Radiation exposure in CB PVI can be markedly reduced without prolonging procedure times, affecting the outcome or complication rates. Moreover, ICE seems to shorten total freezing time.
Aims
Pacing the specific conduction system like the Bundle of His (HB) can lead to more physiologic activation patterns compared to traditional right ventricular apical pacing. The aim of this study was to estimate the feasibility and value of electroanatomical mapping (EAM) for HB pacing during the learning curve and its impact on procedural outcome.
Methods and results
Fifteen consecutive patients were treated using EAM of the His bundle region before implantation. Voltage and activation maps of HB potentials were performed. The activation time from His potential to R wave (ECG-reference) was measured and correlated to the HV interval. The atrial and ventricular potentials were blended so the active window could only see the His potential. After completing the activation map, it was transformed into a peak-to-peak voltage map of the HB. With reversed black and white colour scale, the exact point of the maximal His signal amplitude was visualized. Procedural data for the implantation were analysed using this innovative approach. The average total procedural time and fluoroscopy time was 88.2 ± 19.1 min and 10.9 ± 4.5 min, respectively. The 3D mapping time was 18.4 ± 5.1 min. The 13.9 ± 5.1 His potential points were needed in average to complete the map. No periprocedural complications were seen in this cohort. In 86.7% of cases, His bundle pacing was successful. The average threshold for the His bundle stimulation and the R-wave amplitude was 1.62 ± 1 V (@1.0 ms) and 4.8 ± 3.2 mV, respectively. The pacing impedance was 513.5 ± 102.8 Ω. Average paced QRS complex width was 116.9 ± 20.3ms. On average 2.6 ± 1.6 lead positions were targeted to find the optimal pacing site.
Conclusion
Electroanatomical mapping-guided implantation of His-bundle leads can facilitate the identification of optimal pacing sites and allow to minimize procedure and fluoroscopy times even during the phase of the learning curve.
Background
DiGeorge syndrome, also known as ‘CATCH 22’, is the most common deletion in humans and is one of the velocardiofacial syndromes. It is characterized by a specific facial phenotype, and structural and functional abnormalities in the cardiac and endocrine systems. One form of endocrine system dysfunction is hypocalcaemia, which causes arrhythmic events and can result in a transient loss of consciousness. We present a case highlighting the late diagnosis of DiGeorge syndrome in a patient with recurrent episodes of syncope due to suspected arrhythmic events secondary to hypocalcaemia.
Case summary
A 44-year-old woman was referred for further investigation of recurrent syncope episodes and documented transient QT-prolongation with hypocalcaemia. Previous detailed cardiological examination, including invasive procedures such as coronary angiography and cardiac magnetic resonance tomography, was unremarkable. Slight characteristic facial dysmorphia and transient hypocalcaemia were strongly suggestive of DiGeorge syndrome. The diagnosis was confirmed by genetic testing. Calcium substitution was initiated and no recurrent episodes of syncope or arrhythmic events were reported during 12 months of follow-up.
Discussion
Clinical presentation and time of manifestation of the DiGeorge syndrome varies widely depending on the mutation expression extent. An atypical disease course may delay the diagnosis and appropriate management of affected patients. In this case, confirmation of the diagnosis allowed the initiation of appropriate treatment, reducing the risk for further events. Given that syncope and arrhythmia can be the first and only manifestation of late-onset DiGeorge syndrome, specialists in adult cardiology need to be aware of this presentation.
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