Abnormal Cardiac Innervation in Patients with Idiopathic Ventricular Fibrillation

BIFFI, M., et al .: Abnormal Cardiac Innervation in Patients with Idiopathic Ventricular Fibrillation. Idiopathic ventricular fibrillation (VF) is diagnosed in up to nearly 10% of survivors of out-of-hospital cardiac arrest. The arrhythmogenic substrate is unknown. This study examined the role of cardiac innervation as a possible contributor to this arrhythmia. Eight patients with idiopathic VF were compared with eight normal subjects (controls) by [¹²³] I metaiodobenzylguanidine SPECT (MIBG), measuring peak uptake, late uptake, and clearance of the nuclear tracer. The left ventricle was divided in 13 segments in the bull's-eye target plot. Peak and late MIBG uptake was increased in the anterolateral segments (2,3,7,8) compared to the inferoposterior and septal segments, in controls and in patients. No difference was observed between controls and patients in the inferoposterior and septal segments. In contrast, a significantly higher MIBG uptake was observed in patients compared to controls in the anterolateral segments (   94 ± 4%   vs   81 ± 11%, P < 0.03   for peak uptake;   94 ± 5%   vs   79 ± 12%, P < 0.01   for late uptake). No difference was observed in MIBG clearance in any segment in either study group. Cardiac sympathetic innervation is highly heterogeneous, though predominant in anterolateral segments in normal subjects. Patients with idiopathic VF exhibit the same distribution, though have a significantly greater density of sympathetic terminals in the anterolateral segments than controls, which may promote ventricular arrhythmias. (PACE 2003; 26[Pt. II]:357–360)     

Electrophysiological Evaluation of Sustained Ventricular Tachyarrhythmias in Idiopathic Dilated Cardiomyopathy

Sustained ventricular tachyarrhythmias and sudden death are particularly prevalent in patients with idiopathic dilated cardiomyopathy (IDC). In contrast to patients with ischemic heart disease, the value of electrophysiological stimulation (EPS) in patients with IDC has not yet been established. To clarify the role of EPS in these patients, we studied 19 patients (58 +/- 11 years) with IDC who had symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF). The mean left ventricular ejection fraction was 26 +/- 9%. Ten patients had survived out-of-hospital cardiac arrest, eight had documented sustained monomorphic VT and one patient had non-sustained VT associated with syncope. Thirteen of the 19 patients (68%) had their clinical ventricular tachyarrhythmias induced at EPS (12 VT, 1 VF). In nine of 13 patients (69%), the arrhythmias were subsequently suppressed during serial electrophysiological drug testing. During 17 +/- 11 months of follow-up, 10/19 (53%) patients experienced recurrence of their arrhythmias and nine out of 19 (47%) patients died; six died suddenly and three secondary to heart failure. There was no difference in arrhythmia recurrence between patients with and without inducible ventricular tachyarrhythmias at initial study. Furthermore, suppression of arrhythmia during serial testing did not predict outcome; recurrences were observed in five out of nine patients whose arrhythmias were suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reproducibility of Electrophysiological Testing During Antiarrhythmic Therapy for Ventricular Arrhythmias Unrelated to Coronary Artery Disease

Although electrophysiological studies are commonly used in the management of patients with ventricular tachycardia (VT), the reproducibility of these studies during therapy has not been established in patients in whom VT is associated with conditions other than coronary artery disease. Therefore, we performed confirmation studies during drug therapy in 60 patients (mean age 48 ± 18 years; 41 male) with sustained ventricular arrhythmias induced during initial study to assess the reproducibility of drug effect. The stimulation protocol used included the serial introduction of up to three premature ventricular stimuli during sinus rhythm and with ventricular pacing at two pacing rates. Rapid ventricular pacing techniques were also used. Antiarrhythmic drug efficacy was confirmed in 78% of patients. Sustained VT was induced at repeat electrophysiological study in 18% of patients daring antiarrhythmic therapy that had been felt to be effective on the basis of a single drug study. We conclude that electrophysiological study results during antiarrhythmic therapy exhibit significant day-to-day variability. Sustained VT can be induced during antiarrhythmic therapy previously determined to be effective by electrophysiological techniques in many patients.     

Ventricular Fibrillation Triggered during and after Radiofrequency Energy Delivery to the Site of Origin of Idiopathic Right Ventricular Outflow Tract Arrhythmia

We observed a case of idiopathic ventricular arrhythmias originating from the right ventricular outflow tract (RVOT). The origin of target premature ventricular contraction (PVC) and nonsustained ventricular tachycardia (VT) was within a wide low‐voltage area around the RVOT. During radiofrequency (RF) application to the site of arrhythmia origin, polymorphic VT and ventricular fibrillation were repeatedly triggered by new PVC that had developed near the site of ablation. This electrical storm persisted >30 minutes after cessation of RF current delivery, and was suppressed by additional RF applications to the site of origin of the new PVC.     

Excellent Long‐Term Reproducibility of the Electrophysiologic Efficacy of Quinidine in Patients with Idiopathic Ventricular Fibrillation and Brugada Syndrome

Background: Quinidine is very effective in preventing the reinduction of sustained ventricular fibrillation (VF) during electrophysiologic study (EPS) in patients with idiopathic VF and Brugada syndrome. However, there are no data on the long‐term reproducibility of this EP efficacy. Methods and Results: Nine patients (seven males and two females, aged 21–72 years), who suffered from aborted cardiac arrest (n = 8) or recurrent syncope (n = 1) due to Brugada syndrome (n = 5) or idiopathic VF (n = 4), comprised the study. All patients had inducible sustained VF at baseline that was prevented by quinidine therapy and underwent another EPS on medication after 1.7–23.6 (9.8 ± 6.8) years (>5 years in eight patients). Two patients underwent two late EPS on quinidine. The goal of repeat EPS on quinidine was to ensure persistent long‐term drug efficacy (n = 6) or to elucidate the reason of syncopal episodes during therapy (n = 3). The EPS protocol significantly evolved over the years as it became more aggressive (more pacing sites and/or more ventricular extrastimuli). All nine patients tolerated the medication well and had no recurrent documented arrhythmic events during long‐term follow‐up (mean 15 ± 7 years). No sustained ventricular tachyarrhythmias could be induced in any patient during repeat late EPS. In six patients, a more aggressive stimulation protocol could be tested at repeat EPS. Conclusion: The long‐term reproducibility of the EP efficacy of quinidine in patients with idiopathic VF and Brugada syndrome is excellent. EP‐guided quinidine therapy represents a valuable long‐term alternative to ICD therapy in these patients.     

Ventricular Fibrillation Induction Using Nonsynchronized Low Energy External Shock During Rapid Ventricular Pacing: Method of Induction When Fibrillation Mode of ICD Fails

Third-generation implantable cardioverter defibrillators (ICD) are frequently implanted with non-thoracotomy systems and provide noninvasive methods for electrical stimulation and ventricular fibrillation induction. These modalities facilitate postoperative testing of the ICD. Rapid right ventricular burst pacing via the defibrillator is commonly used for initiation of ventricular tachyarrhythmias. However, with the available third-generation devices, ventricular fibrillation (VF) induction may be impossible in up to 19% of the patients. In these cases, transvenous placement of a right ventricular catheter has been required to generate VF and appropriately evaluate the device. We report a new technique of noninvasive induction of VF using a low energy external nonsynchronized shock delivered during ICD fibrillation induction pacing. In three patients, after all efforts to induce VF by the Ventritex Cadence V-100 had failed, a 20 J nonsynchronized shock was delivered during rapid RV pacing. This resulted in VF on the first attempt in all patients. This noninvasive technique of VF initiation may provide a useful clinical approach to ICD testing that eliminates the costs and risks of an invasive procedure.     

Slowing of Ventricular Tachycardia as a Possible Endpoint for Serial Drug Testing at Electrophysiological Study

Certain patients who cannot be rendered noninducible by serial drug testing during electrophysiology study demonstrate significant slowing of their ventricular tachycardia rate with selected agents. We evaluated the characteristics and outcome of 19 such patients to assess whether this slowing could be considered an acceptable endpoint for treatment. This group consisted of 14 males and 5 females (mean age 63 +/- 9) with a mean ejection fraction of 28 +/- 13% and inducible sustained ventricular tachycardia. Sixteen patients had known coronary artery disease and 13 had prior myocardial infarction. The other three patients had idiopathic cardiomyopathy. Serial drug testing during an electrophysiology protocol that used up to three extrastimuli at two or three cycle lengths at two right ventricular sites was used to select a medication regimen that provided optimal ventricular tachycardia slowing without limiting side effects. Five patients were treated with amiodarone, three with Ic agents (all with ejection fraction greater than 30%), and the remainder with Ia and Ib agents alone or in combination. Mean initial ventricular tachycardia rate was 219 +/- 26 beats/min with posttreatment ventricular tachycardia rate 137 +/- 17 (mean initial cycle length 278 +/- 35 msec, posttreatment 443 +/- 53 msec). Two groups were identified, those who had recurrent (although well-tolerated) ventricular tachycardia (group I, n = 8, mean time to recurrence = 15 months), and those who did not (group II, n = 11, mean follow-up 22 months). Overall sudden death rate was 5%, while total mortality was 11% (all mortality in group I).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of Coronary Artery Bypass Grafting on Ventricular Arrhythmias: Results with Electrophysiological Testing and Long-Term Follow-Up

Myocardial revascularization was performed in 56 patients with coronary artery disease who presented with ventricular tachycardia (VT) (n = 39) or ventricular fibrillation (n = 17). There were 46 men and 10 women, aged 65 ± 10 years. Three vessel (n = 42) or left main disease (n = 4) was present in 82%. Left ventricular ejection fraction averaged 36%± 11%. Electrophysioiogical studies were performed preoperatively in all patients; 50 (89%) had inducible ventricular arrhythmias. Sustained monomorphic VT was induced in 40 patients (cycle length 284 ± 61 msec). Reproducible symptomatic nonsustained VT was induced in four patients and ventricular fibrillation in six patients, while six patients had no inducible arrhythmia. Preoperatively the patients with inducible VT failed 3.3 ± 1.2 drug trials during electrophysiological studies. In addition to coronary bypass, 22 patients also received an automatic implantable cardioverter defibrillator (ICD), 26 patients received prophylactic ICD patches, and 1 patient had resection of a false aneurysm. There were no perioperative deaths. Postoperative electrophysiological studies were performed in all 56 surgical survivors. Ventricular tachyarrhythmia could not be induced in the six patients who had no inducible VT preoperatively and in 13 of 40 (33%) with preoperatively inducible sustained VT or in 19 of 50 (38%) patients with any previously inducible ventricular arrhythmia, thus a totaJ of 25 patients (45%) had no inducible VT postoperatively. Of the remaining, 11 patients were treated with antiarrhythmic drugs alone, 11 had already received an ICD (combined with drugs in 7), and another 9 received the ICD postoperatively (combined with drugs in 4). At a mean foJJow-up of 28 ± 21 months there were 11 deaths (20%): 2 sudden, 5 nonsudden cardiac, and 4 noncardiac deaths. There were 16 nonfatal VT recurrences (29%): 14 among patients with persistently inducible arrhythmias, and onJy 2 among those with no inducible arrhythmia postoperatively (P = 0.004); 13 occurred in patients with an ICD (P = 0.01). Thus among these patients with malignant ventricular arrhythmias who underwent revascuJarization, 45% had no inducible arrhythmia postoperatively with 33% of those with preoperatively inducible sustained VT apparently rendered noninducible by revascularization, while the majority (70%) remained free of major arrhythmic events during long-term follow-up. We conclude that myocardial revascularization alone can result in no ventricular arrhythmia induction in selected patients with VT inducible prior to surgery. Long-term follow-up of such patients indicates a low sudden death and arrhythmia recurrence rate. Furthermore, in patients with persistently inducible ventricular tachyarrhythmias after coronary revascuJarization, the sudden death rate is low despite a high frequency of nonfatal arrhythmia recurrence when antiarrhythmic medications are guided by programmed stimulation or an ICD is used.     

Cellular and Tissue Responses to Recurrent Ventricular Tachycardia and Fibrillation

The effects of rapid rhythms on cellular electrical activity depend on the rate of the rhythm, the cell type, and its condition prior to the arrhythmia. Rapid rates can cause major changes in transmembrane ion concentration gradients and the magnitude of these is a function of the transport capacity of the sodium-potassium pump. Thus digitalis can be expected to exert a prominent effect on rate-induced changes. Some of the rate-induced changes can lead to the generation of arrhythmias, as through calcium overload and the development of delayed afterdepolarizations. Since the actions of antiarrhythmic drugs often show use-dependence, the presence in the heart of local anesthetics or certain slow channel blockers will further modify the effect of rapid and irregular rhythms on cellular electrical activity.     

Idiopathic Left Ventricular Tachycardia: New Insights, into Electrophysiological Characteristics and Radiofrequency Catheter Ablation

KOTTKAMP, H., et.al .: Idiopathic Left Ventricular Tachycardia: New Insights into Electrophysiological Characteristics and Radiofrequency Catheter Ablation . Objectives: This study was performed to investigate the electrophysiological characteristics of idiopathic left ventricular tachycardia and to determine the feasibility of radiofrequency catheter ablation for nonpharmacological cure. Background: The underlying electrophysiological mechanism of idiopathic left ventricular tachycardia with right bundle branch block morphology and left-axis deviation is presently not known. Additionally, only limited data describing the results of radiofrequency catheter ablation for treatment of idiopathic left ventricular tachycardia so far exist. Methods: Electrophysiological studies and radiofrequency catheter ablation were performed in 5 patients (3 male and 2 female, mean age 31 ± 10 years) with idiopathic left ventricular tachycardia (cycle length 376 ± 72 msec). The patients had a history of recurrent palpitations of 4 ± 1 years and had been treated unsuccessfully with 2 ± 1 antiarrhythmic drugs. Sustained ventricular tachycardia with right bundle branch block morphology and left- or right-axis deviation was documented in all patients. Results: Inducibility with critically timed ventricular extrastimuli, inverse relationships of the coupling interval of the initiating extrastimulus and the interval to the first beat of the tachycardia, continuous diastolic or mid-diastolic electrical activity during ventricular tachycardia, and fragmented late potentials during sinus rhythm suggested reentrant activation as the underlying mechanism in three patients. On the other hand, induction dependent on isoproterenol infusion and rapid ventricular pacing and exercise inducibility indicated different electrophysiological characteristics in the remaining two patients. During electrophysiological study, intravenous verapamil terminated ventricular tachycardia in all patients, whereas ventricular tachycardia did not respond to intravenous adenosine, autonomic maneuvers, or intravenous β-blocking agent esmolol. Catheter mapping revealed earliest endocardial activation during ventricular tachycardia in different areas of the left ventricular septum being distributed from the base to the midapical portion of the septum in all patients. In 4 of 5 patients, radiofrequency catheter ablation (median number of pulses 4, range 1–9) resulted in complete abolition of idiopathic left ventricular tachycardia during a follow-up of 4–43 months (median 10) without antiarrhythmic drugs. Successful target sites for catheter ablation included continuous diastolic or mid-diastolic electrical activity during ventricular tachycardia and late potentials during sinus rhythm (2 patients), polyphasic fragmented presystolic potentials during ventricular tachycardia (1 patient), and pace mapping with identical QRS morphology compared to the ventricular tachycardia and “earliest” detectable activity during tachycardia (1 patient). No procedure related complications occurred. Conclusions: Two different patterns of electrophysiological properties of idiopathic left ventricular tachycardia were observed, indicating that this arrhythmia entity does not represent a homogeneous group. The “origin” of the tachycardias as identified by successful radiofrequency catheter ablation was located in different areas of the left ventricular septum and was distributed from the base to the mid-apical region. Radiofrequency catheter ablation was an effective and safe treatment modality in most of these patients. Distinct target site characteristics for successful catheter ablation including polyphasic diastolic activity during tachycardia and fragmented late potentials during sinus rhythm could be identified.     

How Do Physicians Determine When to Perform an "On-Drug" Electrophysiology Study for Efficacy Determination in Patients with Sustained Ventricular Tachyarrhythmias: A Previously Unaddressed Variable That May Affect Efficacy Rates

In patients with ventricular tachyarrhythmias, efficacy rates of antiarrhythmic agents, as judged by serial electrophysiological (EP) tests, have been variable. Factors underlying this variability have been reported to include: specific drug, type of arrhythmia, type of heart disease, left ventricular function, and number of prior drug failures. We hypothesized that variability in physician practice behavior as to when a drug assessment is performed might be another important factor affecting drug efficacy. Using a survey sent to 103 electrophysiology centers we determined from the 46 respondents that this is indeed the case. Twenty-six of the 46 respondents always, 9 of 46 sometimes, and 11 of 46 did not require ectopy reduction on continuous electrocardiographic monitoring before proceeding to an EP study. The ectopy reduction required, however, varies among physicians in percentage and type. Twenty-seven of the 35 respondents who utilize rhythm monitoring also require attainment of an acceptable blood level, a prespecified minimal target dose, and/or one or more ECG interval changes prior to proceeding to EP testing. Fifteen out of 46 do not require "therapeutic" drug levels. Of 11 who don't use rhythm monitoring, 5 also don't use blood levels. The lower value for "therapeutic ranges" varied by up to 3-fold and the upper value by up to 2 1/2-fold for individual drugs. The minimum time for testing varied from 1 half-life to over 10 half-lives. Similarly, the response to failure of a submaximal dose also varied: 9% always retested at a high dose, 2% never tested at a higher dose, and 91 % were inconsistent. Moreover, what was considered the maximal dose for an individual drug varied by 3- to 6- fold for most agents queried. We believe these variations in dose, time, and coassessment factors must have an influence on efficacy rates of antiarrhythmic agents.     

Amiodarone in the Management of Patients with Ventricular Tachycardia and Ventricular Fibrillation

Fifty-eight patients with symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF) were treated with amiodarone. All had clinical episodes of VT/VF or inducible VT during electropharmacologic testing despite treatment with maximumtolerated doses of conventional antiarrhythmic agents. Chronic treatment with amiodarone was begun at a dose of 800–1000 mg per day. Thirty-two patients were also treated with a previously ineffective conventional agent. Thirty patients underwent programmed ventricular stimulation after 2.6 ± 1.7 months (mean ± S. D.) of treatment with amiodarone at a mean daily dose of 588 ± 155 mg. VT was induced in 25 patients (sustained in 20, nonsustained in five). Seventeen patients had a recurrence of VT or VF after 0.5–9 months of treatment with amiodarone (fatal in seven, non-fatal in 10). Forty-one patients (71%) had no recurrence of symptomatic VT or VF while being treated with amiodarone (mean follow-up period, 17.1 ± 12.4 months). Among the 25 patients who had inducible VT with programmed ventricular stimulation while being treated with amiodarone, 19 patients (76%) have had no recurrence of symptomatic VT or VF overa follow-up period of 21.5 ± 7.3 months. Ambulatory electrocardiographic recordings obtained after one week of treatment with amiodarone were not helpful in predicting clinical response. Twenty-two patients (38%) developed ataxia and/or an intention tremor which improved with a decrease in the amiodarone dose. Amiodarone, either by itself or in combination with conventional antiarrhythmic drugs, has a significant therapeutic effect in high risk patients with refractory VT. The finding of inducible VT during electropharmacologic testing in patients taking amiodarone does not preclude a favorable clinical response. Neurologic toxicity is common in patients treated with 600–800 mg per day of amiodarone.     

The Repetitive Ventricular Response: Relationship to Ventricular Fibrillation Threshold in Dogs

The experiments investigated the hypothesis that the occurrence of repetitive ventricular responses elicited by the ventricular extrasystole (VES) technique are an indicator of ventricular vulnerability to fibrillation, A comparison was made between the incidence of repetitive responses elicited by the VES technique and the minimum electrical energy (VFT technique) necessary to elicit repetitive responses and ventricular fibrillation in normal dogs, dogs with acute infarction, and dogs with chronic infarction. The VES technique produced repetitive responses in 14 of 46 sites. Responses were of at least three types: (1) bundle branch re-entry: (2) activation at the pacing site, and (3) activation at the infarct zone. In contrast repetitive responses and the onset of fibrillation produced by the VFT technique appeared to be a single type with earliest activation at the pacing site. There were no differences in the ventricular fibrillation thresholds between dogs with and without repetitive responses produced by the VES technique. Thus the incidence of VES technique-induced repetitive responses is not a reasonable predictor of ventricular vulnerability to fibrillation. However, in 2 dogs with lòwer ventricular fibrillation thresholds, repetitive responses originating at the infarct zone were induced by the VES technique. Occurrence of these repetitive responses may be indicative of ventricular vulnerability to fibrillation.     

Promotion of Ventricular Tachycardia Induction by Procainamide in Dogs with Inducible Ventricular Fibrillation Late After Myocardial Infarction

The influence of procainamide on inducible ventricular tachyarrhythmias was evaluated in 35 dogs with experimental myocardial infarction, and 9 normal dogs. Programmed stimulation was performed from the right ventricular apex via a percutaneously positioned electrode catheter, using up to five extrastimuli before and after intravenous administration of procainamide (15 mg/kg). Procainamide levels in postinfarct dogs were 8.5 +/- 0.7 micrograms/mL (range 5.3-13.6 micrograms/mL). Procainamide exerted its greatest effect in postinfarct dogs with reproducible baseline ventricular fibrillation. Six of nine dogs (P less than 0.05) with ventricular fibrillation had sustained monomorphic ventricular tachycardia (cycle length: 147 +/- 4 msec) induced after procainamide administration. This ventricular tachycardia required significantly more extrastimuli than baseline ventricular fibrillation (3 +/- 0.3 extrastimuli before vs 4 +/- 0.3 extrastimuli after procainamide). Procainamide never converted ventricular fibrillation to ventricular tachycardia in normal dogs. Procainamide had minimal effect on inducible ventricular tachycardia after myocardial infarction. Ventricular tachycardia induction was abolished in only 2 of 17 dogs despite significant prolongation of electrophysiological parameters. Ventricular tachycardia cycle length, and the number of extrastimuli required were unchanged by procainamide in this subgroup. Conclusion: Ventricular tachycardia is insensitive to the antiarrhythmic properties of procainamide in this model. In contrast, procainamide is able to convert postinfarction ventricular fibrillation to ventricular tachycardia, presumably by promoting sustained, organized reentry. This previously undescribed action is an unusual form of proarrhythmic effect, and suggests that this drug should be used cautiously in patients after myocardial infarction.     

Successful Prevention of Recurrent Ventricular Fibrillation by Intravenous Isoproterenol in a Patient with Brugada Syndrome

TANAKA, H., et al. : Successful Prevention of Recurrent Ventricular Fibrillation by Intravenous Isoproterenol in a Patient with Brugada Syndrome. Intravenous administration of isoproterenol restored the ST-segment configuration to nearly normal in the right precordial leads and completely prevented spontaneous VF attacks in a patient with Brugada syndrome. The formation of a Brugada-type ECG has been attributed to the transmural dispersion of repolarization of the right ventricular epicardium and related to modulation of the autonomic nervous system. Our case may provide clues to the pathophysiological mechanism of this syndrome.     

Simultaneous Recording of Atrial and Ventricular Monophasic Action Potentials: Monophasic Action Potential Duration During Atrial Pacing, Ventricular Pacing, and Ventricular Fibrillation

A newly developed transvenous suction electrode was used in dogs to record monophasic action potentials (MAPs) from the right atrium and right ventricle simultaneously. Continuous MAP recordings could be made from the same endocardial site for test periods of 1.5 hours. Left ventricular pacing at increasing heart rates resulted in a statistically significant decrease of right ventricular MAP duration. A high degree of correlation was found between right ventricular MAP duration at 90% of repolarization and the QT interval during both right atrial and left ventricular pacing. At the onset of ventricular fibrillation (VF), right ventricular MAP duration shortened to 25% of the value obtained during left ventricular pacing at a cycle length of 250 ms. A cyclic alternation in amplitude of the right ventricular MAPs was observed during VF. Fast Fourier Transform Analysis of right ventricular MAPs during VF showed a significant dominant frequency at 12 Hz, with no levels of interest beyond this frequency. This observation might prove to be useful in elaborating a new algorithm for the automatic detection of ventricular fibrillation.     

Atrial Electrophysiological Features in Patients with Wolff-Parkinson-White and Atrial Fibrillation: Absence of Rate Adaptation of Intraatrial Conduction Time Parameters

Clinical electrophysiology has not yet clearly defined atrial features that can predict spontaneous occurrence of atrial fibrillation (AF). The aim of this work was to identify atrial electrophysiological features that can distinguish Wolff-Parkinson-White patients with spontaneous AF from those without this arrhythmia. Sixty-nine patients with Wolff-Parkinson-White were divided into three groups: group I (16 patients) with spontaneous AF; group II (35 patients) with reciprocating tachycardia but not AF; and group III (18 patients) asymptomatic without documented arrhythmias. Atrial effective refractory periods (ERPs) and intraatrial conduction times in response to premature extrastimuli were analyzed. The latter were evaluated as the A₁A₂ interval minus the correspondent S₁S₂ interval (A₁A₂-S₁S₂), S₂A₂ and the interval A₁A₂ following the shortest S₁S₂ producing atrial activation (FRP'). All the parameters have been evaluated in two atrial sites and at two atrial pacing cycle lengths (600 and 400 ms). For all the parameters, the difference (“gradient”) was calculated between the values of the same parameter measured at the atrial pacing cycle length of 600 ms and that found at the atrial pacing cycle length of 400 ms in the same recording site in each patient was calculated. Atrial FRP did not differ significantly in the three groups. Intraatrial conduction parameters, evaluated in the high right atrium (HRA), were longer when measured at an atrial pacing of 400 ms and showed a lack of rate adaptation in patients with spontaneous AF. In group I patients in particular, FRP’became longer with the increase of atrial rate, while in groups 2 and 3, it usually shortened. The mean gradient of HRA FRP’was -15.0 ± 19 ms in group I as compared to 5.7 ±13 ms in group II and 6.4± 13 ms in group III (P < 0.001); sensitivity. specificity, and negative predictive value of a negative gradient in the identification of patients with spontaneous AF, were, respectively, 83%, 75%, and 93%. Patients from groups 2 and 3 did not differ in any of the analyzed parameters. Patients with Wolff-Parkinson-White and spontaneous AF showed prolonged intraatrial conduction times and a different behavior in response to modification of heart rate. (PACE 1997;20[Pt. I]:1318-1327)     

Persistent Ventricular Fibrillation During Therapeutic Hypothermia and Prolonged High-Dose Vasopressor Therapy: Case Report

Background: Recent emphasis on high quality prehospital cardiopulmonary resuscitation has resulted in more out-of-hospital cardiac arrest victims surviving to the emergency department. As such, standardized in-hospital post-cardiac arrest care is necessary to assure optimal neurological recovery. Although therapeutic hypothermia has arisen as a key component in the post-cardiac arrest care paradigm, its interaction with other therapies remains poorly defined. Objective: The purpose of this communication is to demonstrate a potential interaction between therapeutic hypothermia and routinely administered resuscitation medications. Case Report: We present a case of idiopathic ventricular fibrillation in a previously healthy 36-year-old man who developed persistent ventricular fibrillation in the setting of mild therapeutic hypothermia and high doses of routine resuscitation medications. Conclusion: This case illustrates the importance of understanding the potential interaction between therapeutic hypothermia and resuscitation medications along with the need for a systematic and standardized, multi-disciplinary approach to post-cardiac arrest care.