Effects of verapamil and lidocaine on two components of the re-entry circuit of verapamil-senstitive idiopathic left ventricular tachycardia. (49/664)

OBJECTIVES: We characterized pharmacologically the slow conduction zone of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) with regard to the late diastolic potential (LDP). BACKGROUND: We showed that the slow conduction zone of ILVT could be divided into two components by LDP; that is, the distal component with a tachycardia-dependent conduction delay property and the proximal one without it. METHODS: Electrophysiologic studies were performed in eight consecutive patients. The LDP was recorded during left ventricular (LV) mapping during ILVT. Entrainment was performed from the right ventricular outflow tract while recording LDP. The effects of lidocaine (1 mg/kg body weight) and verapamil (0.5 or 1.0 mg) were examined during entrainment. RESULTS: The LDPs preceding the Purkinje potential (PP) were serially recorded from the upper third to the middle of the LV septum along the narrow longitudinal line. The ventricular tachycardia (VT) cycle length increased after lidocaine (p < 0.05), and further after verapamil (p < 0.05). The increments in the VT cycle length after administration of the drugs strongly correlated with those in LDP-PP (r > 0.9 for both drugs). The interval from the ventricular potential to LDP was unchanged after administration of the drugs. In one patient, verapamil terminated VT by local conduction block between LDP and PP. The LDP-PP measured during entrainment increased after lidocaine, and further after verapamil, whereas the interval from the stimulus to LDP remained unchanged. CONCLUSIONS: The component distal to LDP is mainly calcium channel-dependent and partly depressed sodium channel-dependent. The proximal component is considered to be sodium channel-dependent (normal).  (+info)

Three dimensional echocardiography documents haemodynamic improvement by biventricular pacing in patients with severe heart failure. (50/664)

OBJECTIVES: To quantify the short term haemodynamic effects of biventricular pacing in patients with heart failure and left bundle branch block by using three dimensional echocardiography. DESIGN: Three dimensional echocardiography was performed in 15 consecutive heart failure patients (New York Heart Association functional class III or IV) with an implanted biventricular pacing system. Six minute walk tests were performed to investigate the effect of biventricular pacing on exercise capacity. Data were acquired at sinus rhythm and after short term (2-7 days) biventricular pacing. RESULTS: Compared with baseline values, biventricular pacing significantly reduced left ventricular end diastolic volume (EDV) by mean (SD) 4.0 (5.1)% (p < 0.01) and end systolic volume (ESV) by 5.6 (6.4)% (p < 0.02). Mitral regurgitant fraction was significantly reduced by 11 (12.1)% (p < 0.003) and forward stroke volume (FSV) increased by 13.9 (18.6)% (p < 0.02). Exercise capacity was significantly improved with biventricular pacing by 48.4 (43.3)% (p < 0.00001). Regression analyses showed that the percentage increase in FSV independently predicted percentage improvement in walking distance (r(2) = 0.73, p < 0.0002). Both basal QRS duration and QRS narrowing predicted pacing efficacy, showing a significant correlation with %DeltaEDV, %DeltaESV, and %DeltaFSV. CONCLUSIONS: In five of 15 consecutive patients with heart failure and left bundle branch block, biventricular pacing induced a more than 15% increase in FSV, which predicted a more than 25% increase in walking distance and was accompanied by an immediate reduction in left ventricular chamber size and mitral regurgitation.  (+info)

Bundle branch and atrioventricular block as complications of acute myocardial infarction in the thrombolytic era. (51/664)

OBJECTIVE: To analyze the incidence of intraventricular and atrioventricular conduction defects associated with acute myocardial infarction and the degree of in hospital mortality resulting from this condition during the era of thrombolytic therapy. METHODS: Observational study of a cohort of 929 consecutive patients with acute myocardial infarction. Multivariate analysis by logistic regression. Was used. RESULTS: Logistic regression showed a greater incidence of bundle branch block in male sex (odds ratio = 1.87, 95% CI = 1.02-3.42), age over 70 years (odds ratio = 2.31, 95% CI = 1.68-5.00), anterior localization of the infarction (odds ratio = 1.93, 95% CI = 1.03-3.65). There was a greater incidence of complete atrioventricular block in inferior infarcts (odds ratio = 2.59, 95% CI 1.30-5.18) and the presence of cardiogenic shock (odds ratio = 3.90, 95% CI = 1.43-10.65). Use of a thrombolytic agent was associated with a tendency toward a lower occurrence of bundle branch block (odds ratio = 0.68) and a greater occurrence of complete atrioventricular block (odds ratio = 1.44). The presence of bundle branch block (odds ratio = 2.45 95%, CI = 1.14-5.28) and of complete atrioventricular block (odds ratio = 13.59, 95% CI = 5.43-33.98) was associated with a high and independent probability of inhospital death. CONCLUSION: During the current era of thrombolytic therapy and in this population, intraventricular disturbances of electrical conduction and complete atrioventricular block were associated with a high and independent risk of inhospital death during acute myocardial infarction.  (+info)

Ventricular tachycardia with QRS configuration similar to that in sinus rhythm and a myocardial origin: differential diagnosis with bundle branch reentry. (52/664)

INTRODUCTION: Tachycardia with a QRS configuration which resembles that in sinus rhythm is usually thought to be supraventricular. Ventricular tachycardia, with a similar QRS configuration to that in sinus rhythm on the 12-lead ECG, can occur. The mechanisms of this form of ventricular tachycardia have not been previously reported. METHODS AND RESULTS: The mechanism of ventricular tachycardia was defined during electrophysiological study in five patients. During sinus rhythm, all patients had a wide QRS complex (>0.12 s) on the 12-lead ECG. The morphology remained grossly unchanged during spontaneous, symptomatic tachycardia. Four of the five patients had coronary artery disease and left ventricular dysfunction. The remaining patient had idiopathic dilated cardiomyopathy. The relationship between the His bundle, deflection, the right bundle branch and the QRS complex was evaluated during tachycardia. Atrial and ventricular pacing, and ventricular activation mapping were performed during tachycardia to define the tachycardia mechanism. The tachycardia induced at electrophysiological testing, which was similar to the clinical tachycardia, was proven to be ventricular tachycardia in each patient. The morphology of ventricular tachycardia was right bundle branch block in two patients and left bundle branch block in three patients. The median tachycardia cycle length was 300 ms (range: 260-480 ms). His bundle activation occurred in a 1:1 relationship with ventricular activation during tachycardia in all patients at least intermittently. The tachycardias were thought initially to be bundle branch reentry tachycardia. With further intervention and continued observation, it became clear that His bundle activation was passive and was not required for the tachycardia to sustain. During tachycardia, His bundle activation appeared to precede the local ventricular activation. Instead, the His bundle was activated slowly from the previous ventricular beat causing a long ventricular-His (VH) interval. This was shown by: (1) activation patterns, (2) response to pacing, (3) intermittent VH dissociation, and (4) termination of ventricular tachycardia. CONCLUSION: A unique form of ventricular tachycardia is described. The QRS complex morphology on the 12-lead ECG during tachycardia was grossly similar to that during sinus rhythm. The His bundle activation was passive and occurred with a long activation time from the ventricle to the His bundle. Although it mimics usual bundle branch reentry, this form of ventricular tachycardia appears to be due to a different mechanism in which the His bundle is not obligatory for the continuation of the reentrant phenomenon.  (+info)

Syncope in pharmacologically unmasked Brugada syndrome: indication for an implantable defibrillator or an unresolved dilemma? (53/664)

A 30-year-old Caucasian male was referred for evaluation of a 2-year history of recurrent post-exertion lightheadedness and near syncopal spells in the setting of a family history of unexplained sudden cardiac death. Cardiac evaluation demonstrated normal heart structure, but the 12-lead surface ECG was suggestive of but not diagnostic of Brugada syndrome. An exercise stress test reproduced the patient's usual symptoms during the recovery period, and was consistent with a typical vasovagal faint. The same symptoms were observed during a head-up tilt table test. However, given the family history and ECG, pharmacological testing with procainamide, isoprenaline and metoprolol, as well as programmed ventricular stimulation, were undertaken. Pharmacological provocation further supported a diagnosis of Brugada syndrome, whereas programmed ventricular stimulation was considered non-diagnostic regarding ventricular tachyarrhythmia susceptibility. Consequently, despite ECG and pharmacological findings suggestive of Brugada syndrome, there appeared to be sufficient evidence to believe that this patient's symptoms were the result of neurally mediated syncope and not due to ventricular tachyarrhythmias. The patient was treated with midodrine, and has remained symptom-free for 16 months. Thus, given the frequency with which vasovagal syncope occurs in young patients, its occurrence is not unexpected in individuals with concomitant diagnoses such as Brugada syndrome. In as much as current recommendations favour implantable defibrillators in symptomatic Brugada syndrome, the identification of other causes of syncope in such patients poses an uncomfortable, and currently unsettled dilemma.  (+info)

Assessment of noninvasive markers in identifying patients at risk in the Brugada syndrome: insight into risk stratification. (54/664)

OBJECTIVES: The aim of this study was to compare the use of various noninvasive markers for detecting risk of life-threatening arrhythmic events in patients with Brugada syndrome. BACKGROUND: The role of conduction disturbance in arrhythmogenesis of the syndrome is controversial, whereas it is well established that repolarization abnormalities are responsible for arrhythmias. The value of noninvasive markers reflecting conduction or repolarization abnormalities in identifying patients at risk for significant arrhythmias has not been shown. METHODS: We assessed late potentials (LP) using signal-averaged electrocardiography (ECG), microvolt T-wave alternans (TWA), and corrected QT-interval dispersion (QTD) in 44 consecutive patients who had ECGs showing a pattern of right bundle branch block and ST-segment elevation in leads V1 to V3 but structurally normal hearts. The patients were compared with 30 normal individuals. RESULTS: Eleven patients were excluded from data analysis because of an absence of ECG manifestations of Brugada syndrome at the time of the tests. A history of life-threatening events defined as syncope and aborted sudden death was present in 19 of 33 patients (58%); in 15 of the 19 patients, stimulation induced ventricular fibrillation or polymorphic ventricular tachycardia. The LP were present in 24 of 33 patients (73%); TWA were present in 5 of 31 patients (16%); and a QTD >50 ms was present in 9 of 33 patients (27%). The incidence of LP in Brugada patients was significantly (p < 0.0001) higher than in the controls, whereas incidences of TWA and QTD were not significantly different. Multivariate logistic regression analysis revealed that the presence of LP had the most significant correlation to the occurrence of life-threatening events (p = 0.006). CONCLUSIONS: Late potentials are a noninvasive risk stratifier in patients with Brugada syndrome. These results may support the idea that conduction disturbance per se is arrhythmogenic.  (+info)

Arrhythmogenic right ventricular cardiomyopathy: a cause of sudden death in young people. (55/664)

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an increasingly recognized cause of ventricular tachycardia and sudden cardiac death in young people, notably young athletes. The best treatment is not clear, although options include antiarrhythmic drugs, radiofrequency ablation, and implantable defibrillators.  (+info)

Acute inferior wall myocardial infarction associated with complete atrioventricular block and left posterior hemiblock. (56/664)

Three cases of acute inferior wall myocardial infarction associated with complete atrioventricular block and junctional escape rhythm showing left posterior hemiblock are presented. The triad appears to consitiute a distinct syndrome. It is postuated that the subsidiary pacemaker is situated either in the bundle of His or the proximal part of the anterior division of the left bundle-branch.  (+info)