Is Transient Ischemic Dilatation a Marker or a Mechanism of Recovery After CTO‐PCI?

We read with great interest the article by Hirai et al. investigating determinants of LVEF improvement after successful CTO-PCI using myocardial perfusion imaging 1. The authors should be commended for focusing on functional recovery rather than angiographic success alone, and for employing MPI-derived parameters to explore predictors of reverse remodeling. Their identification of pre-procedural transient ischemic dilatation (TID) as the strongest predictor of LVEF improvement is particularly intriguing and clinically thought-provoking. However, several aspects merit closer scrutiny. The primary outcome was defined as belonging to the highest quartile of ΔLVEF, representing a relative rather than absolute measure of functional recovery. While this approach may simplify statistical comparisons, categorizing a continuous variable into discrete groups can reduce analytical resolution and introduce interpretive limitations. In particular, quartile-based compartmentalization may obscure the influence of baseline LVEF, whereby small absolute improvements in patients with severely depressed function may be weighted similarly to larger gains in those with moderately impaired systolic performance. This methodological choice may blur clinically meaningful differences in recovery and affect the interpretation of predictors of LVEF improvement 2. The interpretation of TID as a predictor of LVEF recovery also deserves caution. TID is widely recognized as a marker of severe and extensive ischemia rather than a direct mediator of myocardial dysfunction. Its association with LVEF improvement after CTO-PCI may therefore reflect successful ischemic burden reduction rather than a unique pathophysiological substrate primed for recovery. Without a parallel quantitative assessment of ischemic extent reduction, it remains uncertain whether TID adds incremental prognostic value beyond established perfusion metrics such as summed stress or difference scores 3. Another important consideration is the potential for selection bias introduced by restricting the analysis to patients with patent vessels at 1-year follow-up. By excluding individuals who experienced re-occlusion, the study population may be enriched for patients with more favorable procedural outcomes, preserved microvascular integrity, and greater capacity for functional recovery. This survivor-type bias could overestimate the association between baseline MPI parameters and subsequent LVEF improvement, as patients with early failure or adverse remodeling are systematically removed from analysis 4. Consequently, the reported predictors of LVEF recovery should be interpreted within the context of this selected cohort and may not be generalizable to the broader CTO population. Finally, while LVEF improvement is an appealing surrogate endpoint, its clinical relevance depends on translation into hard outcomes. Large randomized trials have shown that revascularization-induced functional or viability improvements do not consistently yield prognostic benefit, especially in stable ischemic heart disease. Integrating clinical endpoints or longer-term outcome data would substantially strengthen the applicability of the current findings. In summary, this study contributes valuable data on functional recovery after CTO-PCI, but its conclusions should be interpreted within the context of outcome definition, ischemic burden assessment, and selection effects. Future studies combining quantitative ischemia reduction, absolute functional gains, and clinical outcomes will be essential to clarify which patients truly benefit from CTO revascularization. The authors declare no conflicts of interest.