English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Cardiac pacing is a common and proven therapy in the treatment of many cardiac conduction abnormalities and arrhythmias. Despite their lifesaving potential, they are limited by device related complications, notably infection and mechanical complications, which includes myocardial perforation. Though rare, perforation may potentially be fatal. Many times, these perforations are acute, occurring within the fi rst twenty-four hours and common sequelae include pneumothorax, hemopericardium, cardiac tamponade and death. While hemothorax has been reported, it is extremely rare. As time progresses, subacute and delayed perforations become even more uncommon and a hemothorax as a complication to a subacute perforation is exceedingly rare [1]. Here, we present a case of a 90-year-old female with a right ventricular perforation and subsequent development of a left hemothorax twenty-nine days after pacemaker insertion. A 90-year-old female with a history signifi cant for coronary artery disease and sick sinus syndrome with a Medtronic pacemaker placed twenty-nine days prior presented to the emergency department with overall lethargy and feeling “unwell”. She complained of shortness of breath, bloating and pleuritic chest pain. A chest x-ray showed a retrocardiac opacity that was initially believed to be pneumonia. However, her heart rate was noted to have several transient episodes of rates into 30s with pauses. Additionally, her hemoglobin and hematocrit were noted to have decreased from a baseline of 9.5 g/dL and 29.3% to 7.1 g/dL and 21.5% respectively. There was no overt evidence of bleeding. An interrogation of her pacemaker showed a malfunctioning right ventricular lead that was unable to capture at 8.0 V in unipolar and bipolar pacing modes. A computed tomography (CT) of the thorax without contrast was obtained and it showed the right ventricular (epicardial) pacemaker lead perforating the apical right ventricular wall and into the lingua along with

An unusual case of a subacute right ventricular perforation from a pacemaker lead with subsequent left hemothorax