[9] Manhenke C, Orn S, Squire I, et al. The prognostic value of circulating markers of collagen turnover after acute myocardial infarction. Int J Cardiol 2011;150(3):27782. [10] Ather S, Peterson LE, Divakaran VG, et al. Digoxin treatment in heart failure - unveiling risk by cluster analysis of DIG data. Int J Cardiol 2011;150(3):2649. [11] Yun KH, Oh SK, Rhee SJ, et al. 12-month follow-up results of high dose rosuvastatin loading before percutaneous coronary intervention in patients with acute coronary syndrome. Int J Cardiol 2011;146(1):6872. [12] Ekblom K, Marklund SL, Jansson JH, et al. Iron stores and HFE genotypes are not related to increased risk of rst-time myocardial infarction: a prospective nested case-referent study. Int J Cardiol 2011;150(2):16972. [13] Tenenbaum A, Shemesh J, Koren-Morag N, et al. Long-term changes in serum cholesterol level does not inuence the progression of coronary calcication. Int J Cardiol 2011;150(2):1304. [14] Erbs S, Beck EB, Linke A, et al. High-dose rosuvastatin in chronic heart failure promotes vasculogenesis, corrects endothelial function, and improves cardiac remodelingresults from a randomized, double-blind, and placebo-controlled study. Int J Cardiol 2011;146(1):5663. [15] Rössig L, Genth-Zotz S, Rau M, et al. Argatroban for elective percutaneous coronary intervention: the ARG-E04 multi-center study. Int J Cardiol 2011;148(2):2149. [16] Suh JW, Chung WY, Kim YS, et al. The effect of intravenous administration of erythropoietin on the infarct size in primary percutaneous coronary intervention. Int J Cardiol 2011;149(2):21620. [17] Williams AD, Anderson MJ, Selig S, et al. Differential response to resistance training in CHF according to ACE genotype. Int J Cardiol 2011;149(3):3304. [18] Ashton E, Windebank E, Skiba M, et al. Why did high-dose rosuvastatin not improve cardiac remodeling in chronic heart failure? Mechanistic insights from the UNIVERSE study. Int J Cardiol 2011;146(3):4047. [19] Porto I, Dato I, Di Vito L, et al. Differential levels of circulating progenitor cells in acute coronary syndrome patients with a rst event versus patients with recurring events. Int J Cardiol 2011;149(1):504. [20] Njike VY, Faridi Z, Shuval K, et al. Effects of sugar-sweetened and sugar-free cocoa on endothelial function in overweight adults. Int J Cardiol 2011;149(1):838. [21] Tousoulis D, Koniari K, Antoniades C, et al. Combined effects of atorvastatin and metformin on glucose-induced variations of inammatory process in patients with diabetes mellitus. Int J Cardiol 2011;149(1):469. [22] Schoenenberger AW, Radovanovic D, Stauffer JC, et al. Acute coronary syndromes in young patients: presentation, treatment and outcome. Int J Cardiol 2011;148(3):3004. [23] Caminiti G, Volterrani M, Marazzi G, et al. Hydrotherapy added to endurance training versus endurance training alone in elderly patients with chronic heart failure: a randomized pilot study. Int J Cardiol 2011;148(2):199203. [24] Ahmed MI, Lainscak M, Mujib M, et al. Gender-related dissociation in outcomes in chronic heart failure: reduced mortality but similar hospitalization in women. Int J Cardiol 2011;148(1):3642. [25] Ferrario M, Arbustini E, Massa M, et al. High-dose erythropoietin in patients with acute myocardial infarction: a pilot, randomised, placebo-controlled study. Int J Cardiol 2011;147(1):12431. [26] Kim HS, Lee JH, Lee SW, et al. Long-term safety and efcacy of sirolimus- vs. paclitaxel-eluting stent implantation for acute ST-elevation myocardial infarction: 3-year follow-up of the PROSIT trial. Int J Cardiol 2011;147(2):2537. [27] Kofoed KF, Kelbæk H, Thuesen L, et al. Left ventricular contractile function after distal protection in primary percutaneous coronary intervention: results from the drug elution and distal protection in ST-elevation myocardial infarction trial. Int J Cardiol 2011;146(3):3958. [28] Koh KK, Quon MJ, Han SH, et al. Additive benecial effects of atorvastatin combined with amlodipine in patients with mild-to-moderate hypertension. Int J Cardiol 2011;146(3):31925. [29] Robinson HJ, Samani NJ, Singh SJ. Can low risk cardiac patients be fast trackedto phase IV community exercise schemes for cardiac rehabilitation? A randomised controlled trial. Int J Cardiol 2011;146(2):15963. 0167-5273/$ see front matter © 2012 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2012.06.045 Vasomotor function and molecular responses following drug-eluting stent in a porcine coronary model Takamitsu Nakamura a, 1 , Chen Jing b, 1 , Yin Xinhua a , Jinsheng Li a , Jack P. Chen c , Spencer B. King III a , Nicolas Chronos a , John F. McDonald d , Dongming Hou a, a Saint Joseph's Translational Research Institute, Saint Joseph's Hospital of Atlanta, Atlanta, GA, United States b Department of Cardiology, Renmin Hospital of Wuhan University, China c The Northside Heart Institute, Atlanta, GA, United States d The School of Biology, Georgia Institute of Technology, Atlanta, GA, United States article info Article history: Received 26 March 2012 Received in revised form 30 May 2012 Accepted 8 June 2012 Available online 21 June 2012 Keywords: Drug-eluting stent Vasomotor function Gene expression The underlying molecular mechanisms of vascular endothelial dysfunction after drug-eluting stent (DES) implantation remain undened so far. In our previous published studies [1], profound localized inammatory reaction, as well as enhanced local oxidative stress were seen to contribute to vasomotor dysfunction following overlapping DES. Our recent work further investigated the effects of overlap DES on coronary vasomotor function and local gene expression in porcine coronary arteries. A total of 19 animals underwent implantation of overlapping bare metal stents (BMS; n=12), sirolimus-eluting stent (SES; n=12), and zotaroliums- eluting stents (ZES; n=13) as previously described [2]. Each animal was randomly assigned two pairs of identical stents, implanted into any of the three epicardial coronary arteries with a 1.1:1 stent to artery ratio, as well as overlap of one-third to one-half of the stent length. One animal from the ZES group was implanted with only one pair of stents. At 28 days, endothelium-dependent vasomotor func- tion was assessed following infusion of incremental doses of acetylcholine (Ach 10 - 6 and 10 - 5 M, 1 ml/min for 2 min). Endothelium-independent function was assessed by nitroglycerin (NTG, 200 μg). Quantitative coronary angiography was analyzed for luminal diameter changes in response to both Ach and NTG and expressed as percent of diameter change as compared with baseline. After termination, stented arteries from two animals in each group were collected for gene expression, and the remaining were used for histological evaluation. Corresponding author at: Saint Joseph's Translational Research Institute, 380-B Northyards Blvd., Atlanta, GA 30313, United States. E-mail address: dmhou@iupui.edu (D. Hou). 1 The rst 2 authors contributed equally to this work. 210 Letters to the Editor