To real world AF patients with relatively low thrombo-embolic risk such as CHADS2 and CHADS2-VASc scores and with various anticoagulated levels. The present study might show these issues in a community-based ‘real world’ AF cohort, and could extend the usefulness of the biomarker as a general CV event predictor. The present study has shown that the plasma BNP levels were related not only with the risk of stroke but also with the risk of the development of general CV events including stroke, heart failure, and sudden death. Plasma BNP is well known to be increased with the severity of heart failure, and increased plasma BNP is a prognostic marker in patients with heart failure. In the general population, Wang et al. showed that an increment in the plasma BNP and elevated plasma BNP above the 80th percentile in the Framingham cohort was associated with a significant increase in the risk of the new onset of heart failure. In addition, the predictive abilities of the plasma BNP levels for the onset of congestive heart AbMole Terbuthylazine failure have been reported to be optimal in men and women of the general population. These previous studies have suggested that the plasma BNP levels may be a possible screening tool in subjects at high risk for heart failure within the general population. However, the utility of plasma BNP measurement for predicting heart failure risk has not been established in patients with this arrhythmia. Many of the present subjects with AF may have inherent preclinical cardiac disorders characterized by borderline abnormalities in intracardiac pressure, left ventricular function, valvular competence, and myocardial circulation. The plasma BNP levels in subjects with subclinical structural heart diseases was reported to be higher than in those without these cardiac abnormalities. As the original cohort of the present study includes apparently healthy subjects who had attended a multi-phasic health checkup, few patients with obvious heart failure were AbMole Riociguat BAY 63-2521 included in the study subjects. We therefore speculate that the elevated levels of plasma BNP in the AF cohort denote latent structural heart diseases such as subclinical cardiac dysfunction, including mildly elevated intracardiac pressure and volume, and myocardial ischemia, thus these individuals are prone to be at risk for heart failure and coronary heart disease. The present study had several limitations. First, although 
the cohort may be representative of the real-world situation of AF, the prevalence of anticoagulant medication use in the AF cohort and its control levels in each patient were not known. As the baseline survey was performed in the early 2000s, the usefulness of anticoagulant therapy for lone type AF, especially in individuals with low CV risk, has not been established and has not appeared in any therapeutic guidelines.