A 20-years-old man was admitted to the emergency department after being resuscitated from SCD while playing football. No personal medical history or daily medication, no alcohol or drugs consumption and no history of medical or food allergy was noted.
During hospitalization stay, a monomorphic ventricular tachycardia with hemodynamic instability was documented and successfully electrically converted to sinus rhythm. The baseline EKG showed a QT interval upper normal limit range. The patient started antiarrhythmic therapy with no recurrence of events.
His older brother had died of SCD at the age of 21 (non-diagnostic autopsy findings). No other family history was reported.
Workup study including transthoracic echocardiography and cardiac magnetic resonance did not reveal any specific structural or functional abnormalities. Coronary artery disease and congenital anomalies were excluded. Genetic testing identified a mutation in the KCNH2 gene of uncertain significance, usually associated to long QT syndrome type 2. He was then referred for a subcutaneous implantable cardiac defibrillator (S-ICD; generator Emblem  MRI A219) implantation for secondary prevention, with no immediate complications.
Four months later, the patient developed suture dehiscence and inflammatory signs through the path of the subcutaneous lead and an infection was assumed. Empirical antibiotic therapy was initiated but blood cultures were consistently negative. Because of the persistence of inflammatory signs, the S-ICD was removed, and an endovascular ICD (generator: Boston Autogen EL  VR D174; Lead: Reliance 4-Front) was implanted without complications. The patient was then discharged symptom-free.
A pocket fragment and lead portion were sent to microbiology, but the results were negative.
Five months later, he was readmitted due to inflammatory signs on the device incision and wound dehiscence (Fig. 1). Systemic infection was excluded, and the ICD was removed again with negative microbiologic results. We noticed a clear straw-colored exudate as we opened the incision. At this point, a hypersensitivity reaction with device rejection was suspected and the patient was referred to Allergy and Clinical Immunology Department. A patch-test was performed with a sparse reaction to some materials, with no evident allergy to a specific one. A localized dermatitis with titanium material was suspected, but repeated testing was negative. A trial with low dose systemic corticosteroid therapy was initiated with a transient improvement of symptoms followed by an early recurrence of cutaneous inflammatory signs.
Despite of inconclusive results, around three months after the explant, it was decided to implant a custom-made gold-coated endovascular ICD (Medtronic Evera  XT DR, DDBB2D4G; coating thickness 0.5 mum, pure 99.9% 24 carat gold). This gold device was, on this occasion, implanted in the right chest wall percutaneously via the right subclavian vein. It has been well tolerated for 3 years since implantation with no signs of rejection or other complications.