Magnetic resonance imaging of takotsubo syndrome triggered by stress

Takotsubo syndrome is a type of reversible acute cardiac dysfunction triggered by psychological or physical stress, mainly present with chest pain and dyspnea. However, it may not be familiar to most clinicians and extremely easily misdiagnosed due to its low incidence. Despite this, timely cardiac magnetic resonance could provide very important clues to its diagnosis. Takotsubo syndrome (TTS) is a clinical syndrome characterized by an acute and transient left ventricular dysfunction that is always triggered by an emotional or physical stimulation.1 TTS is often be misdiagnosed as acute coronary syndrome (ACS). It is reported that approximately 1–3% of all patients who present with symptoms consistent with ACS then undergo coronary angiography, are identified as TTS in the end.2 We report a typical case of TTS and record its detail cardiac magnetic resonance (CMR) imaging to provide reference for clinicians. A 74-year-old female retired teacher presented to our emergency room with acute chest pain after quarreling with others 4 h ago. She has no history of systemic disease, medication usage nor travel, or cluster history. The vital sign showed normal temperature with 36.5°C, a heart rate of 110 beats per minute, tachypnea with a respiratory rate of 20 breaths per minute and relatively low blood pressure (105/63 mmHg). Oxygen saturation was 96% under room air condition. Physical examination was unremarkable. An electrocardiogram showed tachycardia with ST-segment elevation (leads I, leads AVL and leads V4 to V6). Blood tests revealed troponin I increased significantly. Emergency coronary angiography revealed no significant coronary stenosis. CMR showed that a significant decrease in shrinkage movement of the left ventricle with typical apical and mid-ventricular ballooning (Figure 1A and C) with significant edema in the myocardium (Figure 2A), particularly in the subendocardial region, and the left ventricular (LV) ejection fraction was only 37.4% (Figure 1A and C). The patient was treated with liquid recovery, aspirin and oxygen uptake through a nasal catheter and electrocardiograph monitoring. After aggressive treatment, the prior symptoms disappeared. After 10 days of follow-up, the patient reported an improvement in exercise tolerance without oxygen support. CMR examination before discharge showed that a partial recovery of LV systolic function (Figure 1B) and a significantly reduced area of myocardial edema (Figure 2B). There were no obvious late gadolinium enhancement (LGE) was observed in the recovery myocardium (Figure 2C and D). At telephone follow-up 6 months later, the patient reported that his physical strength had completely returned to normal. Cardiac magnetic resonance imaging after admission and before discharge. (A) Systole (24 h after admission); (B) systole (24 h before discharge); (C) diastole (24 h after admission); and (D) diastole (24 h before discharge). Cardiac magnetic resonance imaging after admission and before discharge. (A) Systole (24 h after admission); (B) systole (24 h before discharge); (C) diastole (24 h after admission); and (D) diastole (24 h before discharge). Cardiac magnetic resonance post-processing imaging. (A) Ventricular edema evaluation (24 h after admission) T2 ratio is represent the degree of edema, high ratio represent severe edema, the edematous area are mainly in subendocardial layer; (B) ventricular edema evaluation (24 h before discharge), the edema area decreased after treatment; (C) LGE, no obvious LGE was observed (24 h before discharge); and (D) T1 mapping image demonstrating no fibrosis at the left ventricular wall (24 h before discharge). Cardiac magnetic resonance post-processing imaging. (A) Ventricular edema evaluation (24 h after admission) T2 ratio is represent the degree of edema, high ratio represent severe edema, the edematous area are mainly in subendocardial layer; (B) ventricular edema evaluation (24 h before discharge), the edema area decreased after treatment; (C) LGE, no obvious LGE was observed (24 h before discharge); and (D) T1 mapping image demonstrating no fibrosis at the left ventricular wall (24 h before discharge). TTS is a reversible myocardial functional lesion, and the specific pathogenesis is not very clear. However, it may not be familiar to most clinicians and extremely easily misdiagnosed due to its low incidence. In clinical practice, TTS is most likely to be misdiagnosed as ACS which would causing fear in patients and their families. Therefore, the early identification of TTS is very important. CMR can provide valuable evidence for the diagnosis of cardiomyopathy. In our case, CMR images showed a typical apical and mid-ventricular ballooning changes, and a wide range of myocardial edema mainly in subendocardial without obvious myocardial enhancement in LGE in the acute phase of illness. However, in acute myocardial infarction (AMI), myocardium edema mainly occurs in the infarct-related territory due to myocardial reperfusion injury and is accompanied by delayed myocardial enhancement in LGE.3 Additionally, TTS also would be misdiagnosed as viral myocarditis (VMC), patients with severe TTS are easily misdiagnosed as acute fulminant VMC. However, VMC tends to present subepicardial delayed myocardial enhancement in LGE,4 and LGE contrast enhancement detects scar tissue, usually patchy or diffuse and nodular, and subepicardial or midmyocardial in a noncoronary distribution.5 These findings could provide a reference for further distinguishing TTS, AMI and VMC. Therefore, for the acute chest pain patients without a certain diagnosis, early CMR examination may provide important clues for the diagnosis of the disease. This work was partially supported by grants from the National Natural Science Foundation of China (81873247). The funder had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. Conflict of interest: All other authors have no conflicts of interest. The materials generated during the current study are available from the corresponding author on reasonable request. Consent was obtained from the participant for the publication of this case report (including all data and images).