History, current illness and physical examination
Personal history: 88-year-old male with a personal history of arterial hypertension, VDD pacemaker due to complete AV block implanted 4 months ago, complicated by post-implant cardiac tamponade and recent admission to the Geriatrics Department for pneumonia in the right upper lobe. Baseline situation: independent for basic activities of daily living, without cognitive impairment. Dyspnoea on moderate exertion.

Usual treatment: enalapril 5 mg per day and torasemide 10 mg per day. Present illness: she attended the emergency department for generalised oedema and oligoanuria of three days' evolution, with intense asthenia and anorexia. She also reported catarrhal symptoms, with rhinorrhoea and dry cough, without thermometric fever.
Physical examination: BP 190/80 mmHg, HR 95 bpm, temperature 37.7 oC, saturation with 2-litre nasal spectacles 94%. General condition was fair, mucocutaneous pallor, eupneic at rest. Auscultation revealed a mesosystolic murmur in the lower left sternal border and rhonchi in the right lung base. The rest was unaltered.

Complementary tests
Laboratory tests: Hb 10.3 g/dl, MCV 100, creatinine 3.49 mg/dl (previously 1.4 mg/dl), Na 144, K 5.5 and moderate haematuria in the urine sediment.
Chest X-ray: cardiomegaly, signs of pulmonary congestion and infiltrate in the right lower pulmonary lobe.
ECG: sinus rhythm at 94 bpm with electrostimulated ventricular response.
Transthoracic echocardiogram: left ventricle with severe concentric hypertrophy and moderate systolic dysfunction. Degenerative aortic stenosis. Non-dilated right ventricle. Normopositioned pacemaker lead, with a wart of approximately 1.8 cm2, close to the tricuspid leaflets and synchronous movement with them, with mild tricuspid insufficiency. Estimated pulmonary artery systolic pressure of 31 mmHg. Slight pericardial effusion and severe left pleural effusion.

Clinical course
The patient was admitted in a serious condition with intense asthenia and oligoanuria with worsening renal function. In view of the echocardiographic findings and the diagnosis of endocarditis on the pacemaker lead, antibiotic treatment with rifampicin and daptomycin was started.
It was decided to remove the entire MCP system and reimplant a new device as the patient was in full AVB, but the clinical evolution was very torpid with intense negative mood symptoms and poor functional reserve, and the patient died a few days after admission without being able to remove the pacemaker.

Diagnosis
We present the case of an octogenarian patient with endocarditis on a pacemaker lead with a very torpid evolution.

The postulated pathogenic mechanisms are as follows:
Local contamination of the pacemaker. This is the most frequent mechanism. It usually occurs during implantation of the device. Often the infection starts in the generator pocket and spreads to the lead. The clinical course may be acute or larval, manifesting itself even years later. The duration of the procedure, inadequate asepsis and operator inexperience are responsible factors.
Skin erosion or necrosis of the generator pocket or the skin adjacent to the electrode, which act as a gateway for microorganisms. Factors involved in this mechanism include inadequate technique and site of implantation, generator size, and patient malnutrition.
Haematogenous infection. Arrival of the micro-organism via the blood from another distant infectious source. The source of bacteraemia may be a central venous catheter, a valve prosthesis or invasive therapeutic procedures.

The most frequently isolated microorganisms are staphylococci. S. aureus is the predominant bacterium in cases of acute infection, while coagulase-negative staphylococci are the micro-organisms responsible for the majority of late infections.

Other microorganisms involved include Pseudomonas aeruginosa, enterobacteria, Propionibacterium acnes and Corynebacterium sp., and polymicrobial infections have been described, especially in diabetic patients or those taking corticosteroids. When the pacemaker infection is secondary to left-sided endocarditis, the microbiological profile is different, in line with the microorganisms causing the valve infection.
