The correct answer is downregulation of connexin 43. What are the observations? Well, this is a map of the epicardium of a model of heart failure and a normal heart. These isochrones are more crowded in heart failure, so conduction is slowed compared to the normal heart. That's the main observation here is conduction slowing in this segment of myocardium. Although all of the changes that were described can occur in models of heart failure, including downregulation of delayed rectifier potassium currents and AP prolongation. In fact, if rates get fast enough and the action potential is long enough that can predispose to conduction slowing, but rates have to be fast. Downregulation of beta-adrenergic receptors has also been described and functional altered regulation of sodium-calcium exchanger. In fact, in some models of heart failure, downregulation of the exchanger itself. However, the thing that really is prominent in governing conduction in the myocardium is connexin 43, and particularly in the ventricular myocardium. Connexin 43 is downregulated in heart failure. Not only is it downregulated, but there's alterations in the subcellular localization of connexin 43, further contributing to conduction slowing in the myocardium. Of the answers above, downregulation of connexin 43 is the best answer. That, I think, gives you a flavor for some of the things you might expect to see in the basic science component of the boards. I want to thank you for watching this workshop, and wish you all a good day. Thank you very much.

heart failure

conduction slowing

connexin 43

ventricular myocardium

cardiac conduction