I agree with most of the previous comments and suggestions. I want only to add that this is another example of the fact that TKIs able to inhibit the ABL TK activity can be, in particular in specific patients like this one, toxic and sometimes also highly toxic. This, in my opinion, supports the concept that treatment discontinuation should really become the best goal to be achieved in CML therapy as this will probably have a long-term impact on overall survival (a part all the other advantages).

Even though the evidence that imatinib causes cardiac dysfunction is not convincing, it may be relevant for some patients. He may have a specific susceptibility given his other pathology. If imatinib is the cause of his deterioration then he will be in big trouble if you continue it any longer. Therefore you have a difficult choice. Whatever you choose may be equally or more cardio toxic if ABL is the causative target.
Since he is low Sokal and has achieved CCyR, alpha interferon may maintain his response (not sure if this is OK with his ankylosing spondylitis though). If this is not effective or contraindicated I would consider nilotinib, as long as he is not diabetic and has no vascular risk factors. This is most likely to get him to a deep response quickly, giving him a chance of cessation. Bosutinib is also worth considering.

Always hard to truly assess causality in such a case; I think the possibility exists based on a number of basic science papers but I have seen positive as well as negative remodeling effects cited. I will assume it is based on the fact that imatinib was the only new variable and the degree of change.
Then it becomes a choice :
Nilotinib - global vascular disease seems to raise concerns (could compound current CV issues)
Dasatinib - raises concerns about worsening/accelerating the ankylosing spondylitis (AS).
For the record, are we sure the cardiomyopathy is AS related? I thought it cased aortic insufficiency but does it caused dilated myopathy?
Bosutinib might be a very reasonable option.

This is a difficult one because I think all TKI have a similar potential cardiotoxic effect (myocardial) with imatinib perhaps being the mildest. Thus, I am not sure a change would help. One option is to lower doses (which is always a concern for efficacy, particularly with imatinib) and manage aggressively the heart with close monitoring. If still progressing, maybe a change to bosutinib as it appears to have the least effect (although it could be just a matter of the least follow-up).
I hope this helps.
Best, JC

I have a dilemma with a patient and would ask for some advice. 43yo man diagnosed about 8 months ago with standard CML-CP low Sokal. Started on Gleevec and has CCyR at 6 months (2log reduction). Background of HLA-B27 ankylosing spondylitis with a pre-Gleevec dilated cardiomyopathy EF 45%. Now about 7 months after starting Gleevec, EF is <35%. Cardiologist feels this is Gleevec related. I am aware of work from MDA in the past describing TK induced LV remodeling. This could very well be Gleevec related. If you think it is, are you aware of whether any of the other TKIs might be better? What would you do?
Thanks for the help.
Jeff