Right Ventricular Free Wall Perforation without Tamponade: A Rare Complication of Permanent Pacemaker Lead Placement

2016 ◽  
Vol 1 (1) ◽  
pp. 22-26
Author(s):  
Serkan Burc Deser ◽  
Mustafa Kemal Demirag
Keyword(s):  
Right Ventricular ◽  
Rare Complication ◽  
Permanent Pacemaker ◽  
Ventricular Free Wall ◽  
Pacemaker Lead ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Lead Placement ◽  
Wall Perforation

scholarly journals Fibrin glue patch for pacemaker lead perforation of the right ventricular free wall: A case report

2016 ◽  
Vol 2 (1) ◽  
pp. 80-82 ◽  
Author(s):  
Satoshi Yamaguchi ◽  
Masaki Tabuchi ◽  
Kageyuki Oba ◽  
Hiroshi Doi ◽  
Osamu Arasaki
Keyword(s):  
Case Report ◽  
Right Ventricular ◽  
Fibrin Glue ◽  
Ventricular Free Wall ◽  
Pacemaker Lead ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Lead Perforation ◽  
The Right

Differential regional gene expression from cardiac dyssynchrony induced by chronic right ventricular free wall pacing in the mouse

2006 ◽  
Vol 26 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Kenneth C. Bilchick ◽  
Sudip K. Saha ◽  
Ed Mikolajczyk ◽  
Leslie Cope ◽  
Will J. Ferguson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Right Ventricular ◽  
Differential Expression ◽  
Stem Cell Differentiation ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Cardiac Dyssynchrony ◽  
Clinical Prognosis

Routine clinical right ventricular pacing generates left ventricular dyssynchrony manifested by early septal shortening followed by late lateral contraction, which, in turn, reciprocally stretches the septum. Dyssynchrony is disadvantageous to cardiac mechanoenergetics and worsens clinical prognosis, yet little is known about its molecular consequences. Here, we report the influence of cardiac dyssynchrony on regional cardiac gene expression in mice. Mice were implanted with a custom-designed miniature cardiac pacemaker and subjected to 1-wk overdrive right ventricular free wall pacing (720 beats/min, baseline heart rate 520–620 beats/min) to generate dyssynchrony (pacemaker: 3-V lithium battery, rate programmable, 1.5 g, bipolar lead). Electrical capture was confirmed by pulsed-wave Doppler and dyssynchrony by echocardiography. Gene expression from the left ventricular septal and lateral wall myocardium was assessed by microarray (dual-dye method, Agilent) using oligonucleotide probes and dye swap. Identical analysis was applied to four synchronously contracting controls. Of the 22,000 genes surveyed, only 18 genes displayed significant ( P < 0.01) differential expression between septal/lateral walls >1.5 times that in synchronous controls. Gene changes were confirmed by quantitative PCR with excellent correlations. Most of the genes ( n = 16) showed greater septal expression. Of particular interest were seven genes coding proteins involved with stretch responses, matrix remodeling, stem cell differentiation to myocyte lineage, and Purkinje fiber differentiation. One week of iatrogenic cardiac dyssynchrony triggered regional differential expression in relatively few select genes. Such analysis using a murine implantable pacemaker should facilitate molecular studies of cardiac dyssynchrony and help elucidate novel mechanisms by which stress/stretch stimuli due to dyssynchrony impact the normal and failing heart.

Sign in / Sign up

Export Citation Format

Share Document