Abstract 2518: Hyper Transcardiac Extraction of Aldosterone Promote Ventricular Remodeling and Cardiac Mass in Patients with Primary Aldosteronism
Background Primary aldosteronism (PA) is frequent cause of secondary hypertension. We have reported transcardiac extraction of aldosterone (ALD) induced left ventricular (LV) remodeling in patients (pts) with AMI. Cardiac remodeling and mass increase causes cardiac events. In pts with PA, plasma ALD level was reported to associate with LV mass index (LVMI). However, it is not elucidated whether transcardiac extraction of ALD modulates LV remodeling in pts with PA.
Methods Consecutive 61 pts with PA were studied. PA was verified detection of adrenal grand tumor by MRI, or three times higher levels of ALD in adrenal grand vain. Before administrating drugs, SwanGantz, blood sampling for ALD from aortic root and coronary sinus, contrast LV graphy and UCG were performed. We divided two groups by the median value of transcardiac extraction of ALD into Hi group and Low group.
Result There were no differences between the two groups in pts‘s characteristics including cardiac performance and mean BP (125 in H-g vs. 124 mmHg). Plasma ALD was higher in H-g than in L-g (247 vs 202 pg/ml, P>0.0001). Transcardiac extraction of ALD was 60 pg/ml in H-g and 36 in L-g (P>0.0001). PIIINP, a marker of cardiac fibrosis, was higher in H-g than in L-g (0.53 vs. 0.47 IU/ml, P>0.001). End-diastolic volume index was significant higher in H-g compared with L-g (123 vs. 107 ml/m2, P<0.01) and was significant positive correlation with transcardiac extraction of ALD (r=0.586, P<0.0001). LVMI was significantly higher in H-g than in L-g (159 vs. 138 g/m3, P<0.001). LVMI was significant positive correlation with transcardiac extraction of ALD (r=0.685, P<0.0001) and PIIINP (r=0.861, P<0.0001). According to stepwised multivariate analysis among 14 variables including plasma ALD, only transcardiac extraction of ALD (P>0.001), PIIINP (P>0.001) and mean BP (P>0.001) were independent significant predictor for large LVMI.
Conclusion These results indicated that transcardiac extraction of ALD may be stronger modulator in promotion of LV hypertrophy than plasma level of ALD in pts with PA. In pts with PA, it may play an important role in modulation of LV mass. Considering ALD blocker attenuates extraction of ALD into the heart and improve LV remodeling, ALD blocker may prevent cardiac hypertrophy in pts with PA.