To the Editor:
We read with interest the article by Sharkey et al1 describing the clinical and cardiovascular magnetic resonance (CMR) features of the apical ballooning cardiomyopathy. We have a few concerns about the interpretation of the CMR findings in the article as well as in the related editorial.2
The authors suggest that the lack of mid-wall delayed enhancement in their series should exclude myocardial inflammation as a possible underlying mechanism explaining their findings. We have recently investigated the diagnostic performance of various CMR techniques to identify acute myocarditis3 and found that delayed enhancement occurs in only 44% of these patients, whereas T2-weighted abnormalities reflecting myocardial edema and early global enhancement are noted in >80% of the cases. For this reason, we believe that the CMR approach of the authors does not allow exclusion of myocardial inflammation in those cases with certainty.
The related editorial suggested that the lack of delayed enhancement excludes the presence of myocardial edema in these patients. We have shown in the same report3 that global or focal myocardial edema is frequently observed in the absence of delayed enhancement. We have also previously shown that chronic myocardial scars exhibit delayed enhancement without myocardial edema.4 Furthermore, we recently investigated a female patient with “taku-tsubo” cardiomyopathy and found overt regional high T2 signal intensity without any evidence of delayed enhancement. Accordingly, we believe that no firm conclusion could be drawn about the presence or absence of myocardial edema in these patients in the absence of T2-weighted imaging experiments.
The editorial also suggested that “gadolinium-enhanced MRI … failed to detect regional T2 enhancement which has been shown to detect myocardial inflammation and necrosis.” We have 2 concerns about this statement: First, the enhancement effect of gadolinium is mainly caused by its effect on T1 relaxation time. Second, the article cited to support the statement5 did not include any T2-weighted imaging experiments.
Despite these concerns, we congratulate the authors on their report, which provides many new insights into this rare and yet clinically relevant and novel cardiomyopathy.
References
Response
We appreciate the interest of Dr Abdel-Aty and colleagues in our work.1 These investigators raise the question of whether the absence of postgadolinium-delayed hyperenhancement with T1-weighted cardiac MRI (CMR) reported in our patients with stress (“tako-tsubo”) cardiomyopathy failed to exclude myocardial inflammation because T2-weighted imaging data were not presented.1
For several reasons, we believe that is a highly unlikely scenario for myocarditis to be the undetected and underlying mechanism responsible for stress cardiomyopathy in such a sizeable patient cohort. T1-weighted imaging is the preferred and established technique to assess myocardial viability and exclude infarction and necrosis,2 which was in fact the priority in this particular study. Indeed, 21 of our 22 study patients showed myocardial viability without evidence of delayed hyperenhancement (the other patient had an apical infarct caused by a previous cardiac arrest).
In our group of severely symptomatic patients with stress cardiomyopathy, we did initially perform some T2-weighted scans (in addition to T1-weighted imaging), which are preferable for the interrogation of myocardial edema (consistent with myocarditis). Of the 22 patients, 9 had technically adequate T2-weighted images, and 2 of these (22%) had T2-weighted scans consistent with myocardial edema. We found no difference, however, in clinical profile (including premonitory vital infection and laboratory evidence of systemic inflammation) between the 2 patients with myocardial edema and the 7 patients without this finding; furthermore, 1 of the 2 patients with myocardial edema had a myocardial biopsy that was negative for myocardial inflammation. Finally, and perhaps most importantly, myocarditis is not particularly consistent with the clinical profile evident in each of our patients with stress cardiomyopathy (ie, rapidly reversible apical ballooning with hypercontractile base involving all 3 vascular territories). Therefore, although we appreciate the reasonable insights of Abdel-Aty et al, we do not believe there are any data to substantiate an important role for myocarditis in our patients with stress cardiomyopathy.*
Footnotes
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↵*Original coauthor Dr Jana Lindberg did not participate in the drafting of this letter.
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- Letter Regarding Article by Sharkey et al, “Acute and Reversible Cardiomyopathy Provoked by Stress in Women From the United States”
