br Discussion In the present case dyssynchronization

Discussion In the present case, dyssynchronization between the atrial and ventricular beats resulted in abnormal pacing spikes detected on the surface electrocardiogram, and it is a potentially life-threatening condition. Previous case reports have suggested that this condition might be caused by crosstalk, dislocation of the leads, or inappropriate switching of the connection of the atrial and ventricular leads to the head of the generator [2–5]. Fluoroscopic examination revealed that dislocation of the atrial lead had been causing ventricular capture due to its proximity to the tricuspid valve, causing the ventricular capture to be sensed by the ventricular lead. The diagnosis was confirmed by steady ventricular capture in the AOO mode. As this was not typical crosstalk, the malfunction was resolved by programming the atrial sensing parameter and switching to the VDD mode. AV delay was kept short to prevent inappropriate ventricular spiking as well as to avoid a possible danger of R on T phenomenon caused by sensing of the ventricular activation by the atrial lead before the ventricular lead.
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Case report The Holter recording documented several transient episodes of ST elevation in leads II, III, and aVF, with reciprocal ST depression in leads V5 and V6 during chest discomfort. One of the episodes triggered ventricular premature beats followed by sustained ventricular tachycardia/ventricular fibrillation (VT/VF) requiring cardioversion. Ventricular arrhythmia (VA) onset was preceded by a gradual elevation in the ST compared to previous Tiplaxtinin (Fig. 1A) with marked QRS broadening, most pronounced in leads III and aVF (Figs. 1B–F) where the QRS–ST–T complexes immediately preceding the arrhythmia appeared “triangulated” and lacked distinction between the end of the QRS and beginning of the ST segment (Fig. 1F). Fig. 2A presents a continuous tracing in lead III of the last 3min preceding VA onset. Note that the shortening of the ventricular repolarization not caused by an increased heart rate is clearly revealed by the sinus complex preceding VA in the last row when compared to an earlier sinus complex (arrows). In Fig. 2B, the early (solid line) and late (dotted line) complexes are superimposed and aligned by the ascending QRS limb (arrow). Note the clear separation by >40ms of the descending T wave limbs of both complexes (measured arbitrarily and marked by a horizontal dotted line).
Discussion During the acute phase of myocardial infarction (MI), marked ST elevation with “lambda-like patterns” or monophasic QRS–ST–T complexes similar to those reported here have been strongly associated with VF [1]. Such abnormal ventricular complexes reflect the ischemia-induced slowing of intra-ventricular conduction and abnormal augmentation of repolarization dispersion, as indicated by various alterations in the shape and duration of the action potentials (AP) across the ischemic myocardium (including triangulated APs), which initiates re-entry arrhythmias [2]. These QRS–ST–T patterns (“monophasic” and “triangulated,” among others) are most likely not specific for myocardial ischemia. Arrhythmogenic “lambda-like” ST elevation patterns have been reported in “atypical Brugada syndrome (BrS)” (Brugada changes in the inferior leads) and in acute MI complicated with VF [3]. Moreover, similarities exist between the mechanisms of ST elevation and VF triggers (phase 2 re-entry) during acute ischemia and BrS [4]. Similar “triangulated” (phase 3 prolongation) and unstable (beat-to-beat variability) APs have been induced in experimental studies with Langendorff-perfused hearts treated with AP prolonging or HERG-channel inhibitors [5]; they were predictors of VA [5]. QT shortening of the “triangulated” QRS–ST–T complexes immediately preceding VT onset was possibly important for arrhythmia initiation, because both the AP duration prolongation and shortening in the presence of AP triangulation and instability have been shown to be markedly pro-arrhythmic [5].