Introduction The formation of a coronary thrombus is generally the underlying cause of a myocardial infarction and therefore factors related to coagulation and fibrinolysis may be involved in this pathophysiological process. Results of prospective studies have suggested that levels of fibrinogen and von Willebrand factor are predictors of cardiovascular events in certain populations [1–3]. Others have found that a decrease in fibrinolytic capacity increases the risk of myocardial infarction [4–6]. Cross- sectional studies have also shown that levels of prothrombin fragment 1+2 and thrombin–antithrombin complex are associated with cardiovascular disease [7–9]. It is therefore possible that an increase in activity of the coagulation system or a decrease in fibrinolytic activity contributes to the development of myocardial infarction and that detection of a state of hypercoagulability in patients might be of clinical interest. Most of these studies have concerned either patients with coronary disease or healthy subjects. Data on hypertensive patients are sparse. In a study of elderly men at high and low risks of cardiovascular disease, we found that high levels of fibrinogen, von Willebrand factor, prothrombin fragment 1+2, thrombin–antithrombin complex and plasminogen activator inhibitor activity were associated with cardio- vascular disease [9]. Now that these patients have been followed up for more than 3 years, we wanted to examine, in a hypothesis-seeking study, whether these factors predicted major coronary events (fatal and non-fatal myocardial infarctions and sudden death). Methods Subjects Five hundred and eight male patients with treated primary hypertension were included in a risk factor inter- vention study [10]. The inclusion criteria for the inter- vention study were, apart from treated hypertension and male sex, one or more of the following: hypercholestero- laemia (serum cholesterol level > 6.5 mmol/l), tobacco smoking (one or more cigarettes per day) and diabetes mellitus (fasting blood glucose level > 7 mmol/l) [11]. The patients were representative of high-risk hypertensives in Göteborg insofar as most of them (over 90%) were recruited by screening a random third of all men in their 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 3011 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 3 4 5 6 7111 Original article 537 0263-6352 © 1998 Lippincott-Raven Publishers Prothrombin fragment 1+2 is a risk factor for myocardial infarction in treated hypertensive men Stefan Agewall a , John Wikstrand b and Björn Fagerberg a Background Haemostatic factors may play a part in the development of acute coronary heart disease. Objective To evaluate as predictors of major coronary events (fatal and non-fatal myocardial infarctions and sudden death) levels of fibrinogen, von Willebrand factor, prothrombin fragment 1+2, thrombin–antithrombin complex, plasminogen activator inhibitor activity and C-reactive protein. Methods We studied 131 men, aged 56–77 years, with treated hypertension and at least one additional cardiovascular risk factor (hypercholesterolaemia, diabetes mellitus or smoking). These patients were recruited from a continuing risk factor intervention study. The mean observation time was 3.0 years. Results Fourteen patients died and 16 had a major coronary event during the follow-up period. After adjustments for other risk factors, levels of prothrombin fragment 1+2 and C-reactive protein were independent predictors of major coronary events. The other measured haemostatic variables were not significantly associated with major coronary events during follow-up. Fibrinogen and prothrombin fragment 1+2 levels were independent predictors for mortality. Conclusions Among treated hypertensive men, levels of prothrombin fragment 1+2 and C-reactive protein were independent predictors of major coronary events. J Hypertens 16:537–541 © 1998 Lippincott-Raven Publishers. Journal of Hypertension 1998, 16:537–541 Keywords: C-reactive protein, coagulation, coronary, fibrinolysis, hypertension, myocardial infarction a Department of Medicine and b Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska University Hospital, Göteborg University, Göteborg, Sweden. Sponsorship: This study was supported by grants from the Swedish Medical Research Council (B92-19X-009937-01Aa, B93-19X-09937-02B, B94-19X 09937-02B, B95-19X-09937-04B), the Swedish Heart and Lung Foundation, Göteborg Medical Society, Swedish Medical Society and King Gustaf V and Queen Viktoria Foundation. Correspondence and requests for reprints to Stefan Agewall, MD, PhD, Department of Medicine, Sahlgrenska University Hospital, Göteborg University, S-413 45 Göteborg, Sweden. Received 8 October 1997 Revised 11 December 1997 Accepted 23 December 1997