Figure 1a: Representative echocardiogram image demonstrating apical ballooning and hypokinesis in takotsubo cardiomyopathy.

Figure 1b: Representative image of a takotsubo, Japanese octopus fishing pot.

On the first postoperative night, he was bradycardic between 50-60bpm. He denied any chest pain or shortness of breath. An electrocardiogram (ECG) on POD 1 found sinus bradycardia with sinus arrhythmia and an incomplete right bundle branch block. The patient remained asymptomatic with heart rate as low as 48bpm. A repeat ECG was performed on POD 2 and revealed sinus arrhythmia, moderate ST depression and possible right ventricular hypertrophy. Cardiology was consulted and an echocardiogram was performed. The echocardiogram revealed diffuse hypokinesis of the left ventricle with a reduced ejection fraction of 40-45%, and severe hypokinesis of the mid-apical anterior, apical lateral, and apical myocardium. He was diagnosed with Takotsubo cardiomyopathy and started on benazepril and metoprolol. Psychiatry was also consulted due to concern for anxiety and depression. He was diagnosed with adjustment disorder and started on mirtazapine. The patient remained asymptomatic throughout his postoperative course and was discharged on benazepril and metoprolol.He completed a 1-month course of his cardiac medications and had no long-term sequelae of TTC.

Takotsubo cardiomyopathy is a relatively uncommon diagnosis of transient and self-resolving heart failure typically limited to the elderly, including the head and neck population [1-4]. The development of TTC in our 23-year-old patient is the first patient under the age of 60 to be reported in the head and neck oncologic surgery literature. TTC commonly presents with chest pain and dyspnea and has been reported to occur following significant stressors such as emotional triggers or physical triggers such as malignancy, infection, and surgery [1,6,7]. Some patients may remain asymptomatic, as in our patient, and findings are only found on ECG or echocardiogram [7]. The exact mechanism of TTC remains unknown, yet excess catecholamine release and activation is one of the leading theories which produces oxidative stress on the myocardium [5-7].

ECG and echocardiogram are the two most commonly performed procedures when TTC is suspected.ECG findings vary but often include ST segment elevation, depressions or T-wave inversion [6,7]. The echocardiogram more reliably shows characteristic apical wall changes including hypokinesia, akinesia, or dyskinesia with reduced ejection fractions.7 The Mayo Clinic is a commonly used guidelinefor diagnostic criteria (Figure 2), though many variants of diagnostic criteria exist [6,9]. Management of TTC is primarily supportive. Beta-blockers are often used to counteract the excessive catecholamine release [5,7] and angiotensin-converting enzyme inhibitors (ACE inhibitors) are commonly used to reduce after load and increase ejection fraction [5].