I'd like to take a step back and find out more about the cardiomyopathy. How was it diagnosed and what tests were done to work it up? It is one thing to interpret the results if this is a global effect rather than perhaps a wall motion artifact or something else. I am somewhat confused by how this effect took from 2006 to 2014 to develop while on the drug and then reversed to a large extent in a short period of time after stopping the imatinib, comes back reversibly with a second drug. If this was an abl effect or an off target effect, it should have been there from the beginning and not taken 8 years to develop and then reverse in a matter of months. What changed in this man's history that suddenly brought this reversible event out? Are there other factors that have come into play over the last few years? Other co-comorbidities? Other medications? New diseases. Things that might have made a relatively non-toxic therapy, now toxic.
If a full cardiac work-up with a catheterization and probably endomyocardial biopsy has not been done, I would consider it. Consider a scenario, not necessarily the one here, but where a patient develops a new disease such as amyloid or an autoimmune myocarditis, which is not severe on its own, but in the presence of a drug such as a TKI now tips the patient.
If all this has been done, then I would consider a low dose option such as Jorge has suggested, balancing disease control versus heart failure. On the other hand, something might be discovered which will totally change the approach, have another disease that could be treated, or even direct you to the path of using hydroxyurea just to control counts when necessary.
I definitely agree that with this history and the patient age, an allograft is off the table.