Low order correlations of lipoprotein(a) with other blood lipids and with coagulation and fibrinolysis parameters in hypertensive and diabetic patients

Thrombomodulin and induced tissue factor expression on monocytes as markers of diabetic microangiopathy: A prospective study on hemostasis and lipoproteins in insulin-dependent diabetes mellitus

“…We found increased thrombin generation and fibrin formation that seem to confirm a hypercoagulable state. These results agree with several reports [27,[39][40][41][42] but not with others [29,[43][44][45]. Differences in patient populations and in laboratory methods can explain some of the discrepancies.…”

“…This PAI-1 alteration may cause a lower fibrinolytic response, predisposing the growth of thrombi and increasing the exposure of the vessel walls to clot associated mitogens. An excess of PAI-1 has been previously reported in IDDM patients [27][28][29], as has an increase of PAI-1 determined in vitro after cell stimulation with high concentrations of insulin [30] or glucose [31]. In addition, a stronger lysis-resistance of platelet-rich clots, attributed to a change in platelet PAI-1 activity, has been observed in IDDM [32].…”

“…Fairly well-controlled patients seem to have less pronounced hemostasis alterations [44,46,47] but, even in the studies that did not find increased hypercoagulability markers in IDDM, some groups of patients, such as those with microalbuminuria, can present moderately elevated levels of F 1+2 [44]. In addition, some hypercoagulability markers can be elevated and the remaining persist within the normal range [29]. At present, it is not known if these differences reflect a true different thrombin generation rate or can be explained by the different metabolism and excretion of the markers [40,44].…”

Apolipoprotein(a) Gene Polymorphism in the Korean Population: Is There Any Relevance to Essential Hypertension?

“…Some authors have found normal plasma Lp(a) levels in these subjects [18,19], whereas others have reported increased plasma Lp(a) levels [20][21][22]. In the present study, the mean plasma Lp(a) level of subjects with essential hypertension was not significantly different from that of normotensive subjects.…”

Haemostatic Variables in Arterial Hypertension

“…are signifi Received: August 10, 1994 Accepted in revised form: November 21.1994 cantly higher in people suffering from stable arterial hypertension with a history of minor brain stroke [4] Platelet reactivity was increased in hyper tensive subjects with advancing age as shown by a greater serotonin-induced aggregation and higher (3-thromboglobulin plasma con centration [5,6], Arterial hypertension increases the risk of cerebral, coronary and other vascular complications that frequently involve platelet activation and blood coagula tion. In fact the concentrations of von Willebrand factor, a2-antiplasmin and D-dimer (DD) were significantly higher in the hyper tensive patients compared with the control subjects [7], Alterations in the plasma concentrations of the investigated coagulation and fibrinolysis factors and in the aggregability of the platelets are indicative of an involvement of coagula tion, fibrinolysis and platelets in hyperten sion, which can be considered as partial risk factors for thrombophilia [8], In order to in vestigate possible alterations in the haemo static system at initial stages of the arterial hypertension we measured in patients with essential hypertension and in a control group the plasma levels of thrombomodulin (TM) as a marker of endothelium damage [9], Pthromboglobulin (P-TG) as an indicator of platelet activation which revealed a tendency to increase with advanced progress of hyper tensive vascular lesions [5,6,[10][11][12], DD which increases in hypercoagulable states [13][14][15], tissue-type plasminogen activator (t-PA) and plasminogen activator-inhibitor (PAI-1) as markers of the fibrinolytic system which has been found impaired in hyperten sion [7,8,[16][17][18].…”