Answer: A broken and blocked heart—Takotsubo cardiomyopathy with dynamic left ventricular outflow tract obstruction

Correct Answer. 3. Beta-blocker therapy Left ventriculography showed severe left ventricular dysfunction with mid- to apical akinesia (Supplementary materialonline, Video S1) and a significant 40 mmHg peak to peak left ventricular outflow tract (LVOT) pressure gradient (Figure 1), induced by basal hyperkinesis. Subsequent transthoracic echocardiogram revealed severe mid- and apical wall hypokinesia causing severe left ventricular dysfunction, in keeping with the diagnosis of Takotsubo cardiomyopathy. There was hyperkinesia of the basal walls, leading to systolic anterior motion (SAM) of the anterior mitral leaflet with moderate to severe mitral regurgitation and dynamic LVOT obstruction (LVOTO) with a peak LVOT gradient of 50 mmHg (Supplementary material online, Video S2). The patient was started on regular beta-blocker therapy in addition to intravenous fluid resuscitation. Inotropic support was avoided to prevent worsening LVOTO in the setting of hyperkinetic basal segments. Her blood pressure improved following the commencement of beta-blocker therapy, and she was discharged from the hospital 2 days later. Coronary angiogram pressure waveform. This case highlights the importance of recognizing dynamic LVOTO in hypotensive patients with Takotsubo cardiomyopathy. Dynamic LVOTO is caused by basal hyperkinesia of the left ventricle producing a Venturi effect by systolic narrowing of LVOT with subsequent SAM, which reduces cardiac output.1 Coronary angiogram with haemodynamic assessment and transthoracic echocardiography with Doppler pressure measurement are required for diagnosis.2 Treatment includes fluid administration to improve preload and ventricular filling, and beta-blocker therapy to reduce hyperdynamic basal contraction. It is important to avoid inotropes and/or diuresis as this would augment basal contraction, reduces left ventricular filling, and worsens LVOTO. In situations where hypotension or pulmonary congestion is present, beta-blockers and intravenous fluid should be deferred. Inotropes which purely increase systemic vascular resistance, such as phenylephrine or vasopressin, should be used in this setting. These agents increase afterload and blood pressure without increasing LVOTO.3 Supplementary material is available at European Heart Journal : Acute Cardiovascular Care This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Conflict of interest: none declared.