Wide QRS Tachycardia Research Articles

Taquicardia ventricular bidireccional atípica

A 75-year old male, with the sole cardiovascular risk factor of being an active smoker, was admitted with a several week history of progressive exertional dyspnea. He was not taking any medication on a regular basis. We performed a complete cardiological evaluation and diagnosed the patient with idiopathic dilated cardiomyopathy and severe left ventricular systolic dysfunction. Upon hospitalization, treatment was started with furosemide and captopril; an electrocardiogram revealed sinus rhythm with ventricular extrasystoles. Renal function parameters and serum ion concentrations were within normal limits from admission (creatinine: 0.7 mg/dL; sodium: 139 mEq/L; potassium: 4 mEq/L; magnesium: 1.6 mEq/L). We performed a continuous 24-h electrocardiogram in order to determine the density of ventricular extrasystoles as a possible cause for the cardiomyopathy, and 20% of the complexes corresponded to ventricular extrasystoles with two morphologies, as well as runs of 3-5 beats of nonsustained ventricular tachycardia. We documented one asymptomatic, at-rest episode of tachycardia at 113 bpm, which was a wide QRS tachycardia that alternated between the two morphological QRS types that had been observed in isolated extrasystoles (A). It was electrocardiographically compatible with bidirectional ventricular tachycardia. Although bidirectional ventricular tachycardia is characteristic of digitalis intoxication or familial forms of catecholaminergic ventricular tachycardia, this case was an atypical bidirectional tachycardia caused by a coupled continuous alternation of ventricular extrasystoles in the same patient (B). We started treatment with beta blockers and the ventricular extrasystole density decreased significantly (figure).

The apple does not fall far from the tree: epicardial ventricular tachycardia due to blunt chest trauma

A 62-year-old male was admitted to the emergency department of our centre because of recurrent episodes of palpitations and dizziness. The patient had a history of severe blunt chest trauma with multiple rib fractures (5–10th) due to a tractor fall 2 years before. The electrocardiographic tracing at admission showed ( Panel A ) a wide QRS tachycardia with the right …

A case of wide QRS tachycardia induced by modified electroconvulsive therapy in a patient with depression

A case of wide QRS tachycardia induced by modified electroconvulsive therapy in a patient with depression

Adenosine-induced severe bronchospasm in a patient without pulmonary disease

Adenosine is widely used for the treatment of supraventricular tachycardias for its efficacy and excellent safety, but it has been reported to precipitate severe bronchospasm in patients with pulmonary disease. The drug is therefore contraindicated in asthmatic subjects and should be used with caution in patients with chronic obstructive pulmonary disease. Nevertheless, true bronchospasm is rare and should be distinguished from the much more common occurrence of dyspnea, only as a symptom and without respiratory compromise, which is benign and transient. We describe the occurrence of severe bronchospasm following adenosine administration for a supraventricular tachycardia in a young male without any history of pulmonary disease. To our knowledge, this is the first time such complication is reported in a subject without lung disease. The patient arrived at the emergency department for palpitations with a regular wide QRS tachycardia with a left bundle-branch block morphology. Sinus carotid massage was unsuccessful, and 2 intravenous adenosine boluses were given without effect. A further 12-mg bolus cardioverted the patient, who became increasingly dyspneic and hypoxic, with diffuse bronchospasm. An urgent chest radiograph had normal results. He was treated with oxygen and inhaled and intravenous steroids, but dyspnea and bronchospasm resolved only after intravenous aminophylline. The arrhythmia recurred and was finally terminated by intravenous flecainide. Although dyspnea after adenosine administration is usually a transient, benign phenomenon, physicians should be alert to the presence of objective signs of respiratory distress, which should prompt immediate treatment, even in subjects without previous history of pulmonary disease.

Post-exercise Paroxysmal Tachycardia with QRSs Changing from Wide to Narrow Complexes

A 33-year-old man visited the outpatient clinic complaining of episodic palpitations, which began to develop 3 years earlier but increased frequency lately. Characteristically, the palpitations develop immediately after vigorous exercise and terminate spontaneously within 5min. Each episode was accompanied by chest tightness and dizziness, with cold sweat. Physical examination was unremarkable, and his resting 12-lead EKG showed normal sinus rhythm with normal P, QRS and T morphologies. He then underwent treadmill exercise testing where he walked for 9min and completed stage 3 of the Bruce protocol with the heart rate (HR) reaching 164/min, the 85% predicted maximal HR, without having chest pain or ischemic ST changes. One minute after termination of exercise, the monitoring EKG showed a sudden onset of wide QRS tachycardia with LBBB morphology (Figure 1). He experienced abnormal palpitations and the BP decreased from 160/43 to 96/77mmHg. Twenty seconds later, the wide QRS complexes suddenly changed into narrow QRS complexes associated with a HR increase from 200 to 240/min (Figure 2). The tachycardia soon terminated spontaneously, and the BP returned to 149/89mmHg. What is your diagnosis of the tachycardia?

Ventricular tachycardia in English bulldogs with localised right ventricular outflow tract enlargement

To describe the electrocardiographic characteristics of ventricular tachycardia arising from the right ventricular outflow tract and the particular association between this arrhythmia and the presence of localised right ventricular outflow tract enlargement in English bulldogs. Five English bulldogs were referred with a history of syncope or cardiogenic shock. In all dogs, 12-lead surface ECG, thoracic radiograph and echocardiography were collected. In all but one dog 24-hours Holter monitoring and signal-averaged ECGs was examined and in one dog electrophysiological study and radiofrequency catheter ablation of the VT substrate was performed. Documented arrhythmias included a single sustained monomorphic wide QRS tachycardia in four dogs, and an alternans of two different monomorphic forms in one dog. Mean QRS duration during tachy-cardia was 91·6 ±9·83 milliseconds. QRS complexes manifested a left bundle branch block morphology and an inferior axis (81 ±13·73°). R wave notching was present in the caudal (inferior) leads in three tachy-cardias. Lead I was negative in 3 of 6, positive in 1 of 6 and isodiphasic in 2 of 6. Lead aVL was negative in 5 of 6 and positive in 1 of 6. Signal-averaged electrocardiograms revealed late potentials in three dogs. Echocardiography showed a localised right ventricular outflow tract enlargement in all dogs. Cardiac map-ping established two sites of origin of ventricular tachycardia within the right ventricular outflow tract in one dog: caudal free-wall and cranial-septal. The presence of a localised right ventricular outflow tract enlargement and ventricular tachycardia with left bundle branch block morphology could suggest segmental arrhythmogenic right ven-tricular cardiomyopathy in the English bulldog.

An Interesting Case in Differential Diagnosis of wide-QRS Tachycardia —AV Reciprocating Tachycardia with Enhanced AV Nodal Conduction—

An Interesting Case in Differential Diagnosis of wide-QRS Tachycardia —AV Reciprocating Tachycardia with Enhanced AV Nodal Conduction—

Reciprocal Induction of Long RP and Wide QRS Tachycardias

Reciprocal Induction of Long RP and Wide QRS Tachycardias

The safety of flecainide treatment of atrial fibrillation: long-term incidence of sudden cardiac death and proarrhythmic events

To assess the safety of long-term treatment with flecainide in patients with atrial fibrillation (AF), particularly with regard to sudden cardiac death (SCD) and proarrhythmic events. Retrospective, observational cohort study. Single-centre study at Örebro University Hospital, Sweden. Subjects. A total of 112 patients with paroxysmal (51%) or persistent (49%) AF (mean age 60 ± 11 years) were included after identifying all patients with AF who initiated oral flecainide treatment (mean dose 203 ± 43 mg per day) between 1998 and 2006. Standard exclusion/inclusion criteria for flecainide were used, and flecainide treatment was usually combined with an atrioventricular-blocking agent (89%). Death was classified as sudden or nonsudden according to standard definitions. Proarrhythmia was defined as cardiac syncope or life-threatening arrhythmia. Eight deaths were reported during a mean follow-up of 3.4 ± 2.4 years. Compared to the general population, the standardized mortality ratios were 1.57 (95% confidence interval (CI) 0.68-3.09) for all-cause mortality and 4.16 (95% CI 1.53-9.06) for death from cardiovascular disease. Three deaths were classified as SCDs. Proarrhythmic events occurred in six patients (two each with wide QRS tachycardia, 1 : 1 conducted atrial flutter and syncope during exercise). We found an increased incidence of SCD or proarrhythmic events in this real-world study of flecainide used for the treatment of AF. The findings suggest that further investigation into the safety of flecainide for the treatment of patients with AF is warranted.

Ebstein anomaly in an adult presenting with wide QRS tachycardia: diagnostic and therapeutic dilemmas

A 51-year-old man presented to the emergency department with sustained hemodynamically unstable wide QRS tachycardia and was revived successfully by immediate direct current (DC) cardioversion. There was evidence of previous open heart surgery, possibly atrial septal defect closure. Transthoracic echocardiography showed severe Ebstein anomaly with severe tricuspid regurgitation, no residual atrial septal defect, but with severe right ventricular dysfunction. Subsequent electrocardiograms showed transient atrial fibrillation with no manifest Wolff-Parkinson-White (WPW) accessory pathway during sinus rhythm. The cause of wide QRS tachycardia in this patient may be WPW related or ventricular tachycardia. This case illustrates the diagnostic and therapeutic dilemmas in patients with wide QRS tachycardia and suspected WPW syndrome. In addition, this case demonstrates that unoperated Ebstein anomaly can present in late adult life with tachyarrhythmias.

Curative ablation in a 12-month-old baby with severe ventricular systolic dysfunction and incessant ventricular tachycardia

Cardiomyopathies in the paediatric population portend a poor prognosis being characterized by a particularly accelerated and therapy refractory clinical course.1,2 Recognition and effective treatment of potential secondary causes may play a crucial role, leading to recovery in a not negligible proportion of cases. Left-ventricular dysfunction associated with wide QRS tachycardia is a quite common presentation, depicting two possible clinical pictures: ventricular tachycardia complicating idiopathic cardiomyopathy and primary tachycardiomyopathy. The distinction between the two might be pivotal, particularly in the paediatric population since, recognition of a tachycardiomyopathy must prompt an aggressive rhythm control. In this context, the role of the conduction system is being recognized in many incessant tachycardias with or without an underlying structural heart disease.3,4 The two most clinically relevant scenarios are fascicular tachycardia and junctional ectopic tachycardia (JET).5 The former is usually sustained by a reentry within a diseased Purkinjie network or involving the surrounding ventricular myocardium. The latter is thought to be caused by abnormal automaticity within the atrioventricular junction, and thus usually display a narrow QRS. Although JET is more frequently associated with a known structural injury such as myocarditis or post-operative status, still it should be kept in mind in the differential diagnosis, since isolated-idiopathic cases have been described as well.6 These arrhythmias, when displaying an incessant course may be responsible for systolic impairment, independent of their specific individual prognosis.7 We are describing a case of a 12-month-old baby that presented with a severe systolic dysfunction and almost incessant wide QRS tachycardia causing rapidly worsening heart failure despite full medical therapy. The arrhythmia was finally diagnosed as idiopathic left-ventricular fascicular tachycardia (ILVT) at the invasive electrophysiologic study, and transcatheter ablation through transseptal route was performed. The procedure turned out to be effective both in eliminating the …

Ventricular tachycardia caused by a left ventricular aneurysm in a patient with previous surgery for ventricular septal defect

Ventricular mural aneurysms especially in the left ventricle represent an increased risk for life-threatening arrhythmias. We present a case of ventricular tachycardia originating from an inferobasal left ventricular aneurysm. A 25-year-old male patient presented with complaints of palpitation, breathlessness, and dizziness of two-hour onset. The electrocardiogram showed wide-QRS tachycardia at which time his blood pressure was 80/40 mmHg. The patient suddenly developed collapse and ventricular tachycardia was diagnosed on the monitor, and he returned to sinus rhythm following successful cardioversion. He remained stable during hospitalization. The electrocardiogram was in sinus rhythm with right bundle branch block and small Q waves in inferior leads. He had an eight-year history of surgery for ventricular septal defect closure, during which a ventricular aneurysm was detected but left untreated. Echocardiographic examination showed a dyskinetic aneurysmal region extending from the inferobasal segment to the posterior wall of the left ventricle. Coronary arteries were normal on angiography, and ventriculography confirmed the aneurysm. Electrophysiologic study was recommended, but the patient refused any treatment. He remained asymptomatic during 18 months of follow-up.

A wide QRS tachycardia in a left univentricular pacing system: What is the mechanism?

A 55-year-old man was referred to our institution for cardiac resynchronization therapy-defibrillator (CRT-D) implantation. He had suffered severe ischemic cardiomyopathy with low left ventricular (LV) ejection fraction of 20%, left bundle branch block, and New York Heart Association (NYHA) Class III symptoms despite optimal medical treatment. Magnetic resonance imaging showed a large anterior and lateral scar, with preserved tissue in the septal and posterior regions. In April 2009 he underwent CRT-D implantation with a Boston Scientific COGNIS P107 (Saint-Paul, Minnesota, USA).

Verapamil-Sensitive Left Posterior Fascicular Ventricular Tachycardia Associated with Paroxysmal Atrial Fibrillation

Case Report: A 37-year-old man with the wide QRS tachycardia visited to our hospital. The wide QRS tachycardia had emerged with paroxysmal Atrial fibrillation (pAf). The QRS configuration during the wide QRS tachycardia was a right bundle branch block pattern with left-axis deviation. Verapamil could terminate the wide QRS tachycardia. We diagnosed the wide QRS tachycardia verapamil-sensitive left posterior fascicular Ventricular Tachycardia (VT). Verapamil-sensitive left posterior fascicular VT had always emerged coexistence with pAf. During the electrophysiological study, verapamil-sensitive posterior fascicular VT was induced by programmed atrial stimulation. We performed segmental pulmonary vein antrum isolation during sinus rhythm. After the isolation of pulmonary veins, the radiofrequency application to the VT circuit was performed. VT could be terminated by radiofrequency application where the earliest purkinje potential preceded the onset of earliest surface QRS by 12 ms during VT. No VT was induced after the radiofrequency applications. Conclusions: This VT is the rare case of verapamil-sensitive posterior fascicular VT associated with pAf. We successfully ablated these double tachycardias.

Intermittent Right and Left Bundle Branch Blocks and 2:1 Narrow QRS in a Patient with Uncommon Atrioventicular Nodal Reentrant Tachycardia

The development of bundle branch block, especially left bundle branch block and 2:1 narrow QRS morphology, during atrioventricular nodal reentrant tachycardia (AVNRT) is unusual. We report a case of AVNRT patient with a short tachycardia cycle length, in whom transient wide QRS tachycardia with right and left bundle branch blocks (RBBB and LBBB). The patient was a 28 year-old-male whose chief complaint was palpitation with short of breath and pre-syncope for past 18 years. There was no structural organic heart disease on the echocardiogram. An electrophysiological study was performed without any anti-arrhythmic drugs. Uncommon (fast/slow) AVNRT was induced by atrial burst pacing at 300 ms and atrial programmed extra-stimuli without jump up phenomenon. Spontaneous conversion of QRS morphology from narrow QRS to RBBB and LBBB was observed during tachycardia. There was no change in atrial cycle length by a single premature ventricular stimulus during tachycardia. The wide QRS tachycardia with LBBB was transformed to narrow QRS tachycardia by the introduction of a single premature ventricular stimulus without changing the tachycardia cycle length. Radiofrequency catheter ablation targeting anatomical slow-pathway area was performed and successfully eliminated tachycardia. We speculated that enhanced AV nodal conduction could be closely related with the bundle branch block during AVNRT in this patient.

Chemotherapy-Induced Arrhythmia Which Was Wide QRS Tachycardia Derived from Supra Vena Cava, Atrial Flutter, and Atrial Fibrillation with Syncope

Arrhythmias were reported as a side effect of many chemotherapeutic drugs. Arrhythmias induced by 5-fluorourasil, including ventricular tachycardia, are mostly ischemic in origin and usually occur in the context of coronary spasm produced by this drug. Cisplatin is associated with a very high rate atrial fibrillation. In general, chemotherapy-induced arrhythmia is an existing but poorly recognized and studied entity. A 66-year old male was diagnosed adenocarinoma of the transverse colon (stage IV), and received oxaliplatin (dose 130 mg/m2) and capecitabine (2000 mg/m2). After chemotherapy, the patient developed syncope. The ambulatory electrocardiography data revealed wide QRS tachycardia, but a programmed atrial stimulation induced tachycardia derived from supra vena cava (SVC), atrial fibrillation, and atrial flutter, which was not ventricular tachycardia, were induced by the programmed atrial stimulations in electro physiological study. The patient was performed catheter ablation of cavotricuspid isthmus and SVC isolation without pulmonary vein isolation. After the catheter ablation, tachycardia and syncope was not appeared. We report that chemotherapy induced arrhythmias which was wide QRS tachycardia derived from SVC, atrial flutter, and atrial fibrillation was got well by catheter ablation.

A case of manifest WPW syndrome with RR alternence during wide QRS tachycardia

A case of manifest WPW syndrome with RR alternence during wide QRS tachycardia

Unique Conduction of Left-Lateral Accessory Pathway: A Case Report

A 77-year-old man was admitted to our hospital because of palpitation and dyspnea. The twelve-lead electrocardiogram showed the irregular wide QRS tachycardia. During the sinus rhythm, there were no ventricular preexcitation and no abnormal findings on the twelve-lead electrocardiogram. We performed the electrophysiological study. There was no conduction over the accessory pathway during the high right atrial and ventricular pacing. Venous injection of adenosine could also make the atrio-ventricular conduction block. However, coronary sinus pacing (pacing cycle length=330 ms) could make the antegrade conduction over the left-lateral accessory pathway, and this QRS complex was quite similar to clinical one. We diagnosed his clinical wide QRS tachycardia was preexcited atrial fibrillation. This accessory pathway was eliminated by radiofrequency application. He remained free of any arrhythmias after the procedure.

Mechanisms of Supraventricular Tachycardia

Supraventricular tachycardias (SVT) are represented on electrocardiograms (ECG) as narrow QRS tachycardia. They can be wide QRS tachycardia, when functional bundle branch block occurs. Based on ECG appearance, SVT can be classified into short RP tachycardia or long RP tachycardia. According to underlying mechanisms, SVT can be classified into atrioventricular (AV) reciprocating tachycardia (AVRT), AV nodal reentrant tachycardia (AVNRT) or atrial tachycardia (AT). The two most common SVT, including AVNRT and AVRT, are reentrant and include AV node in the tachycardia circuit. In contrast, AT is independent of AV nodal conduction. In the case of AVRT, antegrade conduction proceeds via the AV node while retrograde conduction occurs via the accessory pathway. As ventricles and atria are sequentially activated, the P waves are usually on the ST-T segment. In the case of AVNRT, the presence of dual AV nodal pathways (fast pathway and slow pathway) underlies the mechanism. During common AVNRT, the antegrade limb passes via the slow pathway, while the retrograde limb passes via the fast pathway. As atria and ventricles are activated simultaneously, the P waves are frequently observed as pseudo-R waves in V1 lead. In the case of AT, the mechanism may be abnormal automaticity, triggered activity or reentry. Adenosine (or adenosine triphosphate) is useful to determine the tachycardia as AV nodal dependent or independent. However, a small dose of adenosine peculiarly terminates some AT.

Wide QRS Tachycardia with Two P Wave Morphologies: What Is the Mechanism?

A 38 years old male complained of occasional palpitation and came to our hospital for help. Twelve-lead electrocardiogram during the palpitation revealed a wide QRS tachycardia with two different P wave morphologies. Two different atrial activation sequences were found in the intracardiac recordings and they were comparable to the two different P wave morphologies from the surface ECG recordings. The first type of atrial activation pattern was retrograde concentric VA conduction with the earliest atrial activation at the proximal coronary sinus which created a negative polarity of P wave in the lead II of ECG. The second type of atrial activation pattern was conducted from the right atrium to the coronary sinus which was considered to be a normal sinus impulse and created a positive polarity of P wave in the lead II of ECG. The idiopathic left ventricular tachycardia was diagnosed by atrioventricular dissociation and the short His-ventricular interval. The catheter ablation was performed during tachycardia. The site of catheter ablation was located at the distal septum of the left ventricle where the characteristic double diastolic potentials as previous studies demonstrated was recorded. The tachycardia was terminated after one pulse of ablation. No further tachycardia could be induced after the ablation even under isoproterenol infusion.