Recently, it has been shown that the mineralocorticoid receptor, which mediates the action of ALD, is expressed in the human heart (16- 19). Although ALD synthase was not detected in the autopsy sample of normal subjects (19), the existence and upregulation of ALD synthase in the heart was reported in rats with MI, suggesting cardiac production of ALD in patients with AMI. However, whether plasma ALD is extracted or produced through the heart in patients with AMI has not been yet elucidated. In this study, we demonstrated for the first time that plasma ALD is extracted through the heart at the acute phase of AMI. We previously reported (14) that about 20% of the plasma ALD level was extracted between the Ao and the CS in patients with CHF, including previous MI more than three months after the onset. This study showed that the ALD extraction ratio through the heart was about 17% and 20% at the acute phase and at one month, respectively. Taken together with our previous study, ALD extraction through the heart was sustained from the acute stage to the chronic stage of MI. Although our findings did not deny the possibility of local ALD production in the heart in patients with AMI, the predominant extraction of ALD was shown because the transcardiac gradient of ALD reflects the total net of ALD extraction and production through the heart. Silvestre et al. (20) reported that both ALD synthase messenger RNA and ALD level increased by 2- to 3.7-fold in the ventricle of rats with MI, while plasma ALD level was not increased compared with that in sham-operated rat. Therefore, local production of ALD in the heart may not be sufficient to increase the plasma ALD level, which is consistent with our findings.