Premature coronary artery disease in young (age <45) subjects: interactions of lipid profile, thrombophilic and haemostatic markers.

BACKGROUND: Intravascular thrombogenesis is influenced by a complex interplay of procoagulant, anticoagulant, fibrinolytic, endothelial damage/dysfunction and inflammatory factors. We hypothesised that abnormalities of these biological systems would contribute to coronary artery disease presenting at a young age.
METHODS: We performed a case-control study of 142 subjects presenting with MI at a young age (<or=45 years; 'cases'), who were compared with 95 controls. We assessed for abnormalities of thrombophilia [total homocysteine (tHcy), lipoprotein (a) [Lp(a)], antiphospholipid antibodies (APA)], lipid profile [total cholesterol, HDL-cholesterol, LDL-cholesterol and triglycerides], fibrinogen and fibrin D-dimer (an index of thrombogenesis), endothelial damage/dysfunction (von Willebrand factor [vWF]), fibrinolysis (tissue plasminogen activator [t-PA antigen] and its inhibitor [PAI-1 antigen]) and inflammation (C-reactive protein [CRP]).
RESULTS: Cases had significantly higher Lp(a) (p=0.008), triglycerides (p=0.001), fibrinogen (p=0.006), fibrin D-dimer (p=0.006) and vWf (p=0.032), but lower HDL-C (p=0.003) levels. There were no significant differences in tHcy, APA titre, total cholesterol or LDL-C, t-PA, PAI-1 and CRP levels (all p=NS). In a multivariate analysis, the only variables independently associated with cases were levels of Lp(a) (p=0.015), fibrinogen (p=0.038) and D-dimer (p=0.005) levels.
CONCLUSIONS: Premature coronary artery disease is characterized by an unfavourable lipid profile, low concentrations of HDL-C and high triglyceride levels, in association with high Lp(a) and a hypercoagulable state (high fibrinogen and D-dimer levels).