Pacemaker lead rupture in a patient with subacute endocarditis: a case report.

BACKGROUND: Cardiac implantable electronic device (CIED)-related infections are associated with severe morbidity and mortality. Few cases have previously documented both lead endocarditis and lead rupture simultaneously. CASE SUMMARY: We describe the case of a 73-year-old man with a dual-chamber pacemaker presenting with subacute endocarditis and recurrent cholangitis. A few months prior, the patient was diagnosed with localized colon cancer and Streptococcus sanguinis lead endocarditis based on nuclear imaging. He was given prolonged antibiotic therapy and lead explantation was to be performed after sigmoidectomy. During the following weeks, his condition worsened and he was readmitted for biliary sepsis. A chest X-ray revealed, incidentally, a complete ventricular lead rupture. Pacemaker electrogram showed ventricular undersensing, loss of ventricular capture, and high impedance. As his health declined, removal of the pacemaker was deemed unreasonable and the patient died of biliary sepsis in the next few weeks. DISCUSSION: We describe the case of an asymptomatic intracardiac lead fracture in the setting of colon cancer and a medically managed Streptococcus lead infection. As this complication occurred during lead infection, bacterial damage may have weakened the lead over time. As illustrated by the patient's outcomes, long-term antibiotic therapy should only be used in cases unsuitable for device removal. Complete hardware removal remains the first-line therapy in patients with CIED-related infections.

Focus on increased serum angiotensin-converting enzyme level: From granulomatous diseases to genetic mutations.

Angiotensin I-converting enzyme (ACE) is a well-known zinc-metallopeptidase that converts angiotensin I to the potent vasoconstrictor angiotensin II and degrades bradykinin, a powerful vasodilator, and as such plays a key role in the regulation of vascular tone and cardiac function. Increased circulating ACE (cACE) activity has been reported in multiple diseases, including but not limited to granulomatous disorders. Since 2001, genetic mutations leading to cACE elevation have also been described. This review takes advantage of the identification of a novel ACE mutation (25-IVS25 + 1G > A) in two Belgian pedigrees to summarize current knowledge about the differential diagnosis of cACE elevation, based on literature review and the experience of our centre. Furthermore, we propose a practical approach for the evaluation and management of patients with elevated cACE and discuss in which cases search for genetic mutations should be considered.