Associazione Nazionale Medici Cardiologi Ospedalieri

CONGRESS ABSTRACT

CONGRESS ABSTRACT

ACQUIRED LQTS WITH VENTRICULAR ARRHYTMIAS IN METHADONE AND CARDIOMYOPATHY AT ONSET

Roagna Edoardo Torino(Torino) – Divisione di Cardiologia, Dipartimento cardiovascolare e Toracico, Città della Salute e della scienza, Torino. Dipartimento di scienze mediche, Università degli studi di Torino | Angelini Filippo Torino(Torino) – Divisione di Cardiologia, Dipartimento cardiovascolare e Toracico, Città della Salute e della scienza, Torino. | Gallone Guglielmo Torino(Torino) – Divisione di Cardiologia, Dipartimento cardiovascolare e Toracico, Città della Salute e della scienza, Torino. Dipartimento di scienze mediche, Università degli studi di Torino

INTRODUCTION: Methadone is associated with QT interval prolongation and increased risk of ventricular arrhythmias such as torsade de pointes (TdP), particularly if associated with other contributing factors. The management is complex, considering that in the majority of cases methadone suspension is impossible.

CLINICAL CASE: man, 39y, history of past cocaine and heroin abuse, in chronic methadone therapy, cames in ED for palpitation and recurrent syncope, after increasing methadone dose from 50 to 130 mg/die. At The ECG sinus rhythm, 83 bpm, wide monomorfic ventricular extrasystolia bigemina, of epicardical origin from the inferior-lateral wall (morphology like BBDx, positive concordance in the precordial leads, negative in DIII and aVF); QTc likely markedly prolonged. During observation recurrent episodes of TdP with external defibrillation; administred ev potassium (K 3.1), MgSO4 and β blocker ev. During hospitalization started nadolol, titrated until 1 mg/kg, and gradually reduced methadone up to 50 mg/die. Executed Holter ECG and ergometric test with evidence of flat and notched T waves with QTc markedly prolonged (> 550 ms) and poor adjustment to chronotropic variations. The echocardiogram shows LVFE 50%, GLS -13% (more reduce at inferior and infero-lateral walls); strongly negative electromechanical window (EMW -232 ms) and pronounced mechanical dispersion (+73 ms). The CMR evidenced late gadolinium enhancement (LGE) of non ischemic pattern, in the same segments with alterated kinesis. Mexiletine oral load test (6 mg/kg) was performed with contemporary ECG and Echo, without significant QTc, EMM or mechanical dispertion variation, suggesting unusefulness of chronic administration. After collective discussion, and considering patient choise, a bicameral ICD was implanted. A wide spectrum genetic test for channellopathies and cardiomyopathies was performed, (NGS and MLPA tecnique), resulted negative. At 1 year follow up (methadone 40 mg/die) persist prolonged QTc (580 ms), without arrhythmic episodes.

CONCLUSIONS: our clinical case illustrates methadone proarrhytmic effect, associated with hypokalaemia and cardiomyopathy at onset, in a subset of prolonged QTc, with elevated electro-mechanical dispersion. Permanent ventricular bigeminism, rare in other acquired or congenital LQTS, is decribed linked with methadone use and its molecular effect of IKr and IK1 block; in our patient there’s correlation between site of origin and site of fibrosis (LGE).