The potential hazard of a non-slip element balloon causing distal longitudinal stent deformation: the first clinical experience and in vitro assessment

Background: A new complication, longitudinal stent deformation (LSD), is increasingly reported withrecent intracoronary stent designs. There have been experiences of unusual cases of distal LSD causedby entrapment of a Lacrosse® non-slip element (NSE) balloon (Goodman Co., Ltd., Nagoya, Japan),which has three flexible nylon elements to prevent slippage. Accordingly, the aim of this study is to reportthe clinical experience of distal LSD caused by the NSE in the documented center and to investigate theincidence and mechanisms involved.Methods: Coronary intervention cases were retrospectively reviewed using the NSE balloon in hospitalbetween May 2014 and June 2017. In bench testing, distal LSD was reproduced in a silicon tube modelto identify its mechanism.Results: A total of 95 patients with 107 lesions underwent coronary interventions with NSE. Of these,72 lesions (12 de-novo lesions and 60 in-stent restenosis) were treated using in-stent dilatation. Twodistal LSD cases occurred, representing an incidence of 2.78% (2/72) among all procedures; 16.7%(2/12) of the de-novo lesions developed LSD. In vitro experimentation allowed indentification of themechanisms involved and bailout strategies.Conclusions: This is the first study to evaluate NSE balloon catheter entrapment complicated by distalLSD in which reconstruction of the deformed stent and retrieval of the NSE could be achieved successfully.There is a potential hazard for distal LSD during post-dilatation using the NSE balloon due to itsstructural characteristics. Careful assessment is needed to prevent this complication

Glutaredoxin-1 Overexpression Enhances Neovascularization and Diminishes Ventricular Remodeling in Chronic Myocardial Infarction

Oxidative stress plays a critical role in the pathophysiology of cardiac failure, including the modulation of neovascularization following myocardial infarction (MI). Redox molecules thioredoxin (Trx) and glutaredoxin (Grx) superfamilies actively maintain intracellular thiol-redox homeostasis by scavenging reactive oxygen species. Among these two superfamilies, the pro-angiogenic function of Trx-1 has been reported in chronic MI model whereas similar role of Grx-1 remains uncertain. The present study attempts to establish the role of Grx-1 in neovascularization and ventricular remodeling following MI. Wild-type (WT) and Grx-1 transgenic (Grx-1Tg/+) mice were randomized into wild-type sham (WTS), Grx-1Tg/+ Sham (Grx-1Tg/+S), WTMI, Grx-1Tg/+MI. MI was induced by permanent occlusion of the LAD coronary artery. Sham groups underwent identical time-matched surgical procedures without LAD ligation. Significant increase in arteriolar density was observed 7 days (d) after surgical intervention in the Grx-1Tg/+MI group as compared to the WTMI animals. Further, improvement in myocardial functional parameters 30 d after MI was observed including decreased LVIDs, LVIDd, increased ejection fraction and, fractional shortening was also observed in the Grx-1Tg/+MI group as compared to the WTMI animals. Moreover, attenuation of oxidative stress and apoptotic cardiomyocytes was observed in the Grx-1Tg/+MI group as compared to the WTMI animals. Increased expression of p-Akt, VEGF, Ang-1, Bcl-2, survivin and DNA binding activity of NF-κB were observed in the Grx-1Tg/+MI group when compared to WTMI animals as revealed by Western blot analysis and Gel-shift analysis, respectively. These results are the first to demonstrate that Grx-1 induces angiogenesis and diminishes ventricular remodeling apparently through neovascularization mediated by Akt, VEGF, Ang-1 and NF-κB as well as Bcl-2 and survivin-mediated anti-apoptotic pathway in the infarcted myocardium