Rhythm-symptom correlation in patients on continuous monitoring after catheter ablation of atrial fibrillation.

INTRODUCTION: Correlation between symptoms and atrial fibrillation (AF) episodes after catheter ablation may have clinical relevance, especially for anticoagulation usage. The aim of our project was to analyze the relationship between symptoms and AF recurrences in unselected patients following AF catheter ablation during long-term follow-up. METHODS AND RESULTS: One hundred and forty-three consecutive patients (mean age 59 ± 9 years, 85% male) were implanted with a continuous cardiac monitor (RevealXT, Medtronic Inc., Minneapolis, MN, USA) following first pulmonary vein ablation procedure. Device data were downloaded every 3 months and correlated to patients' symptom diary. AF was paroxysmal in 55% and persistent in 45%. At a mean follow-up of 14 ± 6 months, 98/143 (69%) patients had at least one AF recurrence. Among these, 53 (54%) reported AF-related symptoms while 45 (46%) were totally asymptomatic. Conversely, 13 (29%) out of 45 patients without AF recurrences reported symptoms. Globally, a significant reduction of symptoms (from 82% at baseline to 44% at last follow-up; P < 0.0001) was observed. SF-12 questionnaire showed a significant improvement of physical and mental functioning (respectively 44.5 ± 8.5 vs 51.0 ± 6.7, and 45.7 ± 9.3 vs 49.2 ± 6.1, P < 0.05 baseline vs last follow-up). At the 12-month follow-up, 80% and 77% of patients were on AAD and anticoagulant drugs, respectively. There were not differences in AAD usage in symptomatic and asymptomatic patients. CONCLUSIONS: Continuous ECG monitoring is a valuable tool for long-term follow-up after AF catheter ablation facilitating reliable assessment of symptomatic and asymptomatic AF episodes. This may have clinical implications with regards to anticoagulation therapy in high-risk patients.

Inferior vena cava loop of the implantable cardioverter defibrillator endocardial lead: a possible solution of the growth problem in pediatric implantation.

The ICD is an important treatment option in adults and children with life-threatening tachyarrhythmias. The possibility of lead displacement caused by growth and the lack of dedicated leads and devices poses special problems in pediatric ICD implantation. We describe our experience in three children in whom we left a redundant lead loop within the inferior vena cava (IVC) is allow for further growth. Since February 1998, three children underwent ICD implantation at our institution. A lead (screw-in) was advanced into the right ventricular apex, and a loop was created in the IVC by progressively withdrawing the stylet and pushing in the lead. Satisfactory sensing and pacing threshold values were obtained and a successful single 16-J defibrillation test was performed. No complications were encountered. After a mean follow-up of 16 months, with a mean increase in body weight and height of 4.1 +/- 0.5 Kg and 6.3 +/- 0.4 cm, respectively, chest X ray showed some release of additional lead length, in the absence of dislodgments, while significant changes in pacing/sensing parameters were not found. In conclusion, the creation of a loop within the IVC allows the lead to adjust for growth in children receiving an ICD. This approach is feasible and safe.

Noncontact system-guided simplified right atrial linear lesions using radiofrequency transcatheter ablation for treatment of refractory atrial fibrillation.

This article describes our experience with a staged "hybrid" approach to the treatment of drug resistant AF, in which the completeness of a single linear lesion in the RA was verified with a noncontact mapping system. Inferior vena cava-tricuspid annulus ablation was performed and followed by the creation of a single intercaval lesion. The study population consisted of 24 patients with a 3.4 +/- 1.6-year history of drug resistant, severely symptomatic, lone paroxysmal (n = 19), or persistent (n = 5) AF. During a follow-up of 8 +/- 2.6 months, 12 (50%) patients remained asymptomatic and 6 (25%) had a significant decrease in AF episodes, while the arrhythmia was unchanged in 5 (21%) patients and aggravated in 1 (4%) patient. Overall, a favorable clinical result was achieved in 18 (75%) patients.

Long-term follow-up after atrioventricular nodal ablation and pacing: low incidence of sudden cardiac death.

Sudden cardiac death (SCD) has been reported in patients with drug refractory AF who underwent AV nodal ablation and pacing. However, whether SCD in these patients is related to the underlying heart disease or to the ablating and pacing procedure remains uncertain. Between May 1987 and January 1997, AV nodal ablation was performed in 585 patients (mean age 66 +/- 11 years) with drug-resistant, paroxysmal (n = 308) or chronic (n = 277) AF in 12 Italian centers. Lone AF was present in 133 patients. After AV junction ablation, patients underwent VVIR (454 patients) or DDDR (131 patients) pacemaker implantation. At a follow-up of 33.6 +/- 24.2 months, 80 (13.7%) deaths were recorded: 40 noncardiac, 23 nonsudden, and 17 sudden cardiac death (3%, 1.04% per year). Among five variables, including age. NYHA functional class, presence of heart disease, paroxysmal or chronic AF, previous embolic events, and LVEF, the presence of heart disease (P = 0.007) and a LVEF < 0.45, (P = 0.003) were associated with a higher risk of SCD. Analysis of SCD-free survival by log-rank test showed a higher incidence of SCD in patients with LVEF < 0.45 (P = 0.0001) and with coronary artery disease (P = 0.005). In this large cohort, a low incidence of long-term SCD after AV nodal ablation and pacing for drug-refractory AF was observed. The presence of underlying heart disease and the extent of baseline LV dysfunction were associated with an increased likelihood of SCD.

Thromboembolism after atrioventricular node ablation and pacing: long term follow up.

OBJECTIVE: To assess the incidence of arterial embolic events in patients with high rate, drug resistant, severely symptomatic paroxysmal and chronic atrial fibrillation who have undergone atrioventricular (AV) node ablation and permanent pacing. DESIGN: Multicentre retrospective cohort study. PATIENTS AND MANAGEMENT: From May 1987 to January 1997, AV node ablation was performed in 585 severely symptomatic patients (mean (SD) age 66 (11) years) with high rate, drug resistant paroxysmal atrial fibrillation (308) or chronic atrial fibrillation (277). Lone atrial fibrillation was present in 133 patients, while the remaining 452 suffered from dilated, ischaemic, or valvar heart disease. Patients underwent VVIR (454) or DDDR (131) pacemaker implantation, after AV node ablation. Antiplatelet agents were given to 202 patients, warfarin to 187 patients. RESULTS: During a follow up of 33.6 (24.2) months, thromboembolic events were observed in 17 patients (3%); the actuarial occurrence rates of thromboembolism were 1.1%, 3%, 4.2%, and 7.4% after one, three, five, and seven years, respectively. Among five variables, univariate analysis showed that only the presence of chronic atrial fibrillation at the time of ablation (relative risk (RR) = 1.8, 95% confidence interval (CI) = 1.02 to 3. 20, p = 0.04) and the need for warfarin treatment (RR = 1.6, 95% CI 1.00 to 2.71, p = 0.048) were associated with a significantly higher risk of occurrence of thromboembolic events. On multivariate analysis the only predictor of embolic events during the follow up was the presence of chronic atrial fibrillation. CONCLUSIONS: Data from this large cohort of patients indicate a fairly low incidence (1.04% per year) of thromboembolic events after AV node ablation and pacing for drug refractory, high rate atrial fibrillation.

Congestive heart failure induced by recipient atrial tachycardia conducted to the donor atrium after orthotopic heart transplantation: complete regression after successful radiofrequency ablation.

We describe the case of a 30-year-old female patient who developed an interatrial tachycardia from the recipient to the donor atrium associated with signs of congestive heart failure 5 years after orthotopic heart transplantation. The patient underwent catheter mapping followed by successful radiofrequency (RF) ablation at the site of the presumed electrical connection between the recipient and the donor atria, through the interatrial surgical suture line, with stable recovery of sinus rhythm and disappearance of signs of left ventricular dysfunction. RF catheter ablation is confirmed to be feasible and safe in the treatment of heart transplant patients even in the presence of rare forms of arrhythmias, thus offering a cure for tachycardia to these patients.

Hypertrophic cardiomyopathy with apical aneurysm: a case of catheter and surgical therapy of sustained monomorphic ventricular tachycardia.

The case is presented of a patient with hypertrophic cardiomyopathy, midventricular obstruction, apical aneurysm, and very frequent episodes of sustained monomorphic ventricular tachycardia (VT) unresponsive to common antiarrhythmic drugs. Left ventricular catheter mapping during sinus rhythm suggested the presence of an extensively scarred apical region; early fractionated ECGs were recorded at the neck of the aneurysm during monomorphic VT, suggesting a possible role of this region as VT substrate. Radiofrequency delivery at these sites stopped the VT and it was no longer inducible; however, it spontaneously recurred the following day. An apical aneurysmectomy, guided by the results of catheter mapping, was performed and was successful in preventing arrhythmic recurrences during 12 months' follow up.

Impaired baroreflex sensitivity is correlated with hemodynamic deterioration of sustained ventricular tachycardia.

OBJECTIVES: The goal of this study was to evaluate clinical and autonomic variables (heart rate variability and baroreflex sensitivity) related to hemodynamic tolerability of VT in patients with sustained monomorphic VT and a healed myocardial infarction. BACKGROUND: Sustained ventricular tachycardia (VT) with hemodynamic deterioration is associated with a worse prognosis than that of well tolerated VT. The causes of hemodynamic deterioration of VT are incompletely understood. METHODS: Twenty-four consecutive patients with sustained monomorphic VT and a healed myocardial infarction (mean age +/- SD 66 +/- 8 years, left ventricular [LV] ejection fraction 37 +/- 11%) were assigned to group 1 if the VT was well tolerated (n = 11) or to group 2 if faintness or syncope occurred or if systolic blood pressure was < 90 mm Hg with clinical signs of shock (n = 13). RESULTS: No difference was found between the two groups in age, LV function, rate and duration of the VT or heart rate variability. However, patients in group 2 had a significantly lower baroreflex sensitivity (3.4 +/- 1.1 vs. 7.1 +/- 3.7 ms/mm Hg, p = 0.003). Multiple logistic regression analysis showed that only the value of baroreflex sensitivity (p = 0.0003)-but not age, LV ejection fraction, VT cycle length or SD of the RR interval (all p > 0.25)-correlated with the tolerability of the VT. Finally, LV ejection fraction (p = 0.0001) and baroreflex sensitivity (p = 0.0003)-but not age, cycle length of the tachycardia or SD of the RR interval-predicted cardiac death or unstable VT during follow-up. CONCLUSIONS: These data suggest that an impaired cardiovascular reflex response may play a key role in the hemodynamic deterioration of sustained VT and that the evaluation of baroreflex sensitivity in patients at high risk for sustained VT may become useful both in risk stratification and in the individualization of treatment.

Influence of residual ischaemia on heart rate variability after myocardial infarction.

Despite the growing evidence for the positive predictive value of depressed baroreflex sensitivity and/or reduced heart rate variability after myocardial infarction, the mechanisms involved in these autonomic alterations are not fully understood. Specifically, the possible influence of residual ischaemia has not been assessed. To address this problem we studied the spectral analysis of heart rate variability in 21 patients with a first myocardial infarction in whom the only clinical correlate was the presence of residual ischaemia, as documented by the positive response to both an exercise stress test and an echocardiographic stress test. Data from these patients were compared with those obtained in a group of postmyocardial infarction patients similar for several risk factors, age, site of myocardial infarction, but without residual ischaemia. Patients positive for residual ischaemia had lower power in the whole spectrum (1146 +/- 158 vs 1631 +/- 159 ms2, P = 0.032) as well as in the low and high frequency bands of heart rate variability. A nocturnal increase in high frequency was observed in those without residual ischaemia (from 167 +/- 35 to 242 +/- 51 ms2, +45%, P = 0.034), but not in those with residual ischaemia (from 111 +/- 19 to 141 +/- 29 ms2, +27%, ns). Thus, residual ischaemia reduces heart rate variability after myocardial infarction. The autonomic effects of residual ischaemia probably contribute to its negative prognostic value after myocardial infarction.

Baroreflex sensitivity, but not heart rate variability, is reduced in patients with life-threatening ventricular arrhythmias long after myocardial infarction.

Low values of heart rate variability (HRV, a marker of vagal tone) and baroreflex sensitivity (BRS, a marker of vagal reflexes) identify patients at higher risk soon after myocardial infarction (MI). However, it is still unknown whether HRV and BRS correlate with malignant arrhythmias after the recovery from the transient post-MI autonomic disturbance. This study assessed whether HRV and BRS would differ in patients with malignant ventricular arrhythmias occurring long after MI compared with those in a control population. Twenty-eight patients entered the study: 14 patients with episodes of sustained ventricular tachycardia or ventricular fibrillation occurring more than 1 year after MI, age (mean +/- SEM) 64 +/- 2 years, and left ventricular ejection fraction 34% +/- 3% (VT/VF group) were compared with 14 similar patients with no ventricular tachycardia (control group). Mean RR interval was not different in the two groups (844 +/- 37 msec in VT/VF and 892 +/- 24 msec in control group). Also, no difference was found in any time- or frequency-domain measure of heart rate variability. However, patients in the VT/VF group had a significantly lower baroreflex sensitivity compared with patients in the control group (4.2 +/- 0.5 vs 8.0 +/- 1.1 msec/mm Hg, p = 0.008). Thus BRS but not HRV was reduced in patients with life-threatening ventricular arrhythmias occurring long after MI. A persistent depression of vagal reflexes may play a role in the occurrence of malignant arrhythmias, and analysis of BRS may potentially be helpful in the identification of patients at high risk long after myocardial infarction.

Scopolamine increases vagal tone and vagal reflexes in patients after myocardial infarction.

OBJECTIVES: The goal of this study was to assess the hypothesis that transdermal scopolamine would increase vagal activity in patients after myocardial infarction. BACKGROUND: In postmyocardial infarction patients, low heart rate variability and reduced baroreceptor reflex sensitivity are associated with increased mortality. Accordingly, there is an increasing interest in a mechanism for shifting the sympathovagal balance toward vagal dominance. METHODS: The effects of transdermal administration of scopolamine on heart rate variability and baroreceptor reflex sensitivity were assessed in 20 patients (mean age 59 +/- 11 years) by pharmacologic washout 14 +/- 3 days after myocardial infarction. Heart rate variability and baroreceptor reflex sensitivity were measured 24 h after application of the scopolamine patch and compared with the values measured before scopolamine and after application of a placebo patch. The following variables were derived from a 15-min electrocardiographic recording: the mean RR interval and its standard deviation, the mean square successive difference, the percent of intervals differing > 50 ms from the preceding RR interval and the low and high frequency areas resulting from power spectral analysis. RESULTS: The placebo patch had no effect on the variables measured. Scopolamine increased both heart rate variability and baroreceptor reflex sensitivity significantly. Specifically, the mean RR interval and its standard deviation increased by 7.1% (p = 0.01) and 25% (p = 0.004), respectively. The mean square successive difference increased by 38% (p = 0.0003) and the percent of intervals differing > 50 ms from the preceding interval by 100% (p = 0.001). The ratio of low to high frequency areas of the power spectrum decreased by 24% (p = 0.02), and baroreceptor reflex sensitivity increased by 42% (p = 0.0006). These effects were also evident in patients with very low initial values. Side effects were minimal. CONCLUSIONS: Transdermal scopolamine increased measures of heart rate variability and baroreceptor reflex sensitivity in patients with a recent myocardial infarction toward values associated with a better prognosis. Pharmacologic modulation of the autonomic balance by scopolamine or related drugs deserves evaluation as a new and promising approach to reduce risk after myocardial infarction.

Early afterdepolarizations induced in vivo by reperfusion of ischemic myocardium. A possible mechanism for reperfusion arrhythmias.

Recent studies in vitro have shown that afterdepolarizations may develop during reperfusion after hypoxia, thus suggesting that these afterdepolarizations may contribute to the genesis of reperfusion arrhythmias. We recorded monophasic action potentials (MAPs) during myocardial ischemia and reperfusion to investigate whether afterdepolarizations develop in vivo when reperfusion arrhythmias occur. In 15 anesthetized cats, 24 trials of 10 minutes of occlusion of the left anterior descending coronary artery were followed by reperfusion. In 13 of 24 (54%) trials, afterdepolarizations developed at the moment of reperfusion, with a mean amplitude of 2.4 +/- 1.1 mV (13 +/- 8% of MAP amplitude). When cycle length was either increased by vagal stimulation or decreased by atrial pacing, early afterdepolarization (EAD) amplitude was modified, according to what has been described for EAD in vitro, with a positive linear correlation between cycle length and EAD amplitude (r = 0.91, p less than 0.0001). The occurrence of EAD was not related to rapid changes in left ventricular pressure. In the eight of 13 (62%) cases in which EAD development was associated with reperfusion arrhythmias, the coupling interval of the EAD and of premature ventricular contractions showed a significant correlation (r = 0.86, p less than 0.0001). However, in five of 13 (38%) cases, occurrence of reperfusion arrhythmias was not accompanied by the presence of EAD on the MAP recording. In two animals, a 2:1 block of EAD conduction was observed, and this was reflected on the intracavitary electrocardiogram as T wave alternans. Thus, EADs occur frequently after reperfusion in vivo, with a time course that parallels the onset of reperfusion arrhythmias. This finding further supports the role of triggered activity in the genesis of reperfusion arrhythmias in vivo.

Delayed afterdepolarizations elicited in vivo by left stellate ganglion stimulation.

Activation of cardiac sympathetic nerves is recognized as a triggering factor for cardiac arrhythmias. However, the mechanisms involved have only been speculated. Because evidence from studies in vitro has established a relation between catecholamines, delayed afterdepolarizations (DAD), and triggered rhythms, it seemed possible that in vivo adrenergic activation also might lead to the development of DAD. Because very little evidence was available for DAD in vivo, we have evaluated whether monophasic action potential (MAP) recording with a contact electrode could be a suitable technique for the detection of DAD from the endocardium of anesthetized cats. In six animals, atrial pacing and graded aortic constriction were performed during MAP recording to assess MAP stability during hemodynamic changes, and in no cases were modifications of the baseline observed. In 11 cats, calcium gluconate (0.5 g) and G-strophanthin (100 micrograms) were administered. Action potential duration at 50% (APD50) and 90% (APD90) repolarization were reduced (from 138 +/- 16 to 122 +/- 18 msec, p less than 0.02, and from 163 +/- 23 to 149 +/- 20 msec, p less than 0.025, respectively). In eight of 11 (73%) animals, DAD were elicited with a mean amplitude of 1.2 +/- 0.4 mV. In 14 cats, the left stellate ganglion was stimulated for 45 seconds. APD50 and APD90 decreased (from 153 +/- 15 to 145 +/- 16 msec, p less than 0.005, and from 176 +/- 18 to 165 +/- 13 msec, p less than 0.001, respectively). DAD were induced in 10 of 14 animals (71%) with a mean amplitude of 1.2 +/- 0.3 mV. These results show that DAD can be induced in vivo by administration of calcium and digitalis and by activation of the cardiac sympathetic nerves. This latter finding further strengthens the existing link between adrenergic activation and ventricular arrhythmogenesis and suggests triggered activity as a likely mechanism.