Cardiovascular Metabolic Syndrome Research Articles

Development of abdominal fat and incipient metabolic syndrome in young healthy men exposed to long-term stress

The sympathetic nervous system may be involved in the pathophysiology of insulin resistance and metabolic cardiovascular syndrome in young men. The aim was to study the effects of long-term stress on different features of the metabolic syndrome (MES) in formerly non-obese healthy young males during 5 months of defined conditions. Sixteen healthy male sailors (mean age 36.5 (SD)+/-7 years) participating in a sailing race around the world were recruited for the study. Investigations were done before the start and at stop overs after finishing laps 1, 2 and 4 (1, 2(1/2) and 5 months, respectively). Anthropometric and blood pressure data as well as biochemical data associated with MES were substantiated. Food intake and exercise were chartered and largely controlled. A mean weight loss of 4.5+/-2 kg (P<0.005), comprising both fat and lean body mass, was recorded during the first lap. Subsequently after 5 months, a weight gain, mainly consisting of 1.2+/-1.1 kg body fat (P<0.05), took place, concomitantly with a protein mass drop of 0.6+/-1.1 kg (P<0.05). The body fat gain accumulated on the abdominal region. Elevated blood levels of HbA1c, insulin and the triglycerides/high-density lipoprotein ratio were also observed during the race. Likewise heart rate and systolic blood pressure increased slightly but to a statistically significant extent. Non-obese healthy young men exposed to long-term stress developed abdominal obesity and signs of a metabolic syndrome in embryo, also emphasized by biochemical and blood pressure alterations. It is suggested that long-term and sustained stress activation might be an additional risk factor for the development of MES, even after control of dietary and exercise habits.

Metabolic syndrome in women with polycystic ovary syndrome

The prevalence of the metabolic syndrome in polycystic ovary syndrome (PCOS) is high across all age groups. Dyslipidemia, particularly a decreased high-density lipoprotein cholesterol level, also is common in women with PCOS.

Cardiovascular metabolic syndrome – an interplay of, obesity, inflammation, diabetes and coronary heart disease

Cardiovascular disease is currently one of the biggest causes of morbidity and mortality facing humanity. Such a paradigm shift of disease pattern over the last century has only worsened due to the alarming global prevalence of obesity and type 2 diabetes. In recent years there is increasing focus on inflammation as one of the key players in the patho-physiology of these disorders. In addition to these overt risk factors new research is unraveling the significance of a constellation of early metabolic abnormalities that include weight gain, insulin resistance, prehypertension and a specific pattern of dyslipidaemia. There exists a complex interrelationship of these various metabolic disorders and their effect on cardiovascular system. Simplified explanation can be that inflammation increases insulin resistance, which in turn leads to obesity while perpetuating diabetes, high blood pressure, prothrombotic state and dyslipidaemia. While inflammation and insulin resistance have direct adverse effects on cardiac muscle, these metabolic abnormalities as a whole cause causes cardiovascular complications; warranting a multi pronged therapeutic and preventive approach for the 'Cardiovascular Metabolic Syndrome' as an entity.

Evidence for an Association Between Metabolic Cardiovascular Syndrome and Coronary and Aortic Calcification Among Women With Polycystic Ovary Syndrome

Evidence for an Association Between Metabolic Cardiovascular Syndrome and Coronary and Aortic Calcification Among Women With Polycystic Ovary Syndrome

Effect of Insulin on NO Production by Monocytes from Patients with Metabolic Cardiovascular Syndrome

Basal and insulin-induced production of NO by monocytes significantly increased in patients with metabolic cardiovascular syndrome. Plasma insulin concentration in these patients was below the control. No intergroup differences were found in C-peptide concentration. A negative correlation was revealed between insulin-induced NO production by monocytes and C-peptide/insulin ratio in patients. The role of monocytes on the regulation of vascular tone via NO production in patients with metabolic cardiovascular syndrome is discussed.

Racial difference in circulating sex hormone–binding globulin levels in prepubertal boys

Racial differences in disease risk (eg, osteoporosis, metabolic cardiovascular syndrome, and prostate cancer) may arise partly on a hormonal basis. While reports of racial differences in gonadal steroid hormone levels in middle-aged men have produced conflicting results, there is evidence that high sex hormone–binding globulin (SHBG) and estradiol levels are more common among young adult African American men than white men. To determine whether this difference relates to pituitary-testicular functioning or to other factors, we conducted a cross-sectional study of 47 healthy prepubertal African American and white boys aged 5 to 9 years at the time of their annual school physical examination. Height, weight, blood pressure, waist and hip circumference, and Tanner staging were determined, and a fasting blood sample was obtained. The African Americans studied were slightly older than the whites (mean ± SD, 82.4 ± 15.0 vs 70.5 ± 10.3 months, P = .003). African Americans were also slightly taller and heavier and had a lower waist-to-hip ratio, but these differences could be explained by the difference in age. Mean SHBG levels were 25% higher ( P = .15) in African Americans than in whites (197 ± 104 vs 157 ± 79 nmol/L), and when adjusted for age, values were 46 nmol/L higher among African Americans. The fifth quintile for SHBG (values > 245 nmol/L) included 1 (4.2%) of 24 whites and 8 (35%) of 23 African Americans studied ( P = .003). There was no significant correlation between age, body mass index, waist circumference, or fasting insulin and SHBG. Total testosterone, the free androgen index, and dehydroepiandrosterone increased with age in both groups, but after adjusting for age, no racial differences were found. Estradiol, estrone, and inhibin B levels, as well as systolic and diastolic blood pressures, were also comparable in both groups. We conclude that high levels of SHBG are more common among African American than in white boys and hypothesize that this difference and its effect on the ratio between bound and free steroid hormones may contribute to racial differences in disease risk in adult men.

Evidence for an Association between Metabolic Cardiovascular Syndrome and Coronary and Aortic Calcification among Women with Polycystic Ovary Syndrome

Women with polycystic ovary syndrome (PCOS) exhibit an adverse cardiovascular risk profile, characteristic of the metabolic cardiovascular syndrome (MCS). The aim of this study was to determine the prevalence of coronary artery (CAC) and aortic (AC) calcification among middle-aged PCOS cases and controls and to explore the relationship among calcification, MCS, and other cardiovascular risk factors assessed 9 yr earlier. This was a prospective study of 61 PCOS cases and 85 similarly aged controls screened in 1993-1994 for risk factors and reevaluated in 2001-2002. The main outcome measures were CAC and AC, measured by electron beam tomography. Women with PCOS had a higher prevalence of CAC (45.9% vs. 30.6%) and AC (68.9% vs. 55.3%) than controls. After adjustment for age and body mass index, PCOS was a significant predictor of CAC (odds ratio = 2.31; P = 0.049). PCOS subjects were also 4.4 times more likely to meet the criteria for MCS than controls. High-density lipoprotein cholesterol and insulin appeared to mediate the PCOS influence on CAC. Interestingly, total testosterone was an independent risk factor for AC in all subjects after controlling for PCOS, age, and body mass index (P = 0.034). We conclude that women with PCOS are at increased risk of MCS and demonstrate increased CAC and AC compared with controls. Components of MCS mediate the association between PCOS and CAC, independently of obesity.

Mechanisms of cardiovascular changes in an experimental model of syndrome X and pharmacological intervention on the renin-angiotensin-system.

Various cardiovascular risk factors and disease states similar to those present in type 2 diabetic patients also seem to be present in non-diabetic individuals. This cluster of risk factors has been called syndrome X, also known as metabolic cardiovascular syndrome or insulin resistance syndrome. Vascular wall components changes, including endothelial dysfunction and vascular smooth muscle cell (VSMC) migration and proliferation, could be involved in the cardiovascular alterations associated with this state. Fructose fed rats (FFR) provide a model of dietary-induced insulin resistance, which has been used to assess the pathophysiological mechanisms of the metabolic and cardiovascular changes associated to the syndrome X. FFR have hyperinsulinemia, insulin resistance (altered glucose tolerance test) and hypertriglyceridemia; they also develop moderate hypertension and cardiac hypertrophy. This has been confirmed in male rats of different strains, such as Wistar and Sprague-Dawley, chronically fed with a 60% fructose-chow or 10% fructose in the drinking water. At different levels of the cardiovascular system, FFR exhibit changes in the nitric oxide generation system and in primary cultured proliferation of VSMC from conduit and resistance arteries. These abnormalities were normalized by long-term treatment with pharmacological agents acting on the renin-angiotensin system (RAS), such as angiotensin converting-enzyme inhibitors or angiotensin-AT(1) receptor antagonists, that also lowered blood pressure to control levels and reversed cardiac hypertrophy. Evidence suggests an important role for the RAS in the pathogenic mechanisms involved in this model of syndrome X. Furthermore, beneficial pharmacological intervention seems to be mediated by AT(2) receptors and kinins.

Oxygen-dependent processes in monocytes and metabolic risk factors for atherogenesis.

Oxygen-dependent processes in peripheral blood monocytes were intensified in patients with metabolic cardiovascular syndrome. This was manifested in increased production of O(2)(*-) and NO. Among metabolic factors (cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triacylglycerols, glucose, etc.), products of glycosylation (fructosamine) and plasma triacylglycerols were most potent in modulating generation of O(2)(*-) and NO by monocytes.

Increased C-reactive protein levels in the polycystic ovary syndrome: a marker of cardiovascular disease.

The polycystic ovary syndrome (PCOS), one of the most common reproductive abnormalities, shares some components of the metabolic cardiovascular syndrome. Therefore, PCOS patients may represent the largest group of women at high risk for the development of early-onset cardiovascular disease (CVD) and/or diabetes. C-reactive protein (CRP) is a strong independent predictor of future CVD and/or stroke. Only one small published study has looked for such an association (17 PCOS patients vs. 15 controls). The objective of this study was to compare the levels of CRP and other risk factors of CVD in a large group of PCOS patients and controls. CRP measurements were undertaken in 116 PCOS patients and 94 body mass index-matched controls with regular menstrual cycles. Whereas 36.8% of the PCOS patients had CRP levels above 5 mg/liter, only 9.6% of the controls exhibited high CRP levels (P < 0.001). The mean +/- SD was 5.46 +/- 7.0 in the PCOS group vs. 2.04 +/- 1.9 mg/liter in the control (P < 0.001). The body mass index, white blood cell count, TSH, glucose, cholesterol, and homocysteine levels were not significantly different between the two groups. CRP levels are elevated in patients with PCOS and may be a marker of early cardiovascular risk in these patients. High CRP levels may explain why some PCOS women may possibly be at an increased risk for the development of early-onset CVD. Consequently, whether treatment regimens directed toward lowering CVD risk factors should be more aggressive for those PCOS women with increased CRP levels, awaits further clinical experience.

High screening blood pressure is related to sympathetic nervous system activity and insulin resistance in healthy young men

The cardiovascular metabolic syndrome is characterized by the presence of several cardiovascular risk factors, including blood pressure (BP) elevation. We aimed to study the relation between mental stress, plasma catecholamines, BP and BP responses to mental stress in healthy young Caucasian men selected from different levels of screening BP. We included 98 men with high and 22 men with normal screening BP. They were examined at baseline in the laboratory, during a hyperinsulinemic, isoglycemic glucose clamp and during mental stress. At baseline in the laboratory, the men with high screening BP were characterized by elevated BP (p < 0.005) and plasma catecholamines (p < 0.05), but unaltered serum lipid levels compared to men with normal screening BP. After 2 h rest the differences almost disappeared, but could be reproduced during a mental arithmetic stress test. The men with elevated screening BP had significantly higher fasting glucose (p = 0.01) and lower insulin sensitivity (p < 0.005). In a multiple regression model, norepinephrine during mental stress (R2 = 0.10, p < 0.05) was the main variable to retrospectively explain allocation to the normal or high screening BP group. In conclusion, young healthy men with elevated screening BP are characterized by increased sympathetic activity and insulin resistance. Norepinephrine during mental stress is the main variable to explain allocation to the normal or elevated screening BP group. We have shown that one single screening BP measurement predicts insulin resistance and elevated fasting glucose in this cohort.

Role of salt sensitivity, blood pressure, and hyperinsulinemia in determining high upper normal levels of urinary albumin excretion in a healthy adult population

Background The objective of this study was to investigate the role of blood pressure (BP), salt sensitivity (SS), and the cardiovascular metabolic syndrome in determining the urinary albumin excretion (UAE) in glucose-tolerant, normoalbuminuric (<20 mg/day) healthy adults. Methods and results We evaluated 177 healthy subjects (age, 38.3 ± 0.9 years; weight, 75.2 ± 1.1 kg; body mass index, 28.8 ± 0.4 kg/m 2; systolic BP, 117 ± 1 mm Hg; diastolic BP, 77.5 ± 0.8 mm Hg; UAE, 8.2 ± 0.3 mg/24 h). Subjects with UAE levels of 15 to 20 mg/day had higher systolic BP, diastolic BP, and pulse pressures than those with UAE levels less than 15 mg/day ( P < .0001). Hypertension (HT) and SS were more prevalent in the high normal UAE group (15 to 20 mg/day) than in groups with lower UAE (47% v 8% for HT and 67% v 24% for SS). In normotensives ( n = 156), no differences in BP were observed among the different UAE strata; yet, the prevalence of SS was greater in the high (57%) compared to the low normal (17% to 21%) UAE groups. Similar levels of UAE, BP, and similar prevalence of SS were found in men with and without abdominal obesity, despite the fact that obesity was associated with hypertriglyceridemia and hyperinsulinemia. Conclusions In healthy normoalbuminuric adults, high normal UAE is associated with SS in normotensives and with SS and higher BP in a mixed population (88% normotensive and 12% hypertensive). Abdominal obesity, hypertriglyceridemia, and hyperinsulinemia were not related to UAE. Therefore, UAE levels of 15 to 20 mg/day should be accepted as microalbuminuria, and these subjects may benefit from early intervention (ie, salt restriction and BP lowering).

Relationship of basic parameters of metaboliccardiovascular syndrome to the degree of carbohydrate metabolic disorders and to the severity of abdominal obesity in males

To study the impact of the degree of carbohydrate metabolic disorders and the severity of abdominal obesity on the basic parameters of the metabolic cardiovascular syndrome, 102 males with had higher body weight not more than first-degree obesity and were insulin resistant with evolving diabetes mellitus were examined The findings suggest that the degree of insulin resistance determines the magnitude of poor changes in lipid metabolism in the metabolic syndrome (without development of diabetes mellitus and in not more than first-degree obesity) to a greater extent than the severity of abdominal obesity does

Effects of topiramate on the progression of experimental metabolic cardiovascular syndrome

Effects of topiramate on the progression of experimental metabolic cardiovascular syndrome

Clustering of cardiovascular risk factors among Omani adults

To determine the distribution and correlates of clustering of cardiovascular disease (CVD) risk factors, data from the Oman National Health Survey, 2000 were analysed. Based on demographic data (blood pressure, fasting blood glucose, serum cholesterol, weight, height, waist and hip measurements), 5660 subjects were grouped according to how many of four CVD risk factors (hypertension, high cholesterol, diabetes, overweight/obesity) they had. We found that 72% of subjects had less than one risk factor and 2% had all four. Older age exacerbated risk, while living in rural areas or being single was protective. Metabolic cardiovascular syndrome is a public health problem in Oman. Increasing awareness in healthcare providers and the wider population by comprehensive dissemination of the survey results is crucial.

Effects of statins on the vasculature: implications for aggressive lipid management in the cardiovascular metabolic syndrome

The cardiovascular metabolic syndrome is a family of risk factors that predispose patients to develop diabetes and cardiovascular disease. Indeed, macrovascular, not microvascular, disease is the leading cause of death in these patients. The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) exert both direct and indirect (cholesterol-lowering) effects on the vasculature. Clinical trials have shown that these agents reduce cardiovascular disease and cerebrovascular disease in persons with diabetes. However, their beneficial effects on diabetic dyslipidemia do not account for all of the observed risk reduction. Positive effects on nitric oxide metabolism, inflammation, coagulability, and adhesion of cells to the vascular endothelium likely contribute to the mechanism of action of these agents. These pleiotropic effects of statins on the vasculature will be discussed in this review.

Obesity and its potential mechanistic basis.

Obesity plays a central role in the development of the thrifty phenotype. The metabolic disturbances of the cardiovascular metabolic syndrome, frequently ascribed to the thrifty phenotype, are rare in the absence of obesity and their expression is generally proportional to the size of the excess fat mass. Thus obesity interacts with early-life programming in the establishment of disease. Surprisingly, the evidence that fetal or infant diet leads to programming of obesity itself is rather weak, though this may be explained by the fact that life-style influences obscure the linkage between metabolic predisposition and maturity-onset obesity. This paper summarises the possible metabolic basis of obesity with special reference to those processes for which there are plausible mechanisms by which long-term programming may operate. It is concluded that the newly-emerging molecular discoveries in body weight regulatory systems point to the need for detailed studies of gene-environment interactions and life-course influences before we will fully understand the aetiology of complex phenotypes such as the metabolic syndrome.

Plasma insulin, leptin, and soluble TNF receptors levels in relation to obesity-related atherogenic and thrombogenic cardiovascular disease risk factors among men

Obesity is related to cardiovascular disease (CVD) morbidity and mortality, however, the mechanisms for the development of obesity-induced CVD risk remain unclear. Hyperinsulinemia and insulin resistance are considered key components in the metabolic cardiovascular syndrome and as independent risk factors for CVD. Plasma leptin and tumor necrosis factor-alpha (TNF-α), two adipocyte products, are also proposed to be associated with the development of CVD risk. The purpose of this study is to evaluate the association of plasma leptin, soluble TNF receptors (sTNF-R), and insulin levels as possible mediators of the effect of obesity on atherogenic and thrombogenic CVD risk factors among men. From the Health Professionals Follow-up Study (HPFS), we selected 268 men, aged 47–83 years, who were free of CVD, diabetes, and cancer (except non-melanoma skin cancer), and who had provided a fasting blood sample in 1994. We measured plasma insulin and leptin levels by radioimmunoassay and sTNF-R levels by ELISA. Men in the highest quintile of body mass index (BMI, mean=30.5 kg/m 2) were less physically active and had a more adverse cardiovascular lipid and homeostatic profile, as indicated by levels of insulin, triglyceride (TG), tissue plasminogen activator (t-PA) antigen levels, and apolipoprotein A1 (Apo-A1). In a multivariate regression model controlling for age, smoking, alcohol intake, physical activity and diet, BMI was inversely associated with HDL-cholesterol (HDL-C) and Apo-A1 and positively associated with TG, Apo-B and t-PA antigen levels. The associations between BMI and these CVD risk factors were only slightly changed after adjusting for leptin and/or sTNF-R; but were substantially attenuated after controlling for insulin levels. These data suggest that the association between obesity and biological predictors of CVD may be mediated through changes in plasma insulin, rather than leptin or sTNF-R levels. However, plasma leptin may still play a role in CVD through independent effects on lipid metabolism.

Metabolic cardiovascular syndrome after renal transplantation.

Cardiovascular disease (CVD) is the major cause of death in renal transplant recipients. Traditional risk factors like hypertension, dyslipidaemia and diabetes mellitus are common, but cannot completely account for the high prevalence of CVD in this population. The aim of the present study was to assess whether post-transplant glucose intolerance, defined as post-transplant diabetes mellitus, impaired glucose tolerance, or impaired fasting glucose, is associated with metabolic disturbances known to increase risk of cardiovascular disease, similar to what has been observed in the general population. One hundred and seventy-three consecutive patients were prospectively examined 10 weeks after transplantation. An oral glucose tolerance test was completed in 167 patients. Questionnaires, medical records, and the results of various blood tests were used to evaluate a number of known cardiovascular risk factors in all patients. Glucose intolerance was present in about one-half the recipients and was associated with age, a positive family history of ischaemic heart disease, acute rejection, higher levels of serum triglycerides, apolipoprotein B and 2-h insulin, and lower levels of serum HDL cholesterol. After adjustment for age and sex, lower HDL cholesterol (P=0.005), higher serum triglycerides (P<0.001), apolipoprotein B (P=0.039) and 2-h insulin (P<0.001) were still associated with post-transplant glucose intolerance. Ten weeks after renal transplantation glucose intolerance is associated with a clustering of cardiovascular risk factors and metabolic abnormalities, consistent with a post-transplant metabolic cardiovascular syndrome.

Metabolic effects of wheat fiber supplementation in diet in subjects with metabolic cardiovascular syndrome

Metabolic effects of wheat fiber supplementation in diet in subjects with metabolic cardiovascular syndrome