Abstract 651: An in Vitro Model to Test Possible Adverse Effects of Electrical Devices on ICD Function

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Madeleine T Friedman ◽  
Theodore J MacVeigh ◽  
Peter L Friedman

Devices such as capsules swallowed to perform video endoscopy (VE-CAP) or cell phones equipped with Bluetooth® (BLUE) emit electrical signals which could have adverse effects on implantable cardiac defibrillators (ICDs). We sought to study whether signals from VE-CAP or BLUE could cause spurious inhibition of ventricular pacing (VP i ) or spurious detection of ventricular fibrillation (VF d ) in an in vitro model. A Medtronic D154ATG single chamber ICD was attached to a Medtronic 6948 lead and placed in a saline bath. The ICD was programmed to perform VVI pacing at 60 beats per minute (bpm) and to detect ventricular fibrillation as rates in excess of 188 bpm, with sensitivity programmed at 0.15 mV. ICD therapies were programmed off. A VE-CAP was placed in the saline bath 1 cm. and 6 cm. from the lead tip (LEAD) and then 1 cm. and 6 cm. from the ICD pulse generator (CAN). Marker channels recorded by wireless telemetry from the ICD were used to determine whether the VE-CAP caused interaction (+) or no interaction (−). BLUE was tested in similar fashion. Radiofrequency (RF) electocautery from a Bovie, which is known to result in VP i and VF d , was applied to the saline bath 1 and 6 cm from the lead and 1 and 6 cm from the pulse generator as a control. The results were as follows: ICD lead tips in the right ventricular apex overlie the diaphragm and are often within 1 cm of the transverse colon. However, even at this distance, interaction between a VE-CAP and an ICD resulting in VP i or VF d is unlikely to occur. Capsule video endoscopy in patients with ICDs should be safe, even in patients who are pacemaker dependent. Similarly, BLUE is unlikely to cause VP i or VF d, and should be safe in such patients.

Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.


2011 ◽  
Vol 71 (05) ◽  
Author(s):  
M Salama ◽  
K Winkler ◽  
KF Murach ◽  
S Hofer ◽  
L Wildt ◽  
...  

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