The Metabolic SYNDROME and the RISK of Venous Thrombosis: RESULTS of AN Individual LEVEL Patient Meta-ANALYSIS

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3177-3177
Author(s):  
Francesco Dentali ◽  
Cihan Ay ◽  
Moon Jang ◽  
Matteo di Minno ◽  
Ingrid Pabinger ◽  
...  

Abstract Abstract 3177 Background: The metabolic syndrome (MS) is a cluster of interrelated risk factors that identify patients at increased risk of cardiovascular events. Recent studies also suggested an association between MS and venous thromboembolism (VTE). However, the role of the individual features of MS and whether MS and its features are more important than obesity alone to predict VTE remain to be established. Methods: We performed an individual patient level meta-analysis of case-control studies comparing the prevalence of MS in patients with unprovoked VTE and in controls. MEDLINE, EMBASE databases, and abstract books were searched up to January 2010. Odds ratios (OR) and 95% confidence intervals of pooled results were calculated. The influence of individual variables (age, sex, BMI and MS) on the likelihood of VTE was compared using logistic regression analysis. Multivariate analysis was subsequently performed including the individual components of MS in the place of MS. The impact of increasing number of individual components of MS on the risk of VTE was investigated. Results: Four studies were identified and analyzed, for a total of 1332 patients (479 cases and 833 controls). Mean age was 53.3 and 52.7, respectively (p=n.s.), 49.5% cases and 42.4% controls were males (p=0.0003), 38.8% and 30.0% were obese (p=0.0001). MS was significantly associated with VTE (OR 1.97, 1.57–2.47), and the association linearly increased with the number of MS features (p for trend <0.001). At multivariate analysis, MS but not obesity remained associated with VTE (OR 1.92, 1.50–2.46 and 1.14, 0.88–1.47, respectively). All individual features of MS, but HDL cholesterol, were independently associated with VTE. Conclusions: The results of this meta-analysis confirm the association between MS and VTE and suggest that MS (and visceral obesity defined by increased waist circumference) could be a more important predictor of VTE than obesity defined by BMI. Disclosures: No relevant conflicts of interest to declare.

2007 ◽  
Vol 30 (4) ◽  
pp. 95
Author(s):  
Valerie Taylor ◽  
Glenda M. MacQueen

Bipolar disorder and major depression are life-shortening illnesses. Unnatural causes such as suicide and accidents account for only a portion of this premature mortality1 Research is beginning to identify that mood disordered patients have a higher incidence of metabolic syndrome, an illness characterized by dyslipidemia, impaired glucose tolerance, hypertension and obesity.2 Metabolic syndrome is associated with an increased risk for a variety of physical illnesses. Hypothesis: Never treated patients with mood disorders have preexisting elevations in the prevalence of the component variables of metabolic syndrome. Central obesity will be especially elevated, predicting increased premature mortality. Methods: We assessed never treated patients with mood disorders for metabolic syndrome and its component variables. Patients were assessed at baseline and followed up at 6-month intervals. All psychiatric pharmacotherapy was documented. Body mass index (BMI) was also obtained and the percentage of deaths attributable to overweight and obesity was calculated using the population attributable risk (PAR). [PAR= ∑[P (RR-1)/RR] Results: Prior to the initiation of treatment, patients did not differ from population norms with respect to metabolic syndrome or BMI. At 2-year follow-up, BMI had increased for unipolar patients 2.02 points and 1.92 points for bipolar patients. (p < .001) This increase in BMI predicted an increase in mortality of 19.4%. Conclusion: An increase in visceral obesity is often the first component of metabolic syndrome to appear and may indicate the initiation of this disease process prematurely in this group. The increase in BMI places patients with mood disorders at risk for premature mortality and indicates a need for early intervention. References 1.Osby U, Brandt L, Correia N, Ekbom A & Sparen P. Excess mortability in bipolar and Unipolar disorder rin Sweden. Archives of General Psychiatry, 2001;58: 844-850 2.Toalson P, Saeeduddin A, Hardy T & Kabinoff G. The metabolic syndrome in patients with severe mental illness. Journal of Clinical Psychiatry, 2004; 6(4): 152-158


2021 ◽  
Vol 8 ◽  
Author(s):  
Zhuo-Ming Huang ◽  
Wen-Rong Chen ◽  
Qi-Wen Su ◽  
Zhuo-Wen Huang

Background: The metabolic syndrome (MS) is significantly associated with the risk of incident heart failure (HF). However, there are still great controversies about the impact of MS on the prognosis in patients with established HF. This meta-analysis aimed to ascertain the effect of MS on the prognosis in patients with HF.Methods: We searched multiple electronic databases, including PubMed, Opengrey, EMBASE, and Cochran Library, for potential studies up to February 15, 2021. Observational studies that reported the impact of MS on the prognosis in patients with established HF were included for meta-analysis.Results: Ten studies comprising 18,590 patients with HF were included for meta-analysis. The median follow-up duration of the included studies was 2.4 years. Compared with HF patients without MS, the risk of all-cause mortality and cardiovascular mortality was not increased in HF with MS (HR = 1.04, 95% CI = 0.88–1.23 for all-cause mortality; HR = 1.66, 95% CI = 0.56–4.88 for cardiovascular mortality, respectively). However, there was a significant increase in composited cardiovascular events in the HF patients with MS compared with those without MS (HR = 1.73, 95% CI = 1.23–2.45).Conclusions: In patients with established HF, the presence of MS did not show an association on the risk of all-cause mortality or cardiovascular mortality, while it may increase the risk of composite cardiovascular events.


Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3068-3068
Author(s):  
Marjolein van Waas ◽  
Sebastian Neggers ◽  
Rob Pieters ◽  
M.M. Van Den Heuvel

Abstract Abstract 3068 Poster Board III-5 Introduction Adult survivors of childhood cancer have been reported to have an increased risk of late sequels. A cluster of abnormalities that contribute to the metabolic syndrome may be expressed at a higher level and therefore result in an increased risk for diabetes mellitus and cardiovascular diseases. Patients and Methods We investigated a single centre cohort of 500 adult survivors (228 females) of childhood cancer, median age 28 years (range 18-59 years) and median follow-up time 19 years (range 6–49 years). This cohort included 164 acute lymphoblastic leukaemia (ALL) survivors (75 females). We measured total cholesterol, high-density lipoprotein-cholesterol (HDL), systolic and diastolic blood pressure, body mass index and the prevalence of diabetes mellitus. Data from the Dutch epidemiologic MORGEN-study were used to calculate standard deviation scores as normative values. Results The criteria of the metabolic syndrome were met in 13% of the total cohort. ALL survivors treated with cranial irradiation had an increased risk of developing the metabolic syndrome compared to ALL survivors not treated with cranial irradiation (23% vs. 7%, P=0.011). ALL survivors who received CRT had higher total cholesterol levels compared to ALL survivors who did not (mean SDS 0.38 vs. mean SDS –0.05, P=0.027), whereas their HDL levels did not differ. Also, ALL survivors treated with CRT were more often hypertensive compared to ALL survivors not treated with CRT (22% vs. 10%, P=0.036) and more often overweight (59% vs. 34%, P=0.003), however they were not more often obese (12% vs. 9%, ns). Conclusions Adult survivors of childhood cancer, especially ALL survivors treated with cranial irradiation, are at increased risk of developing the metabolic syndrome. This increased risk is probably determined by higher prevalence of overweight and hypertension in ALL survivors. Disclosures No relevant conflicts of interest to declare.


2019 ◽  
Vol 123 (1) ◽  
pp. 1-22 ◽  
Author(s):  
‘Mo’ez Al-Islam’ E. Faris ◽  
Haitham A. Jahrami ◽  
Joud Alsibai ◽  
Asma A. Obaideen

AbstractStudies on the impact of Ramadan diurnal intermittent fasting (RDIF) on the metabolic syndrome (MetS) components among healthy Muslims observing Ramadan month have yielded contradictory results. This comprehensive meta-analysis aimed to obtain a more stable estimate of the effect size of fasting during Ramadan on the MetS components, examine variability among studies, assess the generalisability of reported results and perform subgroup analyses for associated factors. We searched the CINAHL, Cochrane, EBSCOhost, Google Scholar, ProQuest Medical, PubMed/MEDLINE, ScienceDirect, Scopus and Web of Science databases for relevant studies published from 1950 to March 2019. The MetS components analysed were: waist circumference (WC), systolic blood pressure (SBP), fasting plasma/serum glucose (FG), TAG, and HDL-cholesterol. We identified eighty-five studies (4326 participants in total) that were conducted in twenty-three countries between 1982 and 2019. RDIF-induced effect sizes for the MetS components were: small reductions in WC (no. of studies K = 24, N 1557, Hedges’ g = −0·312, 95 % CI −0·387, −0·236), SBP (K = 22, N 1172, Hedges’ g = −0·239, 95 % CI −0·372, −0·106), FG (K = 51, N 2318, Hedges’ g = −0·101, 95 % CI −0·260, 0·004) and TAG (K = 63, N 2862, Hedges’ g = −0·088, 95 % CI −0·171, −0·004) and a small increase in HDL-cholesterol (K = 57, N 2771, Hedges’ g = 0·150, 95 % CI 0·064, 0·236). We concluded that among healthy people, RDIF shows small improvement in the five MetS components: WC, SBP, TAG, FG and HDL.


2002 ◽  
Vol 282 (2) ◽  
pp. H630-H635 ◽  
Author(s):  
Stacy D. Beske ◽  
Guy E. Alvarez ◽  
Tasha P. Ballard ◽  
Kevin P. Davy

The influence of excess total and abdominal adiposity on cardiovagal baroreflex gain remains unclear. We tested the hypotheses that cardiovagal baroreflex gain would be reduced in men with 1) higher [higher fat (HF), mass >20 kg, n = 11] compared with lower [lower fat (LF), mass <20 kg, n = 10] levels of total body and abdominal fat and 2) higher abdominal visceral fat (HAVF; n = 10) compared with total body weight- and subcutaneous fat-matched peers with lower abdominal visceral fat (LAVF; n = 7) levels. To accomplish this, we measured cardiovagal baroreflex gain (modified Oxford technique), body composition (dual energy X-ray absorptiometry), and abdominal visceral and subcutaneous fat (computed tomography) in sedentary men (age, 18–40 yr; body mass index, <34.9 kg/m2) across a wide range of adiposity. Cardiovagal baroreflex gain was significantly lower in HF compared with LF (14.3 ± 2.8 vs. 21.4 ± 2.8 ms/mmHg, respectively). In addition, cardiovagal baroreflex gain was lower in HAVF compared with LAVF (13.0 ± 2.0 vs. 21.4 ± 3.6 ms/mmHg, P< 0.05). Therefore, the results of the present study indicate that cardiovagal baroreflex gain is reduced in men with elevated total body and abdominal fat mass. The reduced cardiovagal baroreflex gain in these individuals appears to be linked to their higher level of abdominal visceral fat. Importantly, reduced cardiovagal baroreflex gain may contribute to the increased risk of cardiovascular disease observed in men with the metabolic syndrome.


2019 ◽  
Vol 65 (4) ◽  
pp. 488-497
Author(s):  
Anastasiya Kishkina ◽  
Larisa Kolomiets ◽  
Natalya Yunusova

This literature review is devoted to the relationship of the structural features of the metabolic syndrome in proliferative processes and endometrial cancer (EC), and the identification of the relationship between the individual components of the metabolic syndrome and the development of endometrial cancer. The metabolic syndrome is currently a global medical and social problem, which is due to the wide spread of this symptom complex in the population. Today, the main concept of this syndrome is the concept of a cluster of components associated with an increased risk of developing type 2 diabetes and cardiovascular diseases. It is known that an increase in the mass of adipose tissue above the norm by 20% or more leads to dysfunction of the hypothalamic-pituitary-ovarian system. At the same time, the risk of RE on the background of metabolic syndrome increases by 2-3 times. This probability also largely depends on the severity of proliferation in the endometrium, which is caused by the presence of dyshormonal and metabolic disorders. In addition, this is due to the aggravation of insulin resistance, an increase in the production of androgens by the ovaries, the formation of stable anovulation and, as a result, the progression of pathological changes in the endometrium. With the onset of peri - and postmenopausal endometrial hyperplasia in about 50% of cases progressing to malignant pathology. The role of the system of insulin-like growth factors, adipokines secreted from visceral adipocytes of free fatty acids, local estrogen formation and hyperandrogenization is also recognized in creating a predisposition to the EC formation. According to the results of the study of the functioning of the autocrine-paracrine system of adipose tissue, the risk of endometrial proliferative processes is higher at low levels of adiponectin and high levels of insulin. All this indicates the feasibility of monitoring the status of adipose tissue.


2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Faloia Emanuela ◽  
Michetti Grazia ◽  
De Robertis Marco ◽  
Luconi Maria Paola ◽  
Furlani Giorgio ◽  
...  

The metabolic syndrome is a complex of clinical features leading to an increased risk for cardiovascular disease and type 2 diabetes mellitus in both sexes. Visceral obesity and insulin resistance are considered the main features determining the negative cardiovascular profile in metabolic syndrome. The aim of this paper is to highlight the central role of obesity in the development of a chronic low-grade inflammatory state that leads to insulin resistance, endothelial and microvascular dysfunctions. It is thought that the starting signal of this inflammation is overfeeding and the pathway origins in all the metabolic cells; the subsequent increase in cytokine production recruits immune cells in the extracellular environment inducing an overall systemic inflammation. This paper focuses on the molecular and cellular inflammatory mechanisms studied until now.


2009 ◽  
Vol 26 (2) ◽  
pp. 75-83 ◽  
Author(s):  
Douwe Pons ◽  
Pascalle S. Monraats ◽  
Aeilko H. Zwinderman ◽  
Moniek P. M. de Maat ◽  
Pieter A. F. M. Doevendans ◽  
...  

Variation in theNOS3gene has been related to the development of restenosis. The Glu298Asp polymorphism has previously been investigated for its effect on NO levels and the development of restenosis. However, the variability of findings gave rise to the hypothesis that the functional significance of this polymorphism may only become manifest under conditions of endothelial dysfunction. Since patients with the metabolic syndrome are known to have endothelial dysfunction, we aimed to investigate if the significance ofNOS3polymorphisms may depend on the presence of the metabolic syndrome.We examined the impact of the -949 A/G, the -716 C/T and the Glu298Asp polymorphisms in theNOS3gene on the risk of clinical restenosis in a previously described subpopulation of the GENDER-study, a multicenter prospective study design that enrolled consecutive patients after successful PCI. This subpopulation consisted of 901 patients of whom sufficient data were available to establish absence or presence of the metabolic syndrome. Of these patients, 448 had the metabolic syndrome. Clinical restenosis, defined as target vessel revascularization (TVR), was the primary endpoint.We demonstrated that the minor -949G, -716T and 298Asp alleles were associated with a significantly increased risk of TVR in patients with the metabolic syndrome (HR: 1.58 [95%CI: 1.04–2.40], HR: 1.95 [95%CI: 1.02–3.70] and HR: 1.67 [95%CI: 1.09–2.54], respectively). In the group without the metabolic syndrome we observed no association between the three polymorphisms and TVR.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Hyo-Jeong Ahn ◽  
Kyung-Do Han ◽  
Eue-Keun Choi ◽  
Jin-Hyung Jung ◽  
Soonil Kwon ◽  
...  

Abstract Background The metabolic syndrome (MetS) and its components are associated with the development of atrial fibrillation (AF). However, the impact of time-burden of MetS on the risk of AF is unknown. We investigated the effect of the cumulative longitudinal burden of MetS on the development of AF. Methods We included 2 885 189 individuals without AF who underwent four annual health examinations during 2009–2013 from the database of the Korean national health insurance service. Metabolic burdens were evaluated in the following three ways: (1) cumulative number of MetS diagnosed at each health examination (0–4 times); (2) cumulative number of each MetS component diagnosed at each health examination (0–4 times per MetS component); and (3) cumulative number of total MetS components diagnosed at each health examination (0 to a maximum of 20). The risk of AF according to the metabolic burden was estimated using Cox proportional-hazards models. Results Of all individuals, 62.4%, 14.8%, 8.7%, 6.5%, and 7.6% met the MetS diagnostic criteria 0, 1, 2, 3, and 4 times, respectively. During a mean follow-up of 5.3 years, the risk of AF showed a positive association with the cumulative number of MetS diagnosed over four health examinations: adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) of 1, 2, 3, and 4 times compared to 0 times were 1.18 (1.13–1.24), 1.31 (1.25–1.39), 1.46 (1.38–1.55), and 1.72 (1.63–1.82), respectively; P for trend < 0.001. All five components of MetS, when diagnosed repeatedly, were independently associated with an increased risk of AF: adjusted HR (95% CI) from 1.22 (1.15–1.29) for impaired fasting glucose to 1.96 (1.87–2.07) for elevated blood pressure. As metabolic components were accumulated from 0 to 20 counts, the risk of AF also gradually increased up to 3.1-fold (adjusted HR 3.11, 95% CI 2.52–3.83 in those with 20 cumulative components of MetS), however, recovery from MetS was linked to a decreased risk of AF. Conclusions Given the positive correlations between the cumulative metabolic burdens and the risk of incident AF, maximal effort to detect and correct metabolic derangements even before MetS development might be important to prevent AF and related cardiovascular diseases.


2020 ◽  
Author(s):  
Hyo-Jeong Ahn ◽  
Kyung-Do Han ◽  
Eue-Keun Choi ◽  
Jin-Hyung Jung ◽  
Soonil Kwon ◽  
...  

Abstract Background: The metabolic syndrome (MetS) and its components are associated with the development of atrial fibrillation (AF). However, the impact of time-burden of MetS on the risk of AF is unknown. We investigated the effect of the cumulative longitudinal burden of MetS on the development of AF. Methods: We included 2 885 189 individuals without AF who underwent four annual health examinations during 2009–2013. Metabolic burdens were evaluated in the following three ways: (1) cumulative number of MetS diagnosed at each health examination (0–4 times); (2) cumulative number of each MetS component diagnosed at each health examination (0–4 times per MetS component); and (3) cumulative number of total MetS components diagnosed at each health examination (0 to a maximum of 20). The risk of AF according to the metabolic burden was estimated using Cox proportional-hazards models.Results: Of all individuals, 62.4%, 14.8%, 8.7%, 6.5%, and 7.6% met the MetS diagnostic criteria 0, 1, 2, 3, and 4 times, respectively. During a mean follow-up of 5.3 years, the risk of AF showed a positive association with the cumulative number of MetS diagnosed over four health examinations: adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) of 1, 2, 3, and 4 times compared to 0 times were 1.18 (1.13–1.24), 1.31 (1.25–1.39), 1.46 (1.38–1.55), and 1.72 (1.63–1.82), respectively; P for trend < 0.001. All five components of MetS, when diagnosed repeatedly, were independently associated with an increased risk of AF: adjusted HR (95% CI) from 1.22 (1.15–1.29) for impaired glucose intolerance to 1.96 (1.87–2.07) for elevated blood pressure. As metabolic components were accumulated from 0 to 20 counts, the risk of AF also gradually increased up to 3.1-fold (adjusted HR 3.11, 95% CI 2.52–3.83 in those with 20 cumulative components of MetS), however, recovery from MetS was linked to a decreased risk of AF. Conclusions: Given the positive correlations between the cumulative metabolic burdens and the risk of incident AF, maximal effort to detect and correct metabolic derangements even before MetS development might be important to prevent AF and related cardiovascular diseases.


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