Advertisement

Sign up for our daily newsletter

Advertisement

Pathological cardiac remodeling in obesity – Editorial: Cardiac Remodeling: New Insights in Physiological and Pathological Adaptations

J Med Assoc Thail. Che, C.

Matthew Cox
Monday, March 15, 2021
Advertisement
  • Gradman AH, Alfayoumi F From left ventricular hypertrophy to congestive heart failure: management of hypertensive heart disease.

  • Thus, further studies are needed to assess whether modulation of the microRNA-1 and microRNAc in vivo in the obesity phenotype would play a key role in preventing pathologic cardiac remodeling.

  • Thus, excess adiposity may promote concentric LV geometric changes through factors that are not predicted by BP measured on a single occasion. Impact of obesity and weight loss on cardiac performance and morphology in adults.

  • Among cardiovascular risk factors, age, sex, and hypertension increase the likelihood of diastolic dysfunction, which is demonstrated by what is referred to as the ratio: the ratio of the mitral flow velocities measured in the early diastole and late diastole.

1. Introduction

Owan T Favorable changes in cardiac geometry and function following gastric bypass surgery: 2-year follow-up in the Utah obesity study. Zlochiver, V. Direct multiplexed measurement of gene expression with color-coded probe pairs. Huffman CNovember Reversible cardiomyopathies: A review. There are a number of determinants of LV mass LVMwith the most consistent being an excess adiposity.

Yamaguchi, M. Tissue expression of the leptin receptor, which includes the heart, and signal transduction is similar between mice and humans [ 22 ]. Open in a pathologgical window. HF is classified into Stages A to D, with specific treatment protocols for each stage. Camm, G. In a recent study, HF-fed male rats subjected to aortic valve regurgitation a model of eccentric remodeling had increased cardiac hypertrophy and decreased survival compared with HF-fed rats without aortic value regurgitation [ 45 ], suggesting additive adverse effects of HF feeding and cardiac remodeling. Obesity higher BMI or waist circumference also correlate with higher LV mass compared to age-matched lean individuals [50].

Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice. G protein-coupled receptor kinases in normal and failing myocardium. Our data further define the cellular processes and molecular mechanisms by which GRK2 down-regulation is cardioprotective during diet-induced obesity, reinforcing the protective effect of maintaining low levels of GRK2 under nutritional stress, and showing a role for this kinase in obesity-induced cardiac remodeling and steatosis. Rev Endocr Metab Disord. J Biol Chem.

MeSH terms

Figure 1. However, the gene expression profile in obese postpartum mice with LV hypertrophy reflected the active remodeling of the ECM. Reprints and Permissions. Conflicts of Interest No conflicts of interest are declared by the authors. Arch Physiol Biochem.

  • Cardiac hypertrophy is an independent predictor of CVD. Clinical Presentation: Obesity cardiomyopathy presents with a similar clinical spectrum of HF symptoms to other forms of cardiomyopathies.

  • Full size image.

  • Numerous studies have demonstrated the connection between obesity and the increased risk of cardiac arrhythmias and sudden cardiac death [ 4445 ].

  • Alexander, A.

  • Fibrosis staining and quantitation Fibrosis was quantified in Picro-sirius red-stained sections in order to detect collagen fibers.

Table S2. There is a paucity of data describing the effect obeisty obesity during pregnancy on maternal cardiovascular health. All animals were weighed once a week and the workload was adjusted according to BW variations. Keywords: atrial fibrillation; autonomic regulation; circadian rhythm; ion channel remodeling; long QT syndrome; metabolic disorders. Barretti, and Edilamar M.

Associations among plasma adiponectin, hypertension, left ventricular diastolic function and left ventricular mass index. Burchfield, J. Although Shibata et al. Importance obwsity obesity, race and age to the cardiac structural and functional effects of hypertension. Avelar E, Cloward TV Left ventricular hypertrophy in severe obesity: interactions among blood pressure, nocturnal hypoxemia, and body mass. Cardiac remodeling-concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling.

Jeong, M. Clinical Chemistry Increased LV stroke work due to changes in hemodynamics further stimulates myocardial metabolism setting up a vicious cycle [66]. Karason, H. Influence of left ventricular geometric patterns on prognosis in patients with or without coronary artery disease.

Publication types

The degree of cardiac remodeling correlates with the severity and duration of obesity [53,54]. Prognostic value of left ventricular mass and geometry in systemic hypertension with left ventricular hypertrophy. Metabolism-Clinical and Experimental

Herges et al. Myocardial hypertrophy, fibrosis, focal myocardial disarray, and increased volume of epicardial fat are also parts of the pathological process [ 65 ]. In addition to OCM-specific risk factors, classical risk factors for cardiovascular diseases may increase the risk for HF in obese patients. Left ventricular hypertrophy in severe obesity: interactions among blood pressure, nocturnal hypoxemia, and body mass. Pregnancy late in rodent life has detrimental effects on the heart.

Obesity remodelig the most common problem in obstetrics associated with pregnancy complications [ 6 ], and women with a history of pregnancy complications are at increased risk for future CVD. Epidemiology of heart failure with preserved ejection fraction. The purpose of this study was to determine the long-term effect of obesity during pregnancy on cardiac function and structure in mice. Cristina Murga, Email: se.

Diabetes Mellitus and Its Cardiovascular Complications: New Insights into an Old Disease

Cardiac lipid accumulation associated with diastolic dysfunction in obese mice. Molecular mechanisms underlying cardiac adaptation to exercise. Direct multiplexed measurement of gene expression with color-coded probe pairs. Adeno-associated viral gene transfer of SERCA2a improves heart function in chronic congestive heart failure rats.

Hypertension and obesity independently promote cardiac hypertrophy, and pathological cardiac remodeling in obesity combined effects are additive in both women and men [ 6869 ]. PubMed Google Scholar. Am Heart J. The protection afforded by GRK2 downmodulation is apparent in the presence of concurrent relevant risk factors for insulin resistance and cardiovascular disease such as age and obesity after long-term HFD feeding. Circadian rhythms are involved in many physiological and pathological processes in different tissues, including the heart. Staining of fat depots with Oil red O Fig. Barretti D.

Pooled data from nine studies obesity demonstrated significant pathopogical in LV structure LV reverse remodeling. Kaier TE Ventricular remodelling post-bariatric surgery: is the type of surgery relevant? Goldberg IJ Lipid metabolism and toxicity in the heart. Zeemering, C. It improves insulin resistance and leads to resolution of diabetes mellitus, improve hyperlipidemia and hypertension and may eliminate obstructive sleep apnea [57,]. Pasarica, O. Abrignani, V.

  • Sereda, L. Maesen, S.

  • Selective leptin resistance revisited.

  • From basis to clinical trials. Berkalp B Obesity and left ventricular diastolic dysfunction.

  • Toblli J.

  • Search Strategy: Medical literature was reviewed to identify studies evaluating ventricular dysfunction in obese patients using echocardiographic imaging modalities: conventional and Tissue Doppler Imaging TDI. Venteclef, V.

  • External link. Pathological cardiac hypertrophy with obesity is distinctly different from hypertrophy occurring in response to physiological stimuli, such as pregnancy or exercise.

All animals were weighed once a week pathological cardiac remodeling in obesity the workload was adjusted according to BW variations. Schematic panel of study design a. Exercise Training Protocol Swimming training was performed as described previously [ 4 ]. World J Cardiol. Effect of obesity on left ventricular mass: results from multi-slices computed tomography. Please review our privacy policy. Apelin administration ameliorates high fat diet-induced cardiac hypertrophy and contractile dysfunction.

Am J Cardiol. Figure 5. PubMed Article Google Scholar 6. Abstract Background Over a third of reproductive-age women in the USA are obese, and the prevalence of cardiovascular disease CVD is rising in premenopausal women.

Background

Effect of obesity on left ventricular mass: results from multi-slices computed tomography. Circulating leptin in women: a longitudinal study in the menstrual cycle and during pregnancy. Discussion Obesity is a chronic disease that results from a convergence of genetic, psychological, and social factors. BMC Cardiovascular Disorders.

Although high myocardial TG content is non-toxic, and may initially provide a buffer against Cradiac toxic pathways [79], cardiomyocytes have limited storage and shunt excess FFA into non-oxidative pathways resulting into lipotoxicity and apoptosis of lipid-filled cardiomyocytes [49,79,80]. Qin et al. Messerli FH : Cardiovascular effects of obesity and hypertension. Plasma ceramides and cardiovascular events in hypertensive patients at high cardiovascular risk.

  • Obesity increases both the aldosterone level and the mineralocorticoid receptor expression, which promote interstitial cardiac fibrosis, platelet aggregation, and endothelial dysfunction. Nikolsky, E.

  • American Journal of Physiology.

  • American Diabetes Association Standards of medical care in diabetes Special Issues Frequently Asked Questions.

  • Google Scholar 8.

In conclusion, these results demonstrate that obesity during and after pregnancy promotes marked LV hypertrophy with moderate dilation of the LV chamber. The obesity-associated remodeeling leptin induces hypertrophy in neonatal rat ventricular myocytes. In order to further characterize the cardiac hypertrophy that we detected, we quantified the mRNA expression levels Fig. Optimisation of oil red O staining permits combination with immunofluorescence and automated quantification of lipids. Lipotoxicity in the heart. This could be because the swimming training was most effective to promote this adaptation in obesity phenotype.

Improved fatty acid utilization via dietary modification pathological cardiac remodeling in obesity ameliorates mitochondrial fragmentation and cardiac dysfunction [ 92 ]. Stampfer et al. LV mass was significantly higher in obese patients in all the five studies. Thus, the contribution of blood pressure to increased LV mass in obese postpartum vs nulliparous females is not known. Statistical analysis. Esposito, A. The hair on the chest region was shaved and removed, and electrode cream was applied on the front and hind limbs before being secured with electrical tape to electrodes on the platform.

Report of a WHO consultation. High-fat-fed postpartum mice exhibit increased left ventricular mass with enlargement of the left ventricular chamber. Aerobic exercise training-induced left ventricular hypertrophy involves regulatory microRNAs, decreased angiotensin-converting enzyme-angiotensin ii, and synergistic regulation of angiotensin-converting enzyme 2-angiotensin Hypertension.

Control of stress-dependent cardiac growth and gene expression by a pathological cardiac remodeling in obesity. Given the already mentioned role of GRK2 in fatty acid handling in white and brown adipose tissues [ 2125 ], it is tempting to suggest a similar direct effect of GRK2 downregulation in other organs such as the heart, where fatty acid oxidation is the main source of ATP. Long-term obesity promotes alterations in diastolic function induced by reduction of phospholamban phosphorylation at serine without affecting calcium handling. Google Scholar Reprints and Permissions.

ALSO READ: Heart Disease Obesity Diabetes Metabolism

This article has been cited by other articles in PMC. Obesity is strongly remodeling with pregnancy complications [ 6 ]. MicroRNAs are regulators in various physiological and pathological processes, such as cardiac remodeling [ 22 ]. Reduced levels of GRK2 can protect cardiac tissue from hypertrophy and lipid accumulation after a long term HFD by different mechanisms. Cardiac lipid accumulation associated with diastolic dysfunction in obese mice. Arrows indicate fat red staining. Reprints and Permissions.

Myocardial fibrosis cardoac concomitant with tissue regeneration and inflammation is common in obese individuals obesity cdc charts corresponds with the severity of obesity. Alexander, A. Montori, V. Differences in the types of CVD, timing of onset, and mortality rate have been largely attributed to sex hormones, and more recently, sex chromosomes [ 2 ]. Related articles. Abstract Obesity is a growing health problem worldwide. Futura Publishing Company.

Akt and MAPK signaling mediate pregnancy-induced cardiac adaptation. Arterioscler Thromb Vasc Biol. Thus, we hypothesized that cardiac remodeling induced by obesity is a milder compensatory response than that found in other pathologies, such as CH due to ischemic diseases [ 22 ]. Dysregulation of microRNAs after myocardial infarction reveals a role of miR in cardiac fibrosis.

Barretti, pathological cardiac remodeling in obesity Edilamar M. Front Biosci. Conclusions Our data further define the cellular processes and molecular mechanisms by which GRK2 down-regulation is cardioprotective during diet-induced obesity, reinforcing the protective remodelingg of maintaining low levels of GRK2 under nutritional stress, and showing a role for this kinase in obesity-induced cardiac remodeling and steatosis. Circadian rhythms are involved in many physiological and pathological processes in different tissues, including the heart. Echocardiography Echocardiography was performed on isoflurane-anesthetized LF- and HF-fed female mice at week 20 of diet feeding in postpartum mean of The impact of obesity on left ventricular mass and geometry. All sections were examined using a fluorescence resonance energy transfer FRET equipment coupled to an inverted Axiovert Zeiss, Germany microscope in the Confocal Microscopy Facility of our center.

Catdiac OCM patients with significant LV systolic dysfunction and overt heart failure, management consists treatment of heart failure using conventional heart failure therapy. Value of echocardiographic measurement of left ventricular mass in predicting cardiovascular morbid events in hypertensive men. Twenty four—hour ambulatory BP monitoring was performed on the same day as conventional BP measurements using oscillometric monitors SpaceLabs, Redmond, WA; modelof which the calibration was checked monthly against a mercury manometer. Open Access News and events Contact Us. Pontillo, C. However, there was no effect of diet or pregnancy on the expression of any other angiogenesis-related genes Additional file 1 : Table S2. Published online Dec

The American Journal of Medicine e5-e6. Pradhan, J. Kenchaiah, J.

AMPK activation, a preventive therapeutic target in the transition from cardiac injury to heart failure. It is tempting to hypothesize that the increase in cardiac GRK2 protein levels triggered as a consequence of HFD feeding or in different pathophysiological situations would play a central role allowing progression to maladaptive tissue and metabolic cardiac remodeling due to its unique ability to simultaneously alter GPCR and insulin signaling. BMC Cardiovascular Disorders. Patten IS, Arany Z. Characterization of a mouse model of obesity-related fibrotic cardiomyopathy that recapitulates features of human heart failure with preserved ejection fraction.

  • Subject alert. The increase in circulating blood volume causes an increase in venous return to the right and left ventricles and a subsequent increase in wall tension and chamber dilatation [49].

  • Melo S.

  • Conclusions These results suggest that the combined effects of pregnancy and obesity augment cardiac hypertrophy and promote remodeling. The purpose of the present review and meta-analysis is to synthesize current scholarly and practitioner understanding of IOC with a focus on broadening the knowledge on diagnosis and clinical management.

Google Scholar Exercise Training Protocol Swimming training was performed as described previously [ 4 ]. The online version of this article doi In summary, our obesity point to a protective role of low levels of GRK2 upon obesity-induced cardiac remodeling and steatosis. Lipoapoptosis: its mechanism and its diseases. Lipid droplets in each condition are shown in black and white after image processing. All sections were examined using a fluorescence resonance energy transfer FRET equipment coupled to an inverted Axiovert Zeiss, Germany microscope in the Confocal Microscopy Facility of our center.

Adapted changes in left ventricular structure and function pathological cardiac remodeling in obesity severe uncomplicated obesity. Nat Biotechnol. Effects of aerobic exercise training on pahhological renin-angiotensin system in an obese Zucker rat strain. Consistent with this notion, we report an increase in cardiac GRK2 levels in WT HFD-fed mice that correlates with enhanced cardiac hypertrophy and remodeling. The tissues and tibia were harvested, the heart H was weighed, and carefully, the left ventricle LV free wall plus septum and right ventricle RV were dissected.

A representative blot is shown. High-fat-fed postpartum mice exhibit increased left ventricular mass with enlargement of the left ventricular chamber. Eventually, prolonged persistence of obesity causes both left ventricular systolic and diastolic dysfunctions [ 4 ]. Epicardial and perivascular adipose tissues and their influence on cardiovascular disease: basic mechanisms and clinical associations. Thus, we hypothesized that cardiac remodeling induced by obesity is a milder compensatory response than that found in other pathologies, such as CH due to ischemic diseases [ 22 ].

Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Cardiovascular physiology of pregnancy. Cardiac remodeling-concepts and clinical implications: a consensus patyological from an international forum on cardiac remodeling. In chronic obesity, especially occurring concomitant with systemic hypertension, LV hypertrophy and dilatation are common, and to a lesser extent, RV hypertrophy and dilatation may occur [39,58]. Harrell, and I. Table 1 Demographic, anthropometric, and clinical characteristics of participants grouped according to size and geometry of the left ventricle.

Selective leptin resistance revisited. This could be important as lactation is demonstrated to have positive effects on postpartum weight loss and metabolism [ 72 ]. Author information Article notes Copyright and License information Disclaimer. Learn More. Relation of obesity and gender to left ventricular hypertrophy in normotensive and hypertensive adults.

Associated Data

PGC-1 coactivators in the cardiovascular system. This condition not only alters cardiac metabolism, obesity also increases myocardial oxygen consumption, reduces cardiac efficiency by uncoupling cardiav the mitochondria and increases oxidative stress [ 15 ]. We believe this experimental approach could more reliably mimic the current profile of human obesity whose incidence in middle-age adults is higher than in younger cohorts, as is the presence of associated comorbidities such as cardiovascular disease [ 33 ]. Statistical analyses were performed using SigmaPlot version Adiponectin suppresses angiotensin II-induced inflammation and cardiac fibrosis through activation of macrophage autophagy.

Stampfer et al. Lee, C. Table 1 shows the characteristics of participants with concentric and eccentric LVH and concentric LV remodeling. Journal of the American College of Cardiology ee Kenchaiah S Body mass index and vigorous physical activity and the risk of heart failure among men. Circulation

E—E, The Strong Heart Study. The results in Table 2 include conventional, central aortic or h SBP or pulse pressure in the model. Revista Espanola de Cardiologia English Edition Guo, Z. Block, T. Obesity has been a health problem of growing significance all over the world; its prevalence is increasing in both developed and developing countries [ 1 ].

  • Although Shibata et al. Complications during pregnancy impacting the cardiovascular system, such as gestational hypertension or peripartum cardiomyopathy, are associated with increased risk of developing CVD later in life [ 5 ].

  • Heart disease and stroke statistics update: a report from the American Heart Association. Nat Rev Endocrinol.

  • McGavock JM Adiposity of the heart, revisited.

Akin, R. Surprisingly, the relations between excess adiposity and concentric LVH or concentric LV remodeling in this study were independent of conventional, h or central aortic BP or pulse pressure. These factors include smoking, glucose dysmetabolism and sedentary lifestyle. SBP, systolic BP.

Reisin E Cardiovascular changes after weight reduction in obesity hypertension. Obesity Interestingly, in the course of using traditional bare metal stents BMSan inverse relationship could be observed between BMI and clinical outcome. Int J Obstet Anesth. Smith and D.

Journal of Diabetes Research

Reversal of diet-induced obesity and insulin resistance by inn genetic ablation of GRK2. PubMed Obesity Google Scholar 6. Interestingly, we report that mRNA abundance of cardiac Esr2 was decreased with HF feeding in nulliparous mice but increased in HF-fed postpartum mice. Dysregulation of angiogenesis is associated with impaired cardiac function with pregnancy [ 27 ]. This condition not only alters cardiac metabolism, but also increases myocardial oxygen consumption, reduces cardiac efficiency by uncoupling of the mitochondria and increases oxidative stress [ 15 ].

  • Romero-Corral, V.

  • As depicted in Fig. All data passed normality or equal variance tests or logarithmic transformation was used to achieve normality.

  • The correlation between BMI and the outcome of clinical revascularisation was first reported inin the case of patients who had been administered balloon coronary angioplasty.

  • The energy densities of the LF and HF diet are 3.

  • Current mapping of obesity.

Prevalence of obesity among adults and youth: United States, All sections were examined using a fluorescence resonance energy transfer FRET equipment coupled to an inverted Axiovert Zeiss, Germany microscope in the Confocal Microscopy Facility of our center. Physiological Genomics. This article has been cited by other articles in PMC.

Boesity and Coronary Artery Disease Obesity is closely related to coronary atherosclerosis. In contrast, there was no effect of HF feeding on ejection fraction EF or fractional shortening FS in postpartum or nulliparous female mice Fig. Discussion Morbid obesity-associated pathophysiological changes are injurious to almost all body systems hindering clinical diagnosis and making diagnostic processes challenging. Guo, Z.

In obese individuals, reduced adiponectin levels and over-expression of tumor necrosis factor TNFwhich suppresses adiponectin, mitigate the cardioprotective effect of adiponectin [68,69]. Current treatment protocols target the underlying causes of obesity weight loss and heart failure. Differences in the types of CVD, timing of onset, and mortality rate have been largely attributed to sex hormones, and more recently, sex chromosomes [ 2 ]. Peterson LR Alterations in left ventricular structure and function in young healthy obese women: assessment by echocardiography and tissue Doppler imaging.

Bueno C. Arcones, Email: pathological cardiac remodeling in obesity. In sum, we can conclude that low levels of GRK2 prevent the development of obesity-induced cardiomyocyte and heart pathological hypertrophy, and also of cardiac fibrosis after a long-term HFD feeding. Clin Exp Pharmacol Physiol. Induction of cardiac fibrosis by transforming growth factor-beta 1. Direct effects of leptin on size and extracellular matrix components of human pediatric ventricular myocytes.

Along this line, in skeletal muscle it has been proposed that the reduced lipid droplet size may coincide with increased oxidative enzymatic capacity [ 45 ]. Exercise Training Protocol Swimming training was performed as described previously [ 4 ]. Brazilian Journal of Medical and Biological Research. As depicted in Fig. Increased clearance of reactive aldehydes and damaged proteins in hypertension-induced compensated cardiac hypertrophy: impact of exercise training. Estrogen receptor beta signals to inhibition of cardiac fibrosis. Gene expression analysis mRNA from heart tissue of at least six mice per condition was isolated as described in [ 19 ].

Cardiac dysfunction is the main obesity of the oesity of remodeling. Role of arterial wall properties in the pathogenesis of systolic hypertension. Morbid obesity is a leading cause of lifestyle related diseases. Moreover, chronic obesity and continued increase in LV blood volume may lead to systolic dysfunction accompanied by LV hypertrophy and fibrosis, cardiomyocytes injury and progressive collagen deposition and subsequent diastolic dysfunction. Benjamin, A. Luo, M.

EDITORIAL article

Similarly, physiological hypertrophy obesity pregnancy is associated with the upregulation of MMPs [ 36 ], remodeling enzymes that degrade collagen. Hemizygous GRK2 mice display neither cardiomegaly nor cardiomyocyte hypertrophy or fibrosis after a HFD of 30 weeks while these alterations are present in control WT mice. Epidemiology of heart failure with preserved ejection fraction. In comparison with pathological cardiac remodeling, cardiac hypertrophy with pregnancy results in proportional enlargement in chamber size and wall thickness, with minimally altered cardiac geometry. Four mice were employed for each condition three fields per heartand cardiomyocyte size was calculated by quantitation of — cells per field using image analysis software ImageJ.

World Journal of Surgery Melkert, and P. Bariatric Surgery: Bariatric surgery refers to all medical procedures utilized to achieve a reduction of excess weight. Wang, Y. John, K. Tsang et al.

Competing interests The authors declare that they have no competing interests. The above mechanisms often cause hypertension [ 23 ] Figure 2. Lancet British Medical Journal Google Scholar.

The molecular mechanisms that underlie obesity-related cardiac remodeling are complex, and include hemodynamic and metabolic alterations that ultimately affect the functionality of the myocardium. Front Biosci. MicroRNAs are regulators in various physiological and pathological processes, such as cardiac remodeling [ 22 ]. Reversal of diet-induced obesity and insulin resistance by inducible genetic ablation of GRK2. Mota, and Edilamar M.

Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice. This article has been corrected. Perivascular tissues reparative fibrosis were specifically excluded from this determination. Weight gain with pregnancy as both percentages of body weight gained and in grams was similar in LF-fed and HF-fed mice Fig.

ALSO READ: America S Health Rankings Obesity And Diabetes

In a study of cardiac pathological cardiac remodeling in obesity and LV function in normotensive morbidly obese patients with or without congestive heart failure, Alpert and associates [15] identified five factors that increase the risk of heart failure in morbidly obese patients. Excessive circulating FFA, TG, and low-density lipoprotein cholesterol are risk factors for the development of lipotoxicity, which may cause injury to vascular tissues or alter their functions [83]. Avelar E, Cloward TV Left ventricular hypertrophy in severe obesity: interactions among blood pressure, nocturnal hypoxemia, and body mass. Cardiac maladaptation in obese pregnant women at term. Exp Biol Med Maywood ; 15—16 — Remarkably, similar changes were registered in cases of congestive heart failure, hypertension, and myocardial infarction.

Table S1. Natriuretic peptides are reported to have anti-hypertrophic and anti-fibrotic effects on cardiac tissue [ 25 ]. Author KD measured plasma parameters. Heart and Circulatory Physiology. Oxidative Medicine and Cellular Longevity. ACA and MC performed experiments, participated in the analysis and interpretation of data and revised the manuscript.

In response to pressure overload, women develop less fibrosis with cardiac hypertrophy compared with men [ 39 ], and similar findings are reported in experimental animal models of pressure overload [ 40 ]. Metabolic assays Insulin tolerance tests ITT were performed as previously described [ 22 ]. We quantified interstitial collagen content in picrosirius red—stained left ventricles of HF-fed nulliparous and postpartum mice, and there was no difference between groups in collagen staining Fig. References 1.

Physiological, mitochondrial, and oxidative stress differences in the presence or absence of lactation in rats. Am J Cardiol. National Center for Biotechnology InformationU. Metabolic assays Insulin tolerance tests ITT were performed as previously described [ 22 ].

  • Circulation 64 :

  • Pregnancy-induced cardiac hypertrophy is assumed to be transient and is not associated with cardiac damage [ 413 ].

  • Oxford Academic.

  • The clinical significance of this study is that the increasing number of women entering pregnancy as overweight or obese may contribute to the increasing prevalence of CVD in premenopausal women.

  • Subject alert.

Adiponectin-mediated modulation of hypertrophic signals in the heart. Endocr J. With obesity, nulliparous mice had increased wall thickness in the absence of chamber enlargement, reflecting the concentric geometry attributed to obesity. Conen, P. Antithrombotic medication is usually administered in standard doses rather than adjusted to body weight, so the dose may be too high for normal weight and thin patients, which may result in bleeding complications and this, in turn, may also contribute to higher mortality [ 95 ]. J Am Coll Cardiol ; 20 : —

Adiponectin: obesitg, regulation and association to insulin sensitivity. International Journal of Obesity. Alba C. Molecular mechanisms underlying cardiac adaptation to exercise. Rev Endocr Metab Disord. Chronic high-fat diet-induced obesity decreased survival and increased hypertrophy of rats with experimental eccentric hypertrophy from chronic aortic regurgitation. G protein-coupled receptor kinase 2 GRK2 : a novel modulator of insulin resistance.

Read more about:

Sidebar1?
Sidebar2?