Статті в журналах: "Cardiac metabolic syndrome"

1

Cheng, Tsung O. "Cardiac syndrome X versus metabolic syndrome X." International Journal of Cardiology 119, no. 2 (July 2007): 137–38. http://dx.doi.org/10.1016/j.ijcard.2006.06.062.

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2

Chiavelli, H., M. Lachaux, V. Tardif, A. Dumesnil, L. Nicol, G. Riou, D. Godefroy, et al. "Cardiac lymphatics in metabolic-syndrome related cardiac dysfunstion." Archives of Cardiovascular Diseases Supplements 12, no. 2-4 (October 2020): 239. http://dx.doi.org/10.1016/j.acvdsp.2020.03.095.

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3

Bugger, Heiko, and E. Dale Abel. "The Metabolic Syndrome and Cardiac Function." Advances in Pulmonary Hypertension 7, no. 3 (August 1, 2008): 332–36. http://dx.doi.org/10.21693/1933-088x-7.3.332.

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4

Yavelov, I. S. "SUDDEN CARDIAC DEATH AND METABOLIC SYNDROME." Journal of Clinical Practice 5, no. 4 (December 15, 2014): 53–59. http://dx.doi.org/10.17816/clinpract5453-59.

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In the review epidemiologic data regarding sudden cardiac death in patients with metabolic syndrome are presented. Suspected pathophysiologic mechanisms and approaches to primary prevention of this event are considered.

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5

Chahine, Mohamed. "Cardiac Metabolic State and Brugada Syndrome." Circulation Research 105, no. 8 (October 9, 2009): 721–23. http://dx.doi.org/10.1161/circresaha.109.208405.

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6

Fitchett, David, and Kim A. Connelly. "Impaired Cardiac Function in Metabolic Syndrome." Canadian Journal of Cardiology 30, no. 3 (March 2014): 270–71. http://dx.doi.org/10.1016/j.cjca.2014.01.012.

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7

Lavie, Carl J., and Richard V. Milani. "Metabolic Syndrome, Hostility, and Cardiac Rehabilitation." American Journal of Cardiology 96, no. 11 (December 2005): 1615. http://dx.doi.org/10.1016/j.amjcard.2005.08.001.

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8

Haq, M. Maksumul, and ZA Latif. "'Angry Fat' and Metabolic Syndrome." Ibrahim Cardiac Medical Journal 1, no. 2 (January 30, 2013): 5–6. http://dx.doi.org/10.3329/icmj.v1i2.13543.

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9

Yang, Yijun, Justin Kurian, Giana Schena, Jaslyn Johnson, Hajime Kubo, Joshua G. Travers, Chunya Kang, et al. "Cardiac Remodeling During Pregnancy With Metabolic Syndrome." Circulation 143, no. 7 (February 16, 2021): 699–712. http://dx.doi.org/10.1161/circulationaha.120.051264.

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Background: The heart undergoes physiological hypertrophy during pregnancy in healthy individuals. Metabolic syndrome (MetS) is now prevalent in women of child-bearing age and might add risks of adverse cardiovascular events during pregnancy. The present study asks if cardiac remodeling during pregnancy in obese individuals with MetS is abnormal and whether this predisposes them to a higher risk for cardiovascular disorders. Methods: The idea that MetS induces pathological cardiac remodeling during pregnancy was studied in a long-term (15 weeks) Western diet–feeding animal model that recapitulated features of human MetS. Pregnant female mice with Western diet (45% kcal fat)–induced MetS were compared with pregnant and nonpregnant females fed a control diet (10% kcal fat). Results: Pregnant mice fed a Western diet had increased heart mass and exhibited key features of pathological hypertrophy, including fibrosis and upregulation of fetal genes associated with pathological hypertrophy. Hearts from pregnant animals with WD-induced MetS had a distinct gene expression profile that could underlie their pathological remodeling. Concurrently, pregnant female mice with MetS showed more severe cardiac hypertrophy and exacerbated cardiac dysfunction when challenged with angiotensin II/phenylephrine infusion after delivery. Conclusions: These results suggest that preexisting MetS could disrupt physiological hypertrophy during pregnancy to produce pathological cardiac remodeling that could predispose the heart to chronic disorders.

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10

Asrih, Mohamed, François Mach, Alessio Nencioni, Franco Dallegri, Alessandra Quercioli, and Fabrizio Montecucco. "Role of Mitogen-Activated Protein Kinase Pathways in Multifactorial Adverse Cardiac Remodeling Associated with Metabolic Syndrome." Mediators of Inflammation 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/367245.

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Metabolic syndrome has been widely associated with an increased risk for acute cardiovascular events. Emerging evidence supports metabolic syndrome as a condition favoring an adverse cardiac remodeling, which might evolve towards heart dysfunction and failure. This pathological remodeling has been described to result from the cardiac adaptive response to clinical mechanical conditions (such as hypertension, dyslipidemia, and hyperglycemia), soluble inflammatory molecules (such as cytokines and chemokines), as well as hormones (such as insulin), characterizing the pathophysiology of metabolic syndrome. Moreover, these cardiac processes (resulting in cardiac hypertrophy and fibrosis) are also associated with the modulation of intracellular signalling pathways within cardiomyocytes. Amongst the different intracellular kinases, mitogen-activated protein kinases (MAPKs) were shown to be involved in heart damage in metabolic syndrome. However, their role remains controversial. In this paper, we will discuss and update evidence on MAPK-mediated mechanisms underlying cardiac adverse remodeling associated with metabolic syndrome.

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11

Xu, Xihui, and Jun Ren. "Cardiac Stem Cell Regeneration in Metabolic Syndrome." Current Pharmaceutical Design 19, no. 27 (June 1, 2013): 4888–92. http://dx.doi.org/10.2174/1381612811319270011.

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12

Pechánová, O., Z. V. Varga, M. Cebová, Z. Giricz, P. Pacher, and P. Ferdinandy. "Cardiac NO signalling in the metabolic syndrome." British Journal of Pharmacology 172, no. 6 (December 15, 2014): 1415–33. http://dx.doi.org/10.1111/bph.12960.

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13

ZHU, F. "Cardiac hypertrophy and dysfunction in metabolic syndrome." American Journal of Hypertension 16, no. 5 (May 2003): A181—A182. http://dx.doi.org/10.1016/s0895-7061(03)00565-x.

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14

Saeidi, Marzieh. "GW25-e3568 Cardiac Rehabilitation In Cardiac Patients with Metabolic Syndrome." Journal of the American College of Cardiology 64, no. 16 (October 2014): C209—C210. http://dx.doi.org/10.1016/j.jacc.2014.06.977.

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15

García-Arroyo, Fernando E., Guillermo Gonzaga-Sánchez, Alejandro Silva-Palacios, Francisco Javier Roldán, María L. Loredo-Mendoza, Yamnia Quetzal Alvarez-Alvarez, Jesus A. de los Santos Coyotl, et al. "Osthole Prevents Heart Damage Induced by Diet-Induced Metabolic Syndrome: Role of Fructokinase (KHK)." Antioxidants 12, no. 5 (April 28, 2023): 1023. http://dx.doi.org/10.3390/antiox12051023.

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There is increasing evidence that either ingested or produced fructose may have a role in metabolic syndrome. While not commonly considered a criterion for metabolic syndrome, cardiac hypertrophy is often associated with metabolic syndrome, and its presence carries increased cardiovascular risk. Recently it has been shown that fructose and fructokinase C (KHK) can be induced in cardiac tissue. Here we tested whether diet-induced metabolic syndrome causes heart disease associated with increased fructose content and metabolism and whether it can be prevented with a fructokinase inhibitor (osthole). Male Wistar rats were provided a control diet (C) or high fat/sugar diet for 30 days (MS), with half of the latter group receiving osthol (MS+OT, 40 mg/kg/d). The Western diet increased fructose, uric acid, and triglyceride concentrations in cardiac tissue associated with cardiac hypertrophy, local hypoxia, oxidative stress, and increased activity and expression of KHK in cardiac tissue. Osthole reversed these effects. We conclude that the cardiac changes in metabolic syndrome involve increased fructose content and its metabolism and that blocking fructokinase can provide cardiac benefit through the inhibition of KHK with modulation of hypoxia, oxidative stress, hypertrophy, and fibrosis.

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16

Kim, Yun Gi, Kyungdo Han, Joo Hee Jeong, Seung-Young Roh, Yun Young Choi, Kyongjin Min, Jaemin Shim, Jong-Il Choi, and Young-Hoon Kim. "Metabolic Syndrome, Gamma-Glutamyl Transferase, and Risk of Sudden Cardiac Death." Journal of Clinical Medicine 11, no. 7 (March 23, 2022): 1781. http://dx.doi.org/10.3390/jcm11071781.

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Background: Metabolic syndrome is associated with a significantly increased risk of sudden cardiac death (SCD). However, whether temporal changes in the metabolic syndrome status are associated with SCD is unknown. We aimed to determine whether metabolic syndrome and gamma-glutamyl transferase (ɣ-GTP), including their temporal changes, are associated with the risk of SCD. Methods: We performed a nationwide population-based analysis using the Korean National Health Insurance Service. People who underwent a national health check-up in 2009 and 2011 were enrolled. The influence of metabolic syndrome and ɣ-GTP on SCD risk was evaluated. Results: In 2009, 4,056,423 (848,498 with metabolic syndrome) people underwent health screenings, 2,706,788 of whom underwent follow-up health screenings in 2011. Metabolic syndrome was associated with a 50.7% increased SCD risk (adjusted hazard ratio (aHR) = 1.507; p < 0.001). The SCD risk increased linearly as the metabolic syndrome diagnostic criteria increased. The ɣ-GTP significantly impacted the SCD risk; the highest quartile had a 51.9% increased risk versus the lowest quartile (aHR = 1.519; p < 0.001). A temporal change in the metabolic syndrome status and ɣ-GTP between 2009 and 2011 was significantly correlated with the SCD risk. Having metabolic syndrome in 2009 or 2011 indicated a lower SCD risk than having metabolic syndrome in 2009 and 2011 but a higher risk than having no metabolic syndrome. People with a ≥20-unit increase in ɣ-GTP between 2009 and 2011 had an 81.0% increased SCD risk versus those with a change ≤5 units (aHR = 1.810; p < 0.001). Conclusions: Metabolic syndrome and ɣ-GTP significantly correlated with an increased SCD risk. SCD was also influenced by temporal changes in the metabolic syndrome status and ɣ-GTP, suggesting that appropriate medical treatment and lifestyle modifications may reduce future SCD risk.

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17

Lukitasari, Mifetika, Mohammad Saifur Rohman, Dwi Adi Nugroho, Nila Aisyah Wahyuni, Mukhamad Nur Kholis, and Nashi Widodo. "Improvement of Cardiac Fibrosis Biomarkers through Inflammation Inhibition by Green Tea and Decaffeinated Light Roasted Green Coffee Extract Combination Administration in Metabolic Syndrome Rat Model." F1000Research 10 (October 6, 2021): 1013. http://dx.doi.org/10.12688/f1000research.55468.1.

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Background: Metabolic syndrome is a significant risk factor for cardiovascular diseases. Green tea and green coffee extracts, antioxidant and anti-inflammatory agents may participate in metabolic syndrome-induced cardiac fibrosis alleviation. However, the effect of combination of those extracts still needs exploration. Therefore, this study investigated the effect of green tea and decaffeinated light roasted green coffee extracts and their combination in metabolic syndrome-induced cardiac fibrosis rats. Methods: Metabolic syndrome rat model was i1nduced through high-fat high sucrose diets feeding for 8 weeks and injection of low dose streptozotocin at the 2nd week. The metabolic syndrome rats were divided into 4 experimental groups metabolic syndrome rats (MS); metabolic syndrome rats treated with 300 mg/ kg b.w green tea extract (GT); metabolic syndrome rats treated with 200 mg/ kg b.w decaffeinated light roasted green coffee extract (GC); metabolic syndrome rats treated with the combination of the two extracts (CE); and a normal control (NC) group was added. Angiotensin 2 level was analyzed by ELISA method. Gene expression of NF-κB, TNF-α, IL-6, Tgf-β1, Rac-1, and α-sma were analyzed by touchdown polymerase chain reaction methods. Results: Metabolic syndrome rats treated with green tea and decaffeinated light roasted green coffee significantly decreased angiotensin-2 serum level and cardiac inflammation and fibrosis gene expression level (NF-κB, TNF-α, IL-6, Tgf-β1, Rac-1, and α-sma). More significant alleviation was observed in the combination group. Conclusion: This study suggested that combination of green tea and decaffeinated light roasted green coffee extracts showed better improvement in metabolic syndrome-induced cardiac fibrosis rat model compared to that of single extract administration through inflammation inhibition

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18

Farias Godoy, Alejandra, Andrew Ignaszewski, Jiri Frohlich, and Scott A. Lear. "Predictors of Metabolic Syndrome in Participants of a Cardiac Rehabilitation Program." ISRN Cardiology 2012 (March 28, 2012): 1–7. http://dx.doi.org/10.5402/2012/736314.

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Metabolic syndrome increases the risk of all-cause mortality, cardiovascular mortality and cardiovascular events in patients with cardiovascular disease (CVD). This study assessed the predictors of metabolic syndrome, both its incidence and resolution in a cohort of cardiac rehabilitation program graduates. Methods. A total of 154 and 80 participants without and with metabolic syndrome respectively were followed for 48 months. Anthropometric measurements, metabolic risk factors, and quality of life were assessed at baseline and at 48 months. Logistic regression models were used to assess the predictors of metabolic syndrome onset and resolution. Results. Increasing waist circumference (OR 1.175, P≤0.001) was an independent predictor for incident metabolic syndrome (R2 for model = 0.46). Increasing waist circumference (OR 1.234, P≤0.001), decreasing HDL-C (OR 0.027, P=0.005), and increasing triglycerides (OR 3.005, P=0.003) were predictors of metabolic syndrome resolution. Conclusion. Patients with CVD that further develop metabolic syndrome are particularly susceptible for the cascade of cardiovascular events and mortality. Increasing waist circumference confers a higher risk for future onset of metabolic syndrome in this group of patients. They will require closer follow-up and should be targeted for further prevention strategies after cardiac rehabilitation program completion.

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19

Essick, Eric E., and Flora Sam. "Cardiac Hypertrophy and Fibrosis in the Metabolic Syndrome: A Role for Aldosterone and the Mineralocorticoid Receptor." International Journal of Hypertension 2011 (2011): 1–12. http://dx.doi.org/10.4061/2011/346985.

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Obesity and hypertension, major risk factors for the metabolic syndrome, render individuals susceptible to an increased risk of cardiovascular complications, such as adverse cardiac remodeling and heart failure. There has been much investigation into the role that an increase in the renin-angiotensin-aldosterone system (RAAS) plays in the pathogenesis of metabolic syndrome and in particular, how aldosterone mediates left ventricular hypertrophy and increased cardiac fibrosis via its interaction with the mineralocorticoid receptor (MR). Here, we review the pertinent findings that link obesity with elevated aldosterone and the development of cardiac hypertrophy and fibrosis associated with the metabolic syndrome. These studies illustrate a complex cross-talk between adipose tissue, the heart, and the adrenal cortex. Furthermore, we discuss findings from our laboratory that suggest that cardiac hypertrophy and fibrosis in the metabolic syndrome may involve cross-talk between aldosterone and adipokines (such as adiponectin).

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20

Fujii, Hiromichi, Hirokazu Ohashi, Yasushi Tsutsumi, Takahiro Kawai, Toshihide Tsukioka, and Masateru Onaka. "Myonephropathic Metabolic Syndrome after Cardiac or Aortic Surgery." Japanese Journal of Cardiovascular Surgery 32, no. 4 (2003): 230–33. http://dx.doi.org/10.4326/jjcvs.32.230.

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21

Calik Kutukcu, Ebru, Beyza Nur Durukan, Hilal Uyar, Fatma Rumeysa Kasap, Nurel Erturk, Sezen Kayali, and Naciye Vardar Yagli. "Cardiac Rehabilitation in Metabolic Syndrome: An Update Review." Turkish Journal of Endocrinology and Metabolism 26, no. 3 (September 7, 2022): 165–70. http://dx.doi.org/10.5152/tjem.2022.22027.

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22

Okatan, Esma N., Aysegul Toy Durak, and Belma Turan. "Electrophysiological basis of metabolic-syndrome-induced cardiac dysfunction." Canadian Journal of Physiology and Pharmacology 94, no. 10 (October 2016): 1064–73. http://dx.doi.org/10.1139/cjpp-2015-0531.

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Myocardial contractility is controlled by intracellular Ca2+ cycling with the contribution of sarcoplasmic reticulum (SR). In this study, we aimed to investigate the role of altered SR function in defective regulation of intracellular Ca2+ levels in rats with metabolic syndrome (MetS) induced by a 16-week high-sucrose drinking-water diet. Electric-field stimulated transient intracellular Ca2+ changes in MetS cardiomyocytes exhibited significantly reduced amplitude (∼30%) and prolonged time courses (2-fold), as well as depressed SR Ca2+ loading (∼55%) with increased basal Ca2+ level. Consistent with these data, altered ryanodine receptor (RyR2) function and SERCA2a activity were found in MetS cardiomyocytes through Ca2+ spark measurements and caffeine application assay in a state in which sodium calcium exchanger was inhibited. Furthermore, tetracaine application assay results and hyperphosphorylated level of RyR2 also support the “leaky RyR2” hypothesis. Moreover, altered phosphorylation levels of phospholamban (PLN) support the depressed SERCA2a-activity thesis and these alterations in the phosphorylation of Ca2+-handling proteins are correlated with altered protein kinase and phosphatase activity in MetS cardiomyocytes. In conclusion, MetS-rat heart exhibits altered Ca2+ signaling largely due to altered SR function via changes in RyR2 and SERCA2a activity. These results point to RyR2 and SERCA2a as potential pharmacological targets for restoring intracellular Ca2+ homeostasis and, thereby, combatting dysfunction in MetS-rat heart.

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23

Soares-Miranda, Luisa, Gavin Sandercock, Susana Vale, Rute Santos, Sandra Abreu, Carla Moreira, and Jorge Mota. "Metabolic syndrome, physical activity and cardiac autonomic function." Diabetes/Metabolism Research and Reviews 28, no. 4 (May 2012): 363–69. http://dx.doi.org/10.1002/dmrr.2281.

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24

Sawant, Apurva, Ranjit Mankeshwar, Swarup Shah, Rani Raghavan, Gargi Dhongde, Himanshu Raje, Shoba D'souza, et al. "Prevalence of Metabolic Syndrome in Urban India." Cholesterol 2011 (May 19, 2011): 1–7. http://dx.doi.org/10.1155/2011/920983.

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Background. Metabolic syndrome (MS) is characterised by a constellation of individual risk factors of cardiovascular disease. Materials and Methods. The current study was a population-based survey of cohort of subjects in the metropolitan city of Mumbai. A total of 548 subjects, who attended the CARDIAC evaluation camp, were recruited in the study. Participants with complete fasting lipid profiles, blood glucose, and known cardiac risk markers were evaluated. Results. On applying modified NCEP ATP III, we found out that nearly of the subjects had at least one abnormal parameter. We found the prevalence of MS in our study population to be . The prevalence of MS in males was almost double than females (). The overall prevalence of BMI (>23 kg/m2) was . Increased hypertriglyceridemia and decreased levels of HDL-C were found to be more in males (). Conclusion. The low percentage of subjects with normal and controlled parameters suggests that there is a need for awareness programs and lifestyle interventions for the prevention and control of MS.

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Sadia Nizamani, Khadim Hussain, Ramesh Kumar, Saajan Sawai, and Doulat Singh. "Hyperuricemia in metabolic syndrome." Professional Medical Journal 30, no. 05 (May 2, 2023): 644–48. http://dx.doi.org/10.29309/tpmj/2023.30.05.6963.

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Objective: To determine frequency of hyperuricemia among the patients having metabolic syndrome. Study Design: Cross Sectional study. Setting: Indus Medical College, Tando Muhammad Khan. Period: 28-06-2021 till 28-12-2021. Material & Methods: After informed consent, 246 cases of metabolic syndrome who met the inclusion criteria were included. Inclusion criteria were the known case of metabolic syndrome for more than six months, of age group 20 to 60 years and of either gender. Exclusion criteria were the non-consenting patients as well as the patients with history of hyperthyroidism and hypothyroidism, gout, congestive cardiac failure, chronic renal failure, Post myocardial infarction, chronic liver disease, stroke, COPD & Pregnancy. Data analyzed on IBM SPSS 22.0 and p value< 0.05 taken as statistically significant. Results: Out of 246 patients mean age in our study was 40.80 years with the standard deviation of ±7. Mean FBS, triglycerides, HDL, SBP, DBP and waist circumference was 115.64±10.16 mg/dl, 144.7±10.43 mg/dl, 41.61±4.03 mg/dl, 168.5±4.16, 98.2±2.78 and 101±8.16 cm respectively. 93 (37.8%) were male and 153 (62.2%) were female. Out of 246 patients, 81 (32.9%) had hyperuricemia and 165 (67.1%) did not have hyperuricemia in patients with metabolic syndrome. Conclusion: This study concluded that hyperuricemia is 32.9% common in metabolic syndrome patients.

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26

Reznik, E. V., and I. G. Nikitin. "HYPERTENSION MANAGEMENT IN METABOLIC SYNDROME." Russian Archives of Internal Medicine 9, no. 5 (October 6, 2019): 327–47. http://dx.doi.org/10.20514/2226-6704-2019-9-5-327-347.

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Hypertension is one of the key risk factors for cardiovascular morbidity and mortality. Metabolic syndrome (synonyms: syndrome X, insulin resistance syndrome) is characterized by increased visceral fat mass, decreased sensitivity of peripheral tissues to insulin (insulin resistance) and hyperinsulinemia, which cause disorders of carbohydrate, lipid, and purine metabolism. Hypertension is an integral component of the metabolic syndrome. The severity of hypertension in patients with metabolic syndrome is higher in comparison with patients without metabolic disorders. In patients with metabolic syndrome, the probability of cardiac and brain damage increases fivefold, kidney damage threefold, and the vessels twofold. The presence of diabetes reduces the likelihood of achieving effective control of blood pressure by 1.4 times, hypercholesterolemia — by 1.5 times, obesity — by 1.7 times. In the presence of any three factors, the effectiveness of treatment is reduced twofold. In this article, approaches to the management of patients with hypertension and metabolic syndrome, aspects of non-drug therapy, target blood pressure levels, and the choice of drugs are presented in accordance with evidence-based medicine and current recommendations.

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Dincer, U. Deniz, Alberto Araiza, Jarrod D. Knudson, Chun Hong Shao, Keshore R. Bidasee, and Johnathan D. Tune. "Dysfunction of cardiac ryanodine receptors in the metabolic syndrome." Journal of Molecular and Cellular Cardiology 41, no. 1 (July 2006): 108–14. http://dx.doi.org/10.1016/j.yjmcc.2006.04.018.

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28

Gerber, Lynn, Samuel Powers, Carey Escheik, Jillian Kallman Price, Patrick Austin, Carla Porter, Henry Tran, Marianne Sherman, Zobair Younossi, and Zobair Younossi. "Influence of Metabolic Syndrome on Response to Cardiac Rehabilitation." Medicine & Science in Sports & Exercise 50, no. 5S (May 2018): 193. http://dx.doi.org/10.1249/01.mss.0000535719.21298.3c.

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Sun, Aijun, and Jun Ren. "Estrogen Replacement Therapy and Cardiac Function Under Metabolic Syndrome." Hypertension 59, no. 3 (March 2012): 552–54. http://dx.doi.org/10.1161/hypertensionaha.111.186817.

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30

Raichlin, Eugenia R., Joseph P. McConnell, Amir Lerman, Walter K. Kremers, Brooks S. Edwards, Sudhir S. Kushwaha, Alfredo L. Clavell, Richard J. Rodeheffer, and Robert P. Frantz. "Systemic Inflammation and Metabolic Syndrome in Cardiac Allograft Vasculopathy." Journal of Heart and Lung Transplantation 26, no. 8 (August 2007): 826–33. http://dx.doi.org/10.1016/j.healun.2007.05.008.

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31

Kseneva, S. I., E. V. Borodulina, O. Yu Trifonova, and V. V. Udut. "DYSREGULATION OF THE AUTONOMIC NERVOUS SYSTEM IN THE MECHANISMS OF METABOLIC SYNDROME DEVELOPMENT." Siberian Medical Journal 33, no. 4 (February 13, 2019): 119–24. http://dx.doi.org/10.29001/2073-8552-2018-33-4-119-124.

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The concept of metabolic syndrome as a cluster of risk factors for type 2 diabetes and cardiovascular diseases has undergone a number of evolutionary transformations over the past years. Incorporation of autonomic nervous system dysfunction into the pathogenesis of metabolic syndrome opens an opportunity for inclusion of a number of clinical entities in the cluster of metabolic syndrome as they mutually affect the course and clinical manifestations of pathologies involved in metabolic syndrome. To confirm this notion, a cross-sectional transverse study of a continuous sample of 158 patients with metabolic syndrome was performed. The study showed that, in the presence of metabolic syndrome, the incidence of cardiac autonomic neuropathy reaches 37.5%. A number of features of gastroesophageal reflux disease in patients with metabolic syndrome were found in the structure of complaints where regurgitation predominated. Fibrogastroduodenoscopy demonstrated endoscopically negative form of the disease in 38%, and, according to high DeMeester index by daily pH-metry, the alkaline reflux was present in patients in lying position over 25% of time. Young men with metabolic syndrome had high incidence of prostatic enlargement (increased prostate size and volume) as well as high incidence of the IPSS questionnaire score corresponding to the initial manifestations of prostatic hyperplasia in the presence of insulin resistance and normal androgen levels. The study showed that dysfunction of the autonomic nervous system (along with insulin resistance) was the main converging point in the development of metabolic syndrome. This suggests that cardiac autonomic neuropathy, lower urinary tract symptoms, and gastroesophageal reflux disease may be included in the metabolic syndrome cluster.

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Zandstra, Mirjam, Eva Stekkinger, Maureen J. van der Vlugt, Arie P. van Dijk, Frederik K. Lotgering, and Marc E. A. Spaanderman. "Cardiac Diastolic Dysfunction and Metabolic Syndrome in Young Women After Placental Syndrome." Obstetrics & Gynecology 115, no. 1 (January 2010): 101–8. http://dx.doi.org/10.1097/aog.0b013e3181c4f1e8.

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33

Burroughs Peña, Melissa, Katrina Swett, Neil Schneiderman, Daniel M. Spevack, Sonia G. Ponce, Gregory A. Talavera, Mayank M. Kansal, et al. "Cardiac structure and function with and without metabolic syndrome: the Echocardiographic Study of Latinos (Echo-SOL)." BMJ Open Diabetes Research & Care 6, no. 1 (August 2018): e000484. http://dx.doi.org/10.1136/bmjdrc-2017-000484.

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ObjectiveWe assessed the hypothesis that metabolic syndrome is associated with adverse changes in cardiac structure and function in participants of the Echocardiographic Study of Latinos (Echo-SOL).MethodsNon-diabetic Echo-SOL participants were included in this cross-sectional analysis. Metabolic syndrome was defined according to the American Heart Association/National Heart, Lung, and Blood Institute 2009 Joint Scientific Statement. Survey multivariable linear regression analyses using sampling weights were used adjusting for multiple potential confounding variables. Additional analysis was stratified according to the presence/absence of obesity (body mass index (BMI) ≥25 kg/m2) and the presence/absence of metabolic syndrome.ResultsWithin Echo-SOL, 1260 individuals met inclusion criteria (59% female; mean age 55.2 years). Compared with individuals without metabolic syndrome, those with metabolic syndrome had lower medial and lateral E′ velocities (−0.4 cm/s, (SE 0.1), p=0.0002; −0.5 cm/s (0.2), p=0.02, respectively), greater E/E′ (0.5(0.2), p=0.01) and worse two-chamber left ventricular longitudinal strain (0.9%(0.3), p=0.009), after adjusting for potential confounding variables. Increased left ventricular mass index (9.8 g/m2 (1.9), p<0.0001 and 7.5 g/m2 (1.7), p<0.0001), left ventricular end-diastolic volume (11.1 mL (3.0), p=0.0003 and 13.3 mL (2.7), p<0.0001), left ventricular end-systolic volume (5.0 mL (1.4), p=0.0004 and 5.7 mL (1.3) p<0.0001) and left ventricular stroke volume (10.2 mL (1.8), p<0.0001 and 13.0 mL (2.0), p<0.0001) were observed in obese individuals with and without metabolic syndrome compared with individuals with normal weight without metabolic syndrome. In sensitivity analyses, individuals with normal weight (BMI <25 kg/m2) and metabolic syndrome had worse left ventricular global longitudinal strain (2.1%(0.7), p=0.002) and reduced left ventricular ejection fraction (−3.5%(1.4), p=0.007) compared with normal-weight individuals without metabolic syndrome.ConclusionsIn a sample of US Hispanics/Latinos metabolic syndrome was associated with worse left ventricular systolic and diastolic function. Adverse changes in left ventricular size and function were observed in obese individuals with and without metabolic syndrome but decreased left ventricular function was also present in normal-weight individuals with metabolic syndrome.

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Brandão, Ana Denise, Keila Larissa Pereira Reis, Nathalia Moraes Ribeiro, Patricia Figueiredo, Daniela Martins de Fausto, Antônio Adolfo Mattos de Castro, and Elias Ferreira Porto. "Is it possible that a cardiac rehabilitation program can reduce the cardiovascular risk in individuals with metabolic syndrome?" Revista Brasileira de Fisiologia do Exerc&iacute cio 20, no. 4 (September 9, 2021): 422–32. http://dx.doi.org/10.33233/rbfex.v20i4.4541.

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Background: Metabolic syndrome is a complex disorder represented by a set of cardiovascular risk factors usually related to central fat deposition, insulin resistance, hypertension, and dyslipidemia. It is associated with accelerated atherosclerosis in response to chronic inflammation and vascular endothelial dysfunction, increasing overall mortality. Objective: We aimed to evaluate the effect of a cardiac rehabilitation program on cardiovascular risk factors in patients with metabolic syndrome. Methods: This is prospective interventional study. All patients underwent a 20-session cardiac rehabilitation program with aerobic and resisted exercises as well as an educational program for lifestyle changes. Results: Forty-seven patients participated in the present study. After the cardiac rehabilitation program (CRP), a significant reduction (p = 0,0092) for cardiovascular risk and fatigue (p > 0.001) was observed; 78% of the patients had positive effects on physical capacity, 72% of the patients presented HbA1c reduction, 51% increased HDL-cholesterol, 70% reduced total cholesterol, 63% reduced triglycerides, 61% reduced systolic blood pressure and 53% reduced diastolic blood pressure. Conclusion: Cardiac rehabilitation program with aerobic and resisted exercises associated with educational program for lifestyle changes is an effective approach in the treatment of patients with metabolic syndrome mainly seen by a reduced cardiovascular risk factors and reducing fatigue, improved physical capacity and reduced components of metabolic syndrome.

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Karki, D. B., A. Neopane, S. Joshi, Subash Pant, Lucky Sharma, Pradeep Shrestha, and Rijendra Yogal. "Prevalence of metabolic syndrome in individuals undergoing comprehensive cardiac and general medical check-up at Kathmandu Medical College Teaching Hospital." Journal of Kathmandu Medical College 2, no. 3 (February 27, 2014): 112–16. http://dx.doi.org/10.3126/jkmc.v2i3.9934.

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Background: Metabolic syndrome represents a constellation of metabolic derangements including insulin resistance, diabetes mellitus, obesity, dyslipidaemia and cardiovascular disease. Since it is associated with higher risk of coronary artery disease and diabetes mellitus, timely detection is important. Objectives: The main objective of the study was to find out the prevalence of metabolic syndrome in individuals undergoing comprehensive cardiac and general medical check-up at Kathmandu Medical College Teaching Hospital. The other objectives were to find the gender and ethnic prevalence of this condition. Methods: This is a hospital based cross-sectional study conducted at Kathmandu Medical College Teaching Hospital among 389 healthy participants of both gender and above 20 years of age who underwent comprehensive cardiac and general medical check-up. Metabolic Syndrome was diagnosed using US National Cholesterol Education Program Adult Treatment Panel III. Results: Out of the 389 subjects, 56 persons were found to be having metabolic syndrome (14.40%). Metabolic syndrome was more common in female and obese people and the prevalence did not differ with ethnicity. Conclusion: The prevalence of metabolic syndrome in the present study has been found to be 14.40 %. It is important to diagnose this condition in time so that subsequent complications can be prevented.Journal of Kathmandu Medical College Vol. 2, No. 3, Issue 5, Jul.-Sep., 2013 Page: 112-116DOI: http://dx.doi.org/10.3126/jkmc.v2i3.9934Uploaded date : 2/28/2014

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Lohakare, Akash C., Pawan Mehta, and Shuchi Singh. "Prevalence of cardiac autonomic dysfunction in patients with metabolic syndrome: a cross-sectional, observational study." International Journal of Research in Medical Sciences 7, no. 4 (March 27, 2019): 987. http://dx.doi.org/10.18203/2320-6012.ijrms20191300.

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Background: Cardiovascular autonomic neuropathy (CAN) is a distinguished disorder associated with diabetes mellitus and metabolic syndrome. The pathogenesis of CAN in patients with metabolic syndrome still remains unclear. This study was undertaken to assess the prevalence of cardiac autonomic dysfunction in patients with metabolic syndrome and to correlate different parameters of metabolic syndrome with cardiac autonomic dysfunction.Methods: In this cross-sectional observational study, total 100 consecutive cases meeting the inclusion criteria and attending the Department of Medicine in Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi were enrolled. 50 subjects who satisfied the IDF criteria of metabolic syndrome were taken as cases and remaining 50 subjects (age and gender matched) who did not satisfy the IDF criteria were taken as controls. Comparison of categorical variables was made using chi-square or Fisher’s exact test. P-value <0.05 was considered as statistically significant.Results: Majority of study population (i.e., 42%) belonged to the age group of 41-50 years. Overall prevalence of cardiac autonomic dysfunction (CAD) was 25%. Prevalence of CAD among cases and controls was 38% and 12%, respectively. Overall distribution of various parameters like waist circumference, fasting blood glucose, blood pressure, HDL-C and serum triglycerides was assessed in all subjects with respect to CAD. Statistically significant association of these parameters was seen with CAD (p-value ≤0.01).Conclusions: In this study, strong association was found between CAD and central obesity, impaired fasting glucose, high blood pressure and dyslipidemia. Thus, the metabolic disorders are good predictors of CAD.

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Okamoto, Yoshihisa. "Adiponectin Provides Cardiovascular Protection in Metabolic Syndrome." Cardiology Research and Practice 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/313179.

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Adipose tissue plays a central role in the pathogenesis of metabolic syndrome. Adiponectin (APN) is a bioactive adipocytokine secreted from adipocytes. Low plasma APN levels (hypoadiponectinemia) are observed among obese individuals and in those with related disorders such as diabetes, hypertension, and dyslipidemia. APN ameliorates such disorders. Hypoadiponectinemia is also associated with major cardiovascular diseases including atherosclerosis and cardiac hypertrophy. Accumulating evidence indicates that APN directly interacts with cardiovascular tissue and prevents cardiovascular pathology. Increasing plasma APN or enhancing APN signal transduction may be an ideal strategy to prevent and treat the cardiovascular diseases associated with metabolic syndrome. However, further studies are required to uncover the precise biological actions of APN.

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Axelsen, Lene N., Jacob B. Lademann, Jørgen S. Petersen, Niels-Henrik Holstein-Rathlou, Thorkil Ploug, Clara Prats, Henrik D. Pedersen, and Anne Louise Kjølbye. "Cardiac and metabolic changes in long-term high fructose-fat fed rats with severe obesity and extensive intramyocardial lipid accumulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 6 (June 2010): R1560—R1570. http://dx.doi.org/10.1152/ajpregu.00392.2009.

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Metabolic syndrome and obesity-related diseases are affecting more and more people in the Western world. The basis for an effective treatment of these patients is a better understanding of the underlying pathophysiology. Here, we characterize fructose- and fat-fed rats (FFFRs) as a new animal model of metabolic syndrome. Sprague-Dawley rats were fed a 60 kcal/100 kcal fat diet with 10% fructose in the drinking water. After 6, 12, 18, 24, 36, and 48 wk of feeding, blood pressure, glucose tolerance, plasma insulin, glucose, and lipid levels were measured. Cardiac function was examined by in vivo pressure volume measurements, and intramyocardial lipid accumulation was analyzed by confocal microscopy. Cardiac AMP-activated kinase (AMPK) and hepatic phospho enolpyruvate carboxykinase (PEPCK) levels were measured by Western blotting. Finally, an ischemia-reperfusion study was performed after 56 wk of feeding. FFFRs developed severe obesity, decreased glucose tolerance, increased serum insulin and triglyceride levels, and an initial increased fasting glucose, which returned to control levels after 24 wk of feeding. The diet had no effect on blood pressure but decreased hepatic PEPCK levels. FFFRs showed significant intramyocardial lipid accumulation, and cardiac hypertrophy became pronounced between 24 and 36 wk of feeding. FFFRs showed no signs of cardiac dysfunction during unstressed conditions, but their hearts were much more vulnerable to ischemia-reperfusion and had a decreased level of phosphorylated AMPK at 6 wk of feeding. This study characterizes a new animal model of the metabolic syndrome that could be beneficial in future studies of metabolic syndrome and cardiac complications.

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Bodrova, E. A., A. R. Babaeva, M. A. Osadchuk, and K. S. Solodenkova. "Peculiarities of cardiac remodeling and myocardial dysfunction in metabolic syndrome." Diagnostic radiology and radiotherapy 11, no. 4 (January 12, 2021): 52–59. http://dx.doi.org/10.22328/2079-5343-2020-11-4-52-59.

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Introduction. In 2016, updated recommendations for echocardiographic diagnosis of diastolic dysfunction were developed. It requires a review of the degree of metabolic syndrome (MS) influence on the heart and blood vessels remodeling and the development of left ventricle (LV) diastolic dysfunction (DD).Purpose. Assessment of the MScontribution to the heart and blood vessels remodeling, as well as to the development of LVDD with an analysis of the LV remodeling types and the degree of LVDD.Materials and methods. The main group: 130 patients with MS (62 (47,7%) — men, 68 (52,3%) — women; average age — 59,8±9,5 years) who underwent in-patient examination and treatment in the cardiology department for arterial hypertension (AH) in 2015-2017. The control group included 36 patients with AH (18 (50%) — men, 18 (50%) — women; average age — 56,0±12,7 years) without abdominal obesity, not meeting the criteria of MS International Diabetes Federation.Results. MS is associated with increased prevalence of adverse LV remodeling and DD. In MS group concentric LV hypertrophy was detected significantly commoner than in group without MS, in which concentric remodeling was the most frequent structural abnormality. Eccentric LV hypertrophy was diagnosed only in pts with so-called complete MS. Moreover DD was detected in all pts with complete MS. Type 2 DD was present predominantly in subgroup with complete MS, reflecting relationship between the degree of LV DD and severity of MS in AH pts.Conclusions. Obtained results confirm adverse influence of central obesity and MS on LV myocardial structure and function.

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Miklík, Roman, and Marie Pavlušová. "Cardiac function in hypertensive patients with metabolic syndrome and microalbuminuria." Interní medicína pro praxi 18, no. 4 (September 1, 2016): 184–90. http://dx.doi.org/10.36290/int.2016.042.

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Uhlíř, Petr, Milada Betlachová, and Petra Stará. "Cardiac function in hypertensive patients with metabolic syndrome and microalbuminuria." Medicína pro praxi 13, no. 2 (May 1, 2016): 96–98. http://dx.doi.org/10.36290/med.2016.021.

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Piťha, Jiří. "Cardiac function in hypertensive patients with metabolic syndrome and microalbuminuria." Neurologie pro praxi 17, no. 3 (August 1, 2016): 95–99. http://dx.doi.org/10.36290/neu.2016.033.

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Stejskalová, Jana, Helena Strmeňová, Jana Doležílková, Andrea Holečková, Radoslava Tomanová, and Pavel Vantuch. "Cardiac function in hypertensive patients with metabolic syndrome and microalbuminuria." Pediatrie pro praxi 17, no. 4 (October 1, 2016): 248–50. http://dx.doi.org/10.36290/ped.2016.057.

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Khader, Yousef, Moawiah Khatatbeh, Khalid EL-Salem, Zouhair Amarin, and Anwar Bateiha. "The Metabolic Syndrome Among Patients Undergoing Cardiac Catheterization in Jordan." Journal of the CardioMetabolic Syndrome 3, no. 4 (September 2008): 224–28. http://dx.doi.org/10.1111/j.1559-4572.2008.00020.x.

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Siegmund, Lee Anne, Jonathan Naylor, James Bena, and Mark McClelland. "The relationship between Metabolic Syndrome and adherence to cardiac rehabilitation." Physiology & Behavior 169 (February 2017): 41–45. http://dx.doi.org/10.1016/j.physbeh.2016.11.005.

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Savage, Patrick D., John A. Banzer, Gary J. Balady, and Philip A. Ades. "Prevalence of metabolic syndrome in cardiac rehabilitation/secondary prevention programs." American Heart Journal 149, no. 4 (April 2005): 627–31. http://dx.doi.org/10.1016/j.ahj.2004.07.037.

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Raichlin, E. R., J. P. McConnell, W. K. Kremers, B. S. Edwards, S. S. Kushwaha, A. L. Clavell, R. J. Rodeheffer, and R. P. Frantz. "192: Systemic inflammation and metabolic syndrome in cardiac allograft vasculopathy." Journal of Heart and Lung Transplantation 26, no. 2 (February 2007): S129. http://dx.doi.org/10.1016/j.healun.2006.11.209.

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Kawada, Tomoyuki. "Metabolic syndrome and sudden cardiac death: Validity on risk assessment." International Journal of Cardiology 212 (June 2016): 109. http://dx.doi.org/10.1016/j.ijcard.2016.03.049.

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O'Neill, Elizabeth. "Systemic Lupus, Metabolic Syndrome, Cardiac Disease, and Peripheral Artery Disease." Journal of Clinical Exercise Physiology 12, no. 2 (May 31, 2023): 62–64. http://dx.doi.org/10.31189/2165-6193-12.2.62.

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Solov'eva, Alexandra Viktorovna, and Inessa Ivanovna Dubinina. "Characteristics of metabolic syndrome in women." Diabetes mellitus 15, no. 1 (March 15, 2012): 57–62. http://dx.doi.org/10.14341/2072-0351-5980.

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Aims. To evaluate combination and manifestation sequence of metabolic syndrome (MS) components, as well as cardiovascular riskfactors in women. Materials and methods. We examined 100 female subjects with MS. We assessed anthropometric parameters, glycemic control andlipid metabolism. We also conducted cardiac ultrasound in all participants. Results. 44% of patients developed abdominal obesity after pregnancy, 48% - in perimenopausal period and in 8% of studied casesobesity manifested in combination with arterial hypertension 10 years before menopause (at the average). Family history of type 2diabetes mellitus and obesity, elevation of LDL and TG characterized post pregnancy abdominal obesity. Postmenopausal obesity wasassociated with significantly lower levels of HDL. HDL concentration was also lower in cases of histerectomia and early age of surgicalmenopause. Conclusion. Manifestation of MS in females is associated with periods of hormonal imbalance. Cardiovascular risk positively correlateswith number of pregnancies, duration of abdominal obesity experience, and negatively - with HDL level and age of surgical menopause.Complete form of MS (with all 6 components present) is found more frequently in women with postmenopausal manifestation.

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