scholarly journals Subclinical Impairment of Left Ventricular Function in Young Obese Women: Contributions of Polycystic Ovary Disease and Insulin Resistance

2008 ◽  
Vol 93 (10) ◽  
pp. 3748-3754 ◽  
Author(s):  
Wojciech Kosmala ◽  
Trisha M. O'Moore-Sullivan ◽  
Rafal Plaksej ◽  
Justyna Kuliczkowska-Plaksej ◽  
Monika Przewlocka-Kosmala ◽  
...  

Context: Obesity and insulin resistance (IR) may produce disturbances of left ventricular (LV) function. Obese women with polycystic ovary syndrome (PCO), characterized by hormonal and metabolic abnormalities, are thought to be at particularly increased cardiovascular risk. Objectives: We sought to determine the influence of IR on LV function in obese young women with and without PCO and without other comorbidities. Design: This was a cross-sectional study. Setting: The study was performed at a university hospital. Patients: A total of 150 women aged younger than 40 yr with a body mass index (BMI) of 30 kg/m2 or more was classified into three groups: with both PCO and IR, without PCO and with IR, and without either PCO or IR. Main Outcome Measures: Tissue Doppler-derived myocardial velocities, strain-rate and strain, and metabolic and hormonal measurements were calculated. Results: Subclinical impairment of LV systolic and diastolic function as indicated by lower peak strain (P < 0.001), peak systolic strain rate (P < 0.001), peak early diastolic strain rate (P < 0.001), and peak early diastolic velocity (P < 0.01) was demonstrated in both groups with IR. IR subjects with and without PCO did not differ in any LV function indices. Strain was independently associated with fasting insulin (β = −0.39; P < 0.001), urinary albumin excretion (UAE) (β = −0.36; P < 0.001), and BMI (β = −0.22; P < 0.03), and peak early diastolic strain rate was associated with UAE (β = −0.35; P < 0.001), fasting insulin (β = −0.24; P < 0.02), BMI (β = −0.23; P < 0.02), and SHBG (β = 0.20; P < 0.04). Conclusions: In obese young women, fasting insulin, BMI, SHBG, and UAE are independent correlates of impaired LV performance. The contribution of PCO to LV function abnormalities is linked to IR, but not to other hormonal aberrations associated with this condition.

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Vahabi ◽  
E Kharati-Koopaei ◽  
M Stewart ◽  
H Hancock ◽  
M Norouzi ◽  
...  

Abstract Background Despite the associated dose-dependent cardiotoxicity, anthracyclines continue to form the backbone of modern chemotherapy regimens. Speckle Tracking Echocardiography (STE) has been a popular method of quantifying cardiac function but most studies have focused on left ventricular function. Research into the effects of anthracyclines on left atrial (LA) and right atrial (RA) function continues to be neglected. Purpose To investigate the effects of doxorubicin, a commonly used anthracycline, on both the LA and RA systolic and diastolic strain and strain-rate parameters in two groups of patients with lymphoma: Group 1 (G1) with a conventional drop in ejection fraction (EF <53%), and Group 2 (G2) without. Methods We retrospectively studied 46 patients treated for lymphoma between 2015 and 2018; G1 (n=12) and G2 (n=34). Echocardiograms performed at baseline (T0), mid-chemotherapy (T1), and post-chemotherapy (T2), were analysed by using offline vendor-independent software (TomTec, 2D Cardiac Performance Analysis). Using 2D STE, LA and RA reservoir, conduit and contractile strains, systolic and diastolic strain-rates were measured. Multi-level longitudinal model was used for statistical analysis.This study was ethically approved by the Health Research Association (REC Reference 18/SS/0139). Results Median age was 64 years (IQR 51–74 years) in G1, and 65 years (IQR 57–73 years) in G2. In G1, there was no significant change in LA reservoir strain with time, however a significant decline with an average mean difference of −7.52 was seen between T0 to T2 (p=0.016) in G2. LA conduit strain did not significantly change in either group with incremental doses of doxorubicin. However, LA contraction strain was seen to significantly increase in G1 between T1 to T2 (p=0.045) with an average change of 7.23. LA peak systolic strain rate, and late diastolic strain rate did not show any significant change with time in both groups. Yet, a significant increase was seen in LA early diastolic strain rate between T0 to T2 (p=0.017) in G1 but not G2. No significant changes were seen in the RA strain parameters in both groups. Conclusion In patient with a reduction in LV function, a significant change was noted in the left atrial contraction strain and early diastolic strain rate with incremental doses of doxorubicin. These changes shows the close relationship between the LA and LV, and the importance of LA in providing a compensatory mechanism for a decline in LV function secondary to anthracycline cardiotoxicity. Funding Acknowledgement Type of funding source: None


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Yi Zhang ◽  
Wei-feng Yan ◽  
Li Jiang ◽  
Meng-ting Shen ◽  
Yuan Li ◽  
...  

Abstract Background Functional mitral regurgitation (FMR) is one of the most common heart valve diseases in diabetes and may increase left ventricular (LV) preload and aggravate myocardial stiffness. This study aimed to investigate the aggravation of FMR on the deterioration of LV strain in type 2 diabetes mellitus (T2DM) patients and explore the independent indicators of LV peak strain (PS). Materials and methods In total, 157 T2DM patients (59 patients with and 98 without FMR) and 52 age- and sex-matched healthy control volunteers were included and underwent cardiac magnetic resonance examination. T2DM with FMR patients were divided into T2DM patients with mild (n = 21), moderate (n = 19) and severe (n = 19) regurgitation. LV function and global strain parameters were compared among groups. Multivariate analysis was used to identify the independent indicators of LV PS. Results The T2DM with FMR had lower LV strain parameters in radial, circumferential and longitudinal direction than both the normal and the T2DM without FMR (all P < 0.05). The mild had mainly decreased peak diastolic strain rate (PDSR) compared to the normal. The moderate had decreased peak systolic strain rate (PSSR) compared to the normal and PDSR compared to the mild and the normal. The severe FMR group had decreased PDSR and PSSR compared to the mild and the normal (all P < 0.05). Multiple linear regression showed that the regurgitation degree was independent associated with radial (β = − 0.272), circumferential (β = − 0.412) and longitudinal (β = − 0.347) PS; the months with diabetes was independently associated with radial (β = − 0.299) and longitudinal (β = − 0.347) PS in T2DM with FMR. Conclusion FMR may aggravate the deterioration of LV stiffness in T2DM patients, resulting in decline of LV strain and function. The regurgitation degree and months with diabetes were independently correlated with LV global PS in T2DM with FMR.


Author(s):  
Philippe C. Wouters ◽  
Geert E. Leenders ◽  
Maarten J. Cramer ◽  
Mathias Meine ◽  
Frits W. Prinzen ◽  
...  

AbstractPurpose: Cardiac resynchronisation therapy (CRT) improves left ventricular (LV) function acutely, with further improvements and reverse remodelling during chronic CRT. The current study investigated the relation between acute improvement of LV systolic function, acute mechanical recoordination, and long-term reverse remodelling after CRT. Methods: In 35 patients, LV speckle tracking longitudinal strain, LV volumes & ejection fraction (LVEF) were assessed by echocardiography before, acutely within three days, and 6 months after CRT. A subgroup of 25 patients underwent invasive assessment of the maximal rate of LV pressure rise (dP/dtmax,) during CRT-implantation. The acute change in dP/dtmax, LVEF, systolic discoordination (internal stretch fraction [ISF] and LV systolic rebound stretch [SRSlv]) and systolic dyssynchrony (standard deviation of peak strain times [2DS-SD18]) was studied, and their association with long-term reverse remodelling were determined. Results: CRT induced acute and ongoing recoordination (ISF from 45 ± 18 to 27 ± 11 and 23 ± 12%, p < 0.001; SRS from 2.27 ± 1.33 to 0.74 ± 0.50 and 0.71 ± 0.43%, p < 0.001) and improved LV function (dP/dtmax 668 ± 185 vs. 817 ± 198 mmHg/s, p < 0.001; stroke volume 46 ± 15 vs. 54 ± 20 and 52 ± 16 ml; LVEF 19 ± 7 vs. 23 ± 8 and 27 ± 10%, p < 0.001). Acute recoordination related to reverse remodelling (r = 0.601 and r = 0.765 for ISF & SRSlv, respectively, p < 0.001). Acute functional improvements of LV systolic function however, neither related to reverse remodelling nor to the extent of acute recoordination. Conclusion: Long-term reverse remodelling after CRT is likely determined by (acute) recoordination rather than by acute hemodynamic improvements. Discoordination may therefore be a more important CRT-substrate that can be assessed and, acutely restored.


2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Fernando Cordido ◽  
Jesús Garcia-Buela ◽  
Susana Sangiao-Alvarellos ◽  
Teresa Martinez ◽  
Ovidio Vidal

The aim of the present study was to evaluate the relationship between GHRH-induced GH secretion in obese premenopausal women and cardiovascular risk markers or insulin resistance. Premenopausal obese women, aged 35–52 years, were studied. GH secretion, IGF-I, serum cardiovascular risk markers, insulin, leptin, mid-waist and hip circumference, total body fat, and truncal fat were measured. Subjects were classified as meeting the criteria for GH deficiency (GHD) when peak GH after stimulation with GHRH was≤3 μg/L. Mean total and LDL cholesterol, fasting insulin, and HOMA-IR were all higher, in subjects who would have been classified as GH-deficient compared with GH-sufficient. Peak GH secretion after stimulation was inversely associated with fasting insulin (R=−0.650,P=.012), HOMA-IR (R=−0.846,P=.001), total cholesterol (R=−0.532,P=.034), and LDL cholesterol (R=−0.692,P=.006) and positively associated with HDL cholesterol (R=0.561,P=.037). These data strongly suggest a role for insulin resistance in the decreased GH secretion of obesity and that the blunted GH secretion of central obesity could be the pituitary expression of the metabolic syndrome.


2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Qian Zhang ◽  
Xinhua Xiao ◽  
Jia Zheng ◽  
Ming Li ◽  
Miao Yu ◽  
...  

Increasing evidence shows that diabetes causes cardiac dysfunction. We hypothesized that a glucagon-like peptide-1 (GLP-1) analog, liraglutide, would attenuate cardiac dysfunction in diabetic rats. A total of 24 Sprague–Dawley (SD) rats were divided into two groups fed either a normal diet (normal, n=6) or a high-fat diet (HFD, n=18) for 4 weeks. Then, the HFD rats were injected with streptozotocin (STZ) to create a diabetic rat model. Diabetic rats were divided into three subgroups receiving vehicle (diabetic, n=6), a low dose of liraglutide (Llirag, 0.2 mg/kg/day, n=6), or a high dose of liraglutide (Hlirag, 0.4 mg/kg/day, n=6). Metabolic parameters, systolic blood pressure (SBP), heart rate (HR), left ventricular (LV) function, and whole genome expression of the heart were determined. Diabetic rats developed insulin resistance, increased blood lipid levels and oxidative stress, and impaired LV function, serum adiponectin, nitric oxide (NO). Liraglutide improved insulin resistance, serum adiponectin, NO, HR, and LV function and reduced blood triglyceride (TG), total cholesterol (TC) levels, and oxidative stress. Moreover, liraglutide increased heart nuclear receptor subfamily 1, group H, member 3 (Nr1h3), peroxisome proliferator activated receptor (Ppar) α (Pparα), and Srebp expression and reduced diacylglycerol O-acyltransferase 1 (Dgat) and angiopoietin-like 3 (Angptl3) expression. Liraglutide prevented cardiac dysfunction by activating the PPARα pathway to inhibit Dgat expression and oxidative stress in diabetic rats.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S K Saha ◽  
A Kiotsekoglou ◽  
A Borysenko ◽  
A Gopal ◽  
S C Govind

Abstract Funding Acknowledgements EU GRANT OnBehalf MOPEAD STUDY GROUP Background Although the 2D speckle tracking software (2DSTE-SW) has been irrevocably proved to be useful for quantification of left ventricular (LV) function, the same SW has also been used successfully in a plethora of cardiac illnesses using left atrial (LA) strain and strain rate, even in the absence of a dedicated LA SW. LA peak longitudinal strain during ventricular systole (LA-Reservoir strain%; LA-Res S), and strain rate during early (LA-SRE) and late (LA-SRA) phases constitute respectively the reservoir (LA-RS%), conduit, and booster pump functions of this chamber. The role of this dynamic function has not been investigated to assess cerebral cognition in type 2 diabetes (DM). Methods We enrolled thirty-nine subjects with DM and mild LV dysfunction (76 ± 5 years, 25 F) in the EU- funded MOPEAD (Models of Patient Engagement for Alzheimer’s Disease) project. Fifteen of them underwent standard echocardiography and 2DSTE. We assessed cerebral cognition using the standard MMSE (Mini-Mental Stage Examination) score: we considered a score of less than 28 as a surrogate of mild cognitive impairment (MCI+). Besides LA-Res strain, LA-SRE, LA-SRA, LV-GLS and right ventricular free wall strain (RV-FWS) were also computed (RV-FWS). Routine biochemistry included, among other, HbA1c and NT-proBNP. Results Mean values of the 2D STE measures were LVGLS: 14± 3%, LAVI: 36± 21 ml/m2, LA -RS: 18 ±8 %, LA-SRE: 0.6± 0.3, and LA-SRA: 1.6± 0.4. RV FWS was 20± 5 %. HbA1c was 58 ± 16 mmol/mol. LVEF was 53± 7%. There was no difference in theses variable between MCI+ and those with normal cognition (MCI-). However, in the regression model, LA-Res S had the strongest association with MCI (P &lt; 0.01) (Fig), with excellent strength of association ( R2 = 0.8). LA-SRE, indexed LA volume, and NT-proBNP were not retained by the model (p &gt; 0.05). Conclusion LA reservoir strain may emerge as a useful tool to explore disturbed system biology involving extracardiac organ such as the brain in older adults with type 2 diabetes, in the background of mild LV dysfunction. Abstract P1394 Figure. Fig.Regression analysis


2009 ◽  
Vol 25 (10) ◽  
pp. 640-646 ◽  
Author(s):  
Vasiliki Vervita ◽  
Alexandros D. Saltamavros ◽  
George Adonakis ◽  
Vasilios Tsapanos ◽  
George Decavalas ◽  
...  

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