Author + information
- M. Adnan Nadir, MD∗ ()
- ↵∗Department of Cardiology, Queen Elizabeth Hospital, University of Birmingham, Mindelsohn Way, Birmingham, B15 2TH, United Kingdom
I read the paper by Treibel et al. (1) with great interest. In this elegant study, the authors showed that in patients with aortic stenosis (AS) who had undergone surgical aortic valve replacement, the diffuse fibrosis and myocardial cellular hypertrophy regress with time and that regression is accompanied by structural and functional improvements.
There is increasing appreciation that AS incorporates a disease process that extends beyond the stenotic valve itself, leading to an aortic valvular “heart” disease (2,3). The increasing afterload forces the myocardium to remodel and become hypertrophied in an effort to maintain adequate cardiac output and systolic function. These changes are characterized by cardiomyocyte hypertrophy and extracellular matrix expansion (3).
The renin-angiotensin system has a major influence on myocardial physiology, and there is some evidence for this influence in AS: it regulates the degree of left ventricular hypertrophy and the extent of fibrosis in the myocardium (2,3). Renin-angiotensin system inhibitors reduce left ventricular hypertrophy independent of blood pressure and can reduce the extent of myocardial fibrosis. This reduction, in turn, has a positive influence on future cardiovascular events, including in patients with AS (2,4,5).
In the present study (1), nearly one-half of the patients were taking angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). It would be intriguing to see if the authors could stratify the data according to the use of ACE inhibitors/ARBs and explore the regression of myocardial cellular hypertrophy and myocardial fibrosis. It is plausible that use of ACE inhibitors/ARBs had a positive impact on regression myocardial cellular hypertrophy and myocardial fibrosis and that among patients taking ACE inhibitors/ARBs, the regression may have been more pronounced (2,4,5).
Please note: Dr. Nadir has reported that he has no relationships relevant to the contents of this paper to disclose.
- 2018 American College of Cardiology Foundation
- Treibel T.A.,
- Rebecca Kozor R.,
- Schofield R.,
- et al.
- Nadir M.A.,
- Wei L.,
- Elder D.H.,
- Libianto R.,
- et al.