Inadvertent triggering of supraventricular tachycardia during pacemaker interrogation: Time to lose the magnet?

A 22-year-old male had a dual chamber permanent pacemaker (PPM) implanted for complete heart block following aortic valve replacement for Shone's syndrome 3 months previously. He presented with acute shortness of breath due to severe para-valvular leak with aortic valve dehiscence following a motor vehicle accident. He was scheduled for redo sternotomy and a pre-operative PPM check was undertaken. A programmer wand (Model 2067, Medtronic Inc., Minneapolis, MN, USA) was applied to the patient's PPM site to perform interrogation. During initialization, asynchronous DOO pacing at the magnet rate of 85 bpm was initiated with evidence of both atrial and ventricular capture. Competition from intrinsic rhythm resulted in functional loss of capture. Competitive pacing initiated a narrow complex supraventricular tachycardia at 180 bpm. The tachycardia persisted to result in clinical deterioration until reversion with urgent intravenous metoprolol. Programmer wands from Medtronic (Model 2067 & Encore) and Biotronik (Renamic, Biotronik Inc., Berlin, Germany) have in-built magnets that can cause asynchronous pacing during initialization of interrogation. Removing the magnet in future iterations of PPM programmer wands will mitigate inadvertent arrhythmia induction. .

Aortic plaque defined by contrast transthoracic echocardiography.

The authors explore the use of third generation echo contrast to define plaque in the ascending aorta and exclude more invasive procedures.

An examination of the antibiotic effects of cylindrospermopsin on common gram-positive and gram-negative bacteria and the protozoan Naegleria lovaniensis.

The importance of the toxin cylindrospermopsin to the function and fitness of the cyanobacteria that produce it remains a matter of conjecture. Given that the structure of cylindrospermopsin has commonalities with other antibacterial protein synthesis inhibitors, such as streptomycin, authors tested the possibility that the toxin might act as an antibacterial compound that can kill competing microbes. Escherichia coli, Bacillus subtilis, Staphylococcus aureus, and Pseudomonas aeruginosa were tested by the minimal inhibitory concentration method and significant antibacterial activity was only observed at a cylindrospermopsin concentration of 300 microg mL(-1) after exposure for 5 days. No effect on log phase growth of E. coli was observed for this same toxin concentration. Protein synthesis was inhibited by cylindrospermopsin in E. coli 70S extracts, reduced by 25% compared with controls when treated with 41.5 microg mL(-1) of the toxin; however, a much greater reduction of 97% was observed for chloramphenicol in the same experiment. Naegleria lovaniensis, a phagotrophic protozoan, was more susceptible to cylindrospermopsin, with a decrease in the number of N. lovaniensis plaques after 24-h treatment with 5-50 microg mL(-1) of toxin and an LC(50) of approximately 60 microg mL(-1). Given these results, cylindrospermopsin is clearly not antibacterial at concentrations found in environmental waters, nor will it adversely affect N. lovaniensis at these concentrations. For organisms that are able to ingest cylindrospermopsin-producing cells, the response of N. lovaniensis to the toxin suggests that only a few ingested cells would be enough to kill predatory organisms with similar susceptibility.