We present the case of a 56-year-old woman with a resynchronisation pacemaker who was admitted for device removal due to local infection.

HISTORY, CURRENT DISEASE AND PHYSICAL EXAMINATION

BACKGROUND:
No known drug allergies. No known cardiovascular risk factors.
Cardiological history: rheumatic valve disease with open mitral commissurotomy in 1988. Permanent atrial fibrillation (AF). VVI pacemaker holder since 1998 due to AF that was difficult to control, with generator replacement in 2008 due to battery depletion. Echocardiogram in 2013 showed a moderate-severe double rheumatic mitral lesion with predominant stenosis, with preserved left ventricular ejection fraction (LVEF) and moderate pulmonary hypertension, severe tricuspid insufficiency (TI) and dilatation of the right ventricle (RV) with mild-moderate dysfunction. Surgical intervention was indicated, with mechanical mitral valve replacement and tricuspid annuloplasty, with good results. In the control echocardiogram one year later, the mitral prosthesis is normofunctioning, but a slightly dilated and dysfunctioning LV with LVEF 35% due to diffuse hypokinesia and anomalous septal movement in the context of stimulation is visualised. The patient's functional class worsened (New York Heart Association [NYHA] functional class III), so an upgrade to cardiac resynchronisation therapy was indicated in March 2015.
Possible vertebrobasilar transient ischaemic attack (TIA) in 2012. Normal TSA Doppler.
Myomatous uterus. Total hysterectomy + double adnexectomy in 2011.
Usual treatment: synthroid, furosemide 40 mg c/24 hours, carvedilol 6.25 mg c/12 hours, spironolactone 25 mg c/24 hours, omeprazole, zolpidem.
BFS: higher functions preserved. NYHA II.

CURRENT DISEASE:
After the upgrade to cardiac resynchronisation therapy (CRT), the patient presented a torpid evolution of the surgical wound, with tension haematoma one month after implantation that required drainage, and subsequent dehiscence that required debridement and approximation of the edges.
However, the patient did not evolve satisfactorily and, 5 months later, a subpectoral implant of the generator was indicated for decubitus, also requiring surgical debridement.
He continued to be monitored in cardiac surgery consultations, with good evolution of the surgical wound until, in December 2017, he consulted the emergency department for pain in the area of the generator and increasing local oedema. She did not present fever or elevated infectious markers. She was subsequently assessed by cardiac surgery, which observed signs of incipient decubitus in the pectoral area, with significant skin retraction, without suppuration.
Imaging tests were requested to complete the study and admission was indicated for the start of antibiotic treatment and removal of the resynchronisation device due to infection of the generator area.

PHYSICAL EXAMINATION:
Haemodynamically stable, well perfused. Eupneic. Afebrile. Good general condition. Head and neck: no IY. Chest: induration and pain on palpation in the left infraaxillary area, with skin retraction and trophic changes. No suppuration. Cardiac auscultation: arrhythmic, valvular click. Pulmonary auscultation: preserved ventricular murmur. Abdomen: soft and depressible, without pain or signs of peritoneal irritation. Lower extremities: no oedema or signs of deep vein thrombosis (DVT).

COMPLEMENTARY TESTS
ECG: AF with ventricular rhythm stimulated at 75 bpm.
ANALYTICS: normal renal function with GFR > 90 ml/min and normal ions. CRP 11.8. Normal leukocytes with normal leukocyte formula. Hb 11.8 g/dl. Coagulation without findings.
Transthoracic echocardiography (TTE): left ventricle (V) severely dilated by volumes. No visu asynchrony evident. LVEF 43%. Right ventricle (RV) normal with respect to size and function. Severely dilated left atrium (> 40 cm2).
Moderately dilated right atrium. Mitral prosthesis with good opening and mitral insufficiency (MI) that appears to be intraprosthetic. Normofunctioning tricuspid annulus, with no residual TR so that pulmonary artery pressure (PAP) cannot be estimated. The aortic valve is trivalve, with rheumatic involvement. Mild-moderate valvular aortic stenosis. Mild-moderate aortic insufficiency.
Aortic root of normal size. No pericardial effusion.
Transesophageal echocardiography (TEE): pacemaker lead in LV. Two leads are seen in the RA, following their course to the tricuspid valve without thickening suggestive of endocarditis. The intraventricular section cannot be assessed due to mitral acoustic shadowing. Bivalve mechanical prosthesis with good opening and intraprosthetic washout jets. No stigmata of endocarditis. Trivalve aortic valve.
POSITRON EMISSION TOMOGRAPHY (PET/CT): Heterogeneous increase in activity (early maximum SUV around 4.3 and late around 5.7) around the pacemaker generator located in the left pectoral region and slight activity (early and late SUV around 2.5) in the proximal section of the exit of the pacemaker lead from the generator, in the subcutaneous trajectory reaching the clavicle. Findings that, considering the time that has elapsed since its placement and which are visualised in both the corrected and uncorrected images, suggest active infectious pathology. In the superior mediastinum, a small focal uptake deposit is identified, which shows greater activity in the late images (early SUV = 2.8 and late SUV = 3.8) at the level of the entrance of the pacemaker lead into the superior vena cava. In the clinical context, this finding suggests an active focus of infection. No other abnormal increases in activity were seen in the rest of the pacemaker lead or in the electrodes. There were no abnormal increases in activity at or around the mitral valve suggesting infection-endocarditis.
In the left axilla there are several subcentimetre-sized lymphadenopathies with mild activity (maximum early and late SUV around 1.2) that may correspond to residual or reactive lymphadenopathies that are not very active. One lymph node stands out for its size (maximum diameter around 13mm) which shows greater activity (early SUV = 1.7 and late SUV = 2.6) which may be due to active inflammatory lymphadenopathy.
No other abnormal increases in uptake were identified in the rest of the lymph node territories included in the study, both supra- and infradiaphragmatic. Radiotracer uptake in both lungs is within normal limits. The distribution of activity in the liver and spleen is homogeneous, with no abnormal increases in activity. No pathological findings in the adrenal glands or pancreas. Slight increase in activity along the sternum translating residual reactive changes due to a history of median sternotomy. In the rest of the bone structures included in the study, no abnormal increases in activity are visualised. Reinforcement of uptake adjacent to the right humeral head due to insertional pathology. No significant alterations in the uptake and distribution of the tracer were observed in the rest of the body regions studied. Conclusion: findings compatible with infectious pathology around the pacemaker generator, as well as in the proximal subcutaneous trajectory of the pacemaker lead and in its entry at the level of the superior vena cava in a more focal manner. Lymph node uptake in the left axilla suggestive of reactive-inflammatory ethology.
ANGIO-CT coronary arteries: bicameral pacemaker with the end of the electrodes located in the RV and posterolateral vein. Patent coronary sinus of normal calibre. The posterolateral vein in which the electrode is lodged is of small calibre, and its patency cannot be assessed due to the artefact caused by the electrode. Inferolateral vein of good calibre, 5 mm in diameter, originating 12 mm from the valve of Tebesio and presenting a lateral direction towards the inferolateral segments of the LV, can be seen on the inferior face. Median sternotomy and triple valve replacement. Cardiomegaly. Pulmonary parenchyma without findings.  Conclusions: posterolateral vein in which the electrode is lodged is of small calibre and cannot be assessed due to artefacts caused by the electrode, and its patency cannot be assessed. Inferolateral vein of good calibre.

MICROBIOLOGICAL STUDY:
Blood cultures (on admission): negative.
Pan bacterial PCR 16S rRNA 31/1/18: not detected.
Blood cultures (after episode of phlebitis): positive for Staphylococcus aureus without resistance, with negative results in control cultures after targeted antibiotherapy.
Cultures of vascular material (extracted system): positive for Staphylococcus hominis (DV electrode and subcutaneous swab) and Staphylococcus epidermidis (LV lead, DV lead, subcutaneous swab and generator capsule). Negative control blood cultures.


CLINICAL COURSE
After removal of a cardiac pacing device, it is recommended to re-evaluate the need for reimplantation of the same device or another device with greater or lesser functionalities. The challenge in this patient was to define whether she had responded to resynchronisation therapy, to indicate a resynchronising pacemaker again or, if not, a single-chamber pacing pacemaker. The patient was finally considered a clinical responder due to a slight improvement in functional class (NYHA III to II), but not a responder echocardiographically. Given the positive clinical response, reimplantation of a new cardiac resynchronisation device was indicated.
During admission, the cardiac resynchronisation device was initially scheduled to be explanted and removed at the same time, with periprocedural antibiotic treatment, given that the patient remained afebrile, clinically and haemodynamically stable and without elevation of acute phase reactants. However, while awaiting surgery, she developed bacteraemia due to methicillin-sensitive S. aureus, secondary to phlebitis due to infection of a peripheral vein, so antibiotic therapy with vancomycin was started after drawing blood cultures, and withdrawal and reimplantation was indicated in two stages, after antibiotic therapy. During admission, the patient remained afebrile and haemodynamically stable at all times. Since the patient had a high percentage of pacing with a narrow QRS escape ventricular rhythm at 35 bpm, after removal of the resynchronisation system, a transient right jugular pacemaker was implanted while awaiting reimplantation of the permanent pacemaker. While admitted to the hospital ward, she lost capture due to dislocation of the electrode, which caused decompensation of heart failure requiring continuous isoproterenol perfusion and subsequent replacement of the transient pacing lead, with placement of a temporary active fixation electrode. After the repositioning procedure, she was admitted to the coronary unit, presenting acute pulmonary oedema that responded favourably to diuretic treatment, and she was discharged to the hospital ward in 48-72 hours, where she remained to complete the antibiotic regimen until the reimplantation of the definitive pacemaker.
Finally, in a situation of clinical stability and after approximately 2 weeks of antibiotic treatment, with negative blood cultures, she was scheduled for resynchronisation pacemaker implantation. Unfortunately, the coronary sinus could not be cannulated after multiple attempts, so only one RV electrode connected to a resynchronisation generator was placed on the contralateral side.
The patient was discharged home pending completion of intravenous antibiotic therapy. She is currently clinically stable, has not presented decompensation of heart failure and the control echocardiogram shows no worsening of LVEF. The patient's clinical evolution in the short-medium term is pending re-evaluation, with the aim of considering other therapeutic alternatives should she present poor clinical evolution, such as endocardial left ventricular stimulation, given that she is a patient with an indication for permanent anticoagulation.

DIAGNOSIS
Local infection of the cardiac resynchronisation device.
Removal of the complete system (generator and RV and LV leads).
Implantation of transient right jugular pacemaker.
Implantation of resynchronisation generator and right-sided RV electrode in a second stage.
Right upper extremity phlebitis with methicillin-sensitive S. aureus bacteraemia.
Dilated cardiomyopathy with moderate LV systolic dysfunction.
Rheumatic valve disease with mitral prosthesis and tricuspid annulus without functional alterations. Double mild-moderate aortic lesion.
Permanent AF.
