title: [The heart and metabolic syndrome].
abstract: Most people with the Metabolic Syndrome die from thrombotic complications superimposed to degenerative arterial vascular lesions, mostly myocardial infarction. Type-2-Diabetes is a risk factor per se for such complications, but often clusters with dyslipoproteinemia, hypertension and obesity. This is referred to as "Metabolic Syndrome" and often operates on a genetically programmed susceptibility which accelerates the pathogenesis of coronary artery disease in front of a much wider diabetes specific cardiopathy. From a pathophysiological point of view none of these associated risk factors explains the pathogenetic series of events leading to the precipitation of an occlusive thrombus at sites of complicated coronary plaques. In patients with the Metabolic Syndrome the coagulation system is switched towards a prethrombotic state, involving increased plasmatic coagulation, diminished fibrinolysis, decreased endothelial thromboresistance and predominantly platelet hyperreactivity ("diabetic thrombocytopathy"). Some of these factors are associated with an increased coronary risk (e.g. fibrinogen, PAI-1, platelets), but are also directly linked to the pathogenesis of "atherothrombosis". Altered cardiac remodelling together with adhesion and coagulation mechanisms appears suitable to explain decreased functional performance of infarcted organs, decreased success of acute (reduced fibrinolytic response, no reflow phenomenon) and longterm intervention strategies for vessel patency (PTCA, CABG) in Diabetes. Glucose adjustment alone will not adequately neutralize these complex mechanisms, but in the situation of myocardial infarction eumetabolization with parenteral glucose-insulin-potassium infusion appears mandatory similar to non-diabetics. On the longterm a multidimensional interventional repertoire is required particularly in patients with the Metabolic Syndrome including antihypertensive, antidyslipoproteinemic and antithrombotic drugs, customized according to the individual patients needs as assessed by early diagnostic measures ("early secondary prevention").
authors.affiliation: Diabetes-Forschungsinstitut an der Heinrich-Heine-Universität Arbeitsgruppe Zelluläre Hämostase und Klinische Angiologie, Düsseldorf. tschoepe@uni-duesseldorf.de
authors.forename: D
authors.initials: D
authors.lastname: Tschoepe
authors.forename: P
authors.initials: P
authors.lastname: Roesen
authors.forename: W A
authors.initials: WA
authors.lastname: Scherbaum
mesh_terms: D001786:Blood Glucose / Q000378:metabolism; D003328:Coronary Thrombosis / Q000097:blood / Q000235:genetics*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics*; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics*; D009203:Myocardial Infarction / Q000097:blood / Q000235:genetics; D012307:Risk Factors; D013577:Syndrome; D019851:Thrombophilia / Q000097:blood / Q000235:genetics
chemical_list: D001786:Blood Glucose