High serum level of procollagen type III amino-terminal peptide contributes to the efficacy of spironolactone and angiotensin-converting enzyme inhibitor therapy on left ventricular hypertrophy in essential hypertensive patients.

Abstract

We recently demonstrated that spironolactone may have beneficial effects on left ventricular hypertrophy in selected patients with essential hypertension undergoing treatment with an angiotensin-converting enzyme (ACE) inhibitor. To clarify the possible mechanisms by which spironolactone improves cardiac hypertrophy, we investigated the change in serum procollagen type III amino-terminal peptide (PIIINP) in 11 patients with essential hypertension treated with spironolactone and an ACE inhibitor for 24 weeks. Both blood pressure and serum PIIINP levels were significantly decreased by treatment. There was a statistical significant correlation between the changes in LVMI and those in PIIINP. The reduction in PIIINP was significant in patients whose initial serum PIIINP levels were above the normal range. Before treatment, there were no statistically significant correlations between serum PIIINP levels and either LVMI, blood pressure, or plasma aldosterone concentration. Essential hypertensive patients matched in terms of duration of therapy, blood pressure and LVMI and treated with an ACE inhibitor alone showed no change in serum PIIINP levels. In conclusion, the results of the present study demonstrate that patients with essential hypertension and high serum levels of PIIINP are particularly responsive to MR blockade in terms of left ventricular hypertrophy. Moreover, these results suggest that spironolactone limits cardiac collagen turnover in such patients. Larger studies may provide definitive evidence for the involvement of aldosterone in left ventricular hypertrophy in patients with abnormally high PIIINP levels.