The metabolic cardiovascular syndrome (MS) is a common cluster of metabolic abnormalities (abdominal obesity, hypertension, dyslipidemia and carbohydrate metabolism disorders) that are related to insulin resistance and hyperinsulinemia and are associated with accelerated atherogenesis. Insulin excess is known to promote the development of the whole metabolic cascade. Recently it has been shown that the inflammatory and hemostatic abnormalities, immunological disorders, endothelial dysfunction, hyperhomocysteinemia and hyperuricemia are also important features of MS. Despite the numerous studies of MS its underlying cause is still not established. The dysfunction of visceral adipocytes (adiposopathy) might be genetically determined, and is considered nowadays as the main factor contributing to the development of the MS. Understanding the underlying mechanisms is of particular interest for prevention and target therapy of all the components of MS.

Arterial hypertension in patients with metabolic cardiovascular syndrome (MS) has a number of features which are of great theoretical and practical significance. It has been shown that hypertension is the most frequent component of MS and chronologically follows abdominal obesity while clinical manifestations of atherosclerosis and carbohydrate metabolism disturbances develop much later. In addition, the disorders of hypothalamic-pituitary-adrenal axis contribute to the development of arterial hypertension in patients with abdominal obesity. Besides the abnormalities of central regulatory mechanisms, increased sympathetic tone, insulin resistance and hyperinsulinemia, functional state of adipose tissue is an established important factor for the development of systemic hypertension in patients with abdominal obesity, and in some cases the dysfunction of adipocytes, which can be genetically determined or acquired, may cause the whole cascade of MS. Search for the causes and mechanisms of arterial hypertension in patients with MS can help to find the possible targeted treatment and prevention of the disease.

It is well known that during last 10 years there is a significant growth in the number of patients with diabetes mellitus type 2. Early stages of glucose metabolism impairment such as glucose intolerance should be paid more attention. Diet and life style modification as well as acarbose (Glucobay) intake can result in glycemia normalization and prevent about one third of diabetes cases. Acarbose (Glucobay) can also improve coagulation factors, lipids, diminish oxidative stress, endothelial dysfunction, insulin and proinsulin level due to the decrease of postprandial glycemia and peripheral insulin resistance. As a consequence a reduction of patients' body mass index and cardiovascular risk is observed. We conclude that acarbose (Glucobay) must be administered oftener in patients with prediabetes and diabetes mellitus type 2 as monotherapy in case of postprandial hyperglycemia and as the second drug if normoglycemia is not achieved, as it can be combined with any hypoglycemic drug.

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