Background Takayasu’s arteritis (TA) is a systemic inflammatory disease that affects aorta and its major branches. There are several cardiac manifestations of TA and, recently, an association with Takotsubo syndrome (TTS) was reported Case Presentation A 58–year–old Caucasian female, with history of severe asymptomatic aortic regurgitation (AR) with a recently documented normal LV systolic function and TA in remission under corticosteroids, was admitted in the emergency department with chest pain following an acute intense stressful event. ECG showed sinus tachycardia, T wave inversion in left precordial and lateral leads, and a QTc of 487 ms (Figure 1). Laboratorial evaluation presented high–sensitivity troponin I of 3494 ng/L and B–type natriuretic peptide of 4759 pg/mL. The transthoracic echocardiogram revealed severe dilation of LV with moderate systolic dysfunction, due to apical and midventricular akinesia (“apical ballooning” pattern), and severe AR (Figure 2). The coronary angiography showed normal coronary arteries. An acetylcholine provocative test showed spasm of both the left anterior descending and circumflex arteries, accompanied by chest pain and ST depression in ECG, reverted after intracoronary nitrates administration (Figure 3). The patient was switched to diltiazem and heart failure drug therapy was started. A cardiac magnetic resonance revealed severe dilation of the LV, apical hypokinesia, ejection fraction to 53%, signs of myocardial edema and increased extracellular volume in apical and mid–ventricular anterior and anterolateral walls, and absence of myocardial late gadolinium enhancement, compatible with TTS. Patient was discharged clinically stable, without signs of HF, with progressive reduction of troponin and BNP. A final diagnosis of myocardial infarction with nonobstructive coronary arteries (MINOCA) due to TTS and coronary vasospasm in a patient with TA was done Discussion TA is a rare disease and there are reports of its association both with TTS and coronary vasospasm. Besides that, coronary vasospasm may also be involved in the pathophysiology of TTS. Moreover, in this patient we could not exclude the role coronary diastolic hypoperfusion due to AR in the elicitation of coronary vasospasm. Therefore, although the mechanisms behind these pathologies are not yet fully studied, this case supports their relationship Conclusion We presented a case of a patient with TA admitted with MINOCA due to TTS and coronary vasospasm
Background Eosinophilic granulomatosis with polyangiitis (EGPA), previously known as Churg–Strauss, is a rare multisystem disorder characterized by chronic rhinosinusitis, asthma, and prominent peripheral blood eosinophilia (PE). Cardiac involvement may include eosinophilic myocarditis and it is a serious manifestation of EGPA. Case Presentation A 67–year–old woman presented to the emergency department with 2–weeks history of dyspnea, orthopnea and asthenia. She had history of asthma, PE, adjuvant radiotherapy after right mastectomy (July 2021). The patient was diagnosed with new onset atrial fibrillation in the previous month. At admission, the patient was hemodynamically stable and with signs of congestion. Complementary exams showed sinus rhythm and T–wave inversion on lateral leads; PE (2010/uL), elevated troponin and BNP values; and severe biventricular systolic dysfunction with diffuse hypokinesia and apical akinesia. The patient was admitted to the ICU and was treated with intravenous diuretics and levosimendan. Optimal HF therapy was introduced. Serial echocardiography revealed partial recovery of LVEF and blood analysis showed a decrease in troponin levels, with persistent eosinophilia (6330/uL). Computed tomography (CT) excluded significant coronary disease, and showed bilateral basal ground–glass opacities, areas of air–space consolidation and bilateral reticular–nodular pattern. Cardiac magnetic resonance revealed increased T2 values/signs of myocardial edema in anterior wall, interventricular septum and apex and no late gadolinium enhancement, compatible with myocarditis. An endomyocardial biopsy (EMB) was performed and confirmed the diagnosis of eosinophilic myocarditis. Oral corticosteroids were started. Paranasal CT scan showed signs of chronic sinusitis, without polyposis, and antineutrophil cytoplasmic antibodies were positive, making the diagnosis of EGPA, according to ACR criteria. Discussion In a patient presenting with new onset heart failure and with history of asthma and eosinophilia, it is important to suspect eosinophilic myocarditis, as this is a rare but reversible life–threatening condition. EMB plays an important role in the diagnosis and should be done promptly. Conclusion We described a multidisciplinary management of a case of a patient with eosinophilic myocarditis and EGPA, presenting with severe acute biventricular dysfunction.
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