Dysfunction In Obese Patients Research Articles

The adipo-fibrokine activin A is associated with metabolic abnormalities and left ventricular diastolic dysfunction in obese patients.

AimsLeft ventricular diastolic dysfunction (LVDD) is common in obese subjects, and a relationship between epicardial adipose tissue (EAT), increased adipocytokines, and cardiovascular diseases has been reported. This study sought to examine as to whether the adipo‐fibrokine activin A is a link between increased EAT, the metabolic syndrome (MetS), and LVDD in severely obese subjects.Methods and resultsIn 236 obese subjects (ø body mass index 39.8 ± 7.9 kg/m2) with a variable degree of the MetS and in 60 healthy non‐obese controls (ø body mass index 24.8 ± 3.4 kg/m2), serum activin A levels were measured and correlated with parameters of the MetS, epicardial fat thickness (EFT), and echocardiographic parameters of LVDD. Activin A levels were higher in obese than in non‐obese subjects (362 ± 124 vs. 301 ± 94 pg/mL, P = 0.0004), increased with the number of MetS components (from 285 ± 82 with no MetS component, 323 ± 94 with one or two MetS components, to 403 ± 131 pg/mL with ≥3 MetS components, P < 0.0001) and correlated with EFT (r = 0.41, P < 0.001). Furthermore, activin A levels were related to several parameters of LVDD [e.g. left atrial size (382 ± 117 vs. 352 125 pg/mL, P = 0.024), E/e′ (394 ± 108 vs. 356 ± 127 pg/mL, P = 0.005)]. LVDD was highest in MetS obese subjects with high EFT (44.3%) compared with MetS obese subjects with low EFT (27.0%), non‐MetS obese subjects with high EFT (24.2%), and non‐MetS obese subjects with low EFT (10.6%, P < 0.0001).ConclusionsIn severe obesity, activin A was significantly related to EFT, MetS, and LVDD, implicating MetS‐related alterations in the secretory profile of EAT in the pathogenesis of obesity‐related heart disease.

Obesity-induced activation of JunD promotes myocardial lipid accumulation and metabolic cardiomyopathy.

Metabolic cardiomyopathy (MC)-characterized by intra-myocardial triglyceride (TG) accumulation and lipotoxic damage-is an emerging cause of heart failure in obese patients. Yet, its mechanisms remain poorly understood. The Activator Protein 1 (AP-1) member JunD was recently identified as a key modulator of hepatic lipid metabolism in obese mice. The present study investigates the role of JunD in obesity-induced MC. JunD transcriptional activity was increased in hearts from diet-induced obese (DIO) mice and was associated with myocardial TG accumulation and left ventricular (LV) dysfunction. Obese mice lacking JunD were protected against MC. In DIO hearts, JunD directly binds PPARγ promoter thus enabling transcription of genes involved in TG synthesis, uptake, hydrolysis, and storage (i.e. Fas, Cd36, Lpl, Plin5). Cardiac-specific overexpression of JunD in lean mice led to PPARγ activation, cardiac steatosis, and dysfunction, thereby mimicking the MC phenotype. In DIO hearts as well as in neonatal rat ventricular myocytes exposed to palmitic acid, Ago2 immunoprecipitation, and luciferase assays revealed JunD as a direct target of miR-494-3p. Indeed, miR-494-3p was down-regulated in hearts from obese mice, while its overexpression prevented lipotoxic damage by suppressing JunD/PPARγ signalling. JunD and miR-494-3p were also dysregulated in myocardial specimens from obese patients as compared with non-obese controls, and correlated with myocardial TG content, expression of PPARγ-dependent genes, and echocardiographic indices of LV dysfunction. miR-494-3p/JunD is a novel molecular axis involved in obesity-related MC. These results pave the way for approaches to prevent or treat LV dysfunction in obese patients.

Vitamin D deficiency, insulin resistance and thyroid dysfunction in obese patients: is inflammation the common link?

The aim of this article is to study the possible relation of serum vitamin D concentrations to body mass index (BMI), visceral fat thickness (VFT), insulin resistance (IR), inflammation (serum monocyte chemoattractant protein-1 – MCP-1) and thyroid parameters in obese patients. A total of 158 non-diabetic, obese patients aged 19–68 without a history of thyroid pathology were recruited. Biochemical markers, insulin, 25-OH vitamin D, thyroid parameters (TSH, FT3, FT4, TPO antibodies, TG antibodies) and VFT were measured. Serum MCP-1 evaluated the inflammation. A HOMA-IR cut-off value of 2.5 defined IR. Most patients had severe (70.3%) or moderate (25.3%) vitamin D deficiency. Vitamin D level was negatively associated with BMI (p = .043) and during the cold season with VFT (p = .009). Vitamin D deficiency correlated with Hashimoto’s thyroiditis prevalence during the warm season (p = .047) and was a risk factor for its occurrence (p = .021). At 15 ng/mL cut-off value, vitamin D was negatively correlated with MCP-1 (p = .0006). Also, MCP-1 was positive correlated with HOMA- IR (p = .042), TPO-Ab levels (p = .011) and with Hashimoto’s thyroiditis (p = .027). MCP-1 was a risk factor for vitamin D deficiency (p < .0001). Our study supports a bidirectional interaction between vitamin D and systemic inflammation in obese patients. Moreover, systemic inflammation is related to the severity and frequency of Hashimoto’s thyroiditis. Vitamin D deficiency is the single independent factor associated with Hashimoto’s thyroiditis in obese patients.

Secretory changes and inflammation are associated with vascular dysfunction in obese patients

Aim: A variety of molecules secreted by white (adipokines) and brown (batokines) adipose tissue, liver (hepatokines) and skeletal muscle (myokines) physiologically participate in the control of energy balance and glucose/lipid metabolism, as well as in the regulation of vascular homeostasis. We tested whether changes in their secretory profile couples with inflammation, insulin resistance and vascular dysfunction in obese patients.

Pharmacological inhibition of monoacylglycerol lipase enhances IGM plasma levels and limits atherogenesis in a CB2-dependent manner

Aim: Endocannabinoids are endogenous arachidonic acid-derived lipids binding to cannabinoid receptors CB1 and CB2. Circulating endocannabinoid levels are increased in patients with coronary artery disease, myocardial infarction and chronic heart failure. There is a positive correlation between increased endocannabinoid levels and coronary endothelial dysfunction in obese patients. We aimed to clarify the causal implication of the main endocannabinoid 2-arachidonoyl glycerol (2-AG) in the onset of atherosclerosis.

Endoplasmic reticulum stress and mitochondrial dysfunction in obese patients and their association with metabolic syndrome

Aim: To evaluate whether metabolic syndrome (MetS) influences endoplasmic reticulum (ER) and oxidative stress and inflammation parameters in obese individuals.

Age‐related activation of ADAM17/TNF in adipose tissue leads to remote coronary microvascular dysfunction in obese patients

A disintegrin and metalloproteinase ADAM17 (TNF‐α converting enzyme) regulates soluble TNF levels. Here, we examined whether age‐related changes in adipose tissue (AT)‐expressed ADAM17 contributes to the development of coronary microvascular dysfunction (CMD) in obesity. Human coronary arterioles (CA,~100 μm) and mediastinal AT were examined in patients who underwent open‐heart surgery. CA and AT were also studied in young (6‐month) and aged (24‐month) mice fed a 12‐week high‐fat‐diet (HFD). We found that bradykinin‐induced dilation in isolated human CA significantly declines with age in obese, but not lean patients. Similarly, CA dilation was reduced in aged HFD mice when compared to young. The impaired CA dilation was accompanied by increased ADAM17 activity in AT and elevated serum TNF levels. Transplantation of AT from aged HFD to young mice increased plasma TNF levels and impaired CA dilation in the young recipient mice. In patients we found an age‐related increase in AT ADAM17 activity, which was attributed to expression of ADAM17 in the vascular endothelium of AT, but not adipocytes. Excess release of TNF from AT arteries in older patients was sufficient to impair vasodilator function in a bioassay in which the AT artery was serially connected to a CA. The present study demonstrates age‐related increases in vascular endothelial ADAM17 activity and soluble TNF release in the human and rodent AT, which may contribute to the development of CMD in older obese patients.Support or Funding InformationAHA16PRE27550006

SERUM OMENTIN-1 LEVELS AND ENDOTHELIAL DYSFUNCTION IN OBESITY.

Our aim was to investigate the relationship between serum omentin-1 levels and endothelial dysfunction in obese patients. We evaluated 50 obese patients, and age/gender matched 45 healthy non-obese subjects as controls. Oral glucose tolerance test, lipid parameters, uric acid levels, homeostatic model assessment-insulin resistance (HOMA-IR) index, serum omentin-1 levels and flow mediated dilatation (FMD) % were measured in all subjects. Body compositions were analyzed with bioelectrical impedance method using a Tanita Body Composition Analyzer and ViScan. Serum omentin-1 levels were found significantly lower in obese population compared to the control subjects. FMD response was significantly decreased in obese population. There was a significant positive correlation between serum omentin-1 levels and FMD response (r=0.359, p<0.001). Serum omentin-1 levels were negatively correlated with body mass index (BMI), waist circumference, total fat percentage, visceral fat, fasting insulin and HOMA-IR index. Lower serum omentin-1 levels and decreased FMD response may be an early marker of endothelial dysfunction in obese patients.

Interrelation of Adipokines with Functional State of Kidneys in Patients with Metabolic Syndrome

The aim of this study was to evaluate the effect of adipokines on the formation of kidney disease in patients with obesity and hypertension. The survey included 87 patients with hypertension (stage 1-2): with obesity (n 5 67), without obesity (n 5 20). In control group, there were 25 obese patients without hypertension and metabolic changes and 30 healthy persons (mean age 48.2 6 2.4 years). We investigated the relationship between leptin, resistin, and integral indices of renal damage (glomerular filtration rate [GFR], microalbuminuria [MAU], vascular endothelial growth factor [VEGF]). In obese patients without clinical signs of renal disease, a decrease in GFR was detected in 44.7% of respondents. Levels of leptin and resistin, markers of renal damage (MAU, VEGF), were significantly higher in the group of obesity. Correlation analysis showed the existence of a high degree of direct connection between the level of adipokines and HOMA index, triglycerides (TG), MAU, VEGF in the urine, and a negative correlation with GFR. There was a direct positive relationship between the level of MAU and VEGF in the urine with levels of blood pressure, uric acid, and a negative one with GFR. Levels of MAU and VEGF in urine can be considered as early markers of renal dysfunction in obese patients. The decrease in GFR in patients with obesity was associated with increased levels of leptin and resistin. So, in patients with MS and hypertension, reduction of GFR is linked with the increase in leptin and resistin that is accompanied with the increase of VEGF in urine and MAU. In non-obese patients with hypertension obesity and MS, the increase of VEGF in urine is detected ealier that increase of MAU and reduction of GFR.

Thyroid Function in Obese Children and Adolescents and Its Association with Anthropometric and Metabolic Parameters.

Fat accumulation leads to dysfunction of hypothalamic-pituitary-thyroid axis and to changes in thyroid function. A higher serum level of thyroid stimulating hormone (TSH), with normal levels of thyroid hormones, suggesting subclinical hypothyroidism, is often found in obese individuals. The influence on lipid and glucose metabolism of thyroid dysfunction in obese patients remains unclear. This retrospective study encompassed 110 obese children and 38 healthy non-obese children aged 5-18. Anthropometric measurements, including bioelectrical impedance, were taken in all children. Fasting TSH, fT4, glucose, lipid profile, and a glucose tolerance test in case of the obese individuals, were evaluated. The obese children demonstrated a significantly higher mean concentration of TSH compared with their peers with proper body weight: 2.1 ± 1.0 μIU/ml vs. 1.5 ± 0.6 μIU/ml, p = 0.001. The fT4 was not different between the two groups. In the obese children, TSH correlated with body mass index (BMI) and waist circumference after controlling for age and gender. A multivariate regression analysis showed a relationship of TSH with total cholesterol, LDL cholesterol, triglycerides, and non-HDL after adjusting for BMI. None of these relationships were revealed for fT4. The level of TSH correlated with the degree of abdominal obesity. We conclude that the serum TSH concentration, even remaining within the norm, could adversely affect the lipid profile, irrespective of obesity.

Comorbidity of Obesity and Thyroid Dysfunction: An Association with Greater Cardiovascular Risk Factors

Introduction: Hypothyroidism, metabolic syndrome and central obesity are common diseases known as the risk factors for atherosclerotic cardiovascular disease. The co-existence of thyroid dysfunction in obese patients might substantially increase the cardiovascular risk. The objective of the study was to evaluate the effect of hypothyroidism on the main cardiovascular risk factors in patients with obesity and cardiovascular syndrome. Material and methods: In a cross-sectional clinical study we examined 202 patients with central obesity and metabolic syndrome (160 women, 42 men, aging 43 ± 13 yrs) with BMI ≥ 30 kg/m2 divided in two groups - 101 patients with subclinical or overt hypothyroidism (gr. A-hypot) and 101 eythyroid patients (gr B-eut), diagnosed by TSH, FT4,TPO-Ab. Laboratory assessment included: total cholesterol (TChol), HDL,LDL, triglycerides (3-glyc), serum glucose, standard oral glucose tolerance test (OGTT) and insulin resistance by Homeostasis Model Assessment of Insiline Resistance (HOMA-IR). Serum leptin and C-reactive proteins were estimated in 20 patients of each patients group and in a control group of 20 healthy persons with BMI <25 kg/m2. The supplementation Levothyroxine therapy was carried out of patients with overt and subclinial hypothyroidism. Results: Both compared groups showed similar BMI (mean 37 kg/m2) and HOMA-IR value 3.1 and 3.15, respectively Mean TSH value was found 4-fold higher in gr. A than in gr. B. which significantly correlated with TChol, 3-glyc, CRP and serum leptin The prevalence of arterial hypertension (AH), diabetes type2 or impaired glucose tolerance (IGT) in gr A was 86% and 67% vs. 80% and 70% in gr B, respectively. Significant correlations were established between TSH, TChol, atherogenic lipoproteins, 3-glyc. in patients gr. A but not in gr B. The same parameters decreased significantly after adequate levothyroxin supplementation. The significant positive nonparametric correlations were found also between BMI, TSH, leptin and CRP (p<0.05). Conclusion: Our data demonstrate that hypothyroidism significantly aggravates the lipid metabolisms in patients with obesity or MetS. These disturbances co-existing with higher prevalence of arterial hypertension, DM-T2 or IGT determine the substantially increased cardiovascular risk which correlated with increased insulin resistance, higher levels of leptin and CRP as a marker of chronic inflammation. Consequently clinicians shouid be particularly alert in the possibility of thyroid disfunction in obese patients.

CD51+ endothelial microparticles as a biomarker of endothelial dysfunction in obese patients with hypertension

Endothelial dysfunction plays a crucial role in the development of hypertension. Furthermore, obesity is associated with hypertension and impaired endothelial function [1, 2]. Recent studies have showed that the number of endothelial microparticles (EMPs) is high in patients with obesity and hypertension [3, 4], and EMPs are involved in the pathophysiology of endothelial function in vivo and in vitro [5]. Therefore, EMPs may contribute to hypertension related to obesity; however, EMPs have many phenotypes that exert different functions in various diseases. Currently, the link between obesity and hypertension caused by endothelial dysfunction is unclear. To our knowledge, no study has thus far investigated the specific phenotype to monitor endothelial function in obese patients with hypertension. The aim of the present study was to investigate whether a specific EMP phenotype can be used to monitor endothelial function in obese patients with hypertension and whether this phenotype is characteristic in obese patients with hypertension. We recruited 29 hypertension patients (19 non-obese and 10 obese), and 15 healthy control subjects. Hypertension was diagnosed as systolic/diastolic blood pressure C140/90 mmHg. Obesity was diagnosed according to the proposed body mass index (BMI) criteria of China’s Ministry of Health as follows: normal: 18.5–23.9, overweight: 24–27.9, and obese C28 kg/m. All patients with a history of inflammatory disease, chronic renal failure requiring dialysis, hepatic or hematologic disorders, or autoimmune or malignant diseases were excluded. All patients were not on statins. Healthy subjects were included if they had no known history of medical illness and a normal blood pressure (\140/90 mm Hg), BMI (18.5–23.9 kg/m), and physical examination. The consent procedure was approved by the Ethics Committee at Institute of Microcirculation Peking Union Medical College & Chinese Academy of Medical Sciences. For microparticles isolation and measurements, blood samples were drawn by venipuncture into blue-top vacutainer tubes containing sodium citrate. Within 1 h of blood sampling, whole blood (3 ml per sample) was centrifuged at 1,500 g for 10 min to prepare platelet-rich plasma and further centrifuged at 13,000 g for 10 min to obtain plateletpoor plasma. Samples were stored at -20 C for 1 week and at -80 C thereafter until analysis. One thawing of stock plasma did not affect microparticle (MP) levels. For the EMPs assay, platelet-poor plasma (50 ll) was incubated with the following fluorescent monoclonal antibodies (4 ll each): phycoerythrin (PE)-labeled anti-CD31 (560983, BD Biosciences), fluorescein isothiocyanatelabeled (FITC) anti-CD51/CD61 (integrin alpha v beta3, 110519, eBioscience), and PE-labeled anti-CD144 (VECadherin12-1449, eBioscience). The samples were incubated at room temperature for 20 min, diluted with 1 ml of phosphate-buffered saline buffer, and analyzed using flow cytometer (Accuri C6, Accuri cytometers). For a precise delineation of CD31positive EMPs (as opposed to platelet-derived CD31positive MPs), CD42b-negative MPs were analyzed in platelet-poor plasma. An isotype antibody was used as a negative control in all measurements. EMPs were defined S.-S. Hu H.-G. Zhang (&) Q.-J. Zhang R.-J. Xiu Institute of Microcirculation, Peking Union Medical College & Chinese Academy of Medical Sciences, Key Laboratory of Microcirculation, National Health and Family Planning Commission, Beijing, China e-mail: zhanghg1966126@imc.pumc.edu.cn

0291: Circulating markers of vascular endothelial dysfunction in obese patients

Obesity is a major worldwide health problem associated with several metabolic, inflammatory and oxidative troubles which represent major cardiovascular risk factors. The endothelial dysfunction plays a central role in the physiopathology of cardiovascular diseases. This critical function is generally evaluated through in vivo functional assessment, but emerging new biomarkers, like cell-derived microparticles (MPs,) reflecting alteration of the endothelium are increasingly studied. The aim of this study was to assess the level of circulating MPs in normal weight and obese patients and their relation with different oxidative, inflammatory and endothelial function parameters. Normal weight subjects (n=29, BMI<25kg/m 2 ) and obese patients (n=53, BMI>30 kg/m 2 ), were recruited at F. Hached Hospital (Sousse, Tunisia). Vascular endothelial function was assessed by the exploration of the endotheliumdependent vasodilatation by Laser Doppler Flowmetry and flow cytometry analysis was used for the quantification of circulating MPs. Obese subjects presented an endothelium-dependant vasodilatation significantly lower (21,26+2,89) than in normal weight patients (32,40+6,35) (p=0,008), characteristic to a vascular endothelial dysfunction. Furthermore, obese patients displayed a significantly higher number of circulating MPs (37579+4766 MPs/μl) in comparison to normal weight subjects (12099+934 MPs/μl) (p<0,001). Circulating MPs were positively correlated with anthropometric parameters BMI (r=0,504; p=0,02) and waist-hip ratio (WHC) (r=0,476; p=0,14). A positive correlation was also observed with parameters of inflammation (C-reactive protein (CRP) r=0,374; p=0,045) and oxidative stress (advanced oxidation protein product (AOPP) r=0,487; p=0,04 and total thiols r=0,551; p=0,01). These data demonstrated that circulating MPs could be a good biomarker of vascular endothelial dysfunction in obese patients, however the precise role of MPs in inflammation and oxidative stress has still to be clarified in further studies. Obesity, endothelial dysfunction, microparticles.

Effect of bariatric surgery on microvascular dysfunction associated to metabolic syndrome: a 12-month prospective study

To prospectively evaluate the effect of weight loss after bariatric surgery on microvascular function in morbidly obese patients with and without metabolic syndrome (MetS). A cohort of morbidly obese patients with and without MetS was studied before surgery and after 12 months of surgery. Healthy lean controls were also examined. Microvascular function was assessed by postocclusive reactive hyperemia (PORH) at forearm skin evaluated by laser Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was calculated from laser-Doppler skin blood flow and blood pressure. Regression analysis was performed to assess the contribution of different clinical, metabolic and biochemical parameters to microvascular function. Before surgery, 62 obese patients, 39 with MetS and 23 without MetS, and 30 lean control subjects were analyzed. The absolute area under the hyperemic curve (AUC(H)) CVC of PORH was significantly decreased in obese patients compared with lean control subjects. One year after surgery, AUC(H) CVC significantly increased in patients free of MetS, including patients that had MetS before surgery. In contrast, AUC(H) CVC did not significantly change in patients in whom MetS persisted after surgery. Stepwise multivariate regression analysis showed that only changes in HDL cholesterol (HDL-C) and oxidized LDL (oxLDL) independently predicted improvement of AUC(H) after surgery. These two variables together accounted for 40.9% of the variability of change in AUC(H) CVC after surgery. Bariatric surgery could significantly improve microvascular dysfunction in obese patients, but only in patients free of MetS after surgery. Improvement of microvascular dysfunction is strictly associated to postoperative increase in HDL-C levels and decrease in oxLDL levels.

Systemic inflammation is related to coronary microvascular dysfunction in obese patients without obstructive coronary disease

Background and AimsObesity, systemic inflammation and changes in the heart functions are associated with increased cardiovascular risk. This study aimed to investigate coronary microvascular dysfunction as an early marker of atherosclerosis in obese patients without any evidence of cardiovascular disease. Methods and results86 obese subjects (aged 44 ± 12 years, body mass index (BMI) 41 ± 8 kg m−2), without evidence of heart disease, and 48 lean controls were studied using transthoracic Doppler echocardiography for detecting coronary flow reserve (CFR). A value of CFR ≤ 2.5 was considered abnormal. We measured interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and adiponectin in all patients. Patients with abnormal CFR underwent coronary multislice computed tomography (MSCT) in order to exclude an epicardial stenosis. CFR in obese subjects was lower than in lean subjects (3.2 ± 0.8 vs. 3.7 ± 0.7, p = 0.02) and was abnormal in 27 (31%) obese patients and in one (2%) control (p < 0.0001). All subjects with abnormal CFR showed no coronary stenosis at MSCT. At multivariable analysis, IL-6 and TNF-α were the only determinants of CFR (p < 0.02 and p < 0.02, respectively). At multivariable logistic regression analysis, IL-6 and TNF-α were the only determinants of CFR ≤ 2.5 (p < 0.03 and p < 0.03, respectively). ConclusionsCFR is often reduced in obese subjects without clinical evidence of heart disease, suggesting a coronary microvascular impairment. This microvascular dysfunction seems to be related to a chronic inflammation mediated by adipocytokines. Our findings may explain the increased cardiovascular risk in obesity, independently of BMI.

Resting heart rate is an independent predictor of left ventricular diastolic dysfunction in obese patients with or without arterial hypertension

Background: Left Ventricular Diastolic Dysfunction (LVDD) represents one of the cardiac consequences in overweight and obese patients. Resting heart rate (RHR) is an easy measure but important indicator of cardiovascular health. In this study, we sought to assess if RHR is a reliable determinants of LVDD in obese patients with or without arterial hypertension. Methods and results: A perspective echo-Doppler study was performed in 154 consecutive asymptomatic patients with grade 1-to-3 obesity (body mass index [BMI]: 43±8) who averaged 47 years in age (women 80%). All patients had a LV ejection fraction (EF) ≥50% and no history of heart failure or coronary artery disease. LVDD was identified by an E/A ratio >1.5 and an E/A ratio <0.8. Long-axis function was assessed by global longitudinal strain. For means of comparison, 56 age-matched subjects with or without hypertension were also studied. Prevalence of hypertension was 42% in obese patients, while it was 29% in the control group. LVDD was present in 46 obese patients (30%) and in 12 controls (21%). Patients with grade 3 obesity (BMI ≥40) exhibited higher LV volumes and mass (p<0.0001), cardiac output (p<0.0001), left atrial size (p<0.0001), stroke volume (p<0.0001) and RHR (p<0.0001), and a worse LV long-axis function (p<0.001) as compared to patients with grade 1-2 obesity (BMI between 30 and 40) and the control group. In patients with grade 2-to-3 obesity, BMI directly correlated with stroke volume (r=0.24; p=0.003) and cardiac output (r=0.37; p<0.0001), RHR inversely correlated with LV end-diastolic volume index (r=-0.48; p<0.0001), LV end-systolic volume index (r=-0.42; p<0.0001) and LV mass index (r=-0.40; p<0.0001). RHR (hazard ratio [HR]:1.06, p=0.003) and age (HR: 1.05, p=0.025) were independently associated with LVDD in patients with grade 2-to-3 obesity. Conclusion: In obese patients with or without hypertension, RHR was a major predictor of LVDD and negatively correlated with LV mass and volumes. Obese patients with a disproportionate increase in RHR are likely to carry inadequate allometric scaling of LV mass and volumes relative to their BMI values.

Obesity and hypothyroidism

Obesity and hypothyroidism are common diseases, and consequently clinicians should be particularly alert to the possibility of thyroid dysfunction in obese patients. The relationship between thyroid function and obesity is likely to be bidirectional, with hypothyroidism affecting weight, but obesity also influencing thyroid function. Both serum thyroid-stimulating hormone and fT3 are typically increased in obese individuals, an effect likely mediated by leptin. Following L-T4 treatment for overt hypothyroidism, weight loss appears to be modest and mediated primarily by loss of water weight rather than fat. Selected thyroid analogs might be a means by which to improve weight loss by increasing energy expenditure in obese patients during continued caloric deprivation

Leptin as a mediator between obesity and cardiac dysfunction

Obesity is now recognised as one of the most important risk factors for heart disease. Obese individuals have high circulating levels of leptin, a hormone secreted by adipose tissue and involved in energy homeostasis. Growing evidence suggests that leptin may contribute to the development of cardiac dysfunction. In a large prospective study leptin has been shown to be an independent risk factor for coronary heart disease. An independent positive association has also been found between plasma leptin levels and heart rate in hypertensive patients and heart transplant recipients. In animal studies chronic leptin infusion increased heart rate and blood pressure. It has also been demonstrated that circulating leptin levels are elevated in patients with heart failure. The level of plasma leptin was associated with increased myocardial wall thickness and correlated with left ventricular mass, suggesting a role for this hormone in mediating left ventricular hypertrophy in humans. Moreover, leptin directly induced hypertrophy and hyperplasia in human and rodent cardiomyocytes, accompanied by cardiac extracellular matrix remodelling. Leptin may also influence energy substrate utilisation in cardiac tissue. These findings suggest that leptin acting directly or through the sympathetic nervous system may have adverse effects on cardiac structure and function, and that chronic hyperleptinaemia may greatly increase the risk of cardiac disorders. Additional studies are needed to define the role of leptin in cardiac physiology and pathophysiology, nevertheless the reduction in plasma leptin levels with caloric restriction and weight loss may prevent cardiac dysfunction in obese patients.

Evidence-Based Strategies to Prevent Postoperative Respiratory Dysfunction for Patients with Obstructive Sleep Apnea Undergoing Laparoscopic Bariatric Surgery

Obesity is a major health problem that is associated with significant comorbidities including Obstructive Sleep Apnea (OSA). OSA is a chronic condition characterized by partial or complete collapse of the upper airway during sleep. Laparoscopic bariatric surgery is one of the fastest growing surgical procedures in the United States to promote weight loss in morbidly obese patients. The number of patients undergoing bariatric surgery that have OSA is estimated to be >70%. However, the majority of these patients are neither diagnosed nor appropriately screened for OSA. The purpose of this paper is to discuss evidenced-based strategies to identify patients with OSA and to reduce postoperative respiratory dysfunction in obese patients undergoing laparoscopic bariatric surgery.

Strain imaging in morbid obesity: insights into subclinical ventricular dysfunction.

Obesity has become an important health problem throughout the world. Early detection of cardiovascular abnormalities may be useful in the future for patient management. This study aimed to identify subclinical ventricular dysfunction in obese patients. Morbid obesity is associated with ventricular dysfunction. Doppler echocardiogram was performed in 92 morbidly obese and in 31 healthy controls. Conventional echocardiography and tissue Doppler-based strain imaging were used to analyze ventricular function. Intra- and interobserver strain imaging variabilities were tested on 15 randomly selected cases. Left ventricular (LV) global strain (22.5% ± 3.5 vs 24.4% ± 2.5, P<0.005) and right ventricular (RV) strain (25.8% ± 5.2 vs 28.2% ± 5.2, P<0.029) were lower in obese patients when compared with healthy controls. Echocardiographic parameters of diastolic function were also different from controls. LV strain correlated with LV mass, E/e' ratio, left atrial volume, and RV strain. At multivariate analysis, morbid obesity remained a significant determinant of global LV strain, independently of associated comorbidities. These findings suggest that incipient biventricular dysfunction is present in morbidly obese patients when new echocardiographic indices are used to investigate ventricular function. In addition, strain imaging may provide a more accurate assessment of the ventricular function in obese patients.