The pathophysiological mechanism of TTS remains unclear, but a significant body of research indicates that sympathetic overactivity and catecholamine surge are the most essential pathological mechanism of patho genesis [1, 4]. Acute physical or emotional triggers make sympathetic nervous system overstimulation, resulting in large increases in norepinephrine and epinephrine. At the same time, cortisol and catecholamine bioavailability will increase [5]. A study on animal models shows that a high intravenous epinephrine produces the characteristic reversible apical depression of myocardial contraction coupled with basal hypercontractility [6]. In recent years, it has been hypothesized that the distinctive aberrant apical movement in TTS is caused by the influence of excessive levels of epinephrine on cardiac G protein [7].

The patient in this case is a postmenopausal female. Several illnesses can explain her clinical symptoms following PCI, so distinguishing between them is critical (Table 2). First, the intervention was a success, with no coronary artery dissection, incomplete stent apposition, tissue prolapse, or other complications. Moreover, she was given anticoagulants and antiplatelet agents after the intervention, so postoperative complications (such as coronary artery dissection, stent thrombosis and coronary artery perforation) were unlikely to occur [8]. Second, repeated coronary angiography did not detect neither coronary artery dissection, nor stent thrombosis. Third, abnormalities in ventricular wall motion caused by coronary artery dissection or stent thrombosis are typically restricted to locations innervated by the culprit coronary artery. This patient’s ECG, echocardiography, and CMR show that the distribution of abnormal ventricular wall motion exceeds the area supplied by the left anterior descending artery. Last but not least, all clinical characteristics of the patient can be explained using TTS alone for the following reasons.

The patient’s education level is primary school. She has insufficient awareness of primary disease as a result of having difficult communicating with her doctors, limited knowledge and information, and lack of medical expertise during perioperative time, resulting in negative feelings such as anxiety and fear. Meanwhile, PCI is an invasive treatment that enhanced sympathetic activity and catecholamine release throughout the body. As a result, patients are under emotional and physical distress. Moreover, the ECG showed ST-segment elevation in leads V1-V5 and biphasic T-wave, and blood chemistry showed a significant rise in hs-TnI on the first post-procedure day. Nonetheless, emergency coronary angiography revealed that the blood flow at the stent implantation site was normal. At the same time, echocardiography and CMR revealed that the contractility of the middle and basal segments of the left ventricular septum and of the apex, was decreased, and the patient’s heart function improved rapidly after short-term symptomatic treatment. Therefore, the patient could be diagnosed with TTS based on the 2018 TTS international consensus [1]. This case highlights the difficulty of TTS diagnostic after PCI and the necessity of coronary angiography, echocardiography, and CMR for its differential diagnosis.

Finally, TTS has been regarded as a relatively benign condition with a generally favorable prognosis since its first description. Recent investigation, however, has indicated that patients experienced substantial mortality and morbidity following the acute phase of TTS, with all-cause mortality at 1 year being 5.6% [9]. Therefore, early clinical identification will aid in the development of individualized treatment strategies and clinical management. The primary goal of treating heart failure in TTS patients is to relieve pulmonary congestion and provide hemodynamic support [10, 11]. Treatment of TTS patients differs significantly depending on whether the left ventricular outflow pathway is obstructed or not. We used furosemide to control volume load and beta-blockers to reduce excessive myocardial contraction, decrease left ventricular filling, reduce heart rate, and improve cardiac remodeling in this TTS patient who developed acute heart failure without the left ventricular outflow tract obstruction during the acute phase. A number of randomized clinical trials have indicated that sacubitril/valsartan reduces renal and cardiac adverse events in patients with heart failure with preserved ejection fraction when compared to valsartan alone [12, 13]. Consequently, we began treatment with sacubitril valsartan sodium tablets on the 7th day after PCI. After a follow-up period of 2 mouths the patient was free of cardiac symptoms with a good functional capacity. The left ventricular ejection fraction appears normal.