Another CTO Conundrum: Important Questions Remain

Author(s): 

David R. Ramsdale, MD and Shahid Aziz, MD

This short paper by Moreno et al. claims to show that patients with a chronic total occlusion (CTO) in a non-culprit coronary artery, who also have multivessel disease (MVD) and an acute myocardial infarction (MI) have a worse outcome than those with acute MI and MVD but without a CTO and worse than those with an acute MI but only single vessel disease. This is perhaps a not surprising finding but it is not convincing from this data that the difference is due to the presence of the CTO per se.
Clearly, the study is not randomized and so inevitably some factors that may influence cardiac events during follow up and cardiac death are not present equally in the groups that are being compared. For example, when comparing coronary artery bypass (CABG) surgery in patients in Group 3 to those in Group 2, those in Group 3 had CABG surgery almost 10 times more often. In addition, these patients generally had worse degrees of heart failure and worse left ventricular function. Although previous MI may be responsible for these differences, it is not proven that these effects are a result of the occlusion in the CTO vessel. When comparing Group 1 with Group 2, again patients in Group 2 are older, have had more previous MIs and worse degrees of heart failure than those with single vessel disease (the relative ejection fractions for these two groups are not given). These shortcomings make it difficult therefore to attempt to compare the groups on the basis of coronary anatomy findings alone. Interestingly, the multivariate analysis did not find that the presence of a CTO was predictive of a worse outcome!
We have several other problems with this paper. Firstly, in the context of this study, it is inappropriate to classify left main disease as MVD since this is likely to significantly influence morbidity and mortality as well as the choice of future management. Secondly, most events seem to occur early but there are no data presented to show why. Certainly, GP IIb/IIIa use is surprisingly low (at 30%) for this particular study population. Thirdly, the authors’ findings do not “support the treatment of chronic coronary occlusions in patients with stable ischemic heart disease.” Neither do they support the suggestion that intra-aortic balloon counterpulsation should be used during PCI in this group of patients.
In our view, this subject is an important one, and it would be valuable to know whether patients who present with an acute MI and are found to have a CTO as well as MVD at angiography should be managed by total revascularization by PCI or CABG surgery, by “culprit-lesion” only PCI, or by “as much as is feasible” PCI with drug-eluting stents. It would be important also to know whether a “staged procedure” has any advantages. A large, prospective, multicenter randomized study will be required to answer these questions.


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