P138 ST–SEGMENT ELEVATION, QTC PROLONGATION AND BRUGADA LIKE PATTERN IN THE EMERGENCY DEPARTMENT: A NEW ENTITY FOR US TO KNOW? CASE 1

Abstract

Abstract Introduction ST elevation (STE) usually means acute transmural ischemia by epicardial coronary artery occlusion by a blood clot,so Guidelines recommend rapid reperfusion therapy, possibly within the first hour. Nevertheless,STE due to non–ischemic etiologies has been reported in up to 15% of the general population.We report a case of ‘likely STEMI’ presenting with marked STE,QTc prolongation and Brugada like pattern on ECG but no significant coronary obstruction on angiography.Case 1A 74y woman presented in the ER with syncope and chest pain.History of pulmonary emphysema and Crohn‘s disease previously operated on. On admission:apyretic,BP 80/40, HR130 bpm, SO2 98% on mask O2 12 l/min.WBC 20,000, 84% neut, high D–Dimer 36091 and HS–TnI 99. On transthoracic echo (TTE) akinesis in apical, apical lateral, anteroseptal, and anterior wall and EF 25%.On Chest CT bilateral emphysema,no pulmonary embolism.On ECG sinus tachycardia,frequent PVCs,diffuse deep negative waves and prolonged QTc.While in ER,a new she syncope occurred,and tachycardia with large complex,with spontaneous resolution,was observed.On ICU admission ECG diffuse STE with coved pattern in V1 and prolonged QTc 641 ms;treated with magnesium sulfate,calcium gluconate,metoprolol,ASA,heparin;on urgent coronary angiography subcritical stenosis of left anterior descending artery without blood clot:PCI with drug–eluting stent was performed. Nevertheless,ECG did not change while multiple ventricular fibrillations occurred later, requiring electric shock.Later on, after prolonged treatment with magnesium sulfate, Calcium gluconate, antibiotic, electrolytes correction,QTc,ECG and EF progressively normalized. Discussion The patient reported was labelled as a “TakoTsubo syndrome“ diagnosis,but in fact we think the ECGs (persistent STE, prolonged QTc and Brugada pattern), the TTEs and clinical features can be explained by different nosological entity due to the dysregulated INa, and in particular by increased late sodium current INa late : it leads to impaired cardiac energetics and contractile dysfunction as well as cardiac arrhythmias; acidosis and hypoxia can also increases IN late.As for our patient, unlike Takotsubo syndrome, she had no emotional trigger, no characteristic apical balloon on TTE, while severe physical trigger like hypoxia and acidosis stand out.Patients presenting with these ECG features should not be treated with thrombolysis but referred to a HUB center for coronary angiography.