Objective: The increase of plasminogen activator inhibitor-1 (PAI-1) is known to be associated with atherothrombosis and target organ damage in arterial disease. We, therefore, studied the association of PAI-1 with inflammatory markers in 649 apparently healthy subjects (50+/-10 year-old, 70% male, and 326 hypertensive patients) in relation to development of future cardiovascular (CV) disease in 10 years. Design and methods: We measured circulating levels of hs-CRP, white blood cells (WBC), albumin, and fibrinogen, and PAI-1. Ten-year absolute risk of developing CVD (coronary heart disease) was based on the algorithm of the Framingham risk score. Results: The mean blood pressure (BP) was 135/87 mmHg (156/112 in hypertensives and 115/77 mmHg in normotensives). Hypertensive patients had significantly higher levels of inflammatory changes (p=0.02 for WBC, p=0.001 for fibrinogen, and p=0.04 for log hs-CRP) and PAI-1 (p<0.001), compared to those of age- and sex-matched normotensives. PAI-1 level was positively associated with WBC, fibrinogen and log hs-CRP (p=0.02, p<0.001, and p<0.001) after controlling for traditional CV risk factors. In a logistic regression model that included age, sex, body mass index, cholesterol, and blood pressure, WBC and PAI-1 remained significantly although weakly (棺=0.12, p<0.001 and 棺=0.07, p=0.02, respectively) related to 10-year CV disease. The CV risk correlated, sequentially by stepwise regression, with age, sex, cholesterol, WBC, diastolic BP, and PAI-1 in hypertension group, and sex, age, cholesterol, smoking, WBC and PAI-1 in normotension group. When patients were divided into quartiles according to either WBC or PAI-1, the increased CV risk was associated with higher quartiles of WBC or PAI-1, in conjunction with other inflammatory markers (both p<0.001 for trend). Conclusion: The elevation of PAI-1 is associated with low-grade inflammation. Combined with inflammatory changes, PAI-1 confers additional impact on predicting future cardiovascular events, independent of traditional risk factors in healthy subjects.