White coat hypertension and haemostatic/fibrinolytic balance disorders.

White coat hypertension (WCH) or isolated clinic hypertension is generally accepted to be a benign condition, although some reports have suggested that it may be associated with an increased cardiovascular event rate or other cardiovascular alterations. It has been previously shown that essential hypertension (EH) is associated with abnormalities in haemostatic/fibrinolytic balance and endothelial function. The aim of our study was to assess the impact of WCH on fibrinolytic balance and endothelial function by measuring plasma levels of plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator antigen (tPA), fibrinogen, and thrombomodulin. These markers were determined in 71 patients with EH, 26 with WCH and 87 normotensive healthy control subjects. The three groups were not different with respect to age, gender, smoking habits, BMI and blood lipids. Subjects with WCH were found to have increased plasma levels of PAI-1, tPA, fibrinogen and thrombomodulin compared to controls, but less compared to hypertensive ones. Our results suggest that WCH may be associated with decreased fibrinolytic potential and endothelial dysfunction, indicating that WCH may not be a completely harmless trait.

Parental history of hypertension is associated with coagulation-fibrinolytic balance disorders.

It has been previously shown that essential hypertension (EH) is associated with coagulation-fibrinolytic balance disorders. Our study was conducted in order to investigate disturbances in coagulation-fibrinolysis in offsprings of hypertensive parents. Two groups were studied: 44 healthy normotensive individuals (17 male, 27 female, age range 12-22 years) with a documented family history of hypertension and 33 individuals (14 male, 19 female, age range 11-21 years) without a family history of essential hypertension. The following parameters were determined in both groups: plasminogen activator inhibitor-1 antigen, tissue plasminogen activator antigen, fibrinogen, fibrin degradation products, thrombomodulin, protein S antigen, protein C activity, von Willebrand factor Ag, factor VII and factor XII activity. Additionally, systolic and diastolic blood pressure, insulin levels, blood lipids and heart rate were determined. The two groups were not found to have differences with respect to age, gender, body mass index, blood lipids and insulin levels. Hypertensive offsprings had significantly higher plasma levels of plasminogen activator inhibitor-1 antigen, fibrinogen, fibrin degradation products, protein S antigen and factor XII activity, while no differences were observed to the other haemostatic variables studied. Hence, offsprings of hypertensives had significantly higher diastolic blood pressure and heart rate. In conclusion, alterations regarding blood pressure, heart rate and fibrinolytic function exist in offsprings of hypertensive parents compared to individuals without family history of hypertension.

Markers of risk in young offspring with paternal history of myocardial infarction.

Coronary heart disease clusters within families, but there may be several reasons for this phenomenon to occur. A possible way to elucidate this is to study biological relatives of affected individuals. The aim of our study was thus to compare a number of clinical, metabolic, clotting and immunologic factors between offspring with paternal history of premature myocardial infarction and controls and to propose a model which could safely allow to identify the high risk subgroup among them. Sixty-nine offspring of both sexes mean age 18.1 years old (cases) and thirty-two frequency matched relative to age and gender controls were studied. Cases compared to controls had significantly increased diastolic blood pressure levels (74.0+/-9.9 vs. 67.4+/-8.3 mmHg, P=0.002), leptin plasma levels (11.8+/-10.8 vs. 6.8+/-3 ng/ml, P=0.046) and fibrinogen, plasminogen, fibrin degradation products and plasminogen activator inhibitor-1 plasma levels (306.6+/-52.5 vs. 280.6+/-28.9 mg%, P=0.03, 97.4+/-23.5 vs. 83.6+/-15 mg%, P=0.0007, 292.0+/-148.5 vs. 219.2+/-69.4 ng/ml, P=0.036, 14.7+/-5.3 vs. 8.7+/-3.1 I.U./ml, P=0.0001, respectively), while cases had significantly decreased HDL-cholesterol serum levels (45.9+/-12.5 vs. 50.5+/-8.8 mg%, P=0.03) and protein S plasma levels (89.9+/-17.5 vs. 101.3+/-13.7%, P=0.001). Our findings suggest that offspring of affected individuals may be considered as a high risk group for cardiovascular disease.