Bidirectional Ventricular Tachycardia and Prominent U Waves: Look at Fingers and Muscles and Use Flecainide.

We present a case of bidirectional ventricular tachycardia in a 15-year-old boy asymptomatic for arrhythmias, whose major complaint was muscle weakness. At our first evaluation he was receiving sotalol for his ventricular arrhythmias. In addition to bidirectional tachycardia, electrocardiogram during sinus rhythm showed prominent U waves and prolonged QT-U interval. These electrocardiographic signs, along with the evidence of clinodactyly and mild hypertelorism, led us to the diagnosis of Andersen-Tawil syndrome, confirmed by genetic analysis that revealed a "de novo" missense mutation of KCNJ2 gene. Monotherapy with flecainide was rapidly effective and almost eliminated ventricular arrhythmias. After a 4-year follow-up there were no adverse events, flecainide has been well tolerated without significant modification of the QRS or repolarization, and ventricular arrhythmias have not been relapsed to date. The case highlights the importance of a correct clinical diagnosis, which is crucial for the optimal selection of the most appropriate drug therapy, which is expected not to be harmful, before being beneficial.

Methadone Blockade of Cardiac Inward Rectifier K+ Current Augments Membrane Instability and Amplifies U Waves on Surface ECGs: A Translational Study.

Background Methadone is associated with a disproportionate risk of sudden death and ventricular tachyarrhythmia despite only modest inhibition of delayed rectifier K+ current (IKr), the principal mechanism of drug-associated arrhythmia. Congenital defects of inward rectifier K+ current (IK1) have been linked to increased U-wave amplitude on ECG and fatal arrhythmia. We hypothesized that methadone may also be a potent inhibitor of IK1, contributing to delayed repolarization and manifesting on surface ECGs as augmented U-wave integrals. Methods and Results Using a whole-cell voltage clamp, methadone inhibited both recombinant and native IK1 with a half-maximal inhibitory concentration IC50) of 1.5 µmol/L, similar to that observed for IKr block (half-maximal inhibitory concentration of 2.9 µmol/L). Methadone modestly increased the action potential duration at 90% repolarization and slowed terminal repolarization at low concentrations. At higher concentrations, action potential duration at 90% repolarization lengthening was abolished, but its effect on terminal repolarization rose steadily and correlated with increased fluctuations of diastolic membrane potential. In parallel, patient ECGs were analyzed before and after methadone initiation, with 68% of patients having a markedly increased U-wave integral compared with premethadone (lead V3; mean +38%±15%, P=0.016), along with increased QT and TPeak to TEnd intervals, likely reflective of IKr block. Conclusions Methadone is a potent IK1 inhibitor that causes augmentation of U waves on surface ECG. We propose that increased membrane instability resulting from IK1 block may better explain methadone's arrhythmia risk beyond IKr inhibition alone. Drug-induced augmentation of U waves may represent evidence of blockade of multiple repolarizing ion channels, and evaluation of the effect of that agent on IK1 may be warranted.

Early/Subtle Electrocardiography Features of Acute Coronary Syndrome and ST-Segment Elevation Myocardial Infarction.

Chest pain is one of the most common presenting complaints in the emergency department. Interpreting a 12-lead electrocardiography (ECG) for evidence of ischemia is always challenging. Frank ECG changes such as ST-segment elevation and ST-segment depression can be easily identified by emergency physicians. However, identifying subtle or early features of ACS in the 12-lead ECG is essential in preventing significant mortality and morbidity from ACS. In the following case series, we describe five of the subtle/early ECG changes of ACS, namely (1) T-wave inversion in lead aVL; (2) terminal QRS distortion; (3) hyperacute T-waves; (4) negative U-waves in precordial leads; and (5) loss of precordial T-wave balance. In all these cases, the initial 12-lead ECG showed only subtle/early ECG changes which were followed up with serial ECGs which progressed to STEMI.

Profound repolarization abnormalities after cylindrical battery ingestion: a case report.

BACKGROUND: Cardiac arrhythmias are a serious complication in patients admitted due to intoxication in suicidal attempts. Upon admission, detailed information about the specific kind of intoxication are frequently missing. The differential diagnoses of electrocardiogram (ECG) changes such as elevation of T-waves, prolongation of the QT-interval or elevation of ST-segments in this special subgroup of patients comprise drug-induced electrolyte disorders or direct toxic effects on cardiac excitation and repolarization. CASE SUMMARY: In this clinical report of a 27-year-old male patient, we present a case of unusual ECG alterations mimicking ST-elevation, high amplitude, biphasic T-waves and prolongation of QT-interval. These changes of surface ECG were induced by ingestion of cylindrical batteries in a suicidal attempt and immediately normalized after removal of batteries by esophagogastroduodenoscopy. DISCUSSION: There is limited literature describing changes in surface ECG in patients having ingested cylindrical batteries. We propose two hypotheses for the occurrence of these changes after ingestion of cylindrical batteries: (i) Cardiac movement within the perturbation field induced by the batteries causes electrical changes on a time scale of the heart rate which are above the threshold of the high pass filter. (ii) The batteries' electrotonic potential affects the membrane currents of cardiac myocytes, not inducing an action potential but generating repolarization abnormalities. Individual factors, such as body constitution and localization of the batteries within the stomach, determine the interindividual characteristics of repolarization abnormalities.