Heart disease and metabolic syndrome

Most people with the Metabolic Syndrome die from thrombotic complications s uperimposed to degenerative arterial vascular lesions, mostly myocardial in farction, Type-2-Diabetes is a risk factor per se for such complications, b ut often clusters with dyslipoproteinemia, hypertension and obesity. This i s referred to as "Metabolic Syndrome" and often operates on a genetically p rogrammed susceptibility which accelerates the pathogenesis of coronary art ery disease in front of a much wider diabetes specific cardiopathy. From a pathophysiological point of view none of these associated risk factors expl ains the pathogenetic series of events leading to the precipitation of an o cclusive thrombus at sites of complicated coronary plaques. In patients wit h the Metabolic Syndrome the coagulation system is switched towards a preth rombotic state, involving increased plasmatic coagulation, diminished fibri nolysis, decreased endothelial thromboresistance and predominantly platelet hyperreactivity ("diabetic thrombocytopathy"). Some of these factors are a ssociated with an increased coronary risk (e.g, fibrinogen, PAI-1, platelet s), but are also directly linked to the pathogenesis of "atherothrombosis'' . Altered cardiac remodelling together with adhesion and coagulation mechan isms appears suitable to explain decreased functional performance of infarc ted organs, decreased success of acute (reduced fibrinolytic response, no r eflow phenomenon) and longterm intervention strategies for vessel patency ( PTCA, CABG) in Diabetes. Glucose adjustment alone will not adequately neutr alize these complex mechanisms, but in the situation of myocardial infarcti on eumetabolization with parenteral glucose-insulin-potassium infusion appe ars mandatory similar to non-diabetics. On the longterm a multidimensional interventional repertoire is required particularly in patients with the Met abolic Syndrome including antihypertensive, antidyslipoproteinemic and anti thrombotic drugs, customized according to the individual patients needs as assessed by early diagnostic measures ("early secondary prevention").