Transluminal lead extraction (TLE) is a well-established procedure for the removal of damaged or infected pacing systems. Despite its high efficacy, the procedure is associated with significant risks, some of which may contribute to severe life-threatening complications. Herein, we present the case of a 90-year-old female who was 100% pacemaker-dependent (PM-dependent) and had ventricular lead fragmentation after the TLE procedure. In this elderly patient, after taking into account the whole clinical context—age, frailty syndrome, infection, and high peri- and postprocedural risks—we decided on MICRA VR implantation as well as leaving the remains of the ventricular lead in the right heart chambers. A Leadless pacemaker (LP) is an excellent alternative to PM-dependent individuals, in whom implantation of permanent transvenous PM is precluded due to multiple infectious and non-infectious issues.

On chromosome 10q23 is found the PTEN gene, which encodes a phosphate and tension homologue. The protein dephosphorylates phosphatidylinositol-(3,4,5)-trisphosphate at the plasma membrane to produce inorganic phosphatidylinositol-(4,5)-bisphosphate. This enzymatic activity inhibits the phosphatidylinositol-3-kinase, protein kinase B and mammalian target of the rapamycin signalling cascade. Consequently, essential cellular functions, including metabolic regulation, cellular growth, proliferation and viability, are affected. A mutation in this gene gives rise to hamartoma tumour syndrome, which exhibits a range of phenotypes, including Bannayan-Riley-Ruvalcaba syndrome, Cowden syndrome and proteus-like disease. A man in his late 20s with a PTEN tumour-like arteriovenous malformation in the right thigh was recently diagnosed with lupus nephritis. The patient’s nephritic symptoms, pleural effusion, dyslipidaemia and splenomegaly demonstrate systemic lupus erythematosus (SLE) multisystem involvement. The case report identifies an association between a PTEN mutation and a new diagnosis of SLE that might have been triggered by PTEN-associated immune dysregulation.