Aldosterone Production Is Activated in Failing Ventricle in Humans

TLDR

Aldosterone is known to be produced in extra‑adrenal tissues in animals. The study aimed to determine whether the human heart produces aldosterone. Plasma aldosterone, BNP, and ACE were measured in the anterior interventricular vein, coronary sinus, and aortic root of patients with LV systolic or diastolic dysfunction and controls. In patients with LV dysfunction, aldosterone, ACE, and BNP were higher in the coronary circulation than in the aorta, and the magnitude of these differences correlated positively with LVEDP and negatively with LVEF, indicating ventricular production of these hormones is activated in proportion to heart failure severity.

Abstract

Background —Recent reports have indicated that aldosterone is produced in extra-adrenal tissues in animals. The present study was designed to examine whether aldosterone is produced in human heart. Methods and Results —Plasma levels of aldosterone, BNP, and angiotensin-converting enzyme were measured in anterior interventricular vein (AIV), coronary sinus (CS), and aortic root (Ao), respectively, in 20 patients with left ventricular systolic dysfunction (LVSD), 25 patients with LV diastolic dysfunction (LVDD), and 23 control subjects. Aldosterone levels were significantly higher in AIV and CS than Ao in LVSD (98±10 versus 72±9 pg/mL, P <0.001, and 97±11 versus 72±9 pg/mL, P <0.001, respectively) and LVDD (87±10 versus 71±9 pg/mL, P <0.01, and 84±10 versus 71±9 pg/mL, P <0.01, respectively) groups, but no differences were observed in levels for these sites in the control group. Levels of ACE activity and BNP also were higher in AIV than Ao in both LV dysfunction groups. The difference in aldosterone levels between AIV and Ao and those in BNP and angiotensin-converting enzyme had a significant positive correlation with LVEDP and a significant negative correlation with LV ejection fraction in the LVSD group. Conclusions —Production of aldosterone, angiotensin-converting enzyme, and BNP are activated in failing human ventricle in proportion to severity.