This case report presents a unique scenario of a delayed pacemaker pocket infection occurring three years post-implantation, without positive cultures for any specific pathogen. The absence of pathogen growth in blood and local secretion cultures is particularly notable and warrants discussion. Several factors could contribute to this finding [1]. Firstly, the patient’s prior antibiotic treatment at a local hospital before cultures were taken could have suppressed bacterial growth, making it difficult to identify the causative agent. Additionally, the nature of the infection, possibly being subacute or chronic due to the extended period post-implantation, might have led to low bacterial loads that are difficult to culture.

The patient’s profession as a violinist involves repetitive use of the left shoulder, which likely contributed to mechanical wear and erosion at the pacemaker site, increasing the risk of infection. However, the absence of detectable pathogens in the cultures suggests that the inflammatory response could be partially due to non-infectious factors such as mechanical irritation, although the clinical presentation and response to antibiotics indicate an infectious process.

The unique presentation of VT in this case was associated with the pacemaker lead’s positioning in the right ventricular outflow tract, suggesting that the inflammation around the lead, whether infectious or mechanically induced, could exacerbate arrhythmogenicity [2,3,4]. Although the patient’s ventricular tachycardia (VT) ECG characteristics are not typical, they still suggest a likely origin from the right ventricular outflow tract (RVOT) free wall. The variability in QRS morphology, with lead I showing Rs pattern to rS pattern, leads II, III, aVF showing R pattern, lead V1 showing R pattern, and lead V2 showing rS pattern, may be due to local electrode movement or regional cardiac conduction variations. The termination of VT upon removal of the RVOT free wall electrode further supports this origin despite the atypical ECG presentation [5].

The resolution of symptoms following the removal of the device and administration of antibiotics supports the infectious nature of the inflammation, but also highlights the complexity of diagnosing and treating device-related infections when standard cultures fail to identify a pathogen [6].

The gradual changes in QRS morphology observed during ventricular tachycardia (VT) in this patient with a right ventricular outflow tract (RVOT) pacemaker lead suggest variable contact between the lead tip and myocardial cells. Despite these morphological changes, the VT frequency remains constant, indicating a stable pacing source likely at the lead tip. These observations are independent of body position changes, reinforcing that the QRS variations are due to local contact variations rather than positional changes of the heart. This phenomenon underscores the significant impact of lead tip positioning on QRS waveform characteristics [7,8,9].

Removing a pacemaker lead three years post-implantation carries a risk of cardiac perforation. However, due to pacemaker pocket and lead infection, removal was necessary. We meticulously prepared for potential complications, including pericardiocentesis and cardiac surgery readiness for emergency open-heart intervention. The extraction of the screw-in lead proceeded smoothly, and the patient experienced no postoperative complications such as pericardial effusion [10,11,12].

Given the lack of positive cultures, the decision to use broad-spectrum antibiotics was prudent and based on the common pathogens associated with pacemaker infections, primarily Staphylococcus species. This approach is justified in cases where clinical signs of infection are evident, but no specific pathogens are identified, as it covers a broad range of potential bacteria.

The management of the infection through device removal and broad-spectrum antibiotic therapy [13, 14], in this case, was effective, underlining the importance of a comprehensive approach to suspected infections, especially when empirical treatment is necessary. This case emphasizes the need for careful assessment of occupational factors that may compromise implant sites and highlights the challenges of managing infections when culture results are negative [15].