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    Lipoprotein (a), haemostatic variables and cardiovascular damage in hypertensive patients

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    Objective 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. Methods 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. Results 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. Conclusions 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. J Hypertens 2000, 18:709-716 (C) Lippincott Williams & Wilkins

    Relationship of fibrinogen levels and hemostatic abnormalities with organ damage in hypertension

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    Elevated plasma levels of fibrinogen and activated coagulation pathways are risk factors of cardiovascular disease in the general population. In a cross-sectional study of a case series, we investigated the relationship between fibrinogen and hemostatic markers with target-organ damage (TOD) in patients with arterial hypertension. Prothrombin time, partial thromboplastin time, fibrinogen, fibrin D-dimer, prothrombin fragment 1+2 (F1+2), and antithrombin III were measured in 352 untreated patients with mild to moderate essential hypertension and 92 normotensive controls. Staging of TOD was assessed according to W.H.O. guidelines by clinical evaluation and laboratory tests including measurements of creatinine clearance, proteinuria, ophthalmoscopy, electrocardiography, echocardiography, and ultrasound examination of major arteries. F1+2 concentrations were significantly greater in hypertensive patients than normotensive controls and were positively correlated with blood pressure. Age, blood pressure levels, duration of hypertension, smoking, HDL-cholesterol, triglycerides, and plasma frbrinogen, fibrin D-dimer, and F1+2 levels were significantly related to the presence and severity of TOD in univariate analysis. Plasma fibrinogen and D-dimer levels were related to organ damage independent of age, blood pressure, duration of hypertension, and smoking status. Separate analysis indicated significant association of fibrinogen and D-dimer levels with cardiac, cerebrovascular, peripheral vascular, and renal damage. In conclusion elevated plasma levels of fibrinogen and a prothrombotic state are associated with the presence and severity of TOD in patients with essential hypertension and may contribute to the development of atherosclerotic disease in these patients
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