Infective endocarditis (IE) is a disease of the endocardium, which leads to the appearance of vegetation on the valves, cardiac structures, or, potentially, vascular endothelium of the heart. The risk of IE can be increased more than 140 times by congenital heart disease (50–59% of all IE), particularly if cyanotic. An increase in mortality may result from IE in patients with a complex cardiac pathology or patients with an implanted prosthetic material, most frequently conduits in a pulmonary position. Cardiac implantable electronic devices (CIED) infective endocarditis is a life-threatening complication representing 10% of all cases of endocarditis. Common signs of presentation are often fever and chills; redness and swelling at the pocket of the pacemaker, including the erosion and exteriorization of the device; and life-threatening sepsis. The use of intracardiac echocardiography for the diagnosis of IE is an innovative method. This may be needed, especially in older children undergoing complex cardiac surgery, when transthoracic echocardiography (TTE) and transesophageal echocardiography (TOE) failed to provide a reliable diagnosis. The 2018 European Heart Rhythm Association (EHRA) experts’ consensus statement on transvenous lead extraction recommends complete device removal and antimicrobial therapy for any device-related infection, including CIED-IE. The most detected microorganism was Staphylococcus Aureus. In addition, cardiac surgery and interventional cardiology associated with the placement of prostheses or conduits may increase the risk of IE up to 1.6% for Melody valve implantation. Our manuscript presents a comprehensive review of infective endocarditis associated with cardiac devices and prostheses in the pediatric population, including recent advances in diagnosis and management.

Aims – Frequent premature ventricular complexes (PVCs) may induce/aggravate LV systolic dysfunction (LVD) by tachy(dyssynchrono)cardiomyopathy (tCMP) in patients with/without previous structural heart disease. High arrhythmic burden (i.e. >26%) is the main predictor of tCMP development in patients with previously normal LV function. However, its predictive power is reduced once the arrhythmic burden is below 26%, with considerable overlap between patients at risk for tCMP and those who will maintain normal LV function. We sought to evaluate the predictive power of a composite index that includes PVC burden, PVC duration and PVC coupling interval. Methods – 61 patients referred for radiofrequency ablation (RFA), with frequent PVCs refractory to at least one antiarrhythmic drug (AAD), symptomatic and/or with LV systolic dysfunction (LVEF < 50%) were retrospectively studied. Patients with structural lesions on transthoracic echocardiography (TTE) and/or cardiac magnetic resonance imaging (c-MRI), with sustained ventricular tachycardia/supraventricular tachycardia or severe valvular disease were excluded. A composite parameter dependent on PVC burden, PVC duration and PVC coupling interval was defi ned. Results – Mean PVC burden was 25.80% ± 11.64 (35% ± 8.16 in tCMP subgroup). Chronic PVC suppression was achieved in 89.6% of patients with a mean of 1.44 ± 0.7 procedures with 86.4% of patients requiring one procedure. Septal right ventricular outfl ow tract (RVOT) was the most frequent PVC origin (36.1%). Mean left ventricular ejection fraction (LVEF) in the tCMP group (7 patients) was 38% ± 5.26 which increased 1 month after RF ablation to 54.6% ± 3.64 (87.35% of recovered LVEF), at 3 months to 56% ± 2.23 and at 6 months 57% ± 2.73. LVEF recovery was also present in non-tCMP subgroup, yet statistically insignifi cant. There was no procedure-related mortality. Retrograde ventriculo-atrial (VA) conduction, male gender, non-sustained VT (NSVT), a higher BMI and a higher PVC burden were associated with tCMP development. ROC curve analysis appears to demonstrate higher sensitivity of tCMP prediction by the composite index in comparison to PVC burden in patients with 16.93-25.93% PVCs (i.e. below the formerly described tCMP PVC% cut-off). Conclusions – In patients with a PVC burden lower than the previously described cut offs (i.e. with ~17-25% PVCs) PVC mediated systolic dysfunction seems to be predicted with higher sensitivity by a composite index accounting for PVC burden, PVC duration and PVC coupling interval.

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