Editors' ChoiceAtrial Fibrillation

My Heart's All Aflutter

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Science Translational Medicine  21 Oct 2009:
Vol. 1, Issue 3, pp. 3ec9
DOI: 10.1126/scitranslmed.3000506

Our hearts may flutter when we are in love, but fluttering can also happen when our hearts are not beating correctly. One common type of abnormal heartbeat, atrial fibrillation or A fib, is fairly common among older people (3 to 5%) and can increase the risk of stroke. This disorganized muscle contraction in the upper chambers of the heart occurs when a signal from the adjacent pulmonary vein (instead of the sinoatrial node) initiates the heartbeat. The exact source of this signal has not been clear, but Levin et al. now show that the trigger may be melanocyte-like cells scattered throughout the heart and pulmonary vein of mice and men. These cells express the melanin synthetic enzyme dopachrome tautomerase and other proteins characteristic of melanocytes and their precursors. In genetically altered mice, when dopachrome tautomerase is removed from the melanocyte-like cells, they become hyperexcitable and the mice have frequent episodes of atrial arrhythmia. When these cells are eliminated altogether by removing a key tyrosine kinase receptor (Kit), the mice showed no atrial arrhythmias upon high-frequency electrical stimulation, a treatment that readily induces A fib in normal mice. Like humans, who show autonomic activity before episodes of A fib, autonomic stimulation in mice causes atrial arrhythmias, a response that is much diminished in mice without the melanocyte-like cells. Together, these results build a strong case for an instrumental role for these specialized cells in atrial fibrillation in mice, and perhaps humans. The melanocytes might even be important in love—our romance-activated autonomic nervous system has been known to cause sweaty palms, flushing, and—a fluttering heart.

M. D. Levin et al., Melanocyte-like cells in the heart and pulmonary veins contribute to atrial arrhythmia triggers. J. Clin. Invest. 12 October 2009 (doi:10.1172/JCI39109). [Full Text]

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