Coronary sinus and ascending aortic levels of aldosterone, angiotensin II, and B-type natriuretic peptide in patients with aortic stenosis and in patients with coronary heart disease.

Demonstration that aldosterone synthesis occurs in the myocardium would suggest that the clinical benefits of aldosterone receptor antagonists may extend to patients with normal circulating plasma levels of aldosterone. Previous studies have reported myocardial aldosterone synthesis in patients with heart failure. This study determined whether myocardial aldosterone and angiotensin II release occurs in patients with aortic stenosis (AS) and/or coronary heart disease (CHD) with normal left ventricular ejection fractions and no clinical heart failure. In 19 patients with severe AS and 18 patients with stable CHD, plasma levels of aldosterone, angiotensin II, B-type natriuretic peptide (BNP), and procollagen type III amino terminal peptide (PIIINP) were measured in blood samples taken from the coronary sinus and aortic root before diagnostic coronary angiography. Plasma aldosterone was approximately 20% greater in the coronary sinus than the aorta, respectively, in the 2 patient groups (AS: 120 vs 102 pmol/L, p <0.001; CHD: 94 vs 77 pmol/L, p <0.001). Plasma angiotensin II was also greater in the coronary sinus (AS: 16 vs 11 pmol/L, p <0.001; CHD: 12 vs 9 pmol/L, p <0.001). Plasma levels of BNP in the coronary sinus were approximately double those in the aorta in the 2 groups of patients (p <0.001). In contrast, there was no transmyocardial gradient in the plasma level of PIIINP for either AS or CHD. In conclusion, these results indicate that aldosterone, angiotensin II, and BNP are released into the coronary sinus in severe AS and in stable CHD, even when the left ventricular ejection fraction is normal and there is no clinical heart failure.