Individual Syndrome Components Research Articles

Abdominal obesity is essential for the risk of venous thromboembolism in the metabolic syndrome: the Tromsø study.

The metabolic syndrome is a cluster of cardiovascular risk factors, including abdominal obesity, hypertension, dyslipidemia and insulin resistance, associated with increased risk of cardiovascular diseases and all cause mortality. The purpose of the study was to assess the impact of the metabolic syndrome, and its individual components, on the risk of venous thromboembolism (VTE) in a prospective population-based study. Individual components of the metabolic syndrome were registered in 6170 subjects aged 25-84 years in the Tromsø Study in 1994-1995, and first ever VTE events were registered until 1 September 2007. The metabolic syndrome was present in 21.9% (1350 subjects) of the population. There were 194 validated first VTE events (2.92 per 1000 person-years) during a mean of 10.8 years of follow-up. Presence of metabolic syndrome was associated with increased risk of VTE (HR, 1.65; 95% CI, 1.22-2.23) in age- and gender-adjusted analysis. The risk of VTE increased with the number of components in the metabolic syndrome (P < 0.001). Abdominal obesity was the only component significantly associated with VTE in multivariable analysis including age, gender, and the individual components of the syndrome (HR, 2.03; 95% CI, 1.49-2.75). When abdominal obesity was omitted as a diagnostic criterion, none of the other components, alone or in cluster, was associated with increased risk of VTE. Our study provides evidence for the metabolic syndrome as a risk factor for TE. Abdominal obesity appeared to be the pivotal risk factor among the individual components of the syndrome.

The Metabolic Syndrome

See related article, pages 1078–1083. The metabolic syndrome is a clustering of metabolic abnormalities, which include insulin resistance or diabetes, obesity, hypertension, and dyslipidemia. Although the mechanisms of the underlying abnormalities remain to be clarified, the pathogenesis includes both genetic predisposition and modifiable risk factors such as sedentary lifestyle and dietary intake. Recent estimates suggest that approximately 24% of US adults have the metabolic syndrome.1 In several studies, the metabolic syndrome has been shown to increase the risk of cardiovascular diseases2; however, the strength of its association with stroke is weaker than that for coronary heart disease.3 In the guidelines for the primary prevention of stroke from the American Heart Association/American Stroke Association, the metabolic syndrome is listed as a less–well-documented risk factor.4 But, given the high prevalence of the metabolic syndrome, studying its association with stroke is certainly relevant for 2 reasons: first, to obtain a better etiologic understanding of the causes of stroke; second, to identify individuals at high risk for stroke. This translates into 2 distinct scientific questions: is the metabolic syndrome by itself a risk factor for stroke?; and can we predict which individuals are at increased risk for stroke based on information about the metabolic syndrome? To answer these questions from observational data, one needs 2 distinct model-building strategies that require differences in assumptions of biological associations and statistical considerations.5,6 In this issue of Stroke ,7 Wang and …

Prevention of Cardiovascular Complications of the Metabolic Syndrome: Focus on Pharmacotherapy

The metabolic syndrome increases the risk of atherothrombotic cardiovascular disease (CVD) and diabetes. In turn, diabetes promotes the development of atheroma and is regarded as a coronary heart disease risk equivalent. A multifactorial therapeutic strategy is advocated for patients with the metabolic syndrome to improve cardiovascular risk factor profiles and to reduce the chances of developing type 2 diabetes. Individual components of the syndrome must be addressed using safe, efficacious, and cost-effective measures. There is general agreement that lifestyle modifications, including control of body weight, avoidance of central adiposity, adoption of an antiatherogenic diet, and regular physical activity, are crucial. However, as the magnitude of the individual components of the metabolic syndrome increases with time, lifestyle measures are often insufficient. An individual with metabolic syndrome will often require drug treatment for hyperglycemia, atherogenic dyslipidemia, and high blood pressure, together with antiplatelet therapy. Reducing the need for polypharmacy is an increasingly important consideration for clinicians and the pharmaceutical industry; to date, no single therapy has emerged that targets the root cause(s) of the syndrome. HMG-CoA reductase inhibitors are important agents that reduce CVD morbidity and mortality, in people with impaired fasting glucose or metabolic syndrome. Selective cannabinoid receptor antagonists appear promising because they improve or attenuate several key defects of the syndrome. Thiazolidinediones and metformin are presently licensed for treatment of type 2 diabetes but may prove to have a broader role in future. Novel insulin-sensitizing drugs are under investigation. Drugs that act to prevent or reverse endothelial dysfunction may be of particular utility in preventing cardiovascular disease, especially if initiated before tissue damage has become irreversible. Insulin therapy, which has antiinflammatory and endothelial protective properties, has been shown to reduce morbidity and mortality in high-risk nondiabetic patients during critical illness. Potential synergy between different classes of drugs with metabolic and/or cardiovascular protective properties merits further investigation.