Complete atrioventricular block during ablation of atrial flutter.

We report the case of a 51-year-old patient who developed a complete atrioventricular (AV) block during the isthmic radiofrequency catheter ablation of a typical atrial flutter. The cause was an acute occlusion of the segment three of the right coronary artery. His recanalization was associated with the immediate restoration of a normal AV conduction. The complication is exceptional (one of 740 consecutive atrial flutter ablations). (PACE 2010; 516-519).

Are the results of electrophysiological study different in patients with a pre-excitation syndrome, with and without syncope?

AIMS: Syncope in Wolff-Parkinson-White (WPW) syndrome may reveal an arrhythmic event or is not WPW syndrome related. The aim of the study is to evaluate the results of electrophysiological study in WPW syndrome according to the presence or not of syncope and the possible causes of syncope. METHODS AND RESULTS: Among 518 consecutive patients with diagnosis of WPW syndrome, 71 patients, mean age 34.5 +/- 17, presented syncope. Transoesophageal electrophysiological study in control state and after isoproterenol infusion was performed in the out-patient clinic. Atrioventricular re-entrant tachycardia (AVRT) was more frequently induced than in asymptomatic patients (n = 38, 53.5%, P < 0.01), less frequently than in those with tachycardia; atrial fibrillation (AF) and/or antidromic tachycardia (ATD) was induced in 28 patients (39%) more frequently (P < 0.05) than in asymptomatic patients or those with tachycardia. The incidence of high-risk form [rapid conduction over accessory pathway (AP) and AF or ATD induction] was higher in syncope group (n = 18, 25%, P < 0.001) than in asymptomatic subjects (8%) or those with tachycardias (7.5%). Maximal rate conducted over AP was similar in patients with and without syncope, and higher in patients with spontaneous AF, but without syncope. Results were not age-related. CONCLUSION: Tachycardia inducibility was higher in patients with syncope than in the asymptomatic group. The incidence of malignant WPW syndrome was higher in patients with syncope than in asymptomatic or symptomatic population, but the maximal rate conducted over AP was not higher and another mechanism could be also implicated in the mechanism of syncope.

Increased sensitivity of electrophysiological study by isoproterenol infusion in unexplained syncope.

UNLABELLED: The purpose of the study was to evaluate the interests of electrophysiologic study (EPS) after infusion of isoproterenol in patients with syncope and negative EPS in control state. METHODS: 1350 patients were consecutively admitted for syncope and EPS. Patients were included if they had no history of tachycardia, a normal Holter monitoring, a negative EPS in control state. EPS was repeated after infusion of 2-4 mug/kg of isoproterenol. RESULTS: 256 patients, 35 with exercise-related syncope and 105 with heart disease (HD), were recruited. After isoproterenol, an arrhythmia was identified as the sign associated with syncope in 102 patients (40%): SVT in 32 patients, VT in 36 patients, infrahisian 2nd or 3rd degree AV block in three patients and vasovagal reaction in 31 patients. Arrhythmias were more frequent in patients with HD (50/105) than in those without HD (52/151) (p<0.05); SVT tended to be more frequent in patients without HD (n=23) than in those with HD (n=9) (p<0.1); VT was more frequent in patients with HD (n=26) than in those without HD (n=10) (p<0.001). There was no relationship between a positive isoproterenol testing and occurrence of syncope at exercise (19/35 vs 81/221) (p<0.1). CONCLUSION: isoproterenol infusion increased the sensitivity of EPS in patients with syncope, related or not to exercise, and with negative study in control state, but principally in those with HD. However, SVT was diagnosed in patients without HD and EPS associated with isoproterenol infusion remained an important and rapid tool to establish this diagnosis.

Paradoxical effect of isoprenaline infusion.

BACKGROUND: Isoprenaline (isoproterenol) is a beta-adrenergic drug, used to increase the heart rate and, during electrophysiological study, to facilitate the induction of supraventricular (SVT) and ventricular tachycardias (VT). Decrease in heart rate during isoprenaline infusion is a rare phenomenon. The purpose of the study was to evaluate the incidence, the possible mechanisms, and the significance of a paradoxical bradycardia induced by isoprenaline infusion. METHODS: Electrophysiological study was performed for the evaluation of tachycardias (n = 551) or dizziness/syncope (n = 214) in 765 patients aged from 15 to 85 years. The study was negative in the basal state, and was repeated after isoprenaline infusion (2-4 microg/min). RESULTS: In 714 patients, this perfusion increased the heart rate to 100-140 bpm. A bradycardia was noted in 51 patients (7%). Two bradyarrhythmias were noted: (1) sinus or junctional bradycardia (cycle length - 10%) occurred in 43 patients, aged 15-70 years, generally studied for unexplained syncope (n = 37); a young age (40+/-16 years), syncope (n = 37) and absence of heart disease (n = 27) were more frequent than that in patients without isoprenaline-induced sinus or junctional bradycardia; another arrhythmia (SVT or VT) was induced in seven patients with syncope, five with heart disease and two without; six young patients (<50 years) had no syncope and were studied for SVT or VT; (2) eight patients, aged 65+/-11 years, developed second-degree atrioventricular (AV) block which was supraHisian (n = 4) or infraHisian (n = 4); they were studied for exercise-related syncope; they had no signs of myocardial ischaemia and AV block was reproduced by ajmaline testing: isoprenaline revealed organic conduction disturbance. CONCLUSION: The occurrence of paradoxical bradycardia was a rare finding during isoprenaline infusion (7%); sinus or junctional bradycardia was a sign of hypervagotonia, but was without clinical significance in 35% of these patients. The development of second-degree AV block was always pathological and associated with AV conduction disturbances, which occurred spontaneously during exercise. Isoprenaline infusion appeared to be a simple means to detect organic AV conduction disturbance in patients complaining of exercise or stress-related dizziness/syncope and unable to perform exercise test.

Electrophysiologic characteristics of atria in patients without heart disease.

BACKGROUND: The significance of atrial fibrillation or tachycardia (AF) induction remains debatable. Some believe that the presence of heart disease (HD) increases the sensitivity and decreases the specificity of programmed atrial stimulation (PAS). There are few data in patients without HD. The purpose of the study was to evaluate the results of PAS in asymptomatic patients without HD and in those with documented spontaneous AF, but without HD, to know the diagnosis value of the technique. METHODS: A total of 4,900 PAS were consecutively performed. The control group (I, N=67) was defined by the absence of preexcitation syndrome, dizziness/syncope, hypertension, history of tachycardia, or other documented HD together with a normal 2D echocardiogram and 24-hour Holter monitoring. They were compared to a group (II) of 54 patients with documented paroxysmal AF and without HD. PAS used one and two extrastimuli, delivered during sinus rhythm and two drive rates (600, 400 ms). Atrial-effective refractory periods (ARP), their adaptation to cycle length, and conduction times were noted. AF induction was defined as the induction of AF lasting more than 1 minute. RESULTS: Group I patients (1.4% of 4,900) were younger than group II (51 +/- 17 vs 65 +/- 11 years, P < 0.001). A single extrastimulus never induced sustained AF in group I, but did so in 11 group II patients (20%); sustained AF was induced by two extrastimuli in 15 group I patients (22%) and in 31 group II patients (57%) (P < 0.001). There were no ARP and conduction time differences in group I patients with and without inducible AF, but there was a longer sinus cycle length in patients with inducible AF (977 +/- 164 vs 838 +/- 141 ms, P < 0.02). There were no electrophysiological differences in group II patients with and without inducible AF. No group I patient developed spontaneous AF (follow-up 4 +/- 2 years). The sensitivity of PAS with one extrastimulus was 20% and the specificity 100%; the sensitivity of PAS with two extrastimuli was 57% and the specificity 78%. CONCLUSION: Sustained AF was not induced by one extrastimulus in control patients without symptoms, nor heart disease, but sustained AF was induced by two extrastimuli in 22% of these patients. The induction of a sustained AF by two extrastimuli should be interpreted cautiously, particularly in patients with a relative sinus bradycardia. However, the sensitivity of PAS with one extrastimulus was very low and two extrastimuli were required in patients with spontaneous AF to induce the tachycardia. Other electrophysiological parameters were not useful to differentiate patients with and without inducible AF.

Significance of inducible ventricular flutter-fibrillation after myocardial infarction.

AIM: The purpose of this study was to determine the factors associated with the induction of ventricular flutter/fibrillation (VFl/VF)and its prognostic significance in post-myocardial infarction. METHODS: Programmed ventricular stimulation was performed after myocardial infarction (MI) for syncope (n = 232) or systematically (n = 755); 230 patients had an induced VFl/VF and were followed during 4 +/- 2 years. RESULTS: VFl/VF was induced in 49/232 patients (21%) with syncope versus 181/755 asymptomatic patients (24%) (NS) and 94/410 patients (23%) with left ventricular ejection fraction (LVEF) <40% versus 136/577 patients (22.5%) with LVEF >40% (NS). Cardiac mortality was 9%; LVEF was 33 +/- 15% in patients who died, 43 +/- 13% in alive patients (P < 0.004). In patients with LVEF <40%, induced VFl/VF, mortality rate was 31% in those with syncope, 10% in asymptomatic patients (P < 0.001), because of an increase of deaths by heart failure; patients with LVEF >40% with or without syncope had a low mortality (5% and 3%). After linear logistic regression, VFl/VF and LVEF were predictors of total cardiac mortality, but only LVEF <40% predicted sudden death. CONCLUSION: Syncope and the level of LVEF did not increase the incidence of VFl/VF induction after MI, but modified the cardiac mortality: induced VF increased total cardiac mortality in patients with syncope and LVEF <40%, but did not increase sudden death. In patients with LVEF >40%, induced VFl/VF has no significance neither in asymptomatic patients nor in those with syncope.

Differences in mechanisms and outcomes of syncope in patients with coronary disease or idiopathic left ventricular dysfunction as assessed by electrophysiologic testing.

OBJECTIVES: This study evaluated the causes of syncope and the significance and differences in left ventricular (LV) dysfunction, coronary disease, and idiopathic dilated cardiomyopathy (DCM). BACKGROUND: Risk stratification of and indications for an automated defibrillator could differ according to the cause of LV dysfunction. METHODS: Electrophysiologic study, including atrial and ventricular programmed stimulation, was performed in 119 patients with coronary disease (group I) and 61 patients with DCM (group II) with an left ventricular ejection fraction (LVEF) <40% and syncope. Patients were followed from one to six years (mean 4 +/- 2 years). RESULTS: Sustained monomorphic ventricular tachycardia (VT) was induced in 44 group I patients (37%) and 13 group II patients (21%); ventricular flutter (>270 beats/min) or ventricular fibrillation (VF) was induced in 24 group I patients (19%) and 9 group II patients (15%); and various other arrhythmias were identified. Syncope remained unexplained in 34 group I patients (30%) and 16 group II patients (27%). Prognosis depended on the heart disease: VT or VF induction was a predictive factor of mortality in coronary disease and identified a group with high cardiac mortality (46%), compared with patients with a negative study, who had a lower mortality (6%; p < 0.001) than in other studies. Cardiac mortality was only correlated with LVEF in DCM. CONCLUSIONS: Various causes could explain syncope in 70% of patients with coronary disease and DCM, but differences were noted: VT was frequent in coronary disease with a bad prognosis, and ischemia could explain syncope; in DCM, different causes such as atrial tachycardia could be responsible for syncope, but the prognosis only depended on LVEF.

Absence of change of signal-averaged electrocardiogram identifies patients with ventricular arrhythmias who are non-responders to amiodarone.

OBJECTIVES: The aim of this study was to assess the ability of a non-invasive study, the signal-averaged ECG (SAECG), to predict the effect of amiodarone at ventricular level. BACKGROUND: Amiodarone is the main drug drug used in the treatment of ventricular arrhythmias. Standard ECG does not detect any change in QRS complex resulting from amiodarone therapy. SAECG is more sensitive than ECG for detecting changes in QRS complex. METHODS: The study examined the effects of amiodarone on SAECG in relation to the results of programmed ventricular stimulation in 68 patients with old myocardial infarction, spontaneous and inducible sustained ventricular tachycardia (VT). RESULTS: Amiodarone prolonged the total QRS duration (dur) (129+/-28 vs. 140+/-30 ms, P<0.05) and low amplitude signal (LAS) dur (45+/-20 vs. 51+/-20 ms, P<0.1), whereas the root-mean-square voltage of the last 40 ms of QRS complex (RMS 40) was significantly reduced (20+/-16 vs. 14+/-9 microV, P<0.05). Changes in SAECG parameters did not differ significantly in patients in whom amiodarone prevented the inducibility of VT (n=15) and those in whom VT remained inducible with amiodarone (n=53), but in baseline QRS duration was significantly shorter in patients in whom amiodarone prevented the VT induction (118+/-26 vs. 133+/-28 ms, P<0.05). In patients in whom amiodarone did not prolong the cycle length of VT (n=15), SAECG did not change significantly (QRS dur 131+/-29 vs. 132+/-27 ms, LAS 42+/-20 vs. 42+/-19 ms, RMS 40 22+/-14 vs. 19+/-11 microV). Comparison of the SAECG data in patients with no inducible VT and those with slowed VT differed significantly (P<0.05) between the control state and the recording with amiodarone. CONCLUSIONS: The effects of amiodarone on VT inducibility are predicted by a shorter baseline QRS duration and the degree of drug-induced prolongation of filtered QRS duration. Amiodarone prolonged the QRS duration, LAS duration and decreased RMS 40; this effect was more important in patients with no inducible VT and in those with only slowed VT, than in patients with unchanged or accelerated VT. The absence of changes of QRS duration predicted the induction of a more rapid or not slowed VT with amiodarone with a sensitivity of 87% and a specificity of 83%. Therefore, SAECG appears as an useful and simple means to predict the effects of amiodarone in patients with myocardial infarction and VT.