Conduction system abnormalities in patients with obstructive hypertrophic cardiomyopathy following septal reduction interventions

We observed the impact of percutaneous transluminal septal myocardial ablation (PTSMA) and myectomy on the conduction system in patients with obstructive hypertrophic cardiomyopathy (HC). Septal reduction intervention is capable of eliminating the left ventricular outflow tract obstruction in patients with obstructive HC; however, conduction system abnormalities are frequent consequences of these procedures. A standard 12-lead electrocardiogram and Doppler echocardiogram were obtained in 204 patients who underwent PTSMA (n = 70) or myectomy (n = 134) before and at average of 3 months after intervention. Of 146 patients who had normal conduction systems before intervention, the duration of the QRS complex was significantly prolonged from 98 +/- 15 to 130 +/- 25 ms (p <0.0001), with right bundle branch block (RBBB) developing in 62% patients after PTSMA, and from 100 +/- 13 to 154 +/- 20 ms (p <0.0001), with left bundle branch block (LBBB) developing in 93% patients after myectomy. No significant difference in the QRS duration was found in the remaining 58 patients who had preexisting conduction abnormalities after intervention. In 174 patients without a preexisting permanent pacemaker, a pacemaker was implanted in 22% versus 13% of patients who underwent PTSMA (overall and without preexisting conduction block, respectively) and 10% versus 2% of patients with myectomy. The duration of baseline QRS was an independent predictor for the requirement of a permanent pacemaker (p <0.0001). Thus, RBBB often develops after PTSMA and LBBB is very frequently produced by myectomy. A possible requirement of a permanent pacemaker should always be considered before intervention when patients have preexisting RBBB or LBBB.     

Low energy partial ablation of the atrioventricular node junction in the dog using a suction-ablation catheter

A suction electrode catheter was used for low energy, partial ablation of the atrioventricular (AV) node junction in 12 dogs. In 10 dogs, partial injury of the AV node was induced. In six dogs, delivered energy was measured precisely with use of a specially designed electronic circuit. The total energy required for partial ablation was 225 +/- 91 J. The increase in PR (p less than 0.0001) and AH (p less than 0.001) intervals was proportional to the energy delivered. After ablation, the PR interval increased from 98 +/- 10 to 154 +/- 33 ms (p less than 0.004) and the AH interval from 59 +/- 8 to 102 +/- 16 ms (p less than 0.004). There was no significant change in QRS, QTc, HV or RR intervals. AH and PR intervals were significantly prolonged at 3, 7 and 14 days after ablation (p less than 0.05). Anterograde conduction was significantly altered in 10 dogs. Anterograde AV node effective refractory period increased from 157 +/- 14 to 214 +/- 45 ms (p less than 0.005). Anterograde AV node Wenckebach cycle length increased from 196 +/- 30 to 244 +/- 44 ms (p less than 0.002). Retrograde conduction was assessed in three dogs. Retrograde AV node effective refractory period increased from 156 +/- 21 to 260 ms in two dogs, with complete retrograde block in the third. These changes persisted for up to 2 weeks. Pathologic changes were limited to the region of the AV node. In four dogs adherent thrombus without pulmonary emboli was noted. Partial focal injury to the AV node is feasible in the canine model.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic significance of leftward qrs axis deviation in bifascicular and trifascicular blocks

Background: Intraventricular conduction disturbances determine complete impairment of impulse propagation along the right or left bundle branch or the two left fascicles. Hypothesis: This study was undertaken to investigate the electrophysiologic significance of QRS axis (QRSA) orientation in bifascicular and trifascicular blocks. Methods: A group of 76 subjects, 43 with right bundle-branch block (RBBB) and left anterior hemiblock (LAH) (Group A), and 33 with left bundle-branch block (LBBB) (Group B) was submitted to electrophysiologic evaluation. Results: In Group A, QRSA was inversely related only to intraventricular conduction, while in Group B, QRSA inversely related to infrahisal conduction times. A value of <60° was considered the cut-off point for determin-ing subjects with a considerable leftward QRSA deviation. Of the 27 Group A patients with a QRSA <-60°, 38.5% developed an infrahisal second-degree atrioventricular (AV) block during incremental atrial stimulation (IAS) in comparison with 11.1 % of those with QRSA >-60°. Of the 9 Group B patients with a QRSA <-60°, 44.4% exhibited severe impairment of infrahisal conduction at baseline and 66.6% developed an infrahisal second-degree AV block during IAS, whereas among the remaining 24 with a QRSA >60°, in only 8.3% were both infrahisal (HV1 and HV2) intervals dangerously prolonged, and 23.8% encountered an infrahisal second-degree AV block during IAS. In Group A, atrioventricular conduction time >200 ms exhibited a better predictive accuracy than QRSA <60° for the development of an infrahisal second-degree AV block during IAS, whereas the latter appeared the best noninvasive predictor in Group B with a slightly lesser predictive accuracy than HV >80 ms. Conclusion: The degree of leftward QRSA deviation seems to reflect the entity of intraventricular conduction delay in patients with RBBB + LAH, while it appears to be directly related to infrahisal conduction prolongation in those with LBBB.     

Long-term safety and efficacy of slow pathway ablation in patients with atrioventricular nodal re-entrant tachycardia and pre-existing prolonged PR interval.

The association of atrioventricular nodal re-entrant tachycardia (AVNRT) and pre-existing prolonged PR interval is unusual. Radiofrequency (RF) ablation in such patients may be associated with an increased risk of immediate and delayed AV block. The aim of our study is to assess the long-term efficacy and safety of slow pathway ablation in this population. We studied 10 patients (4 males and 6 females) with pre-existing prolonged PR interval of 68 consecutive patients with AVNRT. All had slow-fast subtype of AVNRT. The mean PR interval was 222 +/- 15 ms before RF. The patients with pre-existing prolonged PR were older (69 +/- 15 vs. 54 +/- 17, P = 0.008) and their tachycardias were slower (387 +/- 102 vs. 323 +/- 73 ms; P < 0.05). Transient complete AV block (<5 s) occurred in two patients. None had permanent complete AV block. One patient had a significant increase in PR interval (from 220 to 320 ms). The mean post-RF PR interval was 232+/-37 ms (P = n.s.). Over a mean follow-up of 39 +/- 21 months, none had a recurrence of tachycardia nor developed higher degree AV block. In conclusion, in patients with AVNRT and pre-existing prolonged PR interval, a slow pathway ablation appeared efficient and safe. From our data, no delayed AV block developed on a long follow-up. Most of the patients with periprocedural transient AV block had no evidence of dual AV node physiology, suggesting that, in this population, absence of dual AV node physiology may be associated with a higher risk of AV block during slow pathway ablation.     

QT interval and repolarization time in patients with intraventricular conduction delay

A prolonged QT interval is an important prognostic indicator for cardiac arrhythmias and sudden death. The conventional QT interval measurement, however, includes in its measure the cardiac depolarization (QRS) as well as the cardiac repolarization (JT) intervals. To evaluate the relative contribution of the depolarization and the repolarization time prolongation to the prolonged QT interval in patients with intraventricular conduction delay (IVCD), the QRS, QT, and JT intervals were measured in 72 subjects with various types of IVCD. The observed intervals in IVCD subjects were compared to similar intervals in 33 healthy individuals in whom there was no evidence for intraventricular conduction abnormalities. The QTc (QT interval corrected for heart rate) in subjects with IVCD were 445 +/- 6.8 msec (mean +/- SEM) in those with LAD, 470 +/- 9.1 msec with RBBB, and 489 +/- 6.9 msec with LBBB. All of these intervals were significantly prolonged compared to 430 +/- 4.3 msec in the control group. The prolongation of QTc interval in each category of IVCD subjects was entirely secondary to a prolonged depolarization time, as the repolarization intervals were not significantly different from those observed in the control group (F = 0.5, p = NS). These observations may provide an explanation for the differential prognosis for subjects with prolonged QT interval with prolonged repolarization time as compared to those with prolonged QT interval with prolonged depolarization time.     

Incidence and predictors of atrioventricular conduction impairment after transcatheter aortic valve implantation

Atrioventricular (AV) conduction impairment is well described after surgical aortic valve replacement, but little is known in patients undergoing transcatheter aortic valve implantation (TAVI). We assessed AV conduction and need for a permanent pacemaker in patients undergoing TAVI with the Medtronic CoreValve Revalving System (MCRS) or the Edwards Sapien Valve (ESV). Sixty-seven patients without pre-existing permanent pacemaker were included in the study. Forty-one patients (61%) and 26 patients (39%) underwent successful TAVI with the MCRS and ESV, respectively. Complete AV block occurred in 15 patients (22%), second-degree AV block in 4 (6%), and new left bundle branch block in 15 (22%), respectively. A permanent pacemaker was implanted in 23 patients (34%). Overall PR interval and QRS width increased significantly after the procedure (p <0.001 for the 2 comparisons). Implantation of the MCRS compared to the ESV resulted in a trend toward a higher rate of new left bundle branch block and complete AV block (29% vs 12%, p = 0.09 for the 2 comparisons). During follow-up, complete AV block resolved in 64% of patients. In multivariable regression analysis pre-existing right bundle branch block was the only independent predictor of complete AV block after TAVI (relative risk 7.3, 95% confidence interval 2.4 to 22.2). In conclusion, TAVI is associated with impairment of AV conduction in a considerable portion of patients, patients with pre-existing right bundle branch block are at increased risk of complete AV block, and complete AV block resolves over time in most patients.     

梗阻性肥厚型心肌病室间隔心肌消融术后心电图变化

目的 :探讨梗阻性肥厚型心肌病经皮腔内室间隔消融术后心电图变化及临床意义。方法 :5例梗阻性肥厚型心肌病患者完成经皮腔内室间隔消融术 ,观察并比较术后不同时间记录的心电图和动态心电图。结果 :5例患者术中和术后均发生右束支传导阻滞 ;术中 3例出现一过性Ⅲ度房室传导阻滞 ,其中 1例发生心室颤动 ,1例出现频发室性期前收缩 ,1例出现Ⅰ度房室传导阻滞 ;术后未见新发Q波 ,QRS时限、QT和QTc间期明显延长 ,Sv1+Rv5显著降低 ,动态心电图随访未见室性心律失常增加。结论 :经皮腔内室间隔消融术致心律失常的发生率较高 ,但常为一过性。 12导联心电图和动态心电图监测是最为实用的诊断手段     

Unterstützung der spontanen atrioventrukulären Überleitung bei Patienten mit DDD(R)-Schrittmachern Effektivität und Sicherheit

AIM: In a prospective and randomized multicenter study using a cross-over protocol we compared the efficacy and the safety of the ELA medical mode-switch algorithm (DDD/AMC = DDD to AAI) to conventional DDD stimulation in patients with spontaneous AV conduction. PATIENTS AND METHOD: Forty-eight patients with a mean age of 67 +/- 13 years were included. Underlying heart disease was present in 54%. Pacemaker indications were paroxysmal AV block (21%), sick-sinus syndrome (46%), paroxysmal AV block + sick-sinus syndrome (31%) and tachycardia-bradycardia syndrome (8%). Patients were excluded from the study in case of a permanent 1st to 3rd degree AV block, a right bundle-branch block with QRS > 120 ms, severe coronary heart disease or idiopathic cardiomyopathy. The programming of the pacemaker was randomized to either DDD/AMC or DDD and was crossed over after 1 month. The AV interval (AVI) which was programmed in conventional DDD pacing was calculated as AVI = PR (or AR) + 30 ms at rest or as AVI = PR (or AR) - 50 ms during exercise. When the DDD/AMC mode was programmed, the AV interval was calculated automatically. We analyzed the AV interval, the frequency of ventricular pacing, the number of pacemaker-induced tachycardias, the number of atrial tachyarrhythmias, and the final programming which was left to the physician's choice. RESULTS: The AV interval after conventional DDD stimulation was 201 +/- 38 ms vs 195 +/- 28 ms with DDD/AMC (p = ns). Ventricular stimulation was significantly less often in the DDD/AMC mode than in the DDD mode (15 +/- 17% vs 48 +/- 37%, p < 0.001). Thereby the DDD/AMC algorithm led to a 69% reduction of ventricular pacing which means an approximately 5.5 months prolongation of the battery lifetime. There was no significant difference in the incidence of pacemaker-induced tachycardias. At the end of the study 77% of the physicians programmed the DDD/AMC mode. CONCLUSION: The analyzed DDD/AMC mode-switch algorithm leads to a significant reduction of ventricular pacing in patients with spontaneous AV conduction or with only paroxysmal AV block. Thereby the battery lifetime is prolonged and the incidence of complications due to ventricular pacing can be reduced.     

Cardiac resynchronization therapy in patients with heart failure and conduction abnormalities other than left bundle-branch block: analysis of the Multicenter InSync Randomized Clinical Evaluation (MIRACLE)

BACKGROUND: Cardiac resynchronization therapy (CRT) has been proposed as a treatment for patients with congestive heart failure (CHF) and prolonged QRS durations. Previous studies have predominantly included patients with left bundle-branch block (LBBB). The Multicenter InSync Randomized Clinical Evaluation (MIRACLE) investigators assessed the efficacy of CRT in patients with CHF with QRS durations > or = 130 ms and found that CRT lead to improvement in several measures of functional capacity and exercise tolerance. HYPOTHESIS: We designed this retrospective study to determine whether patients with CHF who have conduction abnormalities other than LBBB also respond favorably to CRT. METHODS: We divided patients enrolled in the MIRACLE trial into three subgroups according to conduction abnormality--LBBB, right bundle-branch block (RBBB), and nonspecific interventricular conduction delay (IVCD)--and compared the response among and within these groups to CRT or no CRT at baseline and 6-months' follow-up. RESULTS: We found 313 patients with LBBB, 43 with RBBB, and 35 with IVCD. When they received CRT, significant improvement was achieved in functional class (p = 0.001) by patients with RBBB, and in quality of life (p = 0.038) by patients with IVCD. Patients in the RBBB and IVCD groups showed improvement in exercise time and peak oxygen consumption after CRT. Most patients with RBBB (82%) also had either left anterior fascicular block or left posterior fascicular block. CONCLUSIONS: Patients with CHF with RBBB and IVCD do benefit from CRT. Improvement with CRT in patients with RBBB may be due to concomitant left-sided conduction abnormalities. Further subgroup analyses of other CRT trials are necessary to validate these results.     

Evidence that cocaine slows cardiac conduction by an action on both AV nodal and His-Purkinje tissue in the dog

The effects of intravenous cocaine (2 mg/kg) were tested on several indices of cardiac electrical activity in sedated dogs. These included sinus rate, PR, AH, and HV intervals; AV nodal effective refractory period (AVNERP); ventricular effective refractory period; QRS duration; and the QT interval. Cocaine induced significant changes in six control animals with an intact-functioning autonomic nervous systems. After pharmacologic autonomic blockade with propranolol plus propantheline, cocaine increased the PR interval (+ 11 +/- 4.0 ms, p less than 0.05), primarily by slowing conduction at the AV nodal level. However, with constant atrial pacing at a rate above the sinus cycle length, prolongation of both the AH and the HV intervals (+ 15 +/- 2.5 and 6.7 +/- 1.7 ms, respectively) occurred. There was also a significant increase in the AVNERP (+ 29 +/- 5.9 ms, p less than 0.05). Consistent with the observed rate-dependent HV prolongation, cocaine decreased the rate of rise of phase 0 of the transmembrane action potential of Purkinje fibers. These data indicate that cocaine impairs cardiac conduction by direct actions on AV nodal and His-Purkinje cells.     

Diminished left ventricular dyssynchrony and impact of resynchronization in failing hearts with right versus left bundle branch block.

OBJECTIVES: We compared mechanical dyssynchrony and the impact of cardiac resynchronization therapy (CRT) in failing hearts with a pure right (RBBB) versus left bundle branch block (LBBB). BACKGROUND: Cardiac resynchronization therapy is effective for treating failing hearts with conduction delay and discoordinate contraction. Most data pertain to LBBB delays. With RBBB, the lateral wall contracts early so that biventricular (BiV) pre-excitation may not be needed. Furthermore, the magnitude of dyssynchrony and impact of CRT in pure RBBB versus LBBB remains largely unknown. METHODS: Dogs with tachypacing-induced heart failure combined with right or left bundle branch radiofrequency ablation were studied. Basal dyssynchrony and effects of single and BiV CRT on left ventricular (LV) function were assessed by pressure-volume catheter and tagged magnetic resonance imaging, respectively. RESULTS: Left bundle branch block and RBBB induced similar QRS widening, and LV function (ejection fraction, maximum time derivative of LV pressure [dP/dt(max)]) was similarly depressed in failing hearts with both conduction delays. Despite this, mechanical dyssynchrony was less in RBBB (circumferential uniformity ratio estimate [CURE] index: 0.80 +/- 0.03 vs. 0.58 +/- 0.09 for LBBB, p < 0.04; CURE 0-->1 is dyssynchronous-->synchronous). Cardiac resynchronization therapy had correspondingly less effect on hearts with RBBB than those with LBBB (i.e., 5.5 +/- 1.1% vs. 29.5 +/- 5.0% increase in dP/dt(max), p < 0.005), despite similar baselines. Furthermore, right ventricular-only pacing enhanced function and synchrony in RBBB as well or better than did BiV, whereas LV-only pacing worsened function. CONCLUSIONS: Less mechanical dyssynchrony is induced by RBBB than LBBB in failing hearts, and the corresponding impact of CRT on the former is reduced. Right ventricular-only pacing may be equally efficacious as BiV CRT in hearts with pure right bundle branch conduction delay.     

Electrophysiological effects of the combined administration of digoxin and propranolol in man]

The electrophysiological effects of the combined administration of digoxin and propranolol were studied in 40 patients, compared with the effects of digoxin alone and considered in relation to anomalies of the conduction pathways. The cycle of the sinus node was only lengthened by digoxin in patients who had an anomaly of sinus node function. In contrast the addition of propranolol always increased it (from 1 109 +/- 53 ms to 1 232 +/- 58 ms). Sinus node recovery time was only increased by combined administration (from 1 331 +/- 101 ms to 1 450 +/- 68 ms). Changes in sino-atrial conduction intervals were not very marked. The AH interval was increased by digoxin (from 97 +/- 4 ms to 109 +/- 6 ms), with propranolol exerting a synergistic effect (119 +/- 6 ms). When there was pre-existing supra-His block only combined administration increased the conduction defect. The HV interval and QRS duration were not altered. The effective atrial refractory period was increased by combined administration (from 264 +/- 10 ms to 304 +/- 14 ms) except in subjects who had supra-His block. The effective refractory period of the AV node (385 +/- 26 ms) was increased by digoxin (450 +/- 37 ms). This effect was potentiated by propranolol (478 +/- 34 ms) except in those subjects who had supra-His block. In three cases in which there were two conduction pathways at A V node level the refractory periods of the rapid and slow pathways were increased by digoxin, with a synergistic effect from propranolol. The ventriculo-atrial conduction time changed from 151 +/- 24 ms to 172 +/- 22 ms following digoxin, then to 193 +/- 34 ms after the addition of propranolol.     

Left ventricular conduction delays induced by right ventricular apical pacing: effect of left ventricular dysfunction and bundle branch block

Background: RV apical pacing (RVP) may be deleterious, possibly by simulating LBBB, i.e., prolonging QRS duration (QRSd) and LV activation (LVAT). However, determinants of electrical delays are unknown.
Hypothesis: LV dysfunction (LVEF ≤ 40%, HF) and pre-existing conduction system abnormalities may modulate RVP's effects, compared to LBBB.
Methods: RVP-induced QRSd and LVAT were compared in normal LV to HF, with normal QRS (<120 ms), RBBB, or LBBB. LVAT was estimated by interval from QRS onset to basal inferolateral LV depolarization.
Results: During LBBB and RVP, LVAT/QRSd was ≥85%, i.e., LVAT indicated terminal LV depolarization. In normal LV, LVAT during intrinsic conduction (55 ± 18 ms) was delayed by RVP (129 ± 20 ms, n = 58, P < 0.001). RVP's effects were similar to LBBB (P = NS) and unaffected by baseline conduction disease. In HF overall, RVP-induced delays (QRSd 209 ± 27, LVAT 186 ± 26 ms, n = 102) were greater than RVP in normal LV (P < 0.001). When baseline conduction system disease was present, RVP's effects were exaggerated (RVP wide QRS [>120 ms]: QRSd 216 ± 27, LVAT 191 ± 20 ms, [n = 72] vs RVP normal QRS: QRSd 193 ± 24, LVAT 169 ± 24 ms, n = 31, P < 0.001). In patients with LBBB (n = 41), delays during intrinsic conduction (QRSd 163 ± 29, LVAT 137 ± 33 ms, n = 41) were enhanced by RVP (QRSd 218 ± 28, LVAT 191 ± 22 ms, P < 0.001). RVP's effects were similar in patients with LBBB and RBBB (P = NS).
Conclusion: RVP simulated LBBB in normal LV. In HF, RVP induced greater conduction delays than LBBB, enhanced by accompanying conduction disease. These variations may contribute to RVP's mixed clinical effects.     

Narrow QRS Tachycardia with Ventriculoatrial Dissociation Mediated by a Left Fasciculoventricular Fiber

A 30-year-old man presented with narrow QRS tachycardia. The intracardiac electrocardiogram showed an atrial-HIS (AH) interval of 75 msec and a HIS-ventricular (HV) interval of 44 msec during baseline. Atrial incremental pacing revealed HV shortening, with apparent incomplete right bundle branch block (RBBB) morphology without QRS complex axis deviation. The induced tachycardia exhibited several QRS morphologies: a narrow QRS, complete RBBB and complete left bundle branch block (LBBB) morphology. Spontaneous conversion of the QRS pattern from wide to narrow was observed. The cycle length of the tachycardia was significantly shortened (from 316 to 272 ms) from LBBB morphology to narrow QRS complex. The atrial activation was dissociated from the ventricular activation during all tachycardias. Each QRS complex during tachycardia was preceded by a HIS deflection and HV interval was 35 ms, which was shorter than that of sinus rhythm. HIS deflection was earlier than right bundle potential during all kinds of tachycardia. This tachycardia is most likely mediated by a left fasciculoventricular fiber which connects the HIS bundle below the atrioventricular node to the myocardial tissue of the left ventricle. The HIS-Purkinje system is used as an antegrade conduction limb and the fasciculoventricular fiber as a retrograde limb in the tachycardia circuit.     

Effects of magnesium sulfate on cardiac conduction and refractoriness in humans

Magnesium has been used empirically for several decades in the treatment of atrial and ventricular arrhythmias in patients with normal and decreased serum magnesium levels. However, a systematic evaluation of the effects of magnesium on cardiac conduction and refractoriness in humans has not been described. In this study, the electrocardiographic and electrophysiologic effects of magnesium were determined in 10 patients with normal baseline serum magnesium and other electrolyte levels. Six grams of magnesium sulfate was administered intravenously over 6 minutes followed by a continuous infusion of 1 additional gram over 1 hour. Serum magnesium levels rose significantly from a baseline of 2.0 +/- 0.2 to 5.4 +/- 0.4 mg/dl (p less than 0.001). No significant change occurred in heart rate at rest, or in duration of the QRS complex or QT or QTc intervals during sinus rhythm. There were significant increases in sinus node recovery time (1,000 +/- 211 to 1,106 +/- 223 ms, p less than 0.01) and corrected sinus node recovery time (279 +/- 87 to 336 +/- 104 ms, p less than 0.05). Significant increases occurred in atrioventricular (AV) node conduction time during sinus rhythm (82 +/- 22 to 97 +/- 17 ms, p less than 0.02), in the atrial paced cycle length at which AV node Wenckebach block occurred (350 +/- 46 to 419 +/- 65 ms, p less than 0.01) and in the AV node relative refractory period (397 +/- 27 to 422 +/- 18 ms, p less than 0.05), functional refractory period (395 +/- 41 to 415 +/- 33 ms, p less than 0.05) and effective refractory period (306 +/- 67 to 338 +/- 38 ms, p less than 0.05).     

Diastolic mitral regurgitation in patients with atrioventricular conduction abnormalities: a common finding by Doppler echocardiography

M-mode and Doppler echocardiography were performed in 16 patients with first degree atrioventricular (AV) block, 1 patient with second degree (Wenckebach type) and 3 patients with third degree AV block; 20 individuals with a normal PR interval served as control subjects. The time from the onset of the P wave to the mitral valve closure by M-mode and to the end of mitral flow by Doppler echocardiography were obtained. In 20 normal subjects, the P wave to mitral valve closure interval measured 220 +/- 30 ms by M-mode and to the end of mitral flow 225 +/- 29 ms by Doppler technique (p = NS). In patients with first degree AV block, these intervals measured 242 +/- 41 and 249 +/- 36 ms, respectively (p = NS). Late diastolic (before the onset of the QRS complex) mitral regurgitation was detected by pulsed mode Doppler imaging in 9 (56%) of the 16 patients with first degree AV block but in none with a normal PR interval. In the four patients with advanced AV block, intermittent mid or late diastolic mitral regurgitation was found to depend on the position of the P wave in diastole. With early diastolic P waves, the end of mitral valve flow by Doppler technique occurred 230 to 250 ms after the onset of the P wave and was followed by mild diastolic mitral regurgitation of variable duration. With P waves falling in systole, the mitral valve remained open throughout diastole; during most of diastole, however, there was neither forward mitral flow (diastasis) nor diastolic mitral regurgitation detected by Doppler technique.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impact of intraventricular conduction delay on coronary haemodynamics: a study with intracoronary Doppler in patients with bundle branch blocks and normal coronary arteries.

AIMS: The impact of right bundle branch block (RBBB) and left bundle branch block (LBBB) on myocardial perfusion is not completely understood as data are often blurred by underlying cardiac disease. The present study investigates whether conduction delays per se affect coronary perfusion-an indirect measure of myocardial oxygen demand. METHODS AND RESULTS: Intracoronary Doppler and ultrasound were performed in 8 patients with RBBB, 10 patients with LBBB, and 10 control subjects. All patients had angiographically normal coronary arteries and normal left ventricular function. Baseline (bAPV) and adenosine-induced hyperaemic average flow velocity and coronary flow velocity reserve (CFVR) were measured in left anterior descending arteries. Intravascular ultrasound showed no difference in lumen cross-sectional area and plaque burden between groups. Patients with RBBB and LBBB had higher bAPV values than controls (19.0 +/- 4.9, 21.9 +/- 5.1, and 14.6 +/- 2.4 cm/s, respectively; ANOVA P = 0.003). There was no difference between patients with LBBB and RBBB compared with controls in CFVR (2.8 +/- 0.5, 3.0 +/- 1.0, and 3.4 +/- 0.7, respectively; ANOVA P = 0.21). CONCLUSION: Bundle branch blocks, in particular LBBB, are associated with an increased coronary flow velocity, which indicates enhanced myocardial oxygen demand on the basis of mechanoenergetic disturbance. This may contribute to the unfavourable outcome of patients with intraventricular conduction delay.     

Electrophysiologic characteristics of ventricular extrastimulation-induced dissipation of functional bundle branch block associated with supraventricular tachycardia

INTRODUCTION: Linking-related anterograde functional bundle branch block during supraventricular tachycardia (SVT) is due to repetitive concealed retrograde conduction of impulses from the contralateral bundle branch and can be eliminated by a critically timed premature ventricular beat (PVB). We assessed the electrophysiologic characteristics of PVB-induced dissipation of functional bundle branch block during SVT. METHODS AND RESULTS: During SVT with functional bundle branch block, PVB was delivered from the right ventricular apex, scanning the tachycardia cycle length (CL) with 10-msec decrements in the coupling interval in 14 patients (3 AV nodal reentrant tachycardia and 11 orthodromic AV reciprocating tachycardia). Dissipation was achieved in group 1: functional right bundle branch block (RBBB) in 4, functional left bundle branch block (LBBB) in 4, and both functional RBBB and LBBB in 1 with a dissipation zone occupying 4% to 13% (mean 8.5%) of the tachycardia CL. The outer limits were 22+/-16 msec and 68+/-14 msec < tachycardia CL; the inner limits were 56+/-18 msec and 90+/-24 msec < tachycardia CL for RBBB and LBBB, respectively (both P < 0.05). Dissipation could not be achieved in group 2 (4 RBBB and 1 LBBB) due to CL-dependent bundle branch block and/or local ventricular refractoriness. CONCLUSION: During SVT, functional bundle branch block due to "linking" often can be dissipated by timely PVB delivered from the right ventricular apex within a narrow zone of the tachycardia CL. Our findings suggest that the dissipation zone is affected by the pattern of functional bundle branch block relative to the site of PVB delivery.     

Left ventricular electromechanical delay in patients with heart failure and normal QRS duration and in patients with right and left bundle branch block.

AIMS: We sought to define the reference values of intra-left ventricular (LV) electromechanical delay (EMD), and to assess the prevalence (and pattern) of intra-LV dyssynchrony in patients with heart failure (HF) and normal QRS and in patients with right and left bundle branch block. METHODS AND RESULTS: We used tissue Doppler imaging echocardiography and a six-LV wall model to study LV EMD in 103 patients [41 with HF and normal QRS, 22 with right bundle branch block (RBBB), and 40 with left bundle branch block (LBBB)], and in 59 controls. In controls, the median intra-LV EMD was 17 ms, (inter-quartile range 13-30); 95% of controls had a value < or =41 ms. Patients showed a longer intra-LV EMD than controls: 33 ms (20-57) in patients with normal QRS, 32 ms (23-50) in RBBB patients, and 50 ms (30-94) in LBBB patients. Intra-LV dyssynchrony (defined as intra-LV EMD >41 ms) was present in 39, 36, and 60% of the patients, respectively. On average, HF patients showed the same pattern of activation as controls, from the septum to the posterior wall, but activation times were significantly prolonged. In RBBB patients the activation sequence was directed from inferior to anterior and in LBBB from anterior to inferior wall. CONCLUSIONS: Left ventricular dyssynchrony was present in several patients with HF and normal QRS, and in patients with RBBB; conversely, 40% of LBBB patients showed values of LV EMD within the normal range. Left ventricular activation sequence was different between groups. Assessment of LV synchronicity by means of imaging techniques may be more important than QRS duration or morphology in selecting patients for cardiac resynchronization treatment.     

Clinical and electrophysiologic findings in acute ischemic intraHisian bundle-branch block

Clinical and electrophysiologic features of acute ischemic right bundle-branch block (RBBB) that are reversible by His bundle pacing were analyzed in nine patients. All had large anterior myocardial infarctions (mean peak CK-MB = 185 +/- 71 IU/l), and six showed increased pulmonary capillary pressures. The RBBB occurred within 48 hours of infarction, and in six patients it was associated with left fascicular block. The HV intervals that were measured 1 to 4 days after infarction were normal in all patients. Progression to complete atrioventricular (AV) block occurred in three patients, and one patient required permanent cardiac pacing. Sustained ventricular tachycardia developed in two patients, and ventricular fibrillation developed in five. During a mean follow-up period of 26 months, four patients died (three of them suddenly). The RBBB disappeared in only one case. Acute ischemic intraHisian RBBB occurred in the setting of massive myocardial infarctions complicated by ventricular tachycardia or fibrillation and by a high mortality rate during the follow-up period. The RBBB rarely reverted spontaneously, and the His-Purkinje conduction time was frequently normal.