Cryoplasty for the Treatment of Coronary Bifurcation Stenoses Following Main Vessel Stenting

Objectives

This retrospective study sought to assess the safety and clinical efficacy of cryoplasty for treatment of side‐branch stenoses following main vessel stenting in coronary bifurcation lesions.

Background

Cryoplasty prevents restenosis by reducing smooth muscle proliferation and extracellular matrix synthesis. Clinical effectiveness has been demonstrated in the peripheral circulation. Treatment of coronary bifurcation lesions remains a challenge. We used a novel strategy of main vessel stenting combined with side‐branch cryoplasty to treat high‐grade stenoses following main vessel stenting.

Methods

Eighteen patients with bifurcation lesions had significant plaque shift into a side branch after main vessel intervention. Drug‐eluting stents were placed in the main vessel and cryoplasty was performed on the side‐branch vessel. Quantitative coronary analysis was performed on all side‐branch vessels both pre– and post–main vessel stenting. All patients had clinical follow‐up 3 months or more after cryoplasty including either nuclear stress testing or diagnostic coronary angiogram.

Results

Mean percent stenosis decreased from 80.6% post main vessel stenting to 24.8% following cryoplasty (P < 0.0001). Of the 17 patients who had pre‐cryoplasty nuclear stress testing 1 patient had ischemia identified in the distribution of the treated vessel at follow‐up. Five patients had follow up angiography. One patient had restenosis, the other 2 were unchanged. There was a low incidence of MACE.

Conclusions

In this first report of its use in the coronary circulation, cryoplasty for bifurcation side‐branch disease was safe and associated with a low rate of clinical recurrence in carefully selected patients. (J Interven Cardiol 2013;26:239–244)

     

URIC ACID AND TISSUE REPAIR

Uric acid, a metabolic product of purines, may exert a role in tissue healing. In this review we will explore its role as an alarm initiating the inflammatory process that is necessary for tissue repair, as a scavenger of oxygen free radicals, as a mobilizer of progenitor endothelial cells and as supporter of adaptive immune system.     

Randomized clinical trial on acute effects of i.v. iron sucrose during haemodialysis

Aim: Haemodialysis induces endothelial dysfunction by oxidation and inflammation. Intravenous iron administration during haemodialysis could worsen endothelial dysfunction. The aim of this study was to ascertain if iron produces endothelial dysfunction and the possible neutralizing effect of N‐acetylcysteine when infused before iron. The oxidative and inflammatory effects of iron during haemodialysis were also assessed. Methods: Forty patients undergoing haemodialysis were studied in a randomized and cross‐over design with and without N‐acetylcysteine infused before iron sucrose (50 or 100 mg). Plasma Von Willebrand factor (vWF), soluble intercellular adhesion molecule‐1 (sICAM‐1) levels, malondialdehyde, total antioxidant capacity, CD11b/CD18 expression in monocytes, interleukin (IL)‐8 in monocytes and plasma IL‐8 were studied at baseline and during haemodialysis. Results: Haemodialysis produced significant (P < 0.001) increase in plasma vWF, sICAM‐1, malondialdehyde, IL‐8 and CD11b/CD18 expression in monocytes, as well as decrease in total antioxidant capacity. Iron induced significant increase in plasma malondialdehyde and IL‐8 in monocytes, but had no effect on total antioxidant capacity, CD11b/CD18 expression, plasma IL‐8, vWF and sICAM‐1. The addition of N‐acetylcysteine to 50 mg of iron produced a significant (P = 0.040) decrease in malondialdehyde. Conclusion: Standard (100 mg) and low (50 mg) doses of iron during haemodialysis had no effects on endothelium. Iron only had minor effects on inflammation and produced an increase in oxidative stress, which was neutralized by N‐acetylcysteine at low iron dose. Haemodialysis caused a significant increase in oxidative stress, inflammation and endothelial dysfunction markers.