Surgical implications in the current treatment of Wolff-Parkinson-White syndrome.

There are currently two different surgical approaches to the abnormal pathway, Wolff-Parkinson-White (WPW) syndrome-the endocardial (ENDO) and epicardial (EPI) techniques. In recent years, ablation of accessory pathways can be achieved by catheter-induced radiofrequency (RF) current. This study was undertaken to assess our results of surgical treatment for WPW syndrome in the current era of catheter ablation. From 1985 to 1993, 51 patients (33 male and 18 female) with WPW syndrome underwent operations for ablation of accessory pathways. Associated anomalies included Ebstein's anomaly, coronary artery disease, and tricuspid atresia. Preoperatively, 6 patients underwent unsuccessful RF catheter ablation. Fifteen (29%) patients were operated with the ENDO technique and 36 (71%) with the EPI technique. There was no early death in either group. In the immediate postoperative period 40 (78%) patients were in sinus rhythm. The electrophysiological studies revealed successful ablation of the pathway in 50 (98%) patients. On complete late follow-up (mean, 36 months) all patients were back to preoperative levels of activity. Our experience indicates that excellent results can be achieved with each of these two techniques. The left free wall accessory pathways may be ablated in a more reproducible way with the ENDO approach. The concept that surgical ablation of accessory pathways may prevent further atrial fibrillation is supported by the low incidence in this series. Operations for WPW syndrome may become indicated for RF ablation failure, when additional procedures are required. In these cases the surgical skill should be available, and this is a skill that should not be lost.

Effects of intravenous dofetilide on induction of atrioventricular re-entrant tachycardia.

OBJECTIVE: To assess the efficacy and safety of intravenous dofetilide in preventing induction of atrioventricular re-entrant tachycardia. DESIGN: A multicentre, open, dose ranging trial. Fifty one patients with electrically inducible atrioventricular re-entrant tachycardia were allocated to one of five doses of dofetilide (1.5, 3, 6, 9, and 15 microgram/kg), two thirds of the dofetilide dose being given over a 15 minute loading period and the remainder over a 45 minute maintenance period. MAIN OUTCOME MEASURE: Responders were defined as patients in whom dofetilide prevented reinduction of atrioventricular re-entrant tachycardia at the end of the infusion. RESULTS: Intravenous dofetilide had no effect on tachycardia inducibility at the two lower doses (1.5 and 3 microgram/kg) but prevented the reinduction of tachycardia at the three higher doses (6, 9, and 15 microgram/kg) at a rate of 36% (11/31). There was a clear relation between plasma dofetilide concentrations and efficacy (p = 0.009). In non-responders, dofetilide increased the cycle length of induced atrioventricular re-entrant tachycardia. Dofetilide increased the atrial and ventricular effective refractory periods, as well as the antegrade and retrograde effective refractory period of the accessory pathway. Treatment related side effects were reported in four patients, one with a new sustained incessant supraventricular tachycardia. CONCLUSIONS: Dofetilide shows promise as an agent for the prevention of atrioventricular re-entrant tachycardia in patients without structural heart disease.

Time dependent variability of QT dispersion after acute myocardial infarction and its relation to ventricular fibrillation: a prospective study.

OBJECTIVE: To show whether increased QT dispersion on admission predicts ventricular fibrillation after acute myocardial infarction, and to determine the nature of time related changes in QT dispersion. DESIGN: Prospective cohort study. SETTING: Coronary care units of three teaching hospitals in Newcastle-upon-Tyne over an eight month period. PATIENTS: All had acute myocardial infarction according to World Health Organization criteria. INTERVENTIONS: For all patients, QT dispersion (QTd) and Bazett rate corrected QTc dispersion (QTcd) were measured from a high quality 12 lead ECG recorded on admission at a paper speed of 50 mm/s. In a subset, serial ECGs were recorded regularly to show time related changes in QTcd following acute myocardial infarction. MAIN OUTCOME MEASURES: Occurrence of ventricular fibrillation within the first 24 hours after myocardial infarction. RESULTS: Data collected from 201 patients, 12 of whom (6%) developed ventricular fibrillation within 24 hours. Neither QTd nor QTcd differed between those developing ventricular fibrillation and those who did not: QTd mean (SD), 74 (24) ms (95% confidence interval (CI) 59 to 89) v 66 (24) ms (95% CI 62 to 70), respectively; QTcd, 86 (26) ms(0.5) (95% CI 70 to 102) v 77 (29) ms(0.5) (95% CI 72 to 82), respectively. Significant QTcd changes occurred early after myocardial infarction. CONCLUSIONS: Admission QTd and QTcd do not predict ventricular fibrillation after acute myocardial infarction. There are significant changes in QTcd with time, which may account for this measured lack of correlation.

Thoracoscopic mapping and cryoablation of right ventricular tachycardia.

A 14-year-old girl with right ventricular dysplasia and recurrent drug refractory ventricular tachycardia underwent thoracoscopic mapping cryoablation. Good access to the right ventricular free wall was obtained. We suggest this technique may have an important role in the management of patients with right ventricular tachycardia.

Effects of surgery for postinfarction ventricular tachycardia on parameters of left ventricular function.

Heart failure is the leading cause of death in patients after surgery for ventricular tachycardia. This study examines the effects of antiarrhythmic surgery on 4 parameters of left ventricular (LV) function. Global ejection fraction, segmental wall motion score, homogeneity of contraction, and diastolic function were measured in 32 patients by technetium-99m radionuclide ventriculography. Ejection fraction was measured from the left anterior oblique image. Wall motion score was assessed semiquantitatively for 11 LV segments from 3 projections. Homogeneity of contraction was expressed as the SD of the LV phase analysis curve during systole from the left anterior oblique image. Diastolic function was expressed in terms of peak and mean first time derivative of the action potential (dV/dt) of the LV function curve. Subgroup analyses were performed to distinguish the effects of aneurysmectomy, coronary artery bypass grafting, and changes in angiotensin converting enzyme inhibitor therapy. Mean systolic function improved after surgery (ejection fraction 22% vs 32%, p <0001; wall motion score 20 vs 13, p <0.0001; phase analysis 18 vs 12, p <0.03). Mean diastolic function also improved (peak dV/dt 0.83 +/- 0.32 vs 1.49 +/- 0.39, p = 0.006; mean dV/dt 0.41 +/- 0.15 vs 0.76 +/- 0.27, p = 0.006). Improvements were not confined to those who had aneurysmectomy or coronary bypass grafting and were not explained by changes in vasodilator therapy. Thus, antiarrhythmic surgery does not inherently damage LV function. Significant improvements were observed in most patients. Failure to improve indicated a poor longer term prognosis.

Evaluation of antiarrhythmic drug efficacy in patients with an ICD: unlimited potential or replete with complexity and problems?

There are a number of novel ways in which implantable cardioverter defibrillator (ICD) endpoints can be used in clinical trials to evaluate antiarrhythmic drugs. The advances in ICD technology (storage, retrieval, and accurate interpretation of ICD electrograms) expand the potential to include the use of an ICD endpoint as a clinical surrogate for sudden death. The ICD also provides the necessary safety net to test new drugs. The frequent need for antiarrhythmic drugs in patients already fitted with an ICD (e.g., for atrial fibrillation) necessitates knowledge of the drugs' effect on defibrillator threshold. There are interpretative problems and challenges associated with all types of ICD trials. A particular difficult issue is the degree to which the results of data on antiarrhythmic drug efficacy and safety acquired in the context of an ICD endpoint trial might be extrapolated to patient populations in which the device is not used. These and other challenging issues are discussed, with the goal of enhancing the design and interpretation of clinical trials featuring ICD endpoints.

Evaluation of antiarrhythmic drug efficacy in patients with an ICD. Unlimited potential or replete with complexity and problems?

A report from a Study group, proposed by A. J. Camm, London, of the Working Groups on Arrhythmias and Cardiac Pacing of the European Society of Cardiology; co-sponsored by the North American Society of Pacing and Electrophysiology. The Study Group was convened on 29 August 1997 at Saltsjöbaden, near Stockholm. The meeting was chaired by A. J. Camm, London, and C. M. Pratt, Houston. Based on the presentation and discussions, a first draft of the documents was prepared by C. Pratt and J. Camm which was then circulated to all members three times for their review. All members of the Study Group approved the final manuscript. This report represents the opinion of the members of this Study Group and does not necessarily reflect the official position of either society.The meeting of the Study Group was made possible by unrestricted educational grants from Medtronic, Guidant, Proctor & Gamble, Berlex and Sanofi.Also, presented, in part, at the Cardio-Renal Drugs Advisory Board meeting of the Food and Drug Administration, Bethesda, Maryland, on 30 April 1999.

ESCWGA/NASPE/P experts consensus statement: living anatomy of the atrioventricular junctions. A guide to electrophysiologic mapping. Working Group of Arrhythmias of the European Society of Cardiology. North American Society of Pacing and Electrophysiology.

Current nomenclature for the AV junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with anteroposterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, whereas the mouth of the coronary sinus is shown as being posterior. Although this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and AV nodal reentry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology and from the North American Society of Pacing and Electrophysiology. It proposes a new, anatomically sound, nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value for description of the AV junctions and establish the principles of this new nomenclature.

Living anatomy of the atrioventricular junctions. A guide to electrophysiologic mapping. A Consensus Statement from the Cardiac Nomenclature Study Group, Working Group of Arrhythmias, European Society of Cardiology, and the Task Force on Cardiac Nomenclature from NASPE.

Current nomenclature for the atrioventricular (AV) junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with antero-posterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, although the mouth of the coronary sinus is shown as being posterior. Although this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and atrioventricular nodal reentry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. It proposes a new anatomically sound nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value for description of the AV junctions, establishing the principles of this new nomenclature.

Living anatomy of the atrioventricular junctions. A guide to electrophysiological mapping. A Consensus Statement from the Cardiac Nomenclature Study Group, Working Group of Arrythmias, European Society of Cardiology, and the Task Force on Cardiac Nomenclature from NASPE. North American Society of Pacing and Electrophysiology.

Current nomenclature for atrioventricular junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with antero-posterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, while the mouth of the coronary sinus is shown as being posterior. While this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and atrioventricular nodal re-entry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology, and the North American Society of Pacing and Electrophysiology. It proposes a new, anatomically sound, nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value as regards the description of the atrioventricular junctions, establishing the principles of this new nomenclature.

Surgery for postinfarction ventricular tachycardia in the pre-implantable cardioverter defibrillator era: early and long term outcomes in 100 consecutive patients.

OBJECTIVE: To report outcome following surgery for postinfarction ventricular tachycardia undertaken in patients before the use of implantable defibrillators. DESIGN: A retrospective review, with uniform patient selection criteria and surgical and mapping strategy throughout. Complete follow up. Long term death notification by OPCS (Office of Population Censuses and Statistics) registration. SETTING: Tertiary referral centre for arrhythmia management. PATIENTS: 100 consecutive postinfarction patients who underwent map guided endocardial resection at this hospital in the period 1981-91 for drug refractory ventricular tachyarrhythmias. RESULTS: Emergency surgery was required for intractable arrhythmias in 28 patients, and 32 had surgery within eight weeks of infarction ("early"). Surgery comprised endocardial resections in all, aneurysmectomy in 57, cryoablations in 26, and antiarrhythmic ventriculotomies in 11. Twenty five patients died < 30 days after surgery, 21 of cardiac failure. This high mortality reflects the type of patients included in the series. Only 12 received antiarrhythmic drugs after surgery. Perioperative mortality was related to preoperative left ventricular function and the context of surgery. Mortality rates for elective surgery more than eight weeks after infarction, early surgery, emergency surgery, and early emergency surgery were 18%, 31%, 46%, and 50%, respectively. Actuarial survival rates at one, three, five, and 10 years after surgery were 66%, 62%, 57%, and 35%. CONCLUSIONS: Surgery offers arrhythmia abolition at a risk proportional to the patient's preoperative risk of death from ventricular arrhythmias. The long term follow up results suggest a continuing role for surgery in selected patients even in the era of catheter ablation and implantable defibrillators.

Identifying patients at low risk of death from cardiac failure after operation for postinfarct ventricular tachycardia.

BACKGROUND: In unselected patients, cardiac failure accounted for most deaths after antiarrhythmic operation (ER) for postinfarction ventricular tachycardia (VT). This study aimed to determine whether patients at low risk of this outcome could be predicted from a retrospective analysis of variables from 100 consecutive ER patients. METHODS: Thirteen variables suggested by other researchers as predictive of outcome were analyzed. At the time of study, ER was the only therapy available for drug refractory VT. RESULTS: Only emergency ER, wall motion score less than 3 and Killip classification were significantly related to death from cardiac failure. The lack of correlation between emergency ER and variables of ER timing, VT less than 24 hours of ER or VT type implies that the need for emergency ER is also related to ventricular dysfunction. Multivariate analysis identified a group at particularly low risk of death with a specificity of 95%. CONCLUSIONS: Patients at low risk of death after ER can be identified prospectively. In the implantable cardioverter defibrillator era, elective ER is best reserved for such patients. Emergency ER may still be justified in younger patients without comorbidity who will die of VT without it.

Efficacy of new 5-nitroimidazoles against metronidazole-susceptible and -resistant Giardia, Trichomonas, and Entamoeba spp.

The efficacies of 12 5-nitroimidazole compounds and 1 previously described lactam-substituted nitroimidazole with antiparasitic activity, synthesized via SRN1 and subsequent reactions, were assayed against the protozoan parasites Giardia duodenalis, Trichomonas vaginalis, and Entamoeba histolytica. Two metronidazole-sensitive lines and two metronidazole-resistant lines of Giardia and one line each of metronidazole-sensitive and -resistant Trichomonas were tested. All except one of the compounds were as effective or more effective than metronidazole against Giardia and Trichomonas, but none was as effective overall as the previously described 2-lactam-substituted 5-nitroimidazole. None of the compounds was markedly more effective than metronidazole against Entamoeba. Significant cross-resistance between most of the drugs tested and metronidazole was evident among metronidazole-resistant lines of Giardia and Trichomonas. However, some drugs were lethal to metronidazole-resistant Giardia and had minimum lethal concentrations similar to that of metronidazole for drug-susceptible parasites. This study emphasizes the potential in developing new nitroimidazole drugs which are more effective than metronidazole and which may prove to be useful clinical alternatives to metronidazole.

Atrial flutter.

Atrial flutter is a specific electrical entity. It has a now well-established mechanism involving a single macro-re-entrant circuit. Whilst many patients with atrial flutter may develop atrial fibrillation, atrial flutter deserves its own recognition and requires specific management. Acute termination by drugs is possible, although adding pacing improves efficacy. Ibutilide is a new intravenous therapy with considerable efficacy by with a risk of torsade de pointes. For long-term control, radiofrequency ablation is gradually supplanting chronic oral antiarrhythmic strategies.

Atrial fibrillation.

The anatomy, mechanism, presentation and prevalence of atrial fibrillation are now relatively well-established. The arrhythmia can be categorized in many ways, although for the clinician, the grouping into paroxysmal, persistent and permanent has many attractions. For each of these categories, a management strategy is becoming clearer, although there are still considerable deficiencies in our knowledge, particularly in such areas as optimized rate control, medical cardioversion and the use of AV node ablation. These are being addressed by ongoing studies. With their results, we will be closed to an ideal management strategy that will offer the best of rhythm management and the greatest protection from thromboembolism.

Management strategies for a better outcome in unstable coronary artery disease.

Unstable coronary artery disease is a term encompassing both unstable angina and non-Q-wave (non-ST-segment elevation) myocardial infarction. Patients with these conditions are at risk of early progression to acute myocardial infarction and death. Thus, management of these conditions must aim to reduce long-term mortality and morbidity. Risk stratification is crucial for the identification of patients whose risk of early progression is high; they may require coronary angiography and (if suitable) either percutaneous transluminal coronary angioplasty or coronary artery bypass surgery. No single variable can accurately predict risk, but considerable data are emerging to show that biochemical markers of myocardial injury, such as troponin-T and troponin-I, are valuable in combination with electrocardiographic findings and clinical features. Routine early invasive procedures (coronary angiography with or without revascularization) have not yet been shown to have any significant advantage over conservative regimens for the majority of patients. Antiplatelet, anticoagulant, and anti-ischemic agents remain the mainstay of treatment in the acute phase. New agents, such as glycoprotein IIb/IIIa receptor inhibitors and low-molecular-weight heparins, as well as antithrombins and Factor Xa inhibitors add to the treatments currently available. Thrombolytic agents are contraindicated in the absence of ST-segment elevation. After clinical stabilization, ongoing assessment should include exercise testing for all patients who are able; other imaging techniques should be used for patients unable to exercise. A profile indicating a high risk of future events is an indication for elective angiography and consideration for revascularization.