What I don't understand is this:
There are very few beta 2 receptors on the cardiac vasculature, and beta 1 agonists have very slight beta 2 activity, and yet this is enough to offset any potential gain from the decrease in myocardial O2 consumption. I just don't see it, unless doctors are just trying to avoid getting sued.
Whatever, I'll let it go. I don't have time to be looking up articles on it.