| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5603553 | Heart Rhythm | 2019 | 8 Pages |
Abstract
Our findings implicate impaired Ca2+-dependent inactivation in human cardiomyocytes as the plausible mechanism for long QT syndrome associated with 2 novel CaM mutations. The data further expand the spectrum of genotype and phenotype associated with calmodulinopathy.
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Authors
Daniel C. BS, Christopher N. PhD, Gregory MD, MPH, Jurg MD, Florence MD, PhD, Nicole MD, Lisa M. BS, Kateryna V. MS, Daniel M. BA, Walter J. PhD, Lia MD, PhD, Zahurul A. MD, PhD, Alfred L. MD,