"the CYTK drug is trying to increase contractility / force output from the heart, which usually makes things worse in animal models."
Not bored, please expand if you wish. CYTK has gotten to interesting levels, but Zebra's law is possibly in play, as CYTK doesn't have a very advanced pipe. Amgen saw fit to trial this at some expense; would they miss something as basic as you are suggesting? What, specifically, gets worse with critters whose cardiac contractility/output have been therapeutically increased?
No position: tempted, but your stance gives me paws.
Edit: Dunno how much you've kicked the tires in the CYTK garage. The theory is it increases output without increasing intracellular calcium, an effect of beta agonists. Thus you get the output without the increased velocity and shortened systolic ejection time. Interested to hear your take on how those parameters bear on progression to heart failure.
TIA & Regards, RockRat