Interactive Training System for Interventional Electrocardiology Procedures

International audienceRecent progress in cardiac catheterization and devices al-lowed to develop new therapies for severe cardiac diseases like arrhyth-mias and heart failure. The skills required for such interventions are still very challenging to learn, and typically acquired over several years. Vir-tual reality simulators can reduce this burden by allowing to practice such procedures without consequences on patients. In this paper, we propose the first training system dedicated to cardiac electrophysiology, includ-ing pacing and ablation procedures. Our framework involves an efficient GPU-based electrophysiological model. Thanks to an innovative mul-tithreading approach, we reach high computational performances that allow to account for user interactions in real-time. Based on a scenario of cardiac arrhythmia, we demonstrate the ability of the user-guided simulator to navigate inside vessels and cardiac cavities with a catheter and to reproduce an ablation procedure involving: extra-cellular poten-tial measurements, endocardial surface reconstruction, electrophysiology mapping, radio-frequency (RF) ablation, as well as electrical stimulation. This works is a step towards computerized medical learning curriculum

Hypertrophic cardiomyopathy in myosin-binding protein C (MYBPC3) Icelandic founder mutation carriers

Objective: The myosin-binding protein C (MYBPC3) c.927-2A>G founder mutation accounts for >90% of sarcomeric hypertrophic cardiomyopathy (HCM) in Iceland. This cross-sectional observational study explored the penetrance and phenotypic burden among carriers of this single, prevalent founder mutation. Methods: We studied 60 probands with HCM caused by MYBPC3 c.927-2A>G and 225 first-degree relatives. All participants underwent comprehensive clinical evaluation and relatives were genotyped. Results: Genetic and clinical evaluation of relatives identified 49 genotype-positive (G+) relatives with left ventricular hypertrophy (G+/LVH+), 59 G+without LVH (G+/LVH−) and 117 genotype-negative relatives (unaffected). Compared with HCM probands, G+/ LVH+ relatives were older at HCM diagnosis, had less LVH, a less prevalent diastolic dysfunction, fewer ECG abnormalities, lower serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin I levels, and fewer symptoms. The penetrance of HCM was influenced by age and sex; specifically, LVH was present in 39% of G+males but only 9% of G+females under age 40 years (p=0.015), versus 86% and 83%, respectively, after age 60 (p=0.89). G+/LVH− subjects had normal wall thicknesses, diastolic function and NT-proBNP levels, but subtle changes in LV geometry and more ECG abnormalities than their unaffected relatives. Conclusions: Phenotypic expression of the Icelandic MYBPC3 founder mutation varies by age, sex and proband status. Men are more likely to have LVH at a younger age, and disease manifestations were more prominent in probands than in relatives identified via family screening. G+/LVH− individuals had subtle clinical differences from unaffected relatives well into adulthood, indicating subclinical phenotypic expression of the pathogenic mutation

Solar Wind Turbulence and the Role of Ion Instabilities

International audienc