Abstract
Lipoproteins and coagulation factors are independent predictors of atherothrombotic events in the general population and their interaction may contribute to the development of cardiovascular damage. This study was designed to assess relationships between lipoproteins, haemostatic variables, and atherosclerotic complications in hypertensive patients. In 389 untreated essential hypertensive patients recruited at a hypertension clinic, we measured plasma lipids, apolipoproteins, lipoprotein (a), apolipoprotein (a) isoforms, fibrinogen, and parameters that directly reflect the coagulation activation. Hypertensive patients were compared to 92 normotensive controls. Univariate analysis showed log lipoprotein (a) concentrations to be significantly correlated with age (P< 0.02), apolipoprotein B (P< 0.02), plasma fibrinogen (P< 0.001), and fibrin D-dimer (P< 0.001) levels, but not with body mass index, blood pressure, dietary fat intake, cholesterol, triglycerides, apolipoprotein Al, prothrombin fragment 1 + 2, and antithrombin III. The relationship of lipoprotein (a) with fibrinogen and D-dimer was present in both sexes, whereas the relationship of lipoprotein (a) with age and apolipoprotein B was found only in males. Multiple regression analysis showed that both fibrinogen and D-dimer were independently related with lipoprotein (a). Elevated fibrinogen, D-dimer, and lipoprotein (a) levels were significantly and independently associated with clinical evidence of atherosclerotic disease. To investigate whether the relationships of lipoprotein (a) with coagulation parameters are genetically determined, we analysed apolipoprotein (a) phenotypes in a subset of 188 hypertensive patients. While lipoprotein (a) levels were inversely correlated with apolipoprotein (a) isoform protein size, both fibrinogen and D-dimer concentrations were comparable in patients with apolipoprotein (a) isoforms of different size. This study demonstrates a relationship between lipoprotein (a) and clotting variables in hypertensive patients that may contribute to atherosclerotic damage in these patients. There is no evidence of a genetic background for this relationship.
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