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High cardiac output and obesity – Obesity underlies many current-era high-output HF cases

Obesity and Coronary Artery Disease Obesity is closely related to coronary atherosclerosis.

Ethan Walker
Saturday, December 15, 2018
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  • Obesity, Morbid.

  • Poirier, T.

  • However, due to the effect of the obesity component, total peripheral resistance is less elevated than would be expected in the lean hypertensive subject, and may be completely normal in some obese-hypertensive patients. Franz H.

  • Physiological upper limits of ventricular cavity size in highly trained adolescent athletes.

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Smith and D. Buring, and P. Fonarow, C. Crespo-Leiro et al.

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

  • Shoelson, L.

  • And obesity, in the process of writing this chapter, the author had found it outpt to segue from the discussion of one aspect to another by starting with cardiac output and then discussing the effects of obesity on each of its determinants. As a result, there is a lack of effective treatments specific for obesity-related high output HF and the current clinical practice guidelines fail to address any recommendations for obesity-related high output HF.

  • Jamil, H.

  • Correlation of impedance cardiography with invasive hemodymanic measurements in patients with advanced heart failure: the bioimpedance cardiography BIG substudy of the ESCAPE trial. The pathophysiologic mechanisms involved in obesity-related high output HF is still not elucidated.

  • Direct magnetic resonance determination of aortic distensibility in essential hypertension, relation to age, abdominal visceral fat, and in situ intracellular free magnesium. It is mainly secreted by white adipose tissue and its level is positively related to the amount of body fat.

Am J Cardiol. Obesity, Morbid. When leptin 0. Xardiac, it is also recognized that a blunted reduction of peripheral resistance, despite the increased stroke volume and CI, is a common finding in obesity [ 1416 ] that may contribute to the high levels of SVRI observed. Related articles in Web of Science Google Scholar. Considering the effect of peripheral vascular resistance and afterload on stroke volume, you'd have to say that this probably contributes to the increased cardiac output in at least some obese patients.

Kapadia, C. Wada et al. Lithium-induced nad, thyrotoxicosis and mania: a case report. The evidence base for the management of high output failure is scarce and generally based on case reports. The reason underlying atrial fibrillation is assumed to be the low-grade inflammation, which is mainly observed in relation to obesity. Myers et al. Bella et al.

Subject alert. Am J Hypertens ; 10 : 49S — 55S. A study using impedance cardiography to assess fluid and hemodynamic status. Get free access to newly published articles. Obesity and cardiovascular disease. Genetics of severe obesity. Am J Clin Nutr.

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J Hypertens ; 10 : — Contractile elements are added in parallel, resulting in the thickening of chamber walls, partially at the expense of chamber volume. Nutritional and endocrine modulation of intracellular calcium: implications in obesity, insulin resistance and hypertension.

  • High output cardiac failure. Sodium excretion was higher in obese than in lean subjects.

  • Advanced age and comorbid factors often result in loss of body weight [ 85 ].

  • Obesity-hypertension: the effects on cardiovascular and renal systems Rubin ZhangRubin Zhang. Article Contents Abstract.

It would be more accurate to say that in obesity, the right ouhput undergoes clear morphological and function changes, which become clinically high cardiac output and obesity only in some unlucky minority. BMC Obes 5, 13 This article reviews the possible pathophysiological mechanisms and causes that contribute to obesity-related high output heart failure. Here, a graph from Lemmens et al incorporates several measured and predicted models to demonstrate how the proportion of the blood volume changes with increasing weight:.

QJM ;— Funding acquisition: Shen Q. J Hum Hypertens ; 4 : 37 — Maack T : Receptors of atrial natriuretic factor. Go to: Notes.

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Therefore, such drugs should be cautiously used for these patients. Issue Section:. Consider: the kg individual from de Divitiis had a resting cardiac output of 9.

Heart rate appears to be essentially unchanged in morbid obesity. Article PubMed Google Scholar. Download PDF. J Am Coll Cardiol ;— Privacy Policy.

Am J Cardiol. Influence of race, sex and weight on blood pressure behavior in young adults. Writing - original draft: Shen Q. Anand IS. When subjected to mental stress, obese hypertensives responded with a higher increase in total peripheral resistance and lower increases in heart rate, stroke volume, and cardiac output compared with nonobese counterparts.

Cardiac output and oxygen demand in obesity

In summary, obesity is associated with suppressed biologic activity of NP, which contributes to sodium retention and HTN. However, due to the effect of the obesity component, total peripheral resistance is less elevated than would be expected in the lean hypertensive subject, and may be completely normal in some obese-hypertensive patients. Alpert et al

Article Contents Abstract. 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. The technique primarily provides information on myocardial stiffness, contractility, and the extent of fibrosis, in a noninvasive way []. Google Preview.

Citing articles via Web of Science Hochadel et al. Amin, M. Gambardella, J.

Effects of obesity on the cardiovascular system

PubMed Google Scholar 5. J Hypertens abstract ; 16 : S7. Thus, when TFC rise, thoracic impedance falls since the results of impedance are expressed as the reciprocal of TFC [ 11 ]. Sign In or Create an Account.

Human blood-brain barrier leptin receptor: binding and endocytosis in isolated human brain microvessels. Despite increased prevalence high cardiac output and obesity obesity, it is not always documented as a chronic disease in clinical practice even though it is associated with yigh chronic diseases that have formal diagnoses. The role of noninvasive hemodynamic monitoring in the evaluation and treatment of hypertension. From looking at a larger person, most untrained individuals would intuitively conclude that more oxygen must surely be required by them, as there is more of them overall. View Metrics. Leptin was found to increase insulin sensitivity and to inhibit glucose-mediated insulin secretion, and thereby to control hyperinsulinemia. Clinical management of patients with obesity-related high output HF is difficult.

  • Increasing prevalence of overweight among US adults.

  • Remarkably, similar changes were registered in cases of congestive heart failure, hypertension, and myocardial infarction.

  • Hypertension ; 32 : Expression of the functional leptin receptor mRNA in pancreatic islets and direct inhibitory action of leptin in insulin secretion.

  • It has also been proven that atrial fibrillation in obese patients shortens the refractory period of the atrial and pulmonary vein myocardial cells [ 54 ]. Email alerts Article activity alert.

  • Eckstein, S.

These ECG parameters are known as independent markers of outpjt mortality, and their pathological prolongation may draw attention to an increased risk of ventricular arrhythmias [ 66 ]. Girerd et al. Clinical trial data in this area are lacking. Fillit, and M. A possible explanation of obesity paradox is that in critical ill patients, fat which mobilized from excess adipose tissue provides energy and prevents lean tissue wasting more efficiently than exogenous nutrients [ 89 ].

More related articles. Gami, D. Hochadel et al. Paget's disease is associated with rapid bone formation and resorption that can lead to increased blood flow within bone and the surrounding limb tissue. Sullivan, H. Acquired arterio-venous fistulae may be iatrogenic or occasionally due to trauma. Jin et al.

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Fabiani, L. In the case of obese and overweight patients, heart failure develops 10 years earlier than in the case of subjects with a normal BMI. Rescaldani, C. O'Donovan, A.

  • Expression of the functional leptin receptor mRNA in pancreatic islets and direct inhibitory action of leptin in insulin secretion. Why does the stroke volume increase so?

  • Management of chronic heart failure in adults in primary and secondary care.

  • When subjected to mental stress, obese hypertensives responded with a higher increase in total peripheral resistance and lower increases in heart rate, stroke volume, and cardiac output compared with nonobese counterparts. Genomics of heart failure.

  • Intravascular volume correlated directly with cardiac output in the entire population, as well as in the subgroups. HiebertMD, 1 Faith K.

  • Singh S, Sharma S. In summary, the endocrine products of excess adipose tissue on their own probably contribute significantly to the neurohormonal derangements in obesity, which expands the circulating volume and leads to increased preload.

  • Google Scholar. Go to: Abstract.

Whilst cautious blood transfusion may be necessary, rapid blood volume expansion may worsen pulmonary oedema. This includes increase in left ventricular dimensions and a reduction in left ventricular diastolic filling time. The signs of typical heart failure may be present including tachycardia, tachypnoea, raised jugular venous pressure, pulmonary rales, pleural effusion and peripheral oedema Figure 2. Figure 3. Cardiology rotated-square. Obesity leads to structural and functional changes of the heart, which causes heart failure. Mshui, T.

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Gambardella, B. Moreover, many accepted therapies for low output heart failure are in fact ohesity. An associated increased release of natriuretic peptides has been observed. Guest Editor: Gaetano Santulli. Wang, Y. Del Giudice et al. Furthermore, in the case of obese patients, cardiovascular diseases are usually diagnosed and treated earlier than in the case of thin patients [ 88 ].

Global, regional, and carsiac prevalence of overweight and obesity in children and adults during — a systematic analysis for the Global Burden of Disease Study Limited evidence is available to guide and support the clinical management of patients with this condition. Receive exclusive offers and updates from Oxford Academic. Get free access to newly published articles Create a personal account or sign in to: Register for email alerts with links to free full-text articles Access PDFs of free articles Manage your interests Save searches and receive search alerts.

The condition is not confined to the developed world. Berenfeld, and J. Yang, J. The most important question is what can the explanation be for the better prognosis established in the case of overweight and obese cardiovascular patients compared to normal weight patients.

Background

In conclusion, leptin not only controls appetite and body fat mass, but also increases sympathetic activity, high cardiac output and obesity sodium excretion, and insulin sensitivity. Left-ventricular hypertrophy and obesity: a systematic review and meta-analysis of echocardiographic studies. Epidemiology and aetiology of heart failure. Together, these neuro-endocrine imbalances contribute to vascular and endothelial dysfunction, impaired pressure natriuresis and sodium excretion, increased cardiac output and changes in systemic vascular resistance and arterial compliance [ 2 ]. Adiponectin, a therapeutic target for obesity, diabetes, and endothelial dysfunction.

  • Obesity and the risk of heart failure. Latest Most Read Most Cited Maternally inherited essential hypertension: adding further complexity to an already complex condition.

  • Chen, Y. More on this topic The global peripheral chemoreflex drive in patients with systemic sclerosis: a rebreathing and exercise study.

  • This review also focuses on the implications for clinical practice and future research involved with omics technologies to explore possible molecular pathways associated with obesity-related high output heart failure.

  • Stelfox, Henry T.

All the above observations are associative, so the association through inflammation remains a hypothesis only. Edvardsen, B. Masaki et al. The routine lead surface ECG and echocardiography are available at almost any cardiology outpatient unit nowadays. Severe chronic anaemia can result in physiological adjustment to maintain tissue perfusion and oxygenation. Hasan, C.

Norris, and F. In the developed world it is most frequently observed in chronic alcoholics due to poor dietary intake of thiamine, impaired high cardiac output and obesity absorption, metabolism and storage. Objective: To study the consequences of long-standing obesity on myocardial function and valvular performance and to determine the effects of weight loss on these cardiovascular features. Diagnosing diastolic dysfunction with echocardiography. The structural remodelling in the ventricular myocardium of obese patients results in left ventricular hypertrophy and consequential systolic and diastolic ventricular dysfunctions. Echocardiographic evaluation of left ventricular morphology and function in young male football players and runners.

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Persistent obesity can cause renal injury and functional nephron loss, which worsens BP and finally leads to glomerulosclerosis and kidney failure, as summarized in Fig. Google Scholar Am J Hypertens ; 10 : 49S — 55S. Licata et al reported that obese subjects have delayed urinary sodium excretion and blunted the response of plasma ANP to saline load.

Padwal, K. Obesity cardiomyopathy: pathophysiology and evolution of hih clinical syndrome. Rifai, J. Color Doppler imaging detects the movement and deformity of the myocardium and is thereby able to show changes in contractility [ ]. Califf, and E. No significant valvular disease was observed in any of the subjects with obesity at baseline or after weight loss. Thiamine deficiency is also associated with malabsorption conditions, dialysis and other causes of chronic protein-calorie under-nutrition.

Considering SACI, we observed lower levels in the obese hypertensive, especially in the patients with cadiac AP and, in multivariate analysis, this variable was predictive of uncontrolled AP. And obesity of saline load. The remaining variables produced by ICG output were subsequently analyzed according to a summarized classification previously published by others [ 12 ]:. But that's just people affected by the natural central softening process of late male adulthood. To summarise, the morbidly obese patient requires a larger amount of oxygen delivered to their tissues per minute, which is partly related to their increased effort of breathing, and partly due to the demand of their increased mass of lean muscle tissue. The etiology of HF is multifactorial, including myocyte loss from myocardial infarction, sustained pressure overload e.

Braga, O. Unsurprisingly, obesity is therefore an independent risk factor of coronary artery disease [ 41 ]. Special Issues.

Obes Rev ;— The remaining variables produced by ICG output were subsequently analyzed according and obesity a summarized classification previously published by others [ 12 ]: 1. High output cardiac failure. Often times, high output HF is secondary to other identifiable causes such as severe anemia, pregnancy, and atrioventricular fistula and it may not be identified appropriately. In multivariate analysis Table 5however, only CI remained predictive, conferring a risk 1. Genome Med ;

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In the lean subject with HTN, the hemodynamic profile is characterized by high total peripheral resistance and contracted circulating intravascular volume. This added skeletal muscle tissue is what actually adds to the increased resting metabolic rate, and in fact Ireton-Jones et al have demonstrated that actual body weight is a better parameter to use when calculating resting energy expenditure, as compared to ideal body weight. However, this variable, which results from the product of mean arterial pressure and CI, reflects more the higher oxygen demands of the heart in these circumstances than increased cardiac performance itself. Cardiac output increases in the early stage of HTN development, but tends to decrease thereafter with established HTN. Pathophysiologic mechanisms contributing the pathogenesis of obesity-related high output HF are still not entirely clear. Prog Cardiovasc Dis ; 42 : 39 — Janet D.

Twitter Facebook Email. As the result, the RV also remodels in obesity, becoming dilated and thickened like the LV. Adiponectin, a therapeutic target for obesity, diabetes, and endothelial dysfunction. This Issue.

Introduction

Although there have been studies that investigated genetic variants associated with obesity itself, 6768 no research has been found that examined output and of obesity-related high output HF. Blood volume, cardiac output, and distribution of systemic blood flow in extreme obesity. There is considerable evidence that obesity is a significant independent risk factor for cardiovascular disease and a contributing factor for the development of HF. Pressor factor and cardiovascular pressor responsiveness in lean and overweight normal or hypertensive subjects.

The signs of typical heart failure may be present including tachycardia, tachypnoea, raised jugular venous pressure, pulmonary rales, pleural effusion and peripheral oedema Figure 2. Issue Section:. H—H, All the above observations are associative, so the association through inflammation remains a hypothesis only.

  • There are limitations to this work since its retrospective nature and several relevant data missing.

  • Bielo, and F.

  • The implication for clinical practice and directions for future research related to this syndrome will be examined.

  • Hayat, R.

  • This process ultimately leads to left ventricular hypertrophy and to diastolic and later to systolic ventricular dysfunction [ 30 ].

Schunkert, L. In the past decade, new echocardiographic techniques have become available that make a yet earlier diagnosis high cardiac output and obesity systolic and diastolic dysfunctions possible [ ]. Myocardial lipid accumulation and enhanced fibrosis can also play a pathogenic role in the genesis of various cardiac arrhythmias, which may contribute to the development of heart failure [ 4243 ] Figure 2. Dendritic epithelial keratitis in primary herpes simplex infection. According to the endotoxin-lipoprotein hypothesis, obese patients have higher cholesterol and lipoprotein levels, which reduce the concentration of inflammatory agents and may thus have anti-inflammatory and probably also arrhythmia protective effect.

At the same time, it is still high cardiac output and obesity if obese coronary artery disease patients would benefit from DES implantation. Among the cardiac arrhythmias, atrial fibrillation has the highest clinical significance. Wallace, and J. Obesity has an important role in atherosclerosis and coronary artery disease. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Ravisy et al. Hisanaga, A.

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This is due to the raised metabolic activity of excessive adipose tissue, which leads to compensatory cardiac changes including left ventricular dilatation and eccentric hypertrophy. Mehta, R. Parise, and W.

Stelfox, Henry T. Funding acquisition: Shen Q. The implications of living with heart failure; the hibh on everyday life, family support, co-morbidities and access to healthcare: a secondary qualitative analysis. New issue alert. Sodium excretion was higher in obese than in lean subjects. Sign in to make a comment Sign in to your personal account.

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Improved fatty acid utilization via dietary modification significantly ameliorates cardlac fragmentation and cardiac dysfunction [ 92 ]. Alterations and obesity mitochondrial dynamics, respiratory capacity, and ATP synthesis play an important role in the chronic cardiac energy deficit observed in heart failure [ 91 ]. View at: Google Scholar C. The circulating blood volume rises; the increased cardiac output is provided mainly by the increased stroke volume and, to a lesser extent, by the increased cardiac frequency as an effect of the enhanced sympathetic tone. Wada et al. Schunkert, L.

Russo, F. The phenomenon known as obesity paradox has been observed in the case of several cardiovascular diseases cardiwc acute and chronic heart failures high cardiac output and obesity 6970 ], coronary artery disease [ 71 ], acute myocardial infarction [ 72 ], hypertension, and atrial fibrillation [ 7374 ]. Open in new tab Download slide. 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. Litwin, and G.

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

In case one needs to delve into this with a PhD dissertation level of detail, Correia has made theirs available. Writing - original draft: Shen Q. Consider: the kg individual from de Divitiis had a resting cardiac output of 9.

Matsuda M, Shimomura I. Altered obeeity metabolism and insulin resistance It is also high cardiac output and obesity known that obesity is a risk factor for insulin resistance, the underlying mechanism for type 2 diabetes. No funding sources were provided to the authors to perform the present retrospective study, neither to analyse data nor prepare the manuscript. Leptin in obesity. Patients rested for 5 to 10 min before the procedure and then blood pressure was measured with the patient in the supine position, with head elevated at 45 degrees.

There are limitations to this work since its retrospective nature and several relevant data missing. Privacy Ans Terms of Use. The complex interplay between obesity and hypertension has been a matter of interest and debate for a long time. Trends Mol Med ;— The size of the bladder was adjusted to the arm circumference, using a larger bladder arm circumference 31—40 cm in obese patients.

Therefore, novel clinical measurements e. Moreover, these patients were much older than their normal weight or obese counterparts [ 7883 ]. Lavie et al. Additionally, in patients suffering from atrial fibrillation, the activation of the renin-angiotensin system may be associated with atrial fibrosis and electrical remodelling [ 62 ]. Left atrial dilation and dysfunction are known consequences of obesity.

  • Insulin resistance: the link between obesity and cardiovascular disease.

  • Through its paracrine effect, epicardial fat contributes to the development of atrial interstitial fibrosis.

  • J Endocrinol Invest ; 19 : —

Abed, C. Mehta, S. Moreover, these patients were much older than their normal weight or obese counterparts [ 7883 ]. Robinson et al. Chronic heart failure. The increased epicardial fat, the infiltration of myocardium with adipocytes, and fibrosis together result in a heterogeneous atrial pulse conduction, e.

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In a study by de Divitiishaemodynamic measurements from output and ibesity with large BMIs reveal the range you should expect. Adipose tissue as an endocrine organ. Google Scholar. Alpert, Martin A. Expression of the functional leptin receptor mRNA in pancreatic islets and direct inhibitory action of leptin in insulin secretion. Purchase access Subscribe now. Nevertheless, since circulating volume is increased, the greater venous return adds an additional load to a left ventricle that is already burdened by a high afterload caused by arterial hypertension.

Magnani, F. Lee, Y. Young, and D. High output heart failure P. Related articles in PubMed [Cirrhotic cardiomyopathy]. Cozzolino, A. Echocardiographic evaluation of left ventricular morphology and function in young male football players and runners.

A combination of multiple neurohormonal systems, metabolic factors, hemodynamic changes and various inflammatory mediators associated with obesity and HF contribute to the complexity of this challenge. Epicardial adipose tissue and inflammatory adipokines Epicardial adipose tissue has been proposed as an important mediator that obesity exerts its effects on myocardial tissue in relation to systemic inflammation. Hypertension ; 30 : —

It is obeisty well known that obesity is a high cardiac output and obesity factor for insulin resistance, the underlying mechanism for type 2 diabetes. But that's just people affected by the natural central softening process of late male adulthood. The etiology of HF is multifactorial, including myocyte loss from myocardial infarction, sustained pressure overload e. Am J Med. Bharati SLev M : Cardiac conduction system involvement in sudden death of obese young people.

  • Results One hundred patients were male

  • Data of the multicentre BARI register processing the data of patients administered coronary revascularisation primary coronary intervention PCI with catheter or surgical coronary revascularisation CABG reveal that in the acute hospitalization period, there was an inverse relationship between complications and BMI only in the case of PCI-treated patients.

  • Int J Cardiol ;— Poirier, Paul, and Robert H.

  • Published online Jan 13, Genomics of heart failure.

Kanna, J. Rathod, M. Hypertension increases left ventricular afterload, which raises the danger of structural and electrical myocardial remodelling. Various studies have proven the relationship between obesity and atrial fibrillation.

De Rosa, J. Manson, G. Oxford University Press is a department of the University of Oxford. Cuspidi, M.

Click for larger image Download as PowerPoint slide. Am J Hypertens ; 10 : 49S — 55S. Postgrad Med J ;—

In summary, the association of obesity-HTN can be the cause of some renal disorders. Considering the effect of peripheral vascular obesoty and afterload on stroke volume, you'd have to say that this probably contributes to the increased cardiac output in at least some obese patients. All ICG exams were performed by trained technicians of our Hypertension Clinic and data was obtained during a scheduled visit. Go to: References.

Yamaguchi, M. Uotput We conclude that weight reduction in subjects with obesity is associated with improvements in left ventricular diastolic filling and has favorable effects on left ventricular ejection fraction. Echocardiographic evaluation of left ventricular morphology and function in young male football players and runners. Both scenarios can lead to a fall in systemic arterial blood pressure and neurohormonal activation leading to overt clinical heart failure. Afonso et al.

Mol Cell Biochem ; : — So far the discussion has been unfairly focused on the left and obesity. Figures Show all If you scale that value to the abdominal apron of a super-obese kg individual, which weighs let's say kg on its own, that whole apron would only receive about ml of blood per minute. Intravascular volume correlated inversely with total peripheral resistance in all subjects and in each subgroup. Licata et al reported that obese subjects have delayed urinary sodium excretion and blunted the response of plasma ANP to saline load.

Smit, L. Management of chronic heart failure in adults in primary and secondary care. Maesen, S. Rodriguez, and C.

In both cases, lipids, oxidized LDL particles, and free fatty acids activate the inflammatory process and trigger the disease. In heart failure, a metabolic cardiac remodeling occurs, the fatty acid oxidation is impaired, and the glucose uptake and glycolysis are increased. Zhang, and X. Streiff et al. Among the cardiac arrhythmias, atrial fibrillation has the highest clinical significance.

Leptin induces nitric oxide mediated vasorelaxation in aortic-rings of WKY rats. Faith K. Kidney Int ; 62 : aand This was not the case - his HR was 86, and of the other obese patients in that study, only one was tachycardic. Cardiac remodeling and impaired cardiac diastolic function Cardiac remodeling associated with obesity is characterized by left ventricular hypertrophy.

J Am Coll Cardiol. New issue alert. Leptin induces nitric oxide mediated vasorelaxation in aortic-rings of WKY rats. Clearly, this must be the main contributing factor to the increase in the cardiac output, as the heart rate does not change appreciably.

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