P124 A TAKOTSUBO SYNDROME MIMICKING AN APICAL HYPERTROPHIC CARDYOMYOPATHY: A CASE REPORT

Abstract A 70–year–old woman was admitted to our Intensive Care Unit (ICU) with high levels Hs–TnT. Coronaries were normal and ventriculography was suggestive for Takotsubo Syndrome (TS). In the acute phase she developed a cardiogenic shock and transthoracic echocardiography (TTE) showed a dilated left ventricle (LV) with iperkinesia of basal segments and biventricular apex and mid –ventricular akinesia, with a severely reduced left ventricular ejection fraction (LVEF 20%). Seven days after admission to Cardiac Rehabilitation Unit, a TTE showed LV apical hypertrophy (max thickness 18 mm), hypokinesia of hypertrophic segments, hypercontractility of basal segments and LVEF 55%. These features could have been suggestive for a coexisting apical hypertrophic cardiomyopathy (HCM). The EKG showed T wave inversions in precordial and inferior leads, not present at admission, this observation being against the presence of a pre–existing unknown HCM. Cardiac Magnetic Resonance (CMR) showed T1 and T2 mapping imagines for oedema in LV infero–lateral, basal segments and apical region, a subepicardial stria of late gadolinium enhancement in infero–lateral basal segment. These patterns were reported as suggestive for myocarditis rather than TS. Recent infectious or autoimmune diseases were excluded. Further TTE showed reversed LV parameters, normal kinesis of all segments, LVEF 66%, with a persistence of negative T waves at EKG. Discussion Our patient developed a classical TS with LV apical ballooning and hyperkinesia of basal segments with uncommon right ventricular hypokinesia. A peculiar finding was the transient apical LV thickness that was seen through TTE, mimicking an apical hypertrophic cardiomyopathy. Such a finding has already been described in few case reports; however, the nature and the physiopathology of that apical thickness was never proved. Through CMR we noted that, in the same region where TTE detected apical hypertrophy, there was a consistent amount of oedema which could be the reason of pseudo–hypertrophy findings. Our experience confirms the importance of integrating CMR in the diagnostic algorithm as already supported in consensus statements. In our case CMR played a key–role in the exclusion of a coexisting apical hypertrophic cardiomyopathy.