Pacemaker lead related myocardial perforation

Permanent pacemaker (PPM) insertion is widely used to treat cardiac rhythm disorders; approximately 600,000 pacemakers are implanted annually in the US (Wood and Ellenbogen, 2002). Almost 9% of patients who receive a permanent pacemaker, however, experience a variety of medical complications such as infections, battery problems, programming issues, lead migration, or lead fracture (Greenspon et al., 2012). Moreover 1–2% of these patients will encounter severe lead-related problems within 30 days of their pacemaker insertion (Kirkfeldt et al., 2014; Kiviniemi et al., 1999). In this report, we focus on an uncommon but serious complication of PPM insertion: right ventricular lead perforation leading to a pericardial effusion. Although lead perforation is a relatively rare occurrence, this event can be life-threatening, and should be considered in the differential diagnosis when patients present to the emergency department (ED) with relevant symptoms and recent PPM insertion. Specifically, patients who experience complications from pacemaker insertion may present to the ED with a variety of symptoms such as chest pain, syncope, dyspnea, or even dizziness (Squire and Niemann, 2006). Pacemaker complications include pneumothorax, pleural and/or pericardial effusions, and infection, placing the patient at serious risk for significant harm (Squire and Niemann, 2006; Shingaki et al., 2015). The evaluation of a lead-related issue typically involves chest radiography to visualize abnormal lead placement and check for a pneumothorax or pleural effusion, and a 12‑lead electrocardiogram (ECG) to detect pacing errors. We present the case of a patient who presented to the ED three days after his pacemaker insertion with chest pain and dyspnea; he was subsequently diagnosed with a lead perforation into the pericardial space resulting in a pericardial effusion

TREE CANOPY RESEARCH AND STUDENT EXPERIENCES USING THE DOUBLED ROPE CLIMBING METHOD

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Tryptase activates isolated adult cardiac fibroblasts via protease activated receptor-2 (PAR-2)

Protease activated receptor-2 (PAR-2) derived cycloxygenase-2 (COX-2) was recently implicated in a cardiac mast cell and fibroblast cross-talk signaling cascade mediating myocardial remodeling secondary to mechanical stress. We designed this study to investigate in vitro assays of isolated adult cardiac fibroblasts to determine whether binding of tryptase to the PAR-2 receptor on cardiac fibroblasts will lead to increased expression of COX-2 and subsequent formation of the arachodonic acid metabolite 15-d-Prostaglandin J2 (15-d-PGJ2). The effects of tryptase (100 mU) and co-incubation with PAR-2 inhibitor peptide sequence FSLLRY-NH2 (10-6M) on proliferation, hydroxyproline concentration, 15-d-PGJ2 formation and PAR-2/COX-2 expression were investigated in fibroblasts isolated from 9 week old SD rats. Tryptase induced a significant increase in fibroproliferation, hydroxyproline, 15-d-PGJ2 formation and PAR-2 expression which were markedly attenuated by FSLLRY. Tryptase-induced changes in cardiac fibroblast function utilize a PAR-2 dependent mechanism