Elevated levels of lipoprotein (a) in patients suffering from myocardial infarction with carotid atherosclerotic lesions

• Published in: Blood coagulation & fibrinolysis Vol. 10; no. 6; p. 331
• Main Authors: Avellone, G, Di Garbo, V, Abruzzese, G, Campisi, D, Giannola, G, De Simone, R, Raneli, G
• Format: Journal Article
• Language: English
• Published: England 01.09.1999
• Subjects: Apolipoproteins - blood; Arteriosclerosis - blood; Arteriosclerosis - epidemiology; Arteriosclerosis - therapy; Biomarkers - blood; Blood Coagulation - physiology; Body Mass Index; Carotid Artery Diseases - blood; Carotid Artery Diseases - epidemiology; Carotid Artery Diseases - therapy; Cholesterol - blood; Female; Fibrinolysis - physiology; Humans; Lipoprotein(a) - blood; Lipoproteins - blood; Male; Middle Aged; Myocardial Infarction - blood; Myocardial Infarction - epidemiology; Myocardial Infarction - therapy; Risk Factors; Triglycerides - blood
• ISSN: 0957-5235
• DOI: 10.1097/00001721-199909000-00003

The aim of the present study was to evaluate metabolic, coagulation and fibrinolytic parameters in 45 patients [31 men, 14 women, aged 56.5 +/- 3.5 years (mean +/- SD)] who had suffered myocardial infarction more than 6 months earlier, with or without carotid atherosclerotic lesions. After the extracranial carotid arteries had been evaluated using a B-mode Duplex scanning system, patients were subdivided into two groups: group 1 (n = 20) with carotid plaques or measurable intima-media thickness; and group 2 (n = 25) without carotid plaques or measurable intima-media thickness. Twenty-two age- and sex-matched subjects were recruited as controls (group 3). Groups 1 and 2 displayed significantly higher levels of total cholesterol, apolipoprotein B, human autoantibodies against oxidised low-density lipoprotein and the c fraction of the third component system, and significantly lower levels of high-density lipoprotein cholesterol and apolipoprotein A1 than group 3. However, serum levels of triglyceride and lipoprotein (a) were significantly higher in group 1 than in the control group. Moreover, groups 1 and 2 displayed significantly higher levels of factor VII, fibrinogen, fragment 1+2, thrombin-antithrombin complex and plasminogen activator inhibitor after venous occlusion, and significantly lower levels of tissue-type plasminogen activator after venous occlusion than group 3. Significantly higher levels of tissue-type plasminogen activator and plasminogen activator inhibitor before venous occlusion were observed in groups 1 and 2 and significantly lower levels of antithrombin III, protein C and protein S were observed in group 1 compared with the controls. Patients were also analysed according to levels of lipoprotein (a). The lowest levels of tissue-type plasminogen activator after venous occlusion and the highest levels fragment 1 + 2, the c fraction of the third component system, and plasminogen activator inhibitor after venous occlusion were observed in patients with the highest levels of lipoprotein (a). Our data demonstrate an activation of coagulation and deficient fibrinolysis in survivors of myocardial infarction, particularly in those with associated carotid atherosclerotic lesions. We speculate that this thrombophilic state may play a key role in the pathogenesis of atherosclerotic vascular disease and thromboembolic complications.