Determinants of risk factors of atherosclerosis in the postinfarction period: The Tallinn MI Study

Abstract

Environmental as well as genetic factors are involved in the pathogenesis of myocardial infarction. The disease is a frequent cause of mortality in the middle‐aged male population of Estonia. The high prevalence of premature myocardial infarction (PMI) in this country is not fully understood. The association of atherogenic and thrombogenetic risk factors with lifestyle was evaluated in men who had suffered myocardial infarction at⩽55 years of age (n = 71) and in randomly selected corresponding controls (n = 85). Serum routine lipids, apolipoprotein (apo)A‐I, apoB, apoE polymorphism, lipoprotein(a) and fibrinogen levels were determined. Behavioural risk factors, indices of obesity, blood pressure and pedigree data were registered. In 80.6 % of PMI subjects some type of hyperlipidaemia was observed (European Atherosclerosis Society Classification) and lipid‐lowering drugs were taken by 13.9 % of patients. In PMI patients the most common positive determinants of atherogenic lipoprotein indices were waist‐to‐hip ratio and physical inactivity, and in controls, waist‐to‐hip ratio and apoE phenotype. The odds ratio (OR) of PMI was 8.9‐fold greater in the highest tertile of apoB/apoA‐I distribution compared with the lowest tertile. The OR of PMI in the highest tertile of fibrinogen distribution versus the lowest tertile was 6.2 (95 % CI 2.46–15.44), and OR of PMI in the highest Lp(a) tertile versus the lowest was 3.1 (95 % CI 1.31–7.40). Thus, atherogenic dyslipidaemia was the most serious cardiovascular risk factor among PMI patients. From two thrombogenesis‐related markers, the levels of fibrinogen and Lp(a), the first one was more strongly associated with PMI status.

• ApoE polymorphism
• apolipoproteins
• behavioural risk factors
• fibrinogen
• lipids
• lipoprotein(a)
• postinfarction period

Acknowledgements

This study was funded by the Estonian Ministry of Education, project No. 0300847s99. We express our gratitude to Professor Ulrike Beisiegel, Universitäts‐Krankenhaus Eppendorf, Hamburg, Germany, for her personal involvement in the management of the apoE polymorphism studies in Estonia. We also thank Anu Kull, Sirkka Metiäinen, Virva Korhonen and Sari Nuutinen for excellent technical assistance.