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EDITOR
In their editorial on drug treatment in heart failure, Steeds
and Channer state that "all clinical trials of positively inotropic
drugs have either failed to improve symptoms or have increased
mortality in heart failure."1 Even if this statement is
allowed, it is a generalisation too far to conclude that "drugs that
increase the force of contraction of the failing heart result in
increased mortality and...there should be a halt on
further development in this direction."
We believe that there are at least two reasons why attempts to develop
better inotropic drugs should continue. Firstly, basic studies of heart
muscle over the past two decades have shown that there are two cellular
routes to improving the strength of the heart: (a)
increasing intracellular calcium concentrations and (b)
increasing myofilament calcium sensitivity, resulting in stronger contractions for a given amount of calcium.2 All
clinically tested drugs