Author + information
- Kenichi Tsujita, MD, PhD∗ (, )
- Seigo Sugiyama, MD, PhD,
- Hideki Shimomura, MD, PhD,
- Kenshi Yamanaga, MD,
- Koichi Kaikita, MD, PhD,
- Seiji Hokimoto, MD, PhD,
- Hisao Ogawa, MD, PhD,
- for the PRECISE-IVUS Investigators
- ↵∗Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto 860-8556, Japan
We read with great interest the letter by Dr. Giral and colleagues commenting on our recent paper (1). First of all, we all agree with the authors regarding the adverse effects of smoking on cardiovascular disease (CVD), recognizing the importance of campaigns for smoking cessation as a preventable risk factor and prevention of passive smoking in preventing CVD (2). In addition, we recently demonstrated that smokers showed more impaired peripheral endothelial function than never smokers, resulting in a higher rate of in-stent restenosis in smokers (unpublished data). Furthermore, cigarette smoking has been known as a major risk factor in the development of atherosclerosis and has been shown to cause inflammation and modification of the lipid profile. These data seem to be theoretically compatible with the association with cigarette smoking and a higher burden of necrotic core in coronary lesions observed by a cross-sectional intravascular ultrasound (IVUS) study (3). Because coronary plaque progression/regression has been known as a multifactorial process, even in the precisely designed serial IVUS studies, it appears to be difficult to show the direct relationship between smoking and coronary plaque progression during a relatively short study period.
Considering the varying findings of the previous studies, the association between smoking status and coronary plaque progression has still been controversial. As the authors of letter noted, an appropriately designed serial IVUS study evaluating the impact of smoking on coronary plaque progression primarily is definitely warranted.
Please note: This work was supported in part by a Grant-in-Aid for Young Scientists B (22790713, 24790769) and a Grant-in-Aid for Scientific Research C (26461075) from the Ministry of Education, Science, and Culture, Japan (to Dr. Tsujita). Dr. Ogawa has received remuneration for lectures from Bayer, Boehringer Ingelheim, Daiichi-Sankyo, MSD, Pfizer, and Takeda; has received trust research/joint research funds from Bayer, Daiichi-Sankyo, and Novartis; and has received scholarship funds from AstraZeneca, Astellas, Bristol-Myers Squibb, Chugai, Daiichi-Sankyo, Dainippon Sumitomo Pharma, Kowa, MSD, Otsuka, Pfizer, Sanofi, Shionogi, and Takeda. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2016 American College of Cardiology Foundation