Takotsubo cardiomyopathy in an acute surgical patient.

Sir,

Takotsubo cardiomyopathy (TCM) is a considerable differential diagnosis of acute coronary syndrome (ACS), particularly amongst postmenopausal women with preceding stressors. It is characterized by transient hypokinesia or dyskinesia of the left ventricular apical or mid-segments, with basilar hyperkinesis. Diagnosis requires absence of occlusive coronary disease or angiographic evidence of acute plaque rupture. Etiology includes catecholamine surges, with resultant coronary vasospasm or direct myocardial insult. TCM and ACS have specific therapeutic and prognostic implications, necessitating accurate diagnosis.

A 70-year-old female was admitted to the emergency department with acute bowel obstruction. She had previous similar admissions, and thus surgical intervention was proposed if she failed to respond to conservative management.

On the day of admission, she developed severe central chest pain associated with vomiting and diaphoresis. Serial electrocardiography demonstrated dynamic anterolateral ST segment elevation. Troponin-I was 0.14 ng/ml. Cardiac catheterization revealed diffuse but non-obstructive atherosclerotic disease. Left ventriculography demonstrated akinetic mid and apical anterior and inferior walls, with hyper-contractile basal function consistent with TCM [Figure 1]. Transthoracic echocardiography revealed moderate to severely impaired left ventricular (LV) systolic function with apical LV aneurysm. Systolic anterior motion of the mitral valve chordae was noted, with significant left ventricular outflow tract obstruction (LVOTO). An echocardiogram 6 weeks later demonstrated restoration of LV function.

Figure 1

Angiography demonstrating left ventricular systole with mid and apical ballooning (white arrows)

Clinical and electrocardiographic findings in TCM are frequently indistinguishable from those in acute myocardial infarction (AMI). Common presentations include acute sub-sternal chest pain, followed by dyspnea, and less rarely syncope and palpitations.[1] Elevation in creatine phosphokinase and troponin levels is typically less than in AMI. The most frequent electrocardiographic findings are precordial ST elevation and T-wave inversion.[1] QT prolongation and conduction disturbances may also be seen. Higher ST elevation voltage in leads V4–V6 than V1–V3, absence of inferior reciprocal changes, and pathological Q waves were found to be highly sensitive and specific in differentiating TCM from AMI.[2] Dib, et al., however, found that one-third of patients with TCM have no significant electrocardiographic changes.[3]

Prompt diagnosis with coronary angiography was mandatory in this patient to avoid unnecessary fibrinolytic therapy and prolonged anticoagulation for suspected AMI if emergent surgical intervention was warranted. However, the absence of significant coronary stenosis does not exclude AMI with a recanalized coronary artery, or myocarditis. Cardiac magnetic resonance imaging (MRI) has therefore been attributed as a valuable adjunct. This can demonstrate the absence of myocardial necrosis in TCM on late gadolinium-enhanced images, which is not typical of ST-elevation MI or acute myocarditis.[4] Recently, cardiac biomarkers including admission NT-proBNP/myoglobin ratio and peak NT-proBNP/peak TnT ratio have been reported to accurately distinguish TCM from AMI.[5]

Complication rates approximate to 20% in TCM, and include LV failure, pulmonary edema, cardiogenic shock, arrhythmias, ventricular rupture, mural thrombus, LVOTO, mitral insufficiency, and death.[2] In-hospital mortality rate is <2%, with a recurrence rate approximating to 10%.[2] Supportive measures, including beta-blockade and angiotensin-converting enzyme inhibition, are the mainstay of acute management.

This case illustrates the importance of distinguishing TCM from AMI in acute surgical patients. Large-scale studies are required to develop an algorithm to aid differentiation in an acute setting.