ◽  
Vol 8 ◽  
Author(s):  
Mohapradeep Mohan ◽  
Adel Dihoum ◽  
Ify R. Mordi ◽  
Anna-Maria Choy ◽  
Graham Rena ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Strong Predictor ◽  
Sglt2 Inhibitor ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Cardiovascular Morbidity And Mortality ◽  
Risk Patients

Heart failure is an important manifestation of diabetic heart disease. Before the development of symptomatic heart failure, as much as 50% of patients with type 2 diabetes mellitus (T2DM) develop asymptomatic left ventricular dysfunction including left ventricular hypertrophy (LVH). Left ventricular hypertrophy (LVH) is highly prevalent in patients with T2DM and is a strong predictor of adverse cardiovascular outcomes including heart failure. Importantly regression of LVH with antihypertensive treatment especially renin angiotensin system blockers reduces cardiovascular morbidity and mortality. However, this approach is only partially effective since LVH persists in 20% of patients with hypertension who attain target blood pressure, implicating the role of other potential mechanisms in the development of LVH. Moreover, the pathophysiology of LVH in T2DM remains unclear and is not fully explained by the hyperglycemia-associated cellular alterations. There is a growing body of evidence that supports the role of inflammation, oxidative stress, AMP-activated kinase (AMPK) and insulin resistance in mediating the development of LVH. The recognition of asymptomatic LVH may offer an opportune target for intervention with cardio-protective therapy in these at-risk patients. In this article, we provide a review of some of the key clinical studies that evaluated the effects of allopurinol, SGLT2 inhibitor and metformin in regressing LVH in patients with and without T2DM.

scholarly journals Loss of Endothelial Hypoxia Inducible Factor‐Prolyl Hydroxylase 2 Induces Cardiac Hypertrophy and Fibrosis

2021 ◽  
Author(s):  
Zhiyu Dai ◽  
Jianding Cheng ◽  
Bin Liu ◽  
Dan Yi ◽  
Anlin Feng ◽  
...  
Keyword(s):  
Heart Failure ◽  
Endothelial Cells ◽  
Left Ventricular Hypertrophy ◽  
Cardiac Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Hypoxia Inducible Factor ◽  
Left Ventricular ◽  
Sequencing Analysis ◽  
Dependent Manner

Background Cardiac hypertrophy and fibrosis are common adaptive responses to injury and stress, eventually leading to heart failure. Hypoxia signaling is important to the (patho)physiological process of cardiac remodeling. However, the role of endothelial PHD2 (prolyl‐4 hydroxylase 2)/hypoxia inducible factor (HIF) signaling in the pathogenesis of cardiac hypertrophy and heart failure remains elusive. Methods and Results Mice with Egln1 Tie2Cre ( Tie2 ‐Cre‐mediated deletion of Egln1 [encoding PHD2]) exhibited left ventricular hypertrophy evident by increased thickness of anterior and posterior wall and left ventricular mass, as well as cardiac fibrosis. Tamoxifen‐induced endothelial Egln1 deletion in adult mice also induced left ventricular hypertrophy and fibrosis. Additionally, we observed a marked decrease of PHD2 expression in heart tissues and cardiovascular endothelial cells from patients with cardiomyopathy. Moreover, genetic ablation of Hif2a but not Hif1a in Egln1 Tie2Cre mice normalized cardiac size and function. RNA sequencing analysis also demonstrated HIF‐2α as a critical mediator of signaling related to cardiac hypertrophy and fibrosis. Pharmacological inhibition of HIF‐2α attenuated cardiac hypertrophy and fibrosis in Egln1 Tie2Cre mice. Conclusions The present study defines for the first time an unexpected role of endothelial PHD2 deficiency in inducing cardiac hypertrophy and fibrosis in an HIF‐2α–dependent manner. PHD2 was markedly decreased in cardiovascular endothelial cells in patients with cardiomyopathy. Thus, targeting PHD2/HIF‐2α signaling may represent a novel therapeutic approach for the treatment of pathological cardiac hypertrophy and failure.

scholarly journals Prevention of heart failure in hypertension – disentangling the role of evolving left ventricular hypertrophy and blood pressure lowering: the ALLHAT study

2019 ◽  
Author(s):  
Kyle Johnson ◽  
Suzanne Oparil ◽  
Barry R. Davis ◽  
Larisa G. Tereshchenko
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Cox Regression ◽  
Left Ventricular ◽  
Lipid Lowering ◽  
Antihypertensive Medications ◽  
Pressure Lowering

AbstractBackgroundHypertension (HTN) is a known risk factor for heart failure (HF), possibly via the mechanism of cardiac remodeling and left ventricular hypertrophy (LVH). We studied how much blood pressure (BP) change and evolving LVH contribute to the effect that lisinopril, doxazosin, amlodipine have on HF compared to chlorthalidone.MethodsWe conducted causal mediation analysis of Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) data. ALLHAT participants with available serial ECGs and BP measurements were included (n=29,892; mean age 67±4 y; 32% black; 56% men): 11,008 were randomized to chlorthalidone, 5,967 – to doxazosin, 6,593 – to amlodipine, and 6,324 – to lisinopril. Evolving ECG-LVH, and BP-lowering served as mediators. Incident symptomatic HF was the primary outcome. Linear regression (for mediator) and logistic regression (for outcome) models were adjusted for mediator-outcome confounders (demographic and clinical characteristics known to be associated both with both LVH/HTN and HF).ResultsA large majority of participants (96%) had ECG-LVH status unchanged; 4% developed evolving ECG-LVH. On average, BP decreased by 11/7 mmHg. In adjusted Cox regression analyses, progressing ECG-LVH [HR 1.78(1.43-2.22)], resolving ECG-LVH [HR 1.33(1.03-1.70)], and baseline ECG-LVH [1.17(1.04-1.31)] carried risk of incident HF. After full adjustment, evolving ECG-LVH mediated 4% of the effect of doxazosin on HF. Systolic BP-lowering mediated 12% of the effect of doxazosin, and diastolic BP-lowering mediated 10% effect of doxazosin, 7% effect of amlodipine, and borderline 9% effect of lisinopril on HF.ConclusionsEvolving ECG-LVH and BP change account for 4-13% of the mechanism by which antihypertensive medications prevent HF.

scholarly journals Peguero – Lo Presti Criteria from Electrocardiography to Diagnose Left Ventricular Hypertrophy in Patients with Hypertension in Adam Malik Hospital

2020 ◽  
Vol 6 (1) ◽  
pp. 29-33
Author(s):  
Masta N. Ginting ◽  
Cut A. Andra ◽  
Ali N. Nasution ◽  
Harris Hasan ◽  
Nizam Z. Akbar ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Strong Predictor ◽  
Cost Effective ◽  
Cross Sectional Study ◽  
Left Ventricular ◽  
S Wave ◽  
Cross Sectional ◽  
Cardiovascular Morbidity And Mortality ◽  
Female Subjects

Background: Left ventricular hypertrophy (LVH) is a preclinical manifestation of cardiovascular disease and a strong predictor of cardiovascular morbidity and mortality. The electrocardiogram (ECG) is an easily available, easy to use and cost effective tool to evaluate LVH. Peguero – Lo Presti criteria is a newcriteria to diagnose LVH from ECG that has higher sensitivity than the other ECG criteria.Aims: To assess the ability of Peguero – Lo Presti criteria to diagnose LVH and obtain new cut-off point criteria to more accurately diagnose LVH in patients with hypertension in Adam Malik Hospital.Methods: A cross sectional study was conducted on patients with hypertension in cardiac centre Adam Malik Hospital Medan. Electrocardiographic examination was performed to obtain Peguero – Lo Presti point in blinded fashion. LVH was assessed using M-mode method with Cube formula. The analysis of Peguero – Lo Presti criteria was based on the calculation of the deepest S wave in any precordial lead (deepest S wave,SD) and S wave in lead V4 (SV4). A SD + SV4 ≥ 28 mm in male and ≥ 23 mm in female subjects were considered positive for LVH. LVH was defined as left ventricular mass index > 115 gr/m2 in male and > 95 gr/m2 in female subjects.Results: Peguero – Lo Presti criteria had 54.8% sensitivity, 97.6% specificity, 55.4% NPV and 97.6% PPV to diagnose LVH. Lowering the cut-off point of Peguero – Lo Presti criteria to 26 mm in male and 22 mm in female subjects improved the sensitivity from 54.8% to 67.1% with 90.5% specificity, 61.3% NPV and 92.5% PPV to diagnose LVH.Conclusion: Peguero – Lo Presti criteria on ECG could be used to diagnose LVH in patients with hypertension in Adam Malik Hospital Medan.

Abstract 237: Prognostic Significance of Left Ventricular Hypertrophy (lvh) by Electrocardiography in a Minority-predominant Heart Failure (hf) Cohort

2016 ◽  
Vol 9 (suppl_2) ◽  
Author(s):  
Muhammad U Majeed ◽  
Abdullahi Oseni ◽  
Olabisi Akanbi ◽  
Vincent Agboto ◽  
Henry E Okafor
Keyword(s):  
Heart Failure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Prognostic Significance ◽  
Left Ventricular ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
P Value ◽  
Cardiovascular Morbidity And Mortality ◽  
The Impact

Background: Left ventricular Hypertrophy (LVH) has been associated with higher cardiovascular morbidity and mortality but most of these studies were conducted in majority (white) populations. LVH is known to be more common in African Americans (AA) who also have a higher prevalence of cardiovascular morbidity and mortality. The prognostic significance of LVH in AA with Heart Failure (HF) has not been well studied. Methods: We performed a retrospective analysis of a predominantly minority HF cohort (69.3% AA); after obtaining approval from our institutional review board. Our primary goal was to compare the HF outcomes [All-cause hospitalizations (ACH), hospitalizations primarily due to HF and ER visits] in patients with EKG evidence of LVH versus those without LVH. We also examined the racial (Blacks vs Whites), gender (males vs females) and age-based (≥60 Vs <60 years) differential impact of LVH on HF outcomes and determined the prevalence of LVH in the cohort. Levene’s Test and t-test were used to analyze the data for equality of variances and means respectively. Result: Our HF cohort consisted of 599 patients (415 AA, 142 Caucasian, 22 others, 20 unknown). The prevalence of LVH in overall cohort was 26.7%. We noted that black had higher prevalence of LVH ( 31%) vs Whites (15.5%) while prevalence of LVH was not very different in males ( 27.9%) vs females( 25.7%) and ≥60 years of age( 27.5%) vs <60 (27.3%). The analysis showed that there were statistically significant differences in the number of ACH (p-value = 0.014), HF hospitalizations (p-value = 0.019) and ER visits (p-value = 0.001) in the LVH group compared with the non-LVH group. . There were no racial, gender or age-based statistically significant differences in the impact of LVH on HF outcomes. Conclusion: Electrocardiographically determined LVH in a minority - predominant HF cohort is associated with worse outcomes. This needs to be prospectively validated in a larger cohort of HF and could serve as a prognostic marker to guide the care of HF patients.

scholarly journals Association Between the Angiotensin II/Angiotensin (1-7) Imbalance and Left Ventricular Hypertrophy in Patients with Heart Failure

2021 ◽  
Vol 48 (3) ◽  
pp. 12-18
Author(s):  
A. Nikolov ◽  
M. Tzekova ◽  
K. Kostov ◽  
A. Kostadinovska ◽  
S. Blazheva
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Renin Angiotensin System ◽  
Systemic Circulation ◽  
Left Ventricular ◽  
Ang Ii ◽  
Significant Difference ◽  
Patients With Heart Failure

Abstract Introduction: Angiotensin II (AngII) and angiotensin-(1-7) [Ang-(1-7)] are key components of the renin angiotensin system (RAS). They exhibit counter-regulatory effects in the systemic circulation, as well as in tissues important for cardiovascular regulation. Aim: To investigate the association between the AngII/Ang-(1-7) balance and left ventricular hypertrophy (LVH) in patients with heart failure and mid-range ejection fraction (HFmrEF). Material and methods: 56 patients with HFmrEF were included, with a mean age of 65.62 ± 9.69 years and 22 age- and sex-matched healthy subjects, their mean age - 56.4 ± 5.53 years. The patients were divided in two subgroups: subjects with left ventricular hypertrophy (n = 32); (HFmrEF+LVH) and subjects without left ventricular hypertrophy (n = 24); (HFmrEFLVH). AngII and Ang-(1-7) levels were measured with an ELISA kit. Results: Patients with HFmrEF+LVH showed significantly higher levels of AngII: 8.53 pg/mL (1.47 ÷ 13.0) than HFmrEF-LVH – 1.33 pg/mL (0.47 ÷ 6.93) and healthy controls – 1.53 pg/mL (0.27 ÷ 5.21); (KW = 3.48; p = 0.04). There was no significant difference between Ang-(1-7) levels in all patients compared to controls (p > 0.05). AngII/Ang-(1-7) ratio was significantly higher in all patients than controls: 3.81 (2.03 ÷ 6.66) vs. 1.5 (0.93 ÷ 2.06) (KW = 18.68; p < 0.001). Patients with HFmrEF+LVH showed statistically higher AngII/Ang-(1-7) ratio compared with controls (4.7 vs. 1.5). Moreover, subjects with LVH showed the highest AngII/Ang-(1-7) ratio among all particpants in the study. The AngII/Ang-(1-7) ratio correlated with LVH (r = -0.39; p = 0.03), DBP (r = 0.25; p = 0.04), HDL (r = 0.33; p = 0.01), SBP (r = 0.34; p = 0.01). Conclusion: Our study showed an association between AngII/Ang-(1-7) ratio, blood pressure and LVH. The imbalance between Ang-II and Ang-(1-7) could contribute to the mechanisms determining LVH in HFmrEF. Further studies are warranted to clarify whether evaluation of serum Ang-II/Ang-(1-7) ratio could predict LVH development in patients with HFmrEF.

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