Electrocardiographic "precordial pattern break sign" for posterior coronary venous system.

Several general and site‐specific criteria have been proposed to differentiate epicardial from endocardial origin of ventricular arrhythmias (VA), although these criteria are less reliable for VTs arising from the great cardiac vein (GCV) or anterior interventricular cardiac vein (AIV) because of the presence of preferential conduction or intramural origin.1 A useful clue is the presence of a “pattern break” in the precordial lead progression of the R wave consisting of an abrupt loss of the R wave in lead V2 compared to V1 and V3, coinciding with a septal epicardial origin of the VA (opposite lead V2).2 Because the AIV and posterior interventricular (PIV, also referred to as middle cardiac vein‐MCV) veins run along the anterior versus posterior interventricular septum, VAs from these veins primarily create the opposite electrocardiographic features.

A 55‐year‐old woman presented to an outside hospital with a wide complex tachycardia and altered mental status. One shock of 200 J converted her to sinus rhythm. Echocardiography and coronary angiogram were unrevealing. Cardiac MRI showed no evidence of structural heart disease including arrhythmogenic right ventricular cardiomyopathy or sarcoidosis. Electrophysiological study confirmed inducible fast ventricular tachycardia, and a single‐chamber implantable cardioverter‐defibrillator was implanted for protection from sudden cardiac death, and the patient was referred to our department for catheter ablation after receiving multiple shocks from her ICD despite being on beta‐blockers. The ECGs taken during tachycardia showed wide‐QRS tachycardia with a pattern break appearance in V2 (Figure 1A). The earliest ventricular activation was found at near‐apical crux of MCV/PIV. A good match was obtained from that point (Figure 1B), and the radiofrequency with a starting power output of 20 W and maximal temperature set at 40°C was applied with 10 Ω impedance fall resulting in total disappearance of the frequent PVCs after 4.5 seconds and the ablation catheter accompanied the posterior descending coronary artery with a distance of 1.0 cm.3 Neither PVC recurred, even with inducement by isoproterenol infusion 30 minutes after ablation.

Figure 1

Both the ECGs taken during tachycardia (A) and the pace‐mapping (B) show a pattern break appearance in V2

As the right bundle branch block (RBBB) with superior axis ECG morphology is common in patients with idiopathic VA originating from the left posterior fascicle, from the left ventricular posterior papillary muscles, and rarely from the cardiac apical crux, it appears that VAs arising from the basal aspect of the interventricular sulcus are prone to these pattern breaks whether anterior or posterior. There are only few reports involving small numbers of patients describing VA from the crux of the hear.4, 5, 6 It has been reported with some exceptions that VAs ablated from within the proximal coronary sinus or MCV are characterized by left superior axis, deeply negative delta wave caused by the lower spatial location in frontal plane, and activation wave deviated from the inferior leads.4 We reviewed the literature for VAs from MCV/PIV and found the pattern break sign in V2 at Doppalapudi's4 and Kawamura's series6 and at one case report by Yamada et al5 Kawamura et al6 speculated that the QRS morphology could change abruptly from RBBB to left bundle branch block (LBBB) pattern in the apical crux area. The variable QRS morphology in V1 may suggest breakthrough excitation over either the right or the left ventricle.6 Therefore, the variable QRS morphology in V1 suggests that the exit is only to the left ventricle, because the fact that with LBBB morphology, there is abrupt transition by V2 also suggests this mechanism. The ECG of patients with basal crux VA looks like an epicardial pre‐excited posteroseptal accessory pathway (QS in II and R wave in V6). It is further divided into basal crux VT that predominantly has LBBB pattern and has R greater than S in V6 and apical crux VT that can have LBBB or RBBB pattern with R less than S in V6. They have LBBB with early transition or RBBB morphology with QS pattern in leads II and III and precordial MDI > 0.55. Therefore, those with a basal location are recognized by R>S in V6 compared with those with an apical location that have a large R in aVR and R.6 Kamawura et al described a simple stepwise ECG algorithm for predicting the sites of origin of VAs with RBBB and superior axis using MDI > 0.55, R/S ratio in lead V5 and V6, and monophasic R in lead aVR to differentiate apical crux VA from other VAs with RBBB and superior axis.

Basal crux VT can be successfully ablated in the proximal coronary sinus or the mouth of the MCV, whereas apical crux VT requires percutaneous pericardial access for successful ablation. Apical crux VA could not be successfully ablated from the middle MCV (>2 cm) suggesting either a focus remote from the vein or inability to deliver sufficient energy as the MCV. A deep S wave in V6 indicated a more apical VA origin and typically required subxiphoid epicardial access for successful ablation.6 However, target sites of VAs determined by detailed electrophysiological examination are not always in accord with those inferred from surface ECG because clockwise or counterclockwise rotation, displacement of ECG electrodes, or movement of diaphragm may alter the intrathoracic position of the heart, thereby influencing QRS morphology. Electrocardiographic precordial pattern break is a useful electrocardiographic sign and should be kept in mind for origin of VAs originated from PIV.

CONFLICT OF INTEREST

Authors declare no Conflict of Interests for this article.