A 64-year-old man who had undergone cardiac transplantation for ischemic cardiomyopathy 9 years earlier was admitted to the hospital for malaise and fever of unknown origin. His posttransplantation course had been complicated by transplant vasculopathy requiring percutaneous coronary intervention 2 years earlier. His immunosuppressant regimen included cyclosporine, mycophenolate mofetil, and low-dose steroids. On admission, he denied having chest pain, but his high-sensitivity troponin I level was elevated at 17 µg/L (normal range, 0-0.045 µg/L). His ECG was unremarkable. Echocardiography demonstrated extensive posterior wall akinesia but no other regional wall motion abnormalities. Ejection fraction was estimated at 60%. Urgent coronary angiography demonstrated subtotal occlusion of the left circumflex artery. Appropriate antibiotic therapy was initiated, and possible sources of infection were ruled out by transesophageal echocardiography and thoracoabdominal computed tomography scan. Two days later, the patient was taken back to the catheterization laboratory and treated by implantation of a drug-eluting stent.One week later, while still in the hospital, he developed sudden onset of dyspnea accompanied by a drop in oxygen saturation and was admitted to the intensive care unit. His chest x-ray demonstrated pulmonary venous congestion. His aminoterminal pro-brain natriuretic peptide was markedly increased at 40 499 ng/mL (normal range, 0-125 ng/mL). The patient´s cardiac enzymes were as follows: high-sensitivity troponin I, 6.368 µg/L (normal range, 0-0.045 µg/L); creatine phosphokinase, 207 U/L (normal range, 35-171 U/L); and isoenzyme creatine phosphokinase-MB, 22 U/L (normal range, 0-24 U/L). Urgent echocardiography revealed severe akinesia/dyskinesia of the mid and apical portions of both ventricles (Movies I and II in the online-only Data Supplement). Three-dimensional echocardiography performed 1 day later confirmed these findings (Figure [A]). Significant coronary artery obstruction was excluded by repeat coronary angiography (Figure [B]). His ECG demonstrated new T-wave inversions in leads I, II, aVL, aVF, and V 3 through V 6 (Figure [C]). Follow-up echocardiography 10 days later (Movies III and IV in the online-only Data Supplement) showed reversal of all wall motion abnormalities except for posterior wall akinesia/dyskinesia (Figure [D]).Takotsubo cardiomyopathy (TC) is characterized by an acute reversible dysfunction of the myocardium unrelated to obstructive coronary artery disease or myocarditis.Disturbances of myocardial microcirculation and increased sympathetic activity caused by excessive local release of catecholamines (ie, epinephrine, norepinephrine, and dopamine), which in turn may lead to microvascular spasms or myocyte injury, have been implicated in the pathophysiology of this disease entity.
1To the best of our knowledge, our case is the first description of spontaneously occurring biventricular TC in a heart transplantation patient. There is only 1 other report in the literature of TC o...