HRS Policy Statement: Clinical Cardiac Electrophysiology Fellowship Curriculum: Update 2011
Year: 2020
Type: article
Abstract: Progressive cardiac conduction disease (PCCD) 6. Familial atrial fibrillation (FAF) 7. Inferolateral early repolarization syndrome 8. Commotio cordis 23 B. The pathogenetic basis for the cardiac channelopathies including 22,24 : 1. Loss-of-function mutations in potassium channels (Kv7.1 and Kv11.1) explaining two-thirds of all LQTS 2. Loss-of-function mutations in the sodium channel (Nav1.5)explaining ~25% of BrS with the majority of BrS still being genetically elusive 3. Mutations in the RYR2-encoded cardiac ryanodine receptor as the cause for approximately two-thirds of CPVTC. Genotype-phenotype relationships and risk stratification for each channelopathy 7,22,24,25 D. The state of genetic testing for each cardiac channelopathy including [26][27][28] :1. Diagnostic, prognostic, and therapeutic implications 2. The yield of genetic testing 3. Distinguishing true pathogenic mutations from background genetic noise 4. The need for pre-genetic test counseling and acquisition of those skills or partnership with genetic counselors and/or geneticists E. The indications for pharmacotherapy, left cardiac sympathetic denervation therapy, and device therapy for the cardiac channelopathies 7,24,25
DOI: 10.17615/v9c0-gv02
Authors: Kaufman, Elizabeth S., Knight, Bradley P., Anderson, Mark, Haines, David, Callans, David J., Exner, Derek V., Narayan, Sanjiv M., Singh, Jagmeet, Mounsey, J. Paul, Asirvatham, Samuel J., Krahn, Andrew D., Mittal, Suneet, Chugh, Sumeet S., Fisher, John D., Markowitz, Steven M., Al-Ahmad, Amin, Bogun, Frank, Ackerman, Michael, Link, Mark S.
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W4300887281