Treatment of atrial tachycardia arising after superior transseptal approach mitral valve surgery: Insights from ultra-high-density mapping to prevent atrioventricular block.

INTRODUCTION: Mitral valve surgery employing a superior transseptal approach (STA) is associated with arrhythmogenicity and intra-atrial conduction delay, despite being optimal for visualization of the surgical field. It is sometimes difficult to treat atrial tachycardias (AT) that arise after STA. To investigate AT circuits that arise after STA in detail in order to identify the optimal ablation line, using ultra-high-resolution mapping (UHRM). METHODS: We retrospectively analyzed 12 AT from 10 patients (median age 70 years, nine males) who had undergone STA surgery. The tachycardias were mapped using the Rhythmia mapping system (Boston Scientific, Natick, Massachusetts). RESULTS: The 12 STA-related AT (STA-AT) circuits were classifiable as follows according to location of the optimal ablation line: (1) peri-septal incision STA-AT (n = 3), (2) cavotricuspid isthmus (CTI) dependent STA-AT (n = 7), and (3) biatrial tachycardia (n = 2). Radiofrequency (RF) application terminated 11 of the 12 STA-AT. We found that difference in STA-AT circuit type was due to characteristics of the septal incision line made for STA. UHRM was important in identifying optimal ablation sites that did not create additional conduction disturbances in the right atrium (RA). CONCLUSIONS: ATs after STA involve complex arrhythmia circuits due to multiple and long incision lines in the RA. Accurate understanding of the arrhythmia circuit and sinus conduction in the RA after STA is recommended for treating post-surgical tachycardia in a minimally invasive manner.

Noninvasive light emitting diode therapy: A novel approach for postinfarction ventricular arrhythmias and neuroimmune modulation.

BACKGROUND: Sympathetic neural activation plays a key role in the incidence and maintenance of acute myocardial infarction (AMI) induced ventricular arrhythmia (VA). Furthermore, previous studies showed that AMI might induce microglia and sympathetic activation and that microglial activation might contribute to sympathetic activation. Recently, studies showed that light emitting diode (LED) therapy might attenuate microglial activation. Therefore, we hypothesized that LED therapy might reduce AMI-induced VA by attenuating microglia and sympathetic activation. METHODS: Thirty anesthetized rats were randomly divided into three groups: the Control group (n = 6), AMI group (n = 12), and AMI + LED group (n = 12). Electrocardiogram (ECG) and left stellate ganglion (LSG) neural activity were continuously recorded. The incidence of VAs was recorded during the first hour after AMI. Furthermore, we sampled the brain and myocardium tissue of the different groups to examine the microglial activation and expression of nerve growth factor (NGF), interleukin-18 (IL-18), and IL-1ß, respectively. RESULTS: Compared to the AMI group, LED therapy significantly reduced the incidence of AMI-induced VAs (ventricular premature beats [VPB] number: 85.08 ± 13.91 vs 27.5 ± 9.168, P < .01; nonsustained ventricular tachycardia (nSVT) duration: 34.39 ± 8.562 vs 9.005 ± 3.442, P < .05; nSVT number: 18.92 ± 4.52 vs 7.583 ± 3.019, P < .05; incidence rate of SVT/VF: 58.33% vs. 8.33%, P < .05) and reduced the LSG neural activity (P < .01) in the AMI + LED group. Furthermore, LED significantly attenuated microglial activation and reduced IL-18, IL-1ß, and NGF expression in the peri-infarct myocardium. CONCLUSION: LED therapy may protect against AMI-induced VAs by suppressing sympathetic neural activity and the inflammatory response.

Analyses of the Mode of Termination During Diagnostic Ventricular Pacing to Differentiate the Mechanisms of Supraventricular Tachycardias.

OBJECTIVES: The goal of this study was to determine the diagnostic yield of analyzing the mode of termination during ventricular overdrive pacing (VOP) to differentiate the mechanisms of supraventricular tachycardias (SVTs). BACKGROUND: The majority of the diagnostic criteria for VOP rely on successful entrainment, but termination of SVTs is common during VOP. METHODS: We studied 225 SVTs with a 1:1 atrioventricular relationship, including 34 atrial tachycardias, 67 orthodromic reciprocating tachycardias (ORTs) (including 4 ORTs using accessory pathways [APs] with decremental properties), and 124 atrioventricular nodal re-entrant tachycardias. The total pacing prematurity (TPP) needed to reset or terminate the SVT was calculated by using a simplified method, and the post-pacing interval minus the tachycardia cycle length (PPI - TCL) was predicted from the TPP. RESULTS: VOP terminated 87 SVTs (39%). No atrial tachycardias were terminated by VOP in this study. SVT termination occurred after (n = 71) or before (n = 16) atrial resetting. The predicted PPI - TCL was highly correlated with the measured PPI - TCL (r = 0.96; p < 0.001). The TPP had diagnostic accuracy equivalent to the predicted PPI - TCL. The TPP was measurable irrespective of the termination mode and correctly diagnosed ORTs with decremental APs. All ORTs using septal APs and no atrioventricular nodal re-entrant tachycardias had a TPP <125 ms. Considering other criteria evaluable in terminated SVTs, a combined criteria of a TPP <125 ms and atrial capture/termination within the fusion period were specific for ORTs using free-wall APs, except for left anterolateral/lateral sites. CONCLUSIONS: The termination analyses were useful for differential diagnoses of SVTs terminated during VOP.

Meta-analysis of randomized controlled trials on magnesium in addition to beta-blocker for prevention of postoperative atrial arrhythmias after coronary artery bypass grafting.

BACKGROUND: Atrial arrhythmia (AA) is the most common complication after coronary artery bypass grafting (CABG). Only beta-blockers and amiodarone have been convincingly shown to decrease its incidence. The effectiveness of magnesium on this complication is still controversial. This meta-analysis was performed to evaluate the effect of magnesium as a sole or adjuvant agent in addition to beta-blocker on suppressing postoperative AA after CABG. METHODS: We searched the PubMed, Medline, ISI Web of Knowledge, Cochrane library databases and online clinical trial database up to May 2012. We used random effects model when there was significant heterogeneity between trials and fixed effects model when heterogeneity was negligible. RESULTS: Five randomized controlled trials were identified, enrolling a total of 1251 patients. The combination of magnesium and beta-blocker did not significantly decrease the incidence of postoperative AA after CABG versus beta-blocker alone (odds ratio (OR) 1.12, 95% confidence interval (CI) 0.86-1.47, P = 0.40). Magnesium in addition to beta-blocker did not significantly affect LOS (weighted mean difference -0.14 days of stay, 95% CI -0.58 to 0.29, P = 0.24) or the overall mortality (OR 0.59, 95% CI 0.08-4.56, P = 0.62). However the risk of postoperative adverse events was higher in the combination of magnesium and beta-blocker group than beta-blocker alone (OR 2.80, 95% CI 1.66-4.71, P = 0.0001). CONCLUSIONS: This meta-analysis offers the more definitive evidence against the prophylactic administration of intravenous magnesium for prevention of AA after CABG when beta-blockers are routinely administered, and shows an association with more adverse events in those people who received magnesium.

Electrophysiological predictors of propafenone efficacy in prevention of atrioventricular nodal re-entrant and atrioventricular re-entrant tachycardia.

AIM: To assess the efficacy of propafenone in prevention of atrioventricular nodal reentrant tachycardia (AVNRT) and orthodromic atrioventricular tachycardia (AVRT) based on the clinical results of arrhythmia recurrence and find the electrophysiological predictor of propafenone effectiveness. METHODS: This retrospective study included 44 participants in a 12-month period, who were divided in two groups: group A - in which propafenone caused complete ventriculo-atrial block and group B - in which propafenone did not cause complete ventriculo-atrial block. RESULTS: Group A had significantly lower incidence of tachycardia than group B (95% vs 70.8%, P=0.038), and complete ventriculo-atrial block predicted the efficacy of propafenone oral therapy in the prevention of tachycardia (sensitivity 87.5%, specificity 52.8%, positive predictive value 95%, negative predictive value 29.2%). Patients with AVNRT in group B who did not experience the recurrences of tachycardia had significantly shorter echo zone before intravenous administration of propafenone than the patients who experienced episodes of sustained tachycardia (median 40 ms [range 15-60 ms] vs 79 ms [range 50-180 ms], P=0.008). CONCLUSION: In patients with non-inducible tachycardia, complete ventriculo-atrial block can be used as an electrophysiological predictor of the efficacy of propafenone oral therapy in the prevention of tachycardia. In patients with non-inducible AVNRT, but without complete ventriculo-atrial block, propafenone was more effective in patients with shorter echo zone of tachycardia.

Pseudo SVT in the pacemaker patient.

This is an interesting report of a supraventricular tachycardia in a paced patient with intermittent atrioventricular nodal block. Only electrophysiology testing revealed the correct diagnosis. Images explain how pacemaker timing cycles and refractory periods can confuse an otherwise straightforward diagnosis.

Induced atrial tachycardia after circumferential pulmonary vein isolation of paroxysmal atrial fibrillation: electrophysiological characteristics and impact of catheter ablation on the follow-up results.

INTRODUCTION: Atrial tachycardia (AT), including focal and reentrant AT, can occur after circumferential pulmonary vein isolation (CPVI). The aim of this study was to investigate the electrophysiological characteristics of induced AT and its clinical outcome. METHODS AND RESULTS: In our series of 160 patients with paroxysmal atrial fibrillation (AF), 45 ATs were induced by high-current burst pacing after CPVI in 26 patients. All induced ATs were mapped using a three-dimensional (3D) mapping system. Noninducibility was the endpoint of the ablation of the AT. Gap-related AT was considered if the AT was related to the CPVI lesions. A 16-slice multidetector computed tomography scan was performed in all patients to correlate the anatomical structure with electroanatomical mapping. Thirty-five (78%) reentrant ATs and 10 (22%) focal ATs were identified. Of those, 34 were gap-related ATs (24 reentrant and 10 focal ATs). Reentrant AT had more gaps in the left atrial appendage ridge than did focal AT (39.6% vs 0%, P = 0.02). Focal AT had a higher incidence of gap in the PV carina compared with reentrant AT (80% vs 10%, P < 0.001). Reentrant ATs were mostly terminated during the ablation creating the mitral and roof lines with crossing of the gaps. During a mean follow-up of 21 +/- 8 months, only one patient (0.6%) with induced mitral reentry had a recurrent AT. CONCLUSION: The location of the AT gap may be related with the complex anatomy of the LA. The induced ATs after CPVI can be eliminated by catheter ablation.

Pharmacologic prophylaxis for postoperative atrial tachyarrhythmia in general thoracic surgery: evidence from randomized clinical trials.

BACKGROUND: Atrial tachyarrhythmia is the most common complication after general thoracic surgery and is associated with significant morbidity, longer hospital stay, and higher costs. We sought to determine whether the use of antiarrhythmic medications is associated with a reduced rate of postoperative atrial tachyarrhythmia. METHODS: MEDLINE, EMBASE, Cochrane Database of clinical trials (1980-2003), and reference lists of relevant articles were searched for randomized controlled trials with placebo control, general thoracic patients, and noncombined and prophylactic use of the medications. Search, data abstraction, and analyses were performed and confirmed by at least 2 authors. A fixed-effects model was used to perform meta-analyses. RESULTS: There were 11 unique trials (total n = 1294) that met the inclusion criteria. Calcium-channel blockers and beta-blockers reduced the risk of atrial tachyarrhythmia in 4 and 2 trials, respectively (relative risk of 0.50 and 95% confidence interval of 0.34-0.73; relative risk of 0.40 and 95% confidence interval of 0.17-0.95, respectively). However, beta-blockers tended to increase the risk of pulmonary edema (relative risk, 2.15; 95% confidence interval, 0.74-6.23). Magnesium tested in one unblinded trial also reduced the risk of atrial tachyarrhythmia (relative risk, 0.4; 95% confidence interval, 0.21-0.78). On the other hand, digitalis preparations were found to be harmful because they increased the risk of atrial tachyarrhythmia in 3 trials (relative risk, 1.51; 95% confidence interval, 1.00-2.28). Finally, 2 other medications, flecainide and amiodarone, were each tested in a single small trial, and their effects were associated with great uncertainty. CONCLUSIONS: Calcium-channel blockers and beta-blockers are effective in reducing postoperative atrial tachyarrhythmia. The use of these medications should be individualized, and possible adverse events of beta-blockers should be taken into account. Randomized clinical trials do not support the use of digitalis in general thoracic surgery. The value of magnesium as a supplement to a main prophylactic regimen should be explored.

Calcium antagonists reduce cardiovascular complications after cardiac surgery: a meta-analysis.

OBJECTIVES: We sought to determine the efficacy of calcium antagonists (CAs) in reducing death, myocardial infarction (MI), ischemia, and supraventricular tachyarrhythmia (SVT) after cardiac surgery. BACKGROUND: Calcium antagonists may reduce complications after cardiac surgery-namely, death, MI, and renal failure. However, they are underused, possibly due to the results from previous observational studies. METHODS: Both MEDLINE (1966 to December 2001) and EMBASE (1980 to December 2001) were searched, with supplementation by reference list searches. No language restrictions were applied. Included studies were randomized, controlled trials (RCTs) evaluating preoperative, intraoperative, or postoperative (first 48 h) CA use (intravenous or oral) during aortocoronary bypass or valve surgery. Studies were excluded if they exclusively recruited transplant recipients, individuals <18 years old, or patients with pre-existing SVT. Two reviewers independently evaluated study quality by using the Jadad score; a minimal score of 1/5 was required. Forty-one studies, encompassing 3,327 patients, were included. No studies assessed treatment exclusively with short-acting oral nifedipine. Treatment effects were calculated using the random-effects model. Heterogeneity was assessed using the Q test. RESULTS: Calcium antagonists significantly reduced MI (odds ratio [OR] 0.58, 95% confidence interval [CI] 0.37 to 0.91; p = 0.02) and ischemia (OR 0.53, 95% CI 0.39 to 0.72; p < 0.001). Non-dihydropyridines significantly reduced SVT (OR 0.62, 95% CI 0.41 to 0.93; p = 0.02). Calcium antagonists were associated with trends toward decreased mortality during aortocoronary bypass (OR 0.66, 95% CI 0.26 to 1.70, p = 0.4). CONCLUSIONS: Use of CAs during cardiac surgery significantly reduced rates of MI, ischemia, and SVT. Further study using large RCTs is justified.

A beta-blocker, not magnesium, is effective prophylaxis for atrial tachyarrhythmias after coronary artery bypass graft surgery.

OBJECTIVE: To evaluate magnesium as a sole or adjuvant agent with currently used prophylactic drugs in suppressing postoperative atrial tachyarrhythmias (POAT) after coronary artery bypass graft (CABG) surgery. DESIGN: Single-center prospective, randomized clinical trial. SETTING: University hospital. PARTICIPANTS: Patients (n = 400) undergoing CABG surgery. INTERVENTIONS: Patients were randomized among 6 prophylaxis regimens: (1) control (no antiarrhythmics), (2) magnesium only, (3) digoxin only, (4) magnesium and digoxin, (5) propranolol only, and (6) magnesium and propranolol. Patients randomized to a regimen including magnesium received 12 g given during 96 hours postoperatively. Patients in a digoxin regimen received 1 mg after cardiopulmonary bypass and 0.25 mg daily. Patients in a propranolol regimen received 1 mg intravenously every 6 hours until able to take 10 mg orally 4 times a day. Prophylaxis regimens were discontinued after 4 days postoperatively. MEASUREMENTS AND MAIN RESULTS: The primary outcome was a sustained POAT or discharge from the hospital. Control patients had an incidence of POAT (38%) not significantly different from patients in magnesium-only (38%), digoxin-only (31%), and magnesium with digoxin (37%) regimens. Patients treated with propranolol had a significant reduction in POAT. Nearly identical POAT rates in the propranolol-only (18%) and propranolol with magnesium (19%) groups support the lack of efficacy of magnesium in this trial. Study design allowed analysis of and showed a beta-blocker withdrawal effect in addition to suppressive benefit of postoperative beta-blockers. CONCLUSION: beta-Blocker prophylaxis is indicated to reduce the incidence of POAT in CABG surgery patients and to prevent a beta-blocker withdrawal effect in patients receiving these medications preoperatively. Digoxin and magnesium as sole or adjuvant agents do not offer suppressive or ventricular rate reduction benefits in POAT.

Magnesium substitution in elective coronary artery surgery: a double-blind clinical study.

Magnesium may be beneficial in the control of ventricular ectopy and supraventricular tachyarrhythmias after coronary artery bypass graft (CABG) surgery, but it is not known whether a high-dose magnesium regimen is superior to a regimen keeping the patient normomagnesemic. A prospective randomized and double-blind clinical comparison was performed in 81 elective CABG patients in order to assess the effects of two different magnesium infusion regimens on electrolyte balance and postoperative arrhythmias. Forty-one patients (high-dose group, H) received 4.2 +/- 0.7 g (mean +/- SD), of magnesium sulfate before cardiopulmonary bypass, followed by an infusion of 11.9 +/- 2.8 g of magnesium chloride until the first postoperative (PO) morning, and a further 5.5 +/- 1.0 g until the second PO morning. Forty patients (low-dose group, L) received magnesium sulfate only after bypass to a total of 2.9 +/- 0.5 g at the first, and 1.4 +/- 0.1 g at the second PO morning. A blood cardioplegia technique was used in both groups, including bolus doses of magnesium chloride to a total of 2.4 +/- 0.6 g and 2.3 +/- 0.6 g to H and L patients, respectively. Continuous Holter tape-recording was used for 12 to 15 hours preoperatively, and for 48 hours postoperatively. Serum magnesium peaked in H patients on the first PO morning at 1.60 +/- 0.25 mmol/L, whereafter it declined to the normal level on the third PO morning. Patients in the L group were normomagnesemic, except after the start of bypass.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effects of rotundium on clinical electrophysiology in patients with pre-excitation syndrome].

Acute electrophysiologic effects of rotundium were studied with programmed electrical cardiac stimulation in 14 patients with paroxysmal tachyarrhythmias due to preexcitation syndrome after intravenous infusion of 2 mg/kg. The results showed that the drug depressed the function of the atrioventricular node markedly. Significant lengthening of A-H interval (from 75 +/- 19ms to 88 +/- 21ms, P < 0.01), AVNERP (from 246 +/- 47ms to 290 +/- 45ms, P < 0.01), AVNWCL (from 326 +/- 23ms to 388 +/- 42ms, P < 0.01) were seen. But no significant influence on SNRT, CSNRT and SACT (P < 0.05) were observed. Rotundium lengthened A-delta interval (from 97 +/- 18 ms to 106 +/- 19ms, P < 0.05) and the anterograde effective refractory period (ERP) of the accessory pathway (from 287 +/- 36ms to 320 +/- 43ms P < 0.05). It slightly lengthened V-A interval and the retrograde ERP of the accessory pathway. Rotundium lengthened AERP significantly (from 216 +/- 37ms to 244 +/- 41ms, P < 0.02). The effective rate of prevention of supraventricular tachycardia (SVT) by PES in this study was 77.8% (7/9). Rotundium showed no severe side effect in this study.

Train stimulation at the atria for prevention of atrioventricular tachycardia: dependence on accessory pathway location.

In 12 patients with accessory pathway-mediated supraventricular tachycardia, programmed electrical stimulation with a rapid train of 10 stimuli was assessed for prevention of tachycardia induction. Tachycardia was induced with one or two extrastimuli from both the right and the left atrium (by way of the coronary sinus). Preventive train stimulation, with the train delivered after the tachycardia-initiating stimulus, was attempted at the site of tachycardia induction as well as at the opposite site. Prevention at the site of tachycardia induction was successful in all patients when the length of the train (90 ms) exceeded the effective refractory period of the tachycardia-initiating stimulus to achieve single atrial capture within the "preventive zone." However, in patients with a left-sided accessory pathway, preventive stimulation at the right atrium failed when tachycardia was induced from the coronary sinus because of interatrial conduction delay. It is concluded that train stimulation is an effective mode for supraventricular tachycardia prevention, yet the site of preventive stimulation should lie as close as possible to the anatomic site of the reentrant circuit to reduce interatrial conduction delay.