Purpose: The effects of angiotensin II (ANG) on inflammation and haemostasis were examined in 16 otherwise healthy patients with familial hypercholesterolemia (FH) and in 16 healthy controls.

Methods: Plasma markers of inflammation (hs-CRP, IL-6, fibrinogen, leukocyte counts (Lct)), coagulation (thrombin generation: F1+2, Calibrated Automated Thrombogram (CAT), fibrinolysis (plasmin-antiplasmin complexes, PAI-1 activity) were assessed in conjunction to iv ANG infusion (10 ng/kg/min for 3 h). Means ± SD; repeated measures ANOVA, log transformation when appropriate.

Results: Baseline systolic blood pressure was higher in FH than in controls (127±14 vs 115±12 mm Hg, p<0.05), while responses to ANG were similar (+24±10 and +21±7 mm Hg). Baseline hs-CRP, IL-6, Lct, and fibrinogen were similar in FH and controls, and all increased similarly in both groups (p<0.05) during ANG. Baseline CAT (peak and ETP) was higher in FH (367±47 vs 317±60 nM, p=0.01, and 2418±391 vs 2042±358 nM/min, p<0.01, respectively), but ANG did not affect CAT (peak or ETP). Baseline F1+2 was similar in FH and controls (189±41 vs 186±81 pM) and unchanged by ANG. Baseline plasmin-antiplasmin complexes were similar in FH and controls (96±16 vs 93±27 μg/L) and increased (p<0.001) similarly by ANG in both groups. PAI-1 activity was similar in both groups at baseline (1.3±1.3 vs 1.1±1.2 ng/L) and decreased (p<0.001) similarly in both groups, confirming the diurnal variation in fibrinolysis.

Conclusions: Subjects with FH have an increased thrombin generation potential, while an intact fibrinolysis. ANG has proinflammatory effects, similar in FH and healthy controls, but does not affect coagulation or fibrinonlysis.