The Role of CMR in Mid-Ventricular Takotsubo Syndrome

Chonthicha Tanking MD, Sivayos Deetes MD, Rawish Wimolwattanaphan MD

Chulabhorn Hospital, Bangkok, Thailand

Clinical History

A 62-year-old female with a history of diabetes mellitus and hypertension presented to the emergency department with sudden-onset chest tightness after an argument with her daughter. Her initial electrocardiogram (ECG) showed ST-segment elevation in leads I and aVL (Figure 1), accompanied by an elevated high-sensitivity troponin level of 519 ng/L (normal range < 14 ng/L). A transthoracic echocardiogram revealed mildly impaired left ventricular (LV) function with left ventricular ejection fraction (LVEF) of 40% and regional wall motion abnormalities (RWMA) that did not conform to a single epicardial coronary artery distribution (Movie 1). Emergency coronary angiography demonstrated no significant obstructive coronary artery disease (Figure 2).

Figure 1. Twelve lead ECG with ST-segment elevation in leads I and aVL.

Movie 1. Transthoracic echocardiogram in a two-chamber (A), three-chamber (B), four-chamber (C), and mid short axis (D) showed mildly impaired LV function (LVEF 40%) and RWMA of the mid segments.

Figure 2. Coronary angiograms of the right coronary artery (A) and left main coronary artery (B) showed normal coronary arteries.

CMR Findings

Cardiac magnetic resonance (CMR) was done on an Ingenia Ambition X 1.5 T (Philips Healthcare, Best, Netherlands) scanner. Cine imaging showed an LVEF of 51% with a distinct mid-ventricular dyskinesia and compensatory hyperkinesia of the basal and apical segments (Figure 3 and Movie 2).  Critically, CMR provided comprehensive tissue characterization. T2-weighted imaging (Figure 3), and quantitative T2 mapping revealed significant myocardial edema, with a T2 value of 82 ms at 1.5 T (normal T2 mapping 50-60 ms) in the mid-ventricle, substantially higher than the normal apical value of 52 ms (Figure 3). Native T1 mapping also demonstrated an elevated value of 1278 ms (normal native T1 mapping 950-1050 ms) in the mid-ventricular segments, compared to a normal apical value of 1014 ms, consistent with myocardial injury. Most notably, early gadolinium T1 mapping showed a significant shortening (80%), a finding more commonly associated with acute myocarditis due to increasedcapillary permeability and inflammation. This finding, combined with the other CMR results and negative late gadolinium enhancement (LGE) for scar (Figure 3), established a definitive diagnosis of mid-ventricular Takotsubo cardiomyopathy (TCM).

Figure 3. CMR images at presentation (A-F) and 8 weeks later (G-L). Cine images of the LV 2-chamber balanced steady state free precession (bSSFP) during diastole (A) and systole (B) demonstrate mid-ventricular dyskinesia during systole (yellow arrow). T2-weighted imaging (C) shows a hyperintense signal in the mid-ventricle (arrowhead), with a corresponding increased T2 mapping value of 82 ms at 1.5 T (D). LGE is negative for scar (E). Early gadolinium T1 mapping at mid short axis showed markedly shortening of T1 value (F). Follow-up imaging 8 weeks later shows recovery of the mid-ventricular dyskinesia on cine LV 2-chamber bSSFP images during diastole (G) and systole (H). There is also a resolution of the hyperintensity on T2-weighted imaging (I) and normalization of the T2 mapping value in the mid-ventricle (J), with persistently negative LGE for scar (K). Early gadolinium T1 mapping at mid ventricle showed less shortening of T1 value (L).

Movie 2. Cine LV 2 chamber bSSFP showed an LVEF of 51% with a distinct mid-ventricular dyskinesia and compensatory hyperkinesia of the basal and apical segments.

A repeat CMR at eight weeks confirmed complete functional and structural recovery, with a normal LVEF of 64% and no residual RWMAs (Figure 3 and Movie 3). The signs of myocardial edema had fully resolved, as evidenced by normalized T2-weighted images and T2 mapping in the mid-ventricle (51 ms at 1.5 T) (Figure 3). T1 mapping values also normalize to 1010 ms and LGE images did not show any abnormalities (Figure 3). The early gadolinium T1 mapping shortening also decreased to 64%, demonstrating the transient nature of this unique finding. 

Movie 3. A repeat CMR at eight weeks LV 2 chamber cine bSSFP showed a normal LVEF of 64%, no residual RWMA, and complete functional and structural recovery.

Conclusion

For patients with suspected TCM, especially the rare mid-ventricular variant, CMR is an essential diagnostic tool that provides a definitive diagnosis by revealing a unique pattern of reversible myocardial dysfunction and edema. This case not only reinforces the value of CMR but also highlights a novel finding of transient early gadolinium T1 mapping changes, suggesting that the pathophysiology of TCM may include a component of acute microvascular inflammation. This finding has the potential to expand the diagnostic criteria for TCM and provides new insights into this intriguing condition. 

Perspective

This case illustrates the critical role of CMR in the diagnostic workup of patients with suspected TCM, particularly when the presentation is atypical. The definitive CMR diagnosis highlights the limitations of standard imaging modalities in these complex cases [1-3]. CMR offers a superior, multi-parametric approach to diagnosing TCM by combining functional assessment with unparalleled tissue characterization. While elevated native T1 and T2 mapping values provide objective evidence of myocardial edema, a known hallmark of TCM, our case presents a novel finding that challenges the established understanding of TCM pathophysiology [4].

Early gadolinium T1 mapping was acquired 2 minutes after intravenous administration of 0.1 mmol/kg gadobutrol on the short-axis plane (base, mid-ventricle, apical) by using a Modified Look Locker Inversion recovery (MOLLI) sequence with 4-(1) 3-(1)-2 sampling scheme. Percentage of early T1 shortening of the myocardium was calculated by [(early T1 – native T1)/ native T1] x 100. Early T1 indicates early enhanced (2 minutes after contrast administration) myocardial T1 mapping and native T1 indicates myocardial pre contrast T1 mapping.

The significant shortening of the early gadolinium T1 mapping value (cut off 70% or greater) is typically considered a marker of active inflammation and microvascular leak, a finding commonly seen in acute myocarditis [5].  However, in our case this parameter was also elevated acutely and normalized at follow-up. This suggests that TCM may involve a transient component of acute inflammatory response and capillary leak, not just the “neurogenic stunning” or reversible myocyte damage often cited as the sole mechanism. Therefore, early gadolinium T1 mapping could potentially be another quantitative biomarker in diagnostic marker for TCM.

The absence of LGE in our patient was also crucial. Unlike myocarditis or myocardial infarction, TCM is a non-necrotic process, and the lack of LGE distinguishes it from conditions with irreversible damage. Our case reinforces the notion that the findings on CMR are pathognomonic for TCM: reversible dysfunction, edema, and no scar. 

Click here to review the initial CMR on CloudCMR.
Click here to review the 8 week follow-up CMR on CloudCMR. 

References

1. Movahed MR. High Mortality and Complications in Patients Admitted With Takotsubo Cardiomyopathy With More Than Double Mortality in Men Without Improvement in Outcome Over the Years. J Am Heart Assoc. 2025;14(3):e037219.
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3. Ghadri JR, Wittstein IS, Prasad A, Sharkey S, Dote K, Akashi YJ, et al. International Expert Consensus Document on Takotsubo Syndrome (Part I): Clinical Characteristics, Diagnostic Criteria, and Pathophysiology. Eur Heart J. 2018 Jun 7;39(22):2032-2046.
4. Ojha V, Khurana R, Ganga KP, Kumar S. Advanced cardiac magnetic resonance imaging in takotsubo cardiomyopathy. Br J Radiol. 2020 Nov 1;93(1115):20200514.
5. Palmisano A, Benedetti G, Faletti R, Rancoita PMV, Gatti M, Peretto G, et al. Early T1 Myocardial MRI Mapping: Value in Detecting Myocardial Hyperemia in Acute Myocarditis. Radiology. 2020 May;295(2):316-325.