Transient left ventricular apical ballooning syndrome (Takotsubo cardiomyopathy) following orthotopic liver transplantation

We report the first published case of transient left ventricular apical ballooning syndrome (Takotsubo cardiomyopathy) in the setting of orthotopic liver transplantation. A 65-year-old female with end-stage liver disease secondary to nonalcoholic steatohepatitis with stage 2 hepatocellular carcinoma underwent successful total hepatectomy, portal vein thrombectomy, and orthotopic liver transplantation. The patient's past medical history included chronic systemic hypertension without prior history of cardiac disease, diabetes, smoking, hyperlipidemia, or illicit drug use. Pretransplant dobutamine stress echocardiography demonstrated hyperdynamic left ventricular function (ejection fraction 74%) with normal left ventricular size. A double product (defined as maximal systolic blood pressure × heart rate) of 21,714 and heart rate of 91% of maximum predicted were achieved. There were no stress-induced wall motion abnormalities. Cardiac valves were normal. Estimated right ventricular systolic pressure was 36 mm Hg. The intraoperative course was very unremarkable. The patient had an estimated blood loss of 500 mL and received one unit of platelets. The patient did not require pressors during the procedure and had no hemodynamic instability. Thromboelastogram during the procedure did not reveal any evidence of hypercoagulation state. The posttransplantation course was uneventful until 4 hours after transplant when ST elevation was noted on the telemetry monitor. A 12-lead electrocardiogram demonstrated ST segment elevation consistent with an acute anterolateral myocardial infarction (Fig. 1A). The patient was sedated but arousable and denied chest discomfort or dyspnea. An emergent echocardiogram demonstrated anteroapical, apical, and inferoapical akinesis, consistent with an anterior myocardial infarction (Fig. 2A and B). Emergent coronary angiography demonstrated normal coronary arteries and left ventriculography confirmed the apical wall motion abnormalities. A preliminary diagnosis of transient left ventricular apical ballooning syndrome (Takotsubo cardiomyopathy) was made. Peak total creatine kinase levels were 869 U/L (normal 38–176) and troponin levels were 0.15 ng/mL (normal <0.03 ng/mL). The patient's subsequent hospital course was unremarkable. Outpatient transthoracic echocardiogram 6 weeks later (Fig. 2C) showed normal left ventricular function with no wall motion abnormalities, and an electrocardiogram 4 months later (Fig. 1B) demonstrated normal findings with resolution of ST segment elevation. (A) A 12-lead electrocardiogram 4 hours after transplantation demonstrates sinus tachycardia and acute ST elevation in the anterolateral leads. A single premature ventricular complex is also noted. (B) Electrocardiogram 4 months after transplantation shows sinus rhythm and normalization of the ST segment elevation. (A) Echocardiogram apical long axis view (using intravenous contrast) during end-systolic shows a severe apical wall motion abnormality (arrowheads) with normal basilar wall motion (arrows). (B) Same view during end-diastole. (C) End-systolic view 4 months later shows totally normal global and regional wall motion (arrows). Transient left ventricular apical ballooning syndrome or Takotsubo cardiomyopathy is an uncommon cardiac abnormality that characteristically occurs in postmenopausal women following an emotional or physical stressor.1 The clinical presentation is similar to an acute myocardial infarction with chest pain, elevated cardiac biomarkers, and precordial ST elevation on the electrocardiogram. Coronary angiography shows nonobstructive coronary artery disease with ballooning of the apical left ventricle most commonly; however, midventricular ballooning has been reported.2 The pathophysiologic mechanism is not known. Leading hypotheses include catecholamine-mediated myocardial injury, multivessel epicardial spasm, coronary microvascular dysfunction, acute coronary syndrome with reperfusion, impaired fatty acid metabolism, myocarditis, and transient obstruction to left ventricular outflow.3-8 Resolution of the wall motion abnormalities on subsequent evaluation is necessary to make the diagnosis.1 This article contains Supplementary Material available at http://www.mrw.interscience.wiley.com/suppmat/1527-6465/suppmat . Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.