Author + information
- Zhili Shao, MD, PhD,
- Stanley L. Hazen, MD, PhD and
- W.H. Wilson Tang, MD⁎ ()
- ↵⁎Department of Cardiovascular Medicine, Cleveland Clinic, 9500 Euclid Avenue, J3-4, Cleveland, Ohio 44195
We thank Dr. Billecke and colleagues for their interest in our paper (1) and agree that various treatments may directly or indirectly affect asymmetric dimethylarginine levels, and based on our findings we postulated that modulating dimethylarginine dimethylaminohydrolase-1 activity with pharmacotherapy can be a potential therapeutic approach. Nevertheless when comparing between those with chronic versus advanced decompensated heart failure who were on angiotensin-converting enzyme inhibitors, levels of methylated arginine metabolites and arginine bioavailability remained significantly different. This suggested that the underlying disease severity remains an important determinant. Whether proteolysis and protein turnover can contribute to in vivo asymmetric dimethylarginine release, particularly during catabolic or hemolytic processes associated with pulmonary venous hypertension in advanced heart failure, may warrant further investigation.
- American College of Cardiology Foundation