The exact cause of Takotsubo cardiomyopathy isn't fully known. Possible factors include: sympathetic overdrive, coronary spasm, microvascular dysfunction, low estrogen, inflammation, or impaired fatty acid metabolism [2, 3]. Takotsubo cardiomyopathy, frequently associated with emotional and physical stressors, can lead to sympathetic overdrive. Our patient's intense emotional stress episode might have served as a triggering event. The subsequent development of acute pericarditis could potentially arise from the transmural inflammation observed in Takotsubo cardiomyopathy, affecting the adjoining pericardium [4]. Conversely, it's possible that the severe chest pain from pericarditis could trigger a catecholamine surge, predisposing the heart to Takotsubo [5]. Moreover, prior study on murine models by Wu et al. showed that rising catecholamine can induce cardiomyocyte necroptosis that contributes to myocardial injuries [6]. Furthermore, Wang et al. reported a case with fatal pheochromocytoma showing catecholamine-related cardiotoxicity [7]. Noteworthy in our patient’s narrative is the temporal proximity of the two conditions, sans any underlying autoimmune pathology, but intriguingly aligned with an episode of pronounced emotional stress. This intricate chronology leads us to postulate that the onset of Takotsubo cardiomyopathy perhaps paved the way for pericarditis, a conjecture strengthened by the ECG progression. The subsequent resolution of pericarditis, without the intervention of colchicine and no recurrence over a year, further accentuates the distinctiveness of our patient’s clinical journey.

The diagnostic trajectory for our patient emphasized the challenges in differentiating between overlapping cardiac conditions. Utilizing the Mayo Clinic criteria, we identified the transient ventricular abnormalities, ECG changes, and absence of obstructive coronary disease suggestive of Takotsubo cardiomyopathy [3]. The rapid progression from ST elevation to T-wave inversion on the patient's ECG, paired with other clinical signs, was consistent with acute pericarditis. Such concurrent diagnoses emphasize the need for thorough, discerning evaluations in cardiac presentations that might mask as more common entities.

In managing such a multifaceted clinical picture, treatment strategies need to be adaptable. Management of Takotsubo cardiomyopathy lacks definitive guidelines, relying on clinical experience and expert consensus (evidence level C) [8]. Initial treatment mirrors acute coronary syndrome with aspirin, beta-blockers, ACE inhibitors, lipid-lowering agents for 3-6 months, in addition to coronary angiography to rule out artery disease. Anticoagulation is reserved for ventricular thrombus or embolic events [8]. In our patient, the presence of acute chest pain, elevated troponin levels, and ECG changes implied a cardiac event of significant concern. The immediate priority was to rule out obstructive coronary artery disease, thus, an urgent coronary angiography was performed, confirming the absence of such obstruction and pointing toward Takotsubo. With acute pericarditis also on the differential—given the ECG changes—the decision was made to treat both simultaneously. We chose a treatment plan involving aspirin, lisinopril, and metoprolol, covering the primary therapeutic recommendations for both conditions. The patient's rapid improvement, particularly in the left ventricular ejection fraction, further reinforced our treatment approach.

Comparing our case with other reported cases in the literature highlights some different aspects. For example, Kim et al. reported a similar case with both Takotsubo and pericarditis [9]. However, while both displayed ST-segment elevations, the evolution of these changes differed. Kim et al. employed colchicine, resulting in normalized EKG changes and ejection fraction within four weeks [9]. Mori et al. reported a rheumatoid arthritis patient with Takotsubo complicated by pericarditis.¹⁰ In comparison to the 64-year-old woman reported by Mori et al., our patient also demonstrated apical ballooning and pericardial effusion. However, the 64-year-old exhibited more distinct ECG changes, including elevated ST-segments and inverted T-waves, alongside an incomplete right bundle-branch block. Regarding the choice of therapy, Mori et al. treated the patient pericarditis and RA concomitantly with corticosteroid and anticoagulants [10]. Our approach, meanwhile, adopted a broader therapeutic strategy, highlighting the nuanced nature of managing such cases.