Author + information
- Nathan Mewton, MD, PhD⁎ (, )
- Franck Thuny, MD, PhD and
- Pierre Croisille, MD, PhD
- ↵⁎Hôpital Cardiovasculaire Louis Pradel, Cardiology, 28 Avenue Doyen Lépine, Bron, Rhône 69500, France
A few months ago, in an editorial by Raman et al. (1), T2-weighted (T2w) short tau inversion recovery (STIR) imaging, the only validated T2 sequence that was tested against pathology in an experimental setting to assess the myocardial area at risk (AAR), was almost thrown out the window because of its limited accuracy and poor reproducibility due to the high sensitivity to artifacts. However, there was still hope, because better sequences have come out (T2w ACUTE [Acquisition for Cardiac Unified T2 Edema], T2prep steady-state free precession, T2 mapping) with significantly better reproducibility and accuracy. But those sequences have not been validated against pathology.
In a recent issue of iJACC, Fuernau and Eitel et al. (2) have published successively several papers about large groups of acute ST-segment elevation myocardial infarction patients in whom T2wSTIR was used to assess the AAR. Their results showed that T2wSTIR had a significant prognostic value, and it was well correlated to angiographic surrogates of the myocardial AAR. At the same time, we have shown (3) in an experimental model of ischemia reperfusion that T2wSTIR and T2wACUTE were significantly correlated to the AAR by pathology, but significantly overestimated it.
All of these recent publications leave the reader uncertain and confused about the utility and reliability of T2w imaging.
In that same issue of iJACC, Friedrich et al. (4) boldly decided to open the debate between the AAR T2w imaging pro and cons. As always, in such a debate, the truth probably lies somewhere in between.
What are the facts most of us agree on?
• T2w imaging shows myocardial edema as a marker of acute injury.
• T2w imaging is convenient and simple, can be applied retrospectively after reperfusion, and provides incremental data to delayed enhancement imaging.
• T2w imaging and especially the classic T2wSTIR sequence is sensitive to many artifacts that can alter the data interpretation and analysis.
• Myocardial edema detected by T2w cardiac magnetic resonance is correlated to the myocardial AAR, although correlation does not mean causation.
• There currently are no guidelines for post-processing of T2 hyperenhancement and association to delayed-enhancement measurement thresholds.
What are the main points of disagreement?
• T2w imaging provides an accurate measurement of the AAR. If the definition of the AAR is purely perfusional (the area of jeopardized myocardium during the coronary occlusion), then using T2w edema to assess the AAR assumes there is a perfect and direct relationship between the area of edema and the area of jeopardized myocardium. When we put this in a pathophysiological perspective, we know that edema is also influenced by many other factors such as microvascular obstruction, inflammation, reperfusion status, myocardial hemorrhage, reperfusion injury, and other unknown confounders. Therefore, the assumption of a direct linear relationship between the T2w hyperenhanced area and the AAR is potentially submitted to many biases. This assumption ignores that retrospective T2w imaging after reperfusion provides a global assessment of ischemic as well as reperfusion damage, 2 complex but cumulative and nonlinear phenomena. To accept T2w imaging as a method of reference for the assessment of the AAR, you would have either to neglect the effect of factors other than ischemia, such as reperfusion injury, or create a new definition for the AAR.
• The place of interstitial edema in the explanation of T2w enhancement is unclear. Friedrich et al. (4) provide a very elegant explanation of intracellular edema at the acute phase of infarction but do not mention interstitial edema. Edema in the interstitium follows a passive diffusion and would go out of the initial AAR vascular bed bounds as we showed recently (3). If the interstitial space is negligible in comparison to myocardial cells in the healthy myocardium, it increases significantly in the ischemic myocardium and is a probable major player in the well-described overestimation of infarct size by contrast-enhanced cardiac magnetic resonance at the acute phase of myocardial infarction. This is so true that early gadolinium enhancement has recently been compared in iJACC to T2w imaging with acceptable levels of correlation and proposed as a new method to measure the AAR (5).
Like many others, we believe that T2w imaging has a lot to offer for the assessment of acute myocardial infarction patients, but we have to stay close to pathophysiology and not only look at pretty pictures if we want to get closer to truth. (5)
- American College of Cardiology Foundation