2021
DOI: 10.1016/j.clinimag.2021.08.027
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Review of multi-modality imaging update and diagnostic work up of Takotsubo cardiomyopathy

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Cited by 5 publications
(22 citation statements)
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“…In TTC patients, the levels of cardiac enzymes, creatine kinase (CK), CK-MB, and cardiac troponin, and NT-proBNP are increased [13,26]. In addition, the levels of serum catecholamines, neuropeptide-Y, and serotonin are also increased [26].…”
Section: Diagnostic Workup and Findings In Takotsubo Cardiomyopathymentioning
confidence: 99%
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“…In TTC patients, the levels of cardiac enzymes, creatine kinase (CK), CK-MB, and cardiac troponin, and NT-proBNP are increased [13,26]. In addition, the levels of serum catecholamines, neuropeptide-Y, and serotonin are also increased [26].…”
Section: Diagnostic Workup and Findings In Takotsubo Cardiomyopathymentioning
confidence: 99%
“…In TTC patients, the levels of cardiac enzymes, creatine kinase (CK), CK-MB, and cardiac troponin, and NT-proBNP are increased [13,26]. In addition, the levels of serum catecholamines, neuropeptide-Y, and serotonin are also increased [26]. ECG evaluation in these patients usually shows ST elevation or depression, inversion of the T-wave, and prolongation of the QT-interval [13,26].…”
Section: Diagnostic Workup and Findings In Takotsubo Cardiomyopathymentioning
confidence: 99%
See 1 more Smart Citation
“…VTAs are often detected on the left ventricle (LV) but can also be seen on the right ventricle (RV). The etiopathogenesis of VTAs may include myocardial infarction (MI), myocarditis, Chagas disease, and trauma, 1 , 3 , 4 their medical management may consist of anticoagulation to prevent thromboembolism and afterload reduction. Surgical treatment may be considered for large VTAs, a VTA with an increased size during follow-up, angina, rupture, or heart failure.…”
Section: Ventricular Outpouchingsmentioning
confidence: 99%
“…The reaction to stressors depends on individual factors influencing both catecholamine production and myocyte and microvascular response to sympathetic stimulation [24], with estrogen deficiency, genetic factors, and neurologic and psychiatric disorders being predisposing factors to mental and physical triggers [25][26][27][28][29]. Despite the clinical presentation usually mimicking ACS [30], with patients often presenting with chest pain, followed by dyspnea and syncope [31], having electrocardiographic abnormalities (ST-segment elevation, ST-segment depression, T-wave negative conversion, and QT prolongation) [32] and showing a mild elevation of myocardionecrosis enzyme levels, as well as the marked elevation of brain natriuretic peptide (BNP) and N-terminal pro-BNP [33][34][35][36], TTC is formally considered a benign self-limiting state presenting a favorable prognosis [37] and it is generally characterized by a temporary impairment with complete recovery within 3 weeks. However, complications including lethal ventricular arrhythmia, pump failure, outflow tract obstruction, cardiac rupture, and systemic embolization may occur in the acute phase and cause morbidity and mortality.…”
Section: Introductionmentioning
confidence: 99%