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J Am Coll Cardiol, 2006; 47:9-21, doi:10.1016/j.jacc.2005.08.059 (Published online 9 December 2005).
© 2006 by the American College of Cardiology Foundation
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Genomics and Cardiac Arrhythmias

Robert Roberts, MD, FACC*

University of Ottawa Heart Institute, Ottawa, Ontario, Canada


Figure 1
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  		Figure 1 Variation in the precordial lead ST and T waves in a patient with Brugada syndrome. Reprinted with permission from Fuster V, Alexander RW, O’Rourke RA. Hurst’s The Heart. 11th edition. McGraw-Hill Companies, 2004.

 

Figure 2
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  		Figure 2 Schematic of inward and outward ionic currents, pumps, and exchangers that underlie atrial and ventricular action potentials in the mammalian heart. Control and failing (bold line) action potential profiles are shown on top. Each phase of the action potential is labeled. Under the action potential, a schematic of the time course of each current is shown, and the gene product (probable clone) that underlies the current is indicated. Reprinted with permission from Fuster V, Alexander RW, O’Rourke RA. Hurst’s The Heart. 11th edition. McGraw-Hill Companies, 2004.

 

Figure 3
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  		Figure 3 Kaplan-Meier estimates of cumulative survival free of cardiac events among the 580 patients with the long QT syndrome in the risk stratification analysis, according to gender and the QT interval corrected for heart rate (QTc), in the group with a mutation at the LQT1 locus (A), the group with a mutation at the LQT2 locus (B), and the group with a mutation at the LQT3 locus (C). Printed with permission from N Engl J Med 2003;348:1866–74.

 




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