Wide QRS complex tachycardia in a patient with wide QRS complex sinus rhythm due to left bundle branch block pattern.

A 58-year-old man with hypertension and half a year ago documented left bundle branch block (LBBB) in his past history presented with progressive dyspnea. A pre-admission echocardiography showed severely depressed systolic left ventricular function [ejection fraction (EF) = 27%], diffuse hypokinesis and dilated heart chambers consistent with dilated cardiomyopathy (DCM). On admission, he presented with dyspnea on minimal exertion, his blood pressure was 100/70 mmHg, his heart rate was 62 beats/min with occasional mild irregularities suggesting premature beats. The electrocardiogram (ECG) showed a 67 beats/min sinus rhythm with complete LBBB pattern and a QRS duration of 170 ms (Figure 1A). Telemetry first revealed a 170–175 beats/min wide QRS complex tachycardia (WCT) consisting of six beats with right bundle branch block (RBBB) pattern, which followed a 62 beats/min sinus rhythm with LBBB pattern (Figure 1B), later showed two initial sinus beats with a heart rate of 54 beats/min and LBBB pattern and a QRS duration of 170 ms followed by an irregular wide QRS complex rhythm with a 78–102 beats/min mean ventricular rate, with QRS complexes of 150 ms QRS duration and a QRS morphology resembling LBBB (Figure 1C). Apparently at first glance, AV dissociation was not present during the irregular wide QRS complex rhythm, because the number of P-waves and QRS complexes were equal.

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Electrocardiogram and telemetry tracings of the patient recorded at our department.

(A): Electrocardiogram on admission; (B): telemetry tracing showing contralateral bundle branch block during wide QRS complex tachycardia and sinus rhythm; and (C): telemetry tracing showing an irregular wide QRS complex rhythm with narrower QRS complexes than QRS complexes in sinus rhythm. Arrows show the retrograde P-waves. Vertical lines are denoting the onset and end of the QRS complex and small crosses mark the initial and terminal 40 ms of the QRS complex in lead aVR (shown in magnified views at the left lower part of the figure) necessary for the determination of the initial and terminal ventricular activation velocity ratio (vi/vt) in panels B and C. The vi/vt is < 1 in both tracings, suggesting ventricular tachycardia diagnosis. For further explanation see text.

Because the vast majority (95%) of WCTs are either ventricular tachycardia (VT) (up to 80% of cases) or supraventricular tachycardia with aberrant conduction (SVT-A) (15%– 20% of cases), the main differential diagnosis of WCT is to distinguish VT from SVT-A.[ The QRS morphology of the WCT and irregular wide QRS complex rhythm resembling RBBB and LBBB patterns respectively might suggest SVT-A. However, the contralateral bundle branch block (RBBB) in WCT and sinus rhythm (LBBB) in Figure 1B strongly favors VT. The narrower QRS complex during the irregular wide QRS complex rhythm than during the sinus rhythm despite a significantly greater mean ventricular rate of the irregular wide QRS complex rhythm than that of the sinus rhythm also establishes the diagnosis of VT, because a QRS complex that is narrower during WCT than during sinus rhythm suggests VT (Figure 1C). This is a very rare ECG sign suggesting VT in less than 1% of VTs.[ This patient's ECGs are particularly interesting, because the above described two rare and not widely known ECG signs were present in the same patient at approximately the same time and established the VT mechanism of WCTs. The 3rd QRS complex on Figure 1C, which is the first beat of the irregular wide QRS complex rhythm, follows a sinus P-wave with a shorter PR interval (120 ms) than the sinus rhythm PR interval (180 ms), therefore the 3rd QRS complex cannot be a conducted sinus beat, supporting the ventricular origin of the irregular wide QRS complex rhythm. The 4th QRS complex is not preceeded by a P-wave and following the 4th QRS complex, there are retrograde P- waves (predominantly positive P-waves in lead aVR and negative P-waves in the inferior leads) after each QRS complex due to 1:1 VA conduction with different RP intervals inversely proportional with the preceeding RR intervals, also supporting the ventricular rhythm diagnosis. However, the 3rd QRS with the shorter PR interval and the QRS complexes with 1:1 VA conduction of the irregular wide QRS complex rhythm can also be explained by a junctional rhythm with aberrant conduction, this possibility is excluded only by the QRS during WCT narrower than during sinus rhythm phenomenon. Due to the lack of chest leads, the Brugada algorithm and traditional criteria for WCT differential diagnosis cannot be applied in these telemetry ECG tracings, the aVR Vereckei algorithm[ reveals an initial and terminal ventricular activation velocity ratio (vi/vt) < 1 in lead aVR in both wide QRS complex rhythms, also suggesting VT.

Echocardiography at our department revealed identical findings to the pre-admission echocardiography consistent with DCM and additionally showed moderately decreased longitudinal systolic right ventricular (RV) function (TAPSE: 15 mm) and visualized a 18 × 19 mm thrombus at the left ventricular (LV) apex. We optimized the medical treatment for heart failure, which resulted in a significant symptomatic improvement and introduced anticoagulant therapy. Coronary angiography did not reveal coronary artery disease. Continued telemetry revealed premature ventricular beats and additional nonsustained VTs and on the eighth day of his hospital stay ventricular fibrillation developed, which was terminated by DC shock and sinus rhythm was maintained by amiodarone treatment. Cardiac magnetic resonance imaging (MRI) showed significantly depressed LV (LVEF = 18%) and RV (RVEF = 28%) systolic function, diffuse LV and RV hypokinesis, the disappearance of LV apical thrombus, did not reveal any signs suggesting acute myocarditis and showed midmyocardial late gadolinium enhancement (LGE) in the LV basal septal and apical anterior segments and longer native T1 value (950–1065 ms) consistent with DCM. Biventricular pacemaker and implantable cardioverter defibrillator (CRT-D) implantation was performed for secondary prevention.

We diagnosed DCM in our patient, however could not elucidate its exact etiology. Coronary artery disease and acute myocarditis were ruled out and cardiac MRI did not reveal any other possible underlying cause. Alcohol, toxin exposure, autoimmune, metabolic and endocrine underlying causes could not be identified and there were no data in the family history suggesting a hereditary DCM. The LBBB, similarly to RV pacing, by causing significant ventricular dyssynchrony, in itself can cause LV systolic dysfunction and DCM, [ but can be also a consequence of DCM. The significantly depressed systolic LV function (LVEF < 35%), LGE on cardiac MRI and longer T1 value are each an independent predictor of sudden cardiac death and ventricular tachyarrhythmia that occurred in this patient.[ Based only on clinical history, the VT mechanism of WCT in a patient older than 35 years and with structural heart disease is very likely (positive predictive value > 95%).[

Acknowledgments

All authors had no conflicts of interest to disclose.