Frequency of inter- and intraventricular dyssynchrony in patients with heart failure according to QRS width.

AIMS: Cardiac resynchronization therapy (CRT) is an effective treatment for heart failure patients with prolongation of QRS duration. Despite careful patient selection, some do not respond to CRT based on QRS complex duration. We sought to evaluate the presence of left ventricular dyssynchrony using tissue Doppler imaging (TDI) according to QRS duration in heart failure patients. METHODS AND RESULTS: Ninety-nine patients (mean age 52.6 +/- 15.3 years) with severe heart failure [left ventricular (LV) ejection fraction, <35%] were prospectively evaluated. On the basis of QRS width, the patients were divided into two groups. Forty-eight patients (48.5%) had a normal QRS duration (<120 ms), Group I, and 51 (51.5%) had a prolonged QRS duration, Group II. All patients underwent echocardiography coupled with TDI. Spectral displays of six basal and six middle LV segments with pulsed-wave TDI were obtained to assess the time to peak systolic point from R-wave on electrocardiogram (Ts). The standard deviation of Ts (Ts-SD) and the maximal temporal difference of Ts (Ts-diff) were measured. Interventricular dyssynchrony [defined as the presence of an interventricular mechanical delay (IVMD) >40 ms] and intra-LV mechanical delays (defined as Ts-SD >33.4 ms and Ts-diff >100 ms) were correlated with the QRS width and morphology. We found a greater IVMD in Group II patients, compared with patients in Group I (42.5 +/- 22.3 vs. 26.8 +/- 21, respectively, P < 0.001). Intraventricular dyssynchrony defined as Ts-SD > or =33.4 ms was found in 45.1% of patients in Group II compared with 23% of patients in Group I (P = 0.03). Similarly, the Ts-diff was prolonged in Group II patients compared with Group I (P = 0.02). By linear regression analysis, a weak relation was found between Ts-SD and QRS duration (P = 0.055). A substantial portion of patients with prolonged QRS did not exhibit ventricular dyssynchrony defined either as total asynchrony index > or =33.4 ms or as IVMD >40 ms. CONCLUSION: A substantial proportion of patients with prolonged QRS (32.1%) did not exhibit inter- or intraventricular dyssynchrony, which may represent a limitation in identifying the ideal QRS interval for the selection of patients for CRT.

Mid-term follow-up of patients with Brugada syndrome following a cardioverter defibrillator implantation: a single center experience.

BACKGROUND: Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of ST-segment elevation in the right precordial leads and an increase risk of sudden cardiac death. Risk stratification for the life-threatening arrhythmic events in Brugada syndrome is not yet established. In the present study, we report our experience in patients with Brugada syndrome, following an ICD implantation. METHODS AND RESULTS: A total of 12 patients (11 men, 1 woman) with a mean age of 46.5+/-11.8 were studied. At diagnosis, 7 patients had syncope of unknown origin, 2 patients were asymptomatic, 2 patients were survivors of cardiac arrest, and 1 had documented clinical VT requiring direct cardioversion for termination. Age was similar between the symptomatic and asymptomatic patients (46.6+/-13 vs. 46+/-2.8, respectively). Two patients reported a family history of sudden cardiac death. In 3 patients, spontaneous coved-type ECG was found at baseline. In 9 patients, a class I antiarrhythmic drug administration unmasked the characteristic type I ECG. In 4 patients (2 symptomatic with syncope at presentation and 2 asymptomatic), who underwent PES, sustained polymorphic VT or VF was induced. VF was induced by single extrastimuli in 2 symptomatic patients (1 from RV apex and 1 from RVOT). In 2 asymptomatic patients, VF was induced by two and triple ventricular extrastimli (1 from RV apex and 1 from RVOT). None of them experienced an event during follow-up. No significant difference was found between symptomatic and asymptomatic patients (p=NS). The mean follow-up period for the entire study population was 27.83+/-11.25 months. During follow-up, 2 patients (one with prior cardiac arrest and another with syncope) had VF. Both of them had a type I ECG after provocation with a class I antiarrhythmic drug. None of them had undergone programmed ventricular stimulation. Five patients (41.7 %) had inappropriate ICD interventions during follow-up. The cause of inappropriate therapy was sinus tachycardia in 2 patients, AF in 2 patients and T wave oversensing in 1 patient. CONCLUSION: Knowledge about Brugada syndrome is steadily progressing but there are still unanswered issues dealing with the risk stratification and the management of patients.

Resolution of tachycardia-induced cardiomyopathy following ablation of verapamil-sensitive idiopathic left ventricular tachycardia.

Few reports have described tachycardia-induced cardiomyopathy secondary to ventricular tachycardia. We present a 12-year-old boy with dilated cardiomyopathy and incessant verapamil-sensitive idiopathic left ventricular tachycardia. Twelve-lead electrocardiogram showed right bundle branch block QRS morphology with superior axis during tachycardia. Electrophysiology study confirmed the diagnosis, and radiofrequency ablation was done and successfully terminated and prevented induction of ventricular tachycardia. During the follow-up period of 18 months, the patient remained free of symptoms and arrhythmia. Three months after ablation, left ventricular ejection fraction improved and cardiac silhouette became normal on chest x-ray.

Heart rate variability: does it change after RF ablation of reentrant supraventricular tachycardia?

BACKGROUND: Following RF ablation of reentrant supraventricular tachycardia, inappropriate sinus tachycardia may occur. Local parasympathetic denervation is a possible mechanism for these rhythm disturbances. The purpose of this study was to determine the incidence of sinus tachycardia and to determine the relation between endocardial lesions at different ablation sites and alterations in autonomic tone in several different groups of patients with supraventricular tachycardia, using techniques of heart rate variability analysis. METHODS: The subjects of this study were 75 patients (48 women, 27 men) with a mean age of 39.99 (SD = 13.39). They underwent RF ablation of AV nodal slow pathways (40 cases), posteroseptal APs (23 cases), left lateral and right free wall APs (12 cases) because of symptomatic tachycardias. The mean sinus rate and time domain (standard deviation of RR intervals and root mean square of differences of adjacent RR intervals) and frequency domain (low frequency, high frequency and low frequency/high frequency ratio) analyses of heart rate variability were obtained by use of 24 hour Holter monitoring before and 1 month after ablation compared with pre-ablation values. RESULTS: Analysis of 24 hour ambulatory Holter-monitors, performed 1 month after RF ablation, showed no significant changes in time and frequency domain parameters of heart rate variability in different groups. A significant increase in mean heart rate was noted after RF ablation at AV nodal slow pathway group and left freewall/right free wall accessory pathways group. Patients undergoing RF ablation of right or left posteroseptal accessory pathways had no significant increase in the mean heart rate. CONCLUSION: In summary, an increase in sinus tachycardia may be initiated by RF ablation of atrioventricular reentrant tachycardia (AVNRT) and right free wall or left free wall accessory pathways. This finding shows that the modifications of heart rate are not directly related to the posteroseptal region or to the accessory pathways.

Late results of balloon pulmonary valvuloplasty in adults.

This study shows late results of adult patients with pulmonary stenosis after successful balloon pulmonary valvuloplasty. Late results of this procedure are as good as early results.

Differential effects of abrupt cycle length changes on the refractoriness of accessory pathway, His-Purkinje system, atrial and ventricular myocardium in Wolff-Parkinson-White syndrome.

We compared the response of the accessory pathway (AP), the atrial myocardium, the His-Purkinje system (HPS) and the ventricular myocardium during steady state (constant cycle length) and following an abrupt alteration in cycle length in 23 patients with Wolff-Parkinson-White syndrome. The durations of the anterograde and retrograde refractory periods were measured during constant drive cycle lengths of 600 and 400 ms (Method I) and during an abrupt change in cycle length of either short-to-long (400 to 600 ms) (Method II) or long-to-short (600 to 400 ms) (Method III) just before the extra stimulus. The mean durations of the anterograde effective refractory periods of the APs were 295 +/- 43, 243 +/- 39 and 273 +/- 37 ms at 600, 400 and 400 to 600 ms cycle lengths, respectively. For the atrial effective refractory periods at the three cycles, they were 238 +/- 18, 217 +/- 11 and 241 +/- 17 ms, respectively. During ventricular stimulation, the mean durations of the retrograde effective refractory periods of the APs were 263 +/- 25, 245 +/- 19 and 253 +/- 21 ms at cycle lengths of 600, 400 and 400 to 600 ms, respectively. For the relative refractory periods of the HPS, they were 335 +/- 29, 239 +/- 23 and 367 +/- 38 ms, respectively and, for the effective refractory periods of the ventricular myocardium, they were 227 +/- 17, 206 +/- 15 and 215 +/- 18 ms, respectively. The retrograde effective refractory period of the HPS could be measured in only five patients at the three cycles (600, 400 and 400 to 600 ms) and the mean values were 265 +/- 57, 225 +/- 14 and 305 +/- 27 ms, respectively. With Method III, AP and ventricular myocardium responded in a cumulative manner while HPS demonstrated paradoxical effect. Compared to Method I, changes with Methods II and III were statistically significant for all variables measured. During all three cycles, the retrograde effective refractory period of the HPS exceeded the effective refractory period of the AP; and the HPS demonstrated progressive conduction delay while the AP responded to no or minimal delays when the V1V2 intervals were similar. An abrupt cycle length change of the short-to-long type facilitated the induction of orthodromic tachycardia during ventricular pacing.(ABSTRACT TRUNCATED AT 400 WORDS)

Catheter recording of left atrial activation from left pulmonary artery in the Wolff-Parkinson-White syndrome: validation of the technique with intraoperative mapping results.

Accurate localization of accessory pathways (AP) in the Wolff-Parkinson-White (WPW) syndrome requires detailed atrial mapping. Coronary sinus catheterization is so far the most accurate method of left atrial mapping, but it can be technically difficult in some patients. We evaluated the feasibility of left atrial mapping from the left pulmonary artery in 24 patients with WPW syndrome. All patients except one underwent surgical cryoablation of their AP and the results of intraoperative mapping are available for comparison. Mapping in sinus rhythm showed recording of atrial activity in the distal left pulmonary artery occurred 56 +/- 20 ms after activation of high right atrium and 24 +/- 4 ms after activation in the His bundle area, but coincident with left atrial activation in the distal coronary sinus (56 +/- 20 and 53 +/- 13, respectively). Mapping during ventricular pacing or orthodromic tachycardia could differentiate patients as having a right sided, left sided or paraseptal first site of activation. Eleven patients had a left lateral AP, four had a left posterior AP, five had left posteroseptal AP and one had a left anterior AP. The remaining three patients had a right sided AP. Intraoperative results correlated with pre-operative findings in 22 out of 23 (95%) patients who underwent surgical ablation of AP. Thus, recordings form the left pulmonary artery reflect left atrial activity and may be of aid in localizing an AP, especially when coronary sinus recordings cannot be obtained. This technique, however, should not replace the more accurate method of coronary sinus mapping.

Atrioventricular nodal conduction and refractoriness following abrupt changes in cycle length.

The properties of the atrioventricular (AV) nodal conduction and effective refractory period in man are generally evaluated at a constant basic cycle length (CL) and, in most cases, they demonstrate an inverse relationship to the drive cycle. The response of AV node to abrupt change in CL is less defined. We therefore studied the effects of abrupt changes in CL on AV nodal conduction time and refractoriness in 18 patients. AV nodal conduction time, and effective and functional refractory periods were measured during: (1) a constant long CL, (2) a constant short CL, and (3) after an abrupt increase in CL just prior to the introduction of extrastimuli. In 10 of the 18 patients a constant long CL of 600 ms, a constant short CL of 400 ms and a sudden short-to-long change in CL (400 to 600 ms) were tested. AV nodal conduction times (A2H2) were measured at the shortest and longest comparable A1A2 intervals. The mean value of the shortest A2H2 intervals for constant CL of 600 ms was 144 +/- 18 ms; for a constant CL of 400 ms it was 162 +/- 17 ms; after a sudden short-to-long change in CL (400 to 600 ms) it was 142 +/- 14 ms. The mean value of the longest A2H2 intervals at a constant CL of 600 ms was 185 +/- 18 ms; at a constant CL of 400 ms it was 236 +/- 26 ms (p less than 0.01) and after a short-to-long change in CL (400 to 600 ms) 199 +/- 21 ms. AV nodal effective refractory periods measured at the same three CLs had mean values of 279 +/- 13 ms; 300 +/- 15 ms and 294 +/- 13 ms, respectively. Similar results were obtained when other CLs such as 700 to 900, 500 to 900, and 400 to 700 ms were tested. The data suggest that after abrupt short-to-long changes in CL, AV nodal function curves shift from long constant CL toward short constant CL as the coupling intervals decrease, indicating a cumulative pattern. Although the return to baseline conduction time after the fast basic rate is known to be slow, the limitation of this effect to the very early premature beat in the human has not been reported previously.

Tachycardia cycle length and maximum capacity of anterograde and retrograde atrioventricular conduction in paroxysmal supraventricular tachycardia.

Anterograde and retrograde pathways are the two major components of the reentry circuit in patients with paroxysmal supraventricular reentrant tachycardias. Therefore, the capacity of each pathway to maintain 1:1 conduction would be expected to determine the cycle length (CL) of the tachycardia. In this study, the possible relationship between the CL of reentrant tachycardia and the maximum capacities of anterograde and retrograde conduction in the maintenance of a 1:1 response during atrial and ventricular pacing were examined. This relationship was analyzed in 26 patients with orthodromic reentrant tachycardia due to Wolff-Parkinson-White syndrome (group 1) and compared with that in 26 patients with atrioventricular nodal reentrant tachycardia (group 2). There were no statistically significant differences between the two groups in the shortest tachycardia CLs (mean +/- SD, 325 +/- 44 versus 329 +/- 52 ms); in the shortest ventricular pacing CLs with 1:1 response (314 +/- 63 versus 319 +/- 38 ms); nor in the CLs that produced retrograde atrioventricular block (306 +/- 62 versus 301 +/- 37 ms). In contrast, the longest atrial pacing CL that produced Wenckebach's phenomenon and the shortest atrial pacing CL with 1:1 response were significantly shorter for group 1 than for group 2 patients (290 +/- 38 versus 390 +/- 88 ms, P less than 0.001) and (305 +/- 38 versus 406 +/- 90 ms, P less than 0.001), respectively. It was concluded that the CL of orthodromic tachycardia can best be predicted from the shortest atrial pacing CL that maintains 1:1 anterograde conduction via the normal pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Depressant effect on the retrograde atrioventricular nodal conduction of beta-adrenergic blockade by propranolol in humans.

Propranolol is known to have a depressant effect on anterograde atrioventricular (AV) nodal conduction in normal subjects and in those with AV nodal reentrant tachycardia. Using His bundle recording and programmed ventricular stimulation, the effect of propranolol-induced beta-adrenergic blockade (1 mg/kg intravenously) on retrograde AV nodal conduction was studied in 17 patients without (group I) and nine with (group II) AV nodal reentrant tachycardia. During baseline studies the ventricular pacing cycle length that induced ventriculoatrial block was 338 +/- 60 ms (range 260 to 450 ms) in group I and 305 +/- 39 ms (range 260 to 375 ms) in group II patients (not significant). After injection of propranolol, the ventricular pacing cycle length that induced ventriculoatrial block in group I patients was 416 +/- 97 ms (range 300 to 550 ms) (P less than 0.001, compared to baseline state) in 15 patients, and complete block occurred in two patients. In group II patients ventriculoatrial block occurred at a ventricular pacing cycle length of 375 +/- 97 ms (range 260 to 510 ms) (P less than 0.02 compared to baseline value) in eight patients, and complete block occurred in one patient. Retrograde AV nodal conduction expressed as the H2A2 interval was 75 +/- 33 ms (range 35 to 150 ms) in group I and 49 +/- 16 ms (range 20 to 80 ms) in group II patients (P less than 0.05). Following the administration of propranolol, the H2A2 interval was prolonged in group I patients by 10 to 45 ms in 11 patients, no retrograde AV nodal conduction was observed in three patients, and there was no effect in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Efficacy and safety of intravenous and oral diltiazem for Wolff-Parkinson-White syndrome.

The electrophysiologic effects and safety of diltiazem administered either intravenously or orally were studied in 14 patients with Wolff-Parkinson-White syndrome during orthodromic reentrant tachycardia and atrial fibrillation (AF). Anterograde and retrograde effective refractory periods of the accessory pathway did not change significantly from baseline during either i.v. or oral administration. Administration by either route prevented induction of sustained reentrant tachycardia in 8 patients. In 6 patients, the reentrant tachycardia was either nonsustained (2 patients) or sustained at much slower rates than the baseline rates (mean +/- standard deviation, baseline, 290 +/- 41 ms; i.v., 355 +/- 40 ms [p less than 0.001]; and oral, 377 +/- 33 ms [p less than 0.001]). In these patients anterograde atrioventricular conduction was prolonged significantly from the mean baseline value of 163 +/- 36 ms to 212 +/- 35 ms with i.v. administration (p less than 0.005) and 225 +/- 33 ms with oral administration (p less than 0.005). Retrograde conduction via the accessory pathway did not change significantly after administration of diltiazem. The shortest preexcited RR intervals during AF were significantly reduced during i.v. but not during oral administration: control, 327 +/- 47 ms; i.v., 270 +/- 28 ms (p less than 0.001); and oral, 323 +/- 44 ms (difference not significant). In 5 patients AF was sustained for a mean of 20 minutes after i.v. and for 12 minutes after oral administration (p less than 0.20), compared with a baseline mean value of 0.83 minute.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of autonomic nervous system modulation on retrograde atrioventricular nodal conduction in the human heart.

Although the influence of the autonomic nervous system on anterograde atrioventricular nodal conduction is well established, its effect on retrograde atrioventricular nodal conduction has not been examined systematically. Since retrograde atrioventricular nodal conduction in subjects with normal anterograde conduction may vary from intact retrograde conduction to complete retrograde block when assessed during ventricular pacing, in this study patients with (a) intact retrograde atrioventricular nodal conduction (group 1) were studied during parasympathetic (vagal) stimulation by carotid sinus pressure and during sympathetic inhibition (propranolol 0.2 mg.kg-1 intravenously) and (b) retrograde atrioventricular nodal block (group 2) were studied during vagal blockade (atropine 0.04 mg.kg-1 intravenously) and during sympathetic stimulation (isoproterenol 1-4 micrograms.min-1 infusion). In both groups changes in sinus cycle length and anterograde atrioventricular nodal conduction were measured. In group 1 vagal stimulation by carotid sinus pressure in 20 patients caused the cycle length at which retrograde atrioventricular nodal block was induced to be significantly lengthened from a mean(SD) of 375(59) to 451(51) ms in six patients; caused complete retrograde block in 10 patients; and had no effect in four patients. Sympathetic inhibition by propranolol in another 15 patients delayed the onset of pacing induced retrograde atrioventricular nodal block from a mean(SD) of 340(60) to 418(80) ms in 11 patients; caused complete retrograde atrioventricular nodal block in three patients; and had no effect in one patient. In group 2 vagal blockade by atropine caused a 1:1 retrograde response during ventricular pacing up to a mean(SD) cycle length of 470(135) ms in six out of eight patients. The infusion of isoproterenol caused the retrograde atrioventricular nodal block to be abolished and 1:1 conduction to be resumed up to a ventricular pacing mean(SD) cycle length of 364(57) ms in six out of eight patients. It is concluded that (a) the autonomic nervous system modulates retrograde atrioventricular nodal conduction in a similar manner to its anterograde counterpart and (b) that since retrograde atrioventricular nodal conduction was reversible after the administration of either atropine or isoproterenol retrograde atrioventricular nodal block may be dynamic (physiological) rather than fixed (anatomical) in nature.