Stepwise transvenous lead extraction due to pacemaker pocket infection following lactational mastitis complicated with breast abscess.

BACKGROUND: Lactational mastitis is a common painful and debilitating inflammation of breast tissue, generally treated conservatively or with pus puncture in case of breast abscess. However, treating mastitis in patients with implantable surgical material located in the affected breast region can be extremely challenging. We present an unusual case of lactational mastitis complicated by pacemaker pocket infection in a breastfeeding mother. CASE PRESENTATION: A 35-year-old pacemaker-dependent female developed lactational mastitis seven weeks postpartum. Initially, the condition was treated conservatively with analgesics and antibiotics. After abscess formation, pus was aspirated using fine-needle aspiration technique. Four weeks after mastitis resolution, pacemaker pocket infection developed. According to current cardiovascular implantable electronic device infection treatment guidelines a complete surgical extraction of the entire electronic system, followed by targeted antibiotic treatment and reimplantation of a new device after infection resolution, was recommended. However, after thorough discussion with the young woman and her family and after detailed review of surgery-related risks, she declined a potentially high-risk surgical procedure. Thus, only the pulse generator was explanted; pacing leads positioned in the sub-pectoral pocket; new pacemaker implanted on the contralateral side and broad-spectrum antibiotic therapy continued for six weeks. After breastfeeding cessation, and with chronic fistula development at the primary pacemaker implantation site, the possibility of delayed surgical intervention including complete extraction of retained pacemaker leads was again thoroughly discussed with her. After thoughtful consideration the woman consented to the proposed treatment strategy. A surgical procedure including transvenous lead extraction through the primary implantation venous entry site, using hand-powered bidirectional rotational sheaths, was successfully performed, removing all retained leads through the left subclavian venous entry site, and leaving the fully functional and clinically uninfected pacemaker on the contralateral site intact. CONCLUSION: Although patients' decisions for delayed extraction in a case of cardiovascular implantable electronic device infection should be discouraged by attending physicians and members of interdisciplinary teams, our case shows that a stepwise treatment strategy may be successful as a bailout clinical scenario in patients with specific requests, demands and / or clinical needs.

Pulse amplitude adjustment provides immediate pacemaker longevity gain.

OBJECTIVE: Adjusting pacemaker pulse amplitude influences the longevity of the pacemaker. Our aim was to establish the initial longevity gain. METHODS: Forty randomly selected patients with implanted pacemakers were analyzed. Mean age was 65.58+/-13.7 years. All pacemakers were working on factory settings of pulse amplitude 3.5 V and pulse width of 0.4 ms for average of 3 years before the adjustment. Initial mean longevity was projected to 68.61+/-18.86 months, mean battery voltage 2.78 V, and mean battery current 14.21+/-2.61 microA. RESULTS: Pulse amplitude threshold test was performed and average value of 0.632+/-0.22 V was obtained. Pulse amplitude was programmed to 2.5 V and pulse width was left unchanged. New readings of battery data were obtained. Battery voltage did not show immediate changes, and battery current decreased to 11.53+/-1.98 microA. New average longevity was projected to 81.03+/-19.82 months, which presents a 12.42 months of initial longevity gain with statistical significance at 95% confidence interval (p=0.003). Positive correlation was found between the new pulse amplitude and new values of battery current (p<0.01). CONCLUSION: Pulse amplitude decrease of only 1 V provides significant initial longevity gain of more than a year. If found correlations would have any impact on further longevity gains over longer period of time is yet to be established.

Induction of atrioventricular node reentry by simultaneous anterograde conduction over the fast and slow pathways.

Atrio-ventricular node reentry (AVNRT) is typically induced with an anterograde block over the fast pathway (FP) and conduction over the slow pathway (SP), with subsequent retrograde conduction over the FP. Rarely, a premature atrial complex (PAC) conducts simultaneously over the FP and SP to induce AVNRT. Previous publications have reported that conduction over the fast and slow pathway of the atrioventricular node can occur successively one after the other, thus leading to dual ventricular depolarization from what initially was a single atrial impulse. We report a case of an 18-year-old male patient referred for repeated bursts of ectopic activity. Evaluation of the patient's electrocardiographic recordings suggested the presence of dual ventricular activations for each atrial beat. The electrophysiological study revealed that the patient had simultaneous conduction over the fast and slow pathways of the atrioventricular node giving rise to a non-reentrant tachycardia, along with an absence of retrograde (ventriculoatrial) conduction, and a significant atrio-His bundle jump (A-H jump) through the slow pathway from the fast pathway during programmed electrical stimulation from the right atrium. Ablation of the slow pathway at the base of the Koch triangle yielded a cessation of the dual ventricular response, absence of the nonreentrant tachycardia and no A-H jump.