Significant Increase In Left Ventricular Mass Research Articles

Effects of endurance exercise training on left ventricular structure in healthy adults: a systematic review and meta-analysis.

To determine the impact of endurance training (ET) interventions on left ventricular (LV) chamber size, wall thickness, and mass in healthy adults. Electronic databases including CINAHL, MEDLINE, PsycINFO, SPORTDiscus, Cochrane library, and EBM Reviews were searched up to 4 January 2022. Criteria for inclusion were healthy females and/or males (>18 years), ET intervention for ≥2 weeks, and studies reporting pre- and post-training LV structural parameters. A random-effects meta-analysis with heterogeneity, publication bias, and sensitivity analysis was used to determine the effects of ET on LV mass (LVM) and diastolic measures of interventricular septum thickness (IVSd), posterior wall thickness (PWTd), and LV diameter (LVDd). Meta-regression was performed on mediating factors (age, sex, training protocols) to assess their effects on LV structure. Eighty-two studies met inclusion criteria (n = 1908; 19-82 years, 33% female). There was a significant increase in LVM, PWTd, IVSd, and LVDd following ET [standardized mean difference (SMD) = 0.444, 95% confidence interval (CI): 0.361, 0.527; P < 0.001; SMD = 0.234, 95% CI: 0.159, 0.309; P < 0.001; SMD = 0.237, 95% CI: 0.159, 0.316; P < 0.001; SMD = 0.249, 95% CI:0.173, 0.324; P < 0.001, respectively]. Trained status, training type, and age were the only mediating factors for change in LVM, where previously trained, mixed-type training, young (18-35 years), and middle-aged (36-55 years) individuals had the greatest change compared with untrained, interval-type training, and older individuals (>55 years). A significant increase in wall thickness was observed in males, with a similar augmentation of LVDd in males and females. Trained individuals elicited an increase in all LV structures and ET involving mixed-type training and rowing and swimming modalities conferred the greatest increase in PWTd and LVDd. Left ventricular structure is significantly increased following ET. Males, young and trained individuals, and ET interventions involving mixed training regimes elicit the greatest changes in LV structure.

Serum aldosterone effect on left ventricular structure and diastolic function in essential hypertension

Aldosterone has hypertrophic and profibrotic effects on the heart. This study aims to determine the relationship between serum aldosterone concentration (SAC) and aldosterone-to-renin ratio (ARR) with left ventricular (LV) geometry and diastolic function in essential hypertension (EH). We investigated 213 EH patients (50.3±12.6 years; 57.7% male). SAC, ARR measurements, and echocardiographic analysis were performed for participants. Overall, stepwise multiple regression analysis showed significant associations between SAC and interventricular septum, LV posterior wall thickness, LV amass, LV mass index, e' velocity, a' velocity, and E/e' ratio after adjustment of potentially confounding covariates. When patients were divided into three SAC tertiles, multivariate-adjusted analysis of covariance (ANCOVA) demonstrated a significant increase in LV mass (P ˂ 0.001), LV mass index (P ˂ 0.001), relative wall thickness (P=0.003), interventricular septum (P=0.001), LV posterior wall thickness (P=0.001) and E/e' ratio (P ˂ 0.001), but a decrease in e' velocity (P=0.002) from the first to third tertile of SAC. In logistic regression analysis, increased SAC was independently associated with concentric LV hypertrophy [OR: 1.21, 95% CI: 1.11-1.33, P ˂ 0.001]. No significant associations were found between ARR and echocardiographic parameters of LV structure or diastolic function. In conclusion, SAC, but not ARR, is independently associated with echocardiographic indices of LV structure and diastolic function and is also related to concentric LV hypertrophy. Our findings suggest that aldosterone's pro-hypertrophic and myocardial fibrosis effects contribute to alterations in LV structure and diastolic function in EH beyond blood pressure.

The interleukin-1 receptor type I promotes the development of aging-associated cardiomyopathy in mice

BackgroundAging is associated with metabolic and structural changes causing heart failure with preserved ejection fraction (HFpEF). Interleukin-1 (IL-1) is a pro-inflammatory cytokine involved in aging-related inflammation. ObjectiveWe sought to determine whether IL-1 mediates aging-related changes in the heart, as seen in HFpEF. MethodsWe studied age-matched young (4-month-old), middle-aged (14-month-old), and old (23-month-old) wild-type (WT) C57BL/6J and IL-1 receptor type I deficient (IL1RI-KO) male mice. Echocardiography was used to evaluate left ventricular (LV) dimensions and systolic/diastolic function, and a pressure transducer was used to measure the LV end-diastolic pressure. Picrosirius red stain was used to assess for myocardial interstitial fibrosis (MIF) at pathology. ResultsWT and IL-1RIKO mice showed a normal cardiac phenotype at young age, without any differences between the two groups. With aging, the WT mice developed LV concentric hypertrophy (as measured by a significant increase in LV mass [+42%, P < 0.01] and relative wall thickness [+34%, P < 0.01]), whereas the aging IL-1RI-KO mice did not. With aging, the WT mice also developed diastolic dysfunction (as measured by a significant increase in isovolumetric relaxation time [+148%, P < 0.01] and a significantly higher LV end-diastolic pressure [+174%, P < 0.01]), whereas the aging IL1RI-KO did not. Aged WT mice showed a significant increase in MIF (+124%, P < 0.01) at cardiac pathology, whereas the aging IL-1RI-KO did not. ConclusionsGenetically-modified mice lacking the IL-1RI receptor, not responsive to IL-1, are protected from aging-related LV hypertrophy, fibrosis, and diastolic dysfunction. These data support a central role of IL-1 in the pathophysiology of aging-related HFpEF.

Abstract 13208: Deletion of the Type I Interleukin-1 Receptor Prevents the Development of Cardiomyopathy Associated With Aging in Mice

Background: Aging is associated with metabolic and structural changes causing heart failure with preserved ejection fraction (HFpEF). Interleukin-1 (IL-1) is a pro-inflammatory cytokine involved in aging-related inflammation. We sought to determine whether IL-1 mediates aging-related changes in the heart as seen in HFpEF. Hypothesis: We hypothesize that mice with genetic deletion of IL-1RI, not responsive to IL-1β, would be protected from age-associated cardiac dysfunction. Methods: We studied age-matched young (4-month-old), middle-aged (14-month-old) and old (23-month-old) wild-type (WT) C57BL/6J and IL-1 receptor type I deficient (IL1RI-KO) male mice. Echocardiography was used to left ventricular (LV) dimensions and systolic/diastolic function, and a pressure-transducer was used to measure the LV end-diastolic pressure. Picrosirius red stain was used to assess for myocardial interstitial fibrosis (MIF) at pathology. Results: WT and IL-1RIKO mice showed a normal cardiac phenotype at young age, without any differences in between the two groups. With aging, the WT mice developed LV concentric hypertrophy (as measured by a significant increase in LV mass [+42%, P&lt;0.01] and relative wall thickness [+34%, P&lt;0.01]), whereas the aging IL-1RI-KO mice did not (Figure 1a,b). With aging the WT mice also developed diastolic dysfunction (as measured by a significant increase in isovolumetric relaxation time [+148%, P&lt;0.01] and a significantly higher LV end diastolic pressure [+174%, P&lt;0.01]), whereas the aging IL1RI-KO did not (Figure 1c,d). With aging WT mice showed a significant increase in MIF (+124%, P&lt;0.01) at cardiac pathology, whereas the aging IL-1RI-KO did not (Figure 1e). Conclusions: Genetically-modified mice lacking the IL-1RI receptor, not responsive to IL-1, are protected from aging-related LV hypertrophy, fibrosis and diastolic dysfunction. These data support a central role of IL-1 in the pathophysiology of aging-related HFpEF.

Adiponectin‐deficient Mice Demonstrate Impaired Coronary Arteriolar Vasodilation and Subsequent Decline in Cardiac Function

Circulating adiponectin levels have been shown to correlate with microvascular coronary function, suggesting a cardioprotective effect. Our previous work has shown that adiponectin deficiency decreases coronary smooth muscle contractile function and physiological cardiac hypertrophy that is not reversed with exercise training. However, it is unknown if adiponectin deficiency adversely affects endothelial‐dependent coronary vasodilation, leading to cardiac abnormalities. We tested the hypotheses that adiponectin is necessary for acetylcholine (ACh) and flow‐induced vasodilation in coronary arterioles. It was also hypothesized that exercise training would improve cardiac function in exercise trained wild‐type, but not adiponectin knock‐out (AdipoKO) mice.MethodsC57BL/6 wild‐type (WT) or homozygous AdipoKO mice were obtained at 10 weeks of age and underwent treadmill exercise (12 m/min, 5° incline, 1 hour/day, 5 days/week for 8 weeks) or remained sedentary in cages. At the end of the training/sedentary period, coronary resistance arterioles (intraluminal diameter &lt;150 mm) were isolated, cannulated, and placed under an inverted microscope equipped with a video camera and caliper to record luminal diameter. Vasodilatory responses to ACh (1e‐9 to 1e–4M) and changes in flow (Pressure differences = 2–60 cm H2O) were then assessed. Pre/post cardiac function was measured with a high‐resolution imaging system (Vevo 2100), with M‐mode, and was used to assess ejection fraction, fractional shortening, and left ventricular (LV) mass. Pulsed‐wave Doppler was used to calculate isovolumic relaxation (IVRT)/contraction (IVCT) time.Resultsexercise‐trained WT mice demonstrated physiological cardiac hypertrophy, indicated by a significant increase in LV mass (P&lt;0.05). Exercise‐trained WT mice also had a significantly greater ejection fraction and fractional shortening (both; p&lt;0.05). In contrast, cardiac hypertrophy was absent in exercise‐trained AdipoKO mice and a significant decrease in ejection fraction and fractional shortening was found (both; p&gt;0.05). Further, both sedentary groups were shown to have significant declines in fractional shortening and ejection fraction (p&lt;0.05). Exercise‐training maintained both IVRT/IVCT in the WT mice; however, a significant (p&lt;0.05) lengthening of the IVRT/IVCT was shown in exercise‐trained AdipoKO and WT sedentary mice (p&lt;0.05). The sedentary AdipoKO was shown to have an increase in IVRT only (p&lt;0.05). Sedentary WT mice had significantly greater mean vasodilation to ACh compared to sedentary AdipoKO (p&lt;0.01). Exercise‐training led to increased flow‐induced dilation in the WT (p&lt;0.05), but not the AdipoKO mice (p&gt;0.05).Conclusionthese results indicate that adiponectin is necessary for improvements in cardiac function during exercise training in young adult mice. Additionally, adiponectin may help with preserved cardiac function and that flow‐induced coronary arteriolar vasodilation may have contributed to this response.Support or Funding InformationFSU Research FundsThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Isoproterenol-induced heart failure in rat heart: Evaluation and cardioprotective strategy

It is well established that cardiac remodelling plays a pivotal role in the development of heart failure (HF), a leading cause of death worldwide. Meanwhile, a preclinical rat model of isoproterenol (Iso)-induced HF causes sympathetic hyperactivity, an important factor of cardiac remodelling, hemodynamic changes and cardiac fibrosis development. Several studies showed that metoprolol, a β1-adrenergic receptor (β1-AR) blocker prevents cardiac dysfunction following prolonged β-AR stimulation in different preclinical models. We evaluated the cardioprotective effects of metoprolol on cardiac remodelling and diastolic function in a severe Iso-induced HF model using echocardiography and cardiac pressure measurement. Rats received Iso injections (Iso; 5 mg/kg/day, N = 5), metoprolol (Meto; 24 mg/kg/day) + Iso 5 (Iso + Meto, N = 6), or vehicle ( N = 9) for 7 days. Left ventricular (LV) dimensions and function were followed-up by echocardiography before and after the treatment to assess LV hypertrophy. After echocardiography, LV end-diastolic pressure (LVEDP) was recorded to assess ventricular compliance and rat hearts were used for cardiac remodelling analysis. One week of Iso injections significantly increased LVEDP (+ 48%) and was associated with a major LV hypertrophy, characterised by a significant increase in LV mass (+ 33%) and a thickening of the LV walls observed by echocardiography. Simultaneous treatment with metoprolol prevented diastolic dysfunction and LV remodelling. Hypertrophy and fibrosis will be analysed in each group by histology (on-going experiments). Metoprolol afforded a cardioprotective effect on cardiac remodelling and diastolic dysfunction in Iso-induced HF model. Echocardiography and LVEDP measurements validate the reversibility of hypertrophic HF, and Iso-induced HF developed in rat could represent an effective and predictive preclinical model for evaluating antihypertrophic and antifibrotic agents.

Short-Term Evaluation of Left Ventricular Mass and Function in Children With Growth Hormone Deficiency After Replacement Treatment.

Background: Our study was designed to assess the effects of GHD on nutritional and metabolic parameters, brain natriuretic peptide (BNP) levels, and left ventricular mass (LVM) in prepubertal children and after short-term GH replacement therapy.Materials and Methods: This prospective study enrolled 81 children. We compared 40 GHD children (16 males and 24 females) to 41 healthy children (control group) (18 males and 23 females). All subjects were at Tanner Stage I (aged 7–11 years). At the baseline, a blood sample was drawn and echocardiographic images were obtained. These tests were repeated on the GHD subjects after 6 months of GH replacement therapy. Body surface, weight, size, blood pressure, heart rate, glucose, insulin, HOMA-IR, HOMA-β, QUICKI, cholesterol, HDLc, LDLc, triglycerides, IGF1, and IGFBP3 were measured. Indexed LVM, diastolic and systolic diameter (dD-sD), diastolic and systolic LV function, isovolumic relaxation time, right ventricle function, and BNP levels were obtained through echocardiography. These parameters were correlated to growth factors. Data were analyzed using Student's t-test or U-Mann–Whitney-test and Pearson's correlation, considering p < 0.05 to be significant.Results: Indexed LVM was smaller in GHD patients than in controls, whereas diastolic and systolic functions, BNP, metabolic, and nutritional profiles were similar. After treatment, nutritional and metabolic profiles significantly improved, though diastolic and systolic functions did not seem to have changed. There was a significant increase in LVM. Indexed LVM was similar to that of controls. Significant correlations were obtained between LVM-IGF1 and sD-IGFBP3.Conclusions: GHD in childhood is associated with a lower indexed LVM. In the short-term, GH increases the indexed LVM, while maintaining normal systolic and diastolic functions, BNP, and an improved lipid profile.

Disrupted Adiponectin‐Connexin43 Signaling Underlies the Exacerbated Myocardial Dysfunction in Diabetic Female Rats

Women are diagnosed with type 2 diabetes (T2DM) at an increasing rate, and there is renewed interest in estrogen (E2) replacement therapy (ERT). It remains unknown if E2 contributes to the greater susceptibility of women to diabetes‐evoked myocardial dysfunction. In diabetic men and male animals, the formation of connexin43 (Cx43) hemichannels, at the expense of the physiological Cx43‐based gap junction domain, underlies myocardial dysfunctions. While Cx43 constitutes a promising therapeutic target for cardiovascular anomalies, its role and its modulation by adiponectin (APN) in diabetic females remain unknown. APN, an anti‐inflammatory adipokine with higher levels in females, is reduced in T2DM and coronary artery disease. Whether the higher APN‐Cx43 expression and signaling in healthy female hearts becomes paradoxically detrimental when disrupted by T2DM in an E2‐dependent manner has not been studied. Therefore, we tested the hypothesis that E2 exacerbation of diabetes‐evoked disruption of cardiac APN‐Cx43 signaling underlies heightened myocardial dysfunction in diabetic females.We examined eight groups of Wistar rats (n=8 each); divided into DM or control groups with the following designations: i. sham operated (SO), ii. ovariectomized (OVX), iii. ovariectomized with E2 supplementation (OVX+E2), and iv. male. Females underwent OVX or sham surgery at week 0, and DM was induced with a high fat diet (45%), low‐dose streptozotocin regimen (2 injections, one week apart; 35 mg/kg; I.P.). OVX rats received subcutaneous implants of E2 (OVX+E2) or vehicle (OVX). Over the 10‐week study, weekly body weight, food intake and tail cuff blood pressure were collected along with biweekly echocardiography (starting at week 0). Following final echocardiography, IV glucose tolerance testing, femoral and left ventricular (LV) catheterization were conducted for integrative hemodynamic measurements. Results showed significant increases in LV mass and tau, and decreases in LV developed pressure, LV contractility and fractional shortening in the diabetic female E2‐replete groups (SO or OVX+E2), compared to respective nondiabetic controls or E2‐depleted (OVX or male) rats. Biochemical analysis of cardiac tissue (western blots) showed upregulated estrogen receptor α (ERα) expression in all DM groups, with downregulation of APN receptor 1 (AdipoR1) in E2‐depleted DM groups (OVX and male). Cx43 expression was reduced (P&lt;0.05) in E2‐replete DM females (SO or OVX+E2). The present novel findings are the first to implicate E2 in the exacerbated myocardial dysfunction in diabetic females, and to discern malfunction in cardiac APN‐Cx43 signaling as an underlying mechanism for this sex/E2‐specific problem.Support or Funding InformationEast Carolina University, Brody School of Medicine, Department of Pharmacology and ToxicologyGraduate Student FundingThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Cardiac magnetic resonance imaging to assess the impact of maternal habitus on cardiac remodeling during pregnancy

It is well known that the maternal cardiovascular system undergoes profound alterations throughout pregnancy. Interest in understanding these changes has led investigators to use evolving and increasingly sophisticated techniques to study these changes, most recently with 2-dimensional echocardiography. Despite its clinical utility, echocardiography has limitations, and cardiac magnetic resonance imaging (CMRI) has become increasingly used for evaluation of cardiac structure and function. We used CMRI to evaluate cardiac remodeling according to maternal habitus throughout pregnancy and postpartum. This was a prospective, observational study ofnulliparous women aged 18-30 years, without preexisting medical conditions, conducted from October 2012 through December 2014. Women were classified according to prepregnancy body mass index (BMI) as either normal (BMI 18.5-24.9 kg/m(2)) or overweight (BMI 25-35 kg/m(2)). All women underwent CMRI during 5 epochs throughout gestation: 12-16 weeks, 26-30 weeks, 32-36 weeks, at delivery, and 3 months' postpartum. Using left ventricular mass (LVM) as a marker of cardiac remodeling, the 2 cohorts were compared. There were 14 normal-weight (BMI 22.2 ± 1.3) and 9 overweight (BMI 29.1 ± 2.0) women who participated in the study. Beginning at 26-30 weeks and continuing to delivery, LVM of both normal-weight and overweight women was significantly increased compared with the respective first-trimester studies for each cohort (P < .001). LVM of both cohorts returned to their index values by 3 months' postpartum. The geometric ratio of LVM to left ventricular end-diastolic volume was calculated, and both normal-weight and overweight women demonstrated concentric remodeling throughout gestation, however this resolved by 12weeks' postpartum. There is substantial cardiac remodeling during pregnancy with significant increases in LVM that are proportional to maternal size. Left ventricular geometric remodeling was concentric in both normal-weight and overweight women. All changes in cardiac remodeling resolved by 3 months' postpartum.

Heart function disturbances in chronic kidney disease - echocardiographic indices.

IntroductionIn chronic kidney disease (CKD) patients left ventricular (LV) diastolic dysfunction occurs frequently and is associated with heart failure (HF) and higher mortality. Left ventricular systolic dysfunction is associated with coronary artery disease (CAD) and is a major determinant of prognosis. The aim of this study was to assess indices of LV diastolic dysfunction in CKD patients.Material and methodsStudy included 118 CKD patients. All patients underwent transthoracic echocardiography. Diastolic function based on E and A, E/A ratio and pulmonary vein flow velocities as well as EF%, deceleration time, RA, LA volume were assessed. In dialysis patients examination was carried out before and after dialysis.ResultsIn CKD patients the stage of renal failure was associated with the significant increase in LV mass (268.0 ±47.6 CKD I/II vs. 432.7 ±122.4 CKD V/dialysis, p < 0.0001), systolic LV (37.3 ±4.5 vs. 51.2 ±8.9, p < 0.0001) and diastolic LV (CKD I–II 44.7 ±4.1 vs. CKD III 48.5 ±6.7 vs. CKD IV 47.1 ±5.6; p = 0.004) dimensions and in the size of the LA (40.4 ±2.0 vs. 41.9 ±2.7 vs. 42.3 ±3.2 vs. 44.8 ±3.1; p < 0.0001). The increase the E/E’ ratio between groups of patients (6.7 ±1.5 vs. 8.9 ±2.4 vs. 11.5 ±4.0 vs. 13.5 ±5.0; p < 0.0001) was seen in this study. The reduction in deceleration time (247.2 ±34.5 in CKD I/II vs. 197.4 ±61.0 in CKD IV, p = 0.0005) along with the decrease in estimated glomerular filtration rate was also observed in this study.ConclusionsEarly identification of factors involved is necessary to prevent this devastating process. Many indexes of contractility are used and each of them has imperfections. It seems that TVI, E, E/A and E/E’ are good instruments for the early detection of left ventricular hypertrophy and diastolic dysfunction.

Cardiac MRI in the Assessment of Cardiac Injury and Toxicity From Cancer Chemotherapy

During the past 30 years, there has been a significant decrease in cancer mortality rates, predominantly attributable to improvements in treatment options.1 However, survivors are at increased risk of premature cardiac disease,2 both because of the overlap in risk factors for cancer and cardiovascular disease3 and the cardiotoxic effects of cancer chemotherapy. Two chemotherapeutic agent classes that are commonly associated with cardiotoxicity are the anthracyclines and tyrosine kinase inhibitors, both of which can cause left ventricular (LV) dysfunction and heart failure (HF).4,5 Mechanisms of cardiac injury from cancer therapy have been summarized elsewhere.4,6 Briefly, anthracycline cardiotoxicity has been attributed to reactive oxygen species formation, transcriptional changes in intracellular adenosine triphosphate production in cardiac myocytes, and, more recently, through interaction with cardiac topoisomerase IIβ.4,6 Trastuzumab cardiotoxicity seems to be because of inhibition of cardiomyocyte human epidermal growth factor receptor 2, resulting in ATP depletion and contractile dysfunction.4 Other proposed mechanisms include immune-mediated destruction of cardiomyocytes.4,6 At the tissue level, early anthracycline toxicity has been associated with myocardial inflammation,7–9 vacuolization,9–12 and cell swelling/edema.11,13 These changes seem to occur before myocardial functional abnormalities.11,13 Later stages of toxicity are associated with myocardial fibrosis.14,15 Unfortunately, the use of myocardial biopsy is not feasible for diagnostic purposes in this setting. However, once HF manifests, the 2-year mortality can be as high as 60%.16 This emphasizes the importance of early recognition of cardiac injury and institution of cardioprotective therapy in an effort to prevent development of HF and allow uninterrupted completion of cancer therapy.17 Thus, the diagnosis is dependent on either direct evidence of myocardial damage or functional disturbance. Either signal may be identified …

The Effect of Recombinant Human Growth Hormone Therapy on Left-Ventricular Chamber Size and Function in Children With Growth Hormone Deficiency

This study was designed to assess the effect of recombinant human growth hormone (rhGH) therapy on left-ventricular (LV) chamber size and function in children with idiopathic isolated growth hormone deficiency (GHD) using conventional echocardiography and tissue Doppler imaging (TDI). Thirty patients (19 boys and 11 girls) with idiopathic isolated GHD were followed-up for 12 months. Mean age of patients was 11.0 ± 2.6 years (range 6.3-15.5). At baseline and at 3, 6, and 12 months of treatment, the structure of the left ventricle was assessed by conventional echocardiography and myocardial rates and time intervals by TDI. There was a significant increase in LV mass (LVM) compared with pretreatment values. Like LVM, relative wall thickness (RWT) was also increased significantly. The significant increase in LVM indexed to body surface area and RWT became apparent at month 3 of treatment with a significant increase in LVM indexed to height(2.7) at treatment month 6. Normalized LVM increased as early month 3 of treatment, and a steady increase was observed until month 12. However, no patient had LVM > +2 standard deviation scores at month 12 of treatment. No significant differences were observed in functional parameters of the left ventricle and the interventricular septum. The results of this study showed that rhGH therapy causes an increase in myocardial mass without changing the geometry or function of the myocardium. Therefore, the increase in myocardial mass appears to be concentric, thus causing remodeling instead of hypertrophy.

The Relationship between Body Mass Index and Left Ventricular Structure and Function in Healthy Adults

Background: There is considerable evidence which associate cardiovascular morbidity and mortality with obesity, however, a direct effect of uncomplicated obesity on cardiac function is not well established.Objective: To evaluate the relationship between body mass index (BMI) and left ventricular structure and function.Methods: This cross-sectional study was carried out on (146) apparently healthy adults from both sexes (85 male and 61 female) aged 20-59 years(36.49±9.92 ). Subjects were grouped according to BMI into1.normal weight group included 47 subjects (BMI=18.5-24.9Kg/m2);2. Overweight group included 43 subjects (BMI=25-29.5 Kg/m2) and 3. obese group included (56) subjects(BMI≥30). Echocardiographic indices of left ventricular structure and function were obtained. This study was performed between October 2009 till April 2010 at the Echocardiography Unit in Ibn Sina Teaching Hospital in Mosul.Results: There was a significant increase in LVM(left ventricular mass), LVMI(left ventricular mass index), LVIDD(left ventricular internal dimension in diastole) and PWT(posterior wall thickness) among over weight and obese subjects (P&lt; 0.001),however, both contractility indices [LVEF%(left ventricular ejection fraction percent) and LVFS %(left ventricular fractional shortening percent)] seemed unchanged significantly. The left ventricular diastolic function [E/A ratio(ratio of passive to active velocity inflow)] has significantly decreased among the obese group (P&lt; 0.001). This observed decrease in E/A ratio with increasing BMI coincided with a statistically significant increase (P&lt; 0.001) in LAD (left atrial dimensions).Conclusions: Increased body weight is positively correlated with LVM but not with systolic dysfunction. All subjects with isolated obesity have subclinical left ventricular diastolic dysfunction; this correlates with BMI.

Serum aldosterone and its relationship to left ventricular structure and geometry in patients with preserved left ventricular ejection fraction

Cardiac remodelling might be an important mechanism for aldosterone-mediated cardiovascular (CV) morbidity and mortality. Previous studies relating aldosterone to left ventricular (LV) structure however revealed conflicting results. We aimed to evaluate the relationship of serum aldosterone concentration (SAC) and aldosterone-to-renin ratio (ARR) with echocardiographic parameters of LV remodelling in CV risk patients with preserved left ventricular ejection fraction (LVEF). We studied 1575 participants (54.1% female) with CV risk factors and LVEF >50% (61.7 ± 6.1%). Of the total, 94.7% of patients had no overt heart failure. All patients underwent measurement of SAC, ARR, and comprehensive echocardiographic analysis. Overall, multivariate adjusted analysis of covariance (ANCOVA) showed a significant increase in LV mass (P= 0.001), LV mass index (P= 0.001), relative wall thickness (P= 0.011), and LV posterior wall thickness (P< 0.001) with increasing SAC. This overall association of SAC and LV remodelling was driven by a statistic significant effect exclusively in women. In multivariate logistic regression analysis higher SAC levels were independently related to concentric LV hypertrophy [odds ratio (OR; with 95% CI) by comparing SAC levels in the third gender-specific tertile with the first tertile: 1.87; 95% CI: 1.31-2.68; P= 0.001]. Higher SAC levels were positively related to concentric LVH in either sex. We observed no significant associations between the ARR and echocardiographic parameters of LV remodelling. Circulating aldosterone but not ARR levels are independently related to echocardiographic parameters of LV structure, particularly in women. Higher SAC however was related to concentric LVH in either sex. Our findings in a large CV risk cohort with preserved LVEF indicate aldosterone-mediated pro-hypertrophic effects as a potential pathway for structural alterations of the left ventricular myocardium.

Temporal Evaluation of Cardiac Myocyte Hypertrophy and Hyperplasia in Male Rats Secondary to Chronic Volume Overload

The temporal myocardial remodeling induced by chronic ventricular volume overload in male rats was examined. Specifically, left ventricular (LV) cardiomyocyte length and width, sarcomere length, and number of nuclei were measured in male rats (n = 8 to 17) at 1, 3, 5, 7, 21, 35, and 56 days after creation of an infrarenal aortocaval fistula. In contrast to previously published reports of progressive increases in cardiomyocyte length and cross-sectional area at 5 days post-fistula and beyond in female hearts, cardiomyocyte length and width did not increase significantly in males during the first 35 days of volume overload. Furthermore, a significant decrease in cardiomyocyte length relative to age-matched controls, together with a reduced number of sarcomeres per cell, was noted in male hearts at 5 days post-fistula. There was a concurrent increase in the percentage of mononucleated cardiomyocytes from 11.6% to 18% at 5 days post-fistula. These initial differences could not be attributed to cardiomyocyte proliferation, and treatment with a microtubule stabilizing agent prevented them from occurring. The subsequent significant increase in LV weight without corresponding increases in cardiomyocyte dimensions is indicative of hyperplasia. Thus, these findings indicate hyperplasia resulting from cytokinesis of cardiomyocytes is a key mechanism, independent of hypertrophy, that contributes to the significant increase in LV mass in male hearts subjected to chronic volume overload.

Effects of Body Size and Body Fatness on Left Ventricular Mass in Children and Adolescents: Project HeartBeat!

Left ventricular mass (LVM) is a strong predictor of cardiovascular disease in adults. Available study findings on effects of body fatness on LVM in children are inconsistent. Understanding the impact of body fat on LVM in children may help prevent excessive LVM through measures to reduce overweight and obesity. Healthy children (n=678) aged 8, 11, and 14 years at baseline were examined at 4-month intervals for up to 4 years (1991-1995); 4608 valid measurements of LVM were obtained with M-mode echocardiography. A multilevel linear model was used for analysis. The impact of body size was examined by adding separately nine body-size indicators to a basic LVM-gender-age model. The impact of body fatness was tested by introducing four body-fatness indicators into the nine models, yielding 36 models. All body-size indicators showed strong, positive effects on LVM. In models containing weight or body surface area (measuring both fat-free and fat contributions to body size), additional effects of body fatness were negative; in models containing fat-free mass (FFM) or height (both measuring body size independent of body fat), increased body fatness was related to a significant increase in LVM. For example, in models with FFM as a body-size indicator, a 1-SD increase in percent body fat or fat mass was related to a 5.4- or 7.2-g increase in LVM, respectively. Effects of body size on LVM attributable to fat-free body mass can be distinguished from those attributable to fat body mass; both are independent, positive predictors, but the former is the stronger determinant. When a body-size indicator not independent of body fat is used as a predictor, effects of fat-free body mass and fat body mass are forced to relate to the same indicator; because their magnitudes are estimated to be equal, the effect of fat body mass is overestimated. Thus, when an additional body-fatness indicator is included in the prediction of LVM, the additional estimated effect related to the indicator appears to be negative.

Ventricular dysfunction after pressure overload is associated to impaired CD4 CD8 recruitment in diabetic mice

Cardiac hypertrophy and diabetes mellitus (DM) are independent risk factors for the development of heart failure. We induced left ventricular (LV) pressure overload by transverse aortic constriction (TAC) in wild-type mice (WT) and in mice homozygous for a mutation in leptin receptor (db/db) showing type II DM phenotype. Seven days after TAC WT but not db/db mice showed a significant increase in LV mass calculated by LV weight to body weight (BW) ratio despite a similar pressure gradient (51.7 mm Hg in WT vs. 52 mm Hg in db/db NS). TAC did not change LV end diastolic (ED) and end systolic (ES) diameter (D) in WT (2.80 mm vs. 2.87 mm and 1.17 mm vs. 1.21 mm after TAC) whereas db/db showed a significant increase (2.9 mm vs. 3.7 mm p<0.05 and 1.39 vs. 1.82 mm p<0.05). Beta adrenergic receptor (βAR) kinase 1 expression was significantly augmented in WT after TAC, but not in db/db, suggesting that other mechanisms rather than βAR dysfunction are responsible for the early LV dilatation. It is known that in WT CD8+ T cells contribute to collateral development after hind limb ischemia recruiting CD4+ T cells through IL-16 production. Moreover, disruption of coordinated tissue growth and angiogenesis in the heart contribute to the progression from adaptive cardiac hypertrophy to heart failure. In the present study we found a marked increase in CD4+, CD8+ T cells and interleukin-16 (IL-16) in WT hearts. CD4+CD8+ T cells recruitment and IL-16 production were significantly blunted in db/db suggesting that the consequent impaired angiogenic response after TAC could be responsible for the early LV dilatation.

Alterations in the peripheral circulation in COPD patients

Although various factors influence peripheral circulation in chronic obstructive pulmonary disease (COPD) patients, little is known about the vasomotor changes in these subjects. The present study was designed to assess alterations in the brachial circulation of COPD patients. Twenty-five COPD patients and 25 healthy subjects were studied. Brachial artery (BA) blood flow and indices of BA stiffness were investigated by two-dimensional ultrasonography and pulsed Doppler. Cardiac dimensions, left ventricular (LV) function and cardiac output were assessed by pulsed Doppler echocardiography. A significant increase in LV mass was observed in the COPD group despite normal arterial pressure. Total arterial compliance and BA compliance were significantly decreased in COPD patients in comparison with healthy subjects. Heart rate was increased in COPD patients and was inversely correlated with PaO(2) and forced expiratory volume in the first second (FEV(1)). A decrease in LV preload was expressed by a reduction in LV diastolic diameters and LV stroke volume. Patients with severe COPD have a lower BA surface area than patients with moderate COPD. FEV(1) and PaO(2) were significantly related to BA compliance. In COPD patients, significant alterations in the peripheral circulation were observed. Moreover, the magnitude of changes in the peripheral circulation was related to the severity of COPD.

A High Fat Diet, But Not a High Sucrose Diet, Prevents Pressure Overload Induced Cardiac Dysfunction and Hypertrophy

Currently, a high carbohydrate/low fat diet is recommended to prevent cardiovascular disease; however the effect of dietary fat and carbohydrate on the left ventricular (LV) adaptation to pressure overload is still unclear. Male Wistar rats were fed standard chow (SC, 52% cal from cornstarch), high sugar (HS, 60% cal from sucrose) or high fat (HF, 60% from fat). After 1 week on the diet rats underwent abdominal aorta banding (AB) or sham surgery (n=9-11/group). LV function was assessed by echocardiography before surgery and after 8 wks. There were no differences in these parameters between the groups prior to surgery and body weight was not different among group throughout study. As show in the table, AB caused significant increase in LV mass, LV end systolic volume (sV) and decline in ejection fraction (EF) and velocity of circumferential flow (Vcf) in both standard and high sucrose chows. High fat prevented AB induced effects on LV function and blunted the increase in LV mass. In conclusion, high fat feeding prevented pressure overload induced cardiac contractile dysfunction and reduced LV hypertrophy. High sucrose feeding did not prevent the effects of pressure overload on the LV.

Magnetic resonance imaging of progressive cardiomyopathic changes in the db/db mouse

The db/db mouse is a well-established model of diabetes. Previous reports have documented contractile dysfunction (i.e., cardiomyopathy) in these animals, although the extant literature provides limited insights into cardiac structure and function as they change over time. To better elucidate the natural history of cardiomyopathy in db/db mice, we performed cardiac magnetic resonance (CMR) scans on these animals. CMR imaging was conducted with a 4.7-T magnet on female db/db mice and control db/+ littermates at 5, 9, 13, 17, and 22 wk of age. Gated gradient echo sequences were used to obtain cineographic short-axis slices from apex to base. From these images left ventricular (LV) mass (LVM), wall thickness, end-diastolic volume (LVEDV), and ejection fraction (LVEF) were determined. Additionally, cardiac [(18)F]fluorodeoxyglucose ([(18)F]FDG) PET scanning, pressure-volume loops, and real-time quantitative PCR on db/db myocardium were performed. Relative to control, db/db mice developed significant increases in LVM and wall thickness as early as 9 wk of age. LVEDV diverged slightly later, at 13 wk. Interestingly, compared with the baseline level, LVEF in the db/db group did not decrease significantly until 22 wk. Additionally, [(18)F]FDG metabolic imaging showed a 40% decrease in glucose uptake in db/db mice. Furthermore, contractile dysfunction was observed in 15-wk db/db mice undergoing pressure-volume loops. Finally, real-time quantitative PCR revealed an age-dependent recapitulation of the fetal gene program, consistent with a myopathic process. In summary, as assessed by CMR, db/db mice develop characteristic structural and functional changes consistent with cardiomyopathy.