Cardiovascular disease management in people with diabetes outside North America and Western Europe in 2006 and 2015.

AIM: Optimal treatment of cardiovascular disease is essential to decrease mortality among people with diabetes, but information is limited on how actual treatment relates to guidelines. We analysed changes in therapeutic approaches to anti-hypertensive and lipid-lowering medications in people with Type 2 diabetes from 2006 and 2015. METHODS: Summary data from clinical services in seven countries outside North America and Western Europe were collected for 39 684 people. Each site summarized individual-level data from outpatient medical records for 2006 and 2015. Data included: demographic information, blood pressure (BP), total cholesterol levels and percentage of people taking statins, anti-hypertensive medication (angiotensin-converting enzyme inhibitors, calcium channel blockers, angiotensin II receptor blockers, thiazide diuretics) and antiplatelet drugs. RESULTS: From 2006 to 2015, mean cholesterol levels decreased in six of eight sites (range: -0.5 to -0.2), whereas the proportion with BP levels > 140/90 mmHg increased in seven of eight sites. Decreases in cholesterol paralleled increases in statin use (range: 3.1 to 47.0 percentage points). Overall, utilization of anti-hypertensive medication did not change. However, there was an increase in the use of angiotensin II receptor blockers and a decrease in angiotensin-converting enzyme inhibitors. The percentage of individuals receiving calcium channel blockers and aspirin remained unchanged. CONCLUSIONS: Our findings indicate that control of cholesterol levels improved and coincided with increased use of statins. The percentage of people with BP > 140/90 mmHg was higher in 2015 than in 2006. Hypertension treatment shifted from using angiotensin-converting enzyme inhibitors to angiotensin II receptor blockers. Despite the potentially greater tolerability of angiotensin II receptor blockers, there was no associated improvement in BP levels.

Severe acute respiratory syndrome (SARS): knowledge, attitudes, practices and sources of information among physicians answering a SARS fever hotline service.

In June 2003, Taiwan introduced a severe acute respiratory syndrome (SARS) telephone hotline service to provide concerned callers with rapid access to information, advice and appropriate referral where necessary. This paper reports an evaluation of the knowledge, attitude, practices and sources of information relating to SARS among physicians who staffed the SARS fever hotline service. A retrospective survey was conducted using a self-administered postal questionnaire. Participants were physicians who staffed a SARS hotline during the SARS epidemic in Taipei, Taiwan from June 1 to 10, 2003. A response rate of 83% was obtained. All respondents knew the causative agent of SARS, and knowledge regarding SARS features and preventive practices was good. However, only 54% of respondents knew the incubation period of SARS. Hospital guidelines and news media were the major information sources. In responding to two case scenarios most physicians were likely to triage callers at high risk of SARS appropriately, but not callers at low risk. Less than half of all respondents answered both scenarios correctly. The results obtained suggest that knowledge of SARS was generally good although obtained from both medical and non-medical sources. Specific knowledge was however lacking in certain areas and this affected the ability to appropriately triage callers. Standardized education and assessment of prior knowledge of SARS could improve the ability of physicians to triage callers in future outbreaks.

Clinical and electrophysiological characteristics in children with atrioventricular nodal reentrant tachycardia.

Atrioventricular (AV) nodal reentrant tachycardia is one of the most common supraventricular tachycardias in childhood. However, information about AV nodal reentrant tachycardia in childhood is limited, especially about the variant and multiple forms. The purpose of this retrospective study was to investigate the clinical and electrophysiological characteristics in pediatric patients with AV nodal reentrant tachycardia. Forty-eight pediatric patients with AV nodal reentrant tachycardia were included (ages 11-18 years; 25 males and 23 females). The age of onset and duration of symptoms were significantly younger and shorter in pediatric patients, respectively. A higher incidence of antegrade dual AV nodal pathways was found in adult patients than pediatric patients (72.9 vs 52.1% p = 0.003). Both antegrade and retrograde slow pathway functions were better in pediatric than adult patients. There was no significant difference between children and adults in the occurrence of variant and multiple forms of AV nodal reentrant tachycardia. This study demonstrated that pediatric patients have different electrophysiologic characteristics from those of adult patients.

Mechanisms of transition between double paroxysmal supraventricular tachycardias.

INTRODUCTION: Coexistence of double tachycardias in one patient has been infrequently reported. Furthermore, the mechanisms of transition between double paroxysmal supraventricular tachycardias have not been well studied. METHODS AND RESULTS: Thirty-five patients with two paroxysmal supraventricular tachycardias were studied. Group IA consisted of 3 patients with spontaneous transition between AV reciprocating tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT). Group IB consisted of 13 patients without spontaneous transition between AVRT and AVNRT. Group IIA consisted of 5 patients with spontaneous transition between AVNRT and atrial tachycardia (AT). Group IIB consisted of 14 patients without spontaneous transition between AVNRT and AT. The absolute values of differences between the two tachycardia cycle lengths were significantly smaller in patients with than in those without transition between the two tachycardias (25+/-8 msec vs 90+/-46 msec, P < 0.05, IA vs IB; 21+/-25 msec vs 99+/-57 msec, P < 0.01, IIA vs IIB). The cutoff point of 25 msec had 80% positive predictive value for transition between the two tachycardias. Transition between two tachycardias occurred due to a spontaneous premature atrial complex (30%), conduction block at one limb of tachycardia (20%), or tachycardia-induced tachycardia (50%). Absence of transition between two tachycardias might be explained by the absence of a spontaneous premature atrial complex, longer cycle length of the first tachycardia, larger difference between two tachycardia cycle lengths, or induction of each tachycardia under different situations. CONCLUSION: Double supraventricular tachycardias with similar tachycardia cycle lengths are vulnerable to transition between different tachycardias.

Atrial tachycardias originating from the atrial septum: electrophysiologic characteristics and radiofrequency ablation.

INTRODUCTION: The characteristics of atrial tachycardia (AT) have varied widely among different reports. The anatomic locations of ATs may bias the results. We propose that septal ATs and free-wall ATs have different characteristics. METHODS AND RESULTS: One hundred forty-one patients with AT underwent electropharmacologic study, endocardial mapping, and radiofrequency ablation. Forty-nine (34.7%) patients had septal AT originating from the anteroseptal, mid-septal, and posteroseptal areas. Tachycardia cycle length was similar between septal AT and free-wall AT (367 +/- 46 msec vs 366 +/- 58 msec, P > 0.05). More patients with septal AT required isoproterenol to facilitate induction (44.9% vs 31.5%, P <.0.05). Septal AT was more sensitive to adenosine than free-wall AT (84.4% vs 67.8%, P < 0.05). Only posteroseptal AT showed a positive P wave in lead V1 and negative P wave in all the inferior leads (II, III, aVF). Radiofrequency catheter ablation had a comparable success rate for septal AT and free-wall AT (96% vs 95%) without impairment of AV conduction. During follow-up of 49 +/- 13 months (range 17 to 85), the recurrence rate was similar for septal AT and free-wall AT (3.2% vs 4.6%, P = 0.08). CONCLUSION: Septal AT has electrophysiologic characteristics that are distinct from those of free-wall AT. Catheter ablation of the septal AT is safe and effective.

Shortening of cardiac action potentials in endotoxic shock in guinea pigs is caused by an increase in nitric oxide activity and activation of the adenosine triphosphate-sensitive potassium channel.

OBJECTIVE: To investigate the roles of nitric oxide and adenosine triphosphate (ATP)-sensitive potassium channels (KATP) in the shortening of cardiac action potential in endotoxic shock. DESIGN: Prospective animal study with concurrent controls. SETTING: University animal research laboratory. SUBJECTS: Adult Hartley guinea pigs, weighing 300-400 g. INTERVENTIONS: Guinea pigs were anesthetized and mechanically ventilated for 6 hrs. Lipopolysaccharide (LPS) or saline (sham group) were given intravenously. Drug effects were examined at the end of 6 hrs. MEASUREMENTS AND MAIN RESULTS: Plasma nitrate concentration was measured hourly, while guanosine 3',5'-cyclic monophosphate (cGMP) content and action potential duration at 90% of repolarization (APD90) of papillary muscle were examined every 2 hrs in the 6-hr endotoxemia in both the sham and the LPS-treated groups. The basal levels of these three variables showed no difference in the two groups. In the sham group, these variables did not change significantly (n = 14 for plasma nitrate determination; n = 5 for cGMP content measurement; n = 5-14 for APD90 measurement; all p > .05). But in the LPS-treated group, both plasma nitrate concentration and cGMP content of papillary muscle showed time-dependent increases and they were significantly higher than those in the sham group (at the 6th hr, plasma nitrate: 42.6 +/- 7.7 vs. 21.8 +/- 3.1 micromol/L, both n = 14, p < .01; cGMP: 1.52 +/- 0.15 vs. 0.73 +/- 0.08 pmol/mg protein, both n = 5, p < .01). In contrast, APD90 revealed a time-dependent decrease compared with that in the sham group (at the 6th hr, 137.1 +/- 52 vs. 188.2 +/- 4.8 msecs, both n = 14, p < .001). In the following 60-min in vitro recording of action potentials after the end of 6-hr endotoxemia, the shortened APD90 in the LPS-treated group did not recover and remained shorter compared with that in the sham group, in which the APD90 showed no significant changes (at the 60th min, 165.1 +/- 5.7 vs. 200.2 +/- 3.8 msecs, each n = 14, p < .01). However, in the presence of glibenclamide, a specific KATP blocker (100 micromol/L; n = 10), the APD90 could be reversed almost completely to the same value as that in the sham group (n = 14) (196.6 +/- 3.5 vs. 200.2 +/- 3.8 msecs; p > .05), despite glibenclamide having no effect on the APD90 in the sham group. In the LPS-treated group, NG-nitro-L-arginine methyl ester (1 mmol/L; n = 4), methylene blue (10 micromol/L; n = 5), and aminoguanidine (100 micromol/L; n = 4) significantly prolonged the shortened APD90 (192.5 +/- 3.1, 195.0 +/- 3.3, and 176.5 +/- 3.3 msecs, respectively; p < .01, p < .01, and p < .05, respectively, compared with that without these agents, 165.1 +/- 5.7 msecs, n = 14). These agents had negligible effects on the APD90 in the sham group (all p > .05). Furthermore, 8-bromoguanosine-3',5'-cyclic monophosphate (500 micromol/L; n = 5) decreased APD in intact papillary muscle (mean reduction of APD90, 13.5 +/- 3.5%, n = 5; p < .05), an effect abolished by pretreatment with glibenclamide (100 micromol/L; n = 5) that did not have an effect by itself. CONCLUSIONS: In this experimental model, we provide reasonably convincing evidence to suggest that in endotoxic shock, an increase in nitric oxide activity may activate KATP, which plays a major role in the shortening of APD, presumably through a cGMP-dependent pathway.

The long QT syndromes: genetic basis and clinical implications.

It is becoming clear that mutations in the KVLQT1, human "ether-a-go-go" related gene, cardiac voltage-dependent sodium channel gene, minK and MiRP1 genes, respectively, are responsible for the LQT1, LQT2, LQT3, LQT5 and LQT6 variants of the Romano-Ward syndrome, characterized by autosomal dominant transmission and no deafness. The much rarer Jervell-Lange-Nielsen syndrome (with marked QT prolongation and sensorineural deafness) arises when a child inherits mutant KVLQT1 or minK alleles from both parents. In addition, some families are not linked to the known genetic loci. Cardiac voltage-dependent sodium channel gene encodes the cardiac sodium channel, and long QT syndrome (LQTS) mutations prolong action potentials by increasing inward plateau sodium current. The other mutations cause a decrease in net repolarizing current by reducing potassium currents through "dominant negative" or "loss of function" mechanisms. Polymorphic ventricular tachycardia (torsade de pointes) is thought to be initiated by early after-depolarizations in the Purkinje system and maintained by reentry in the myocardium. Clinical presentations vary with the specific gene affected and the specific mutation. Nevertheless, patients with identical mutations can also present differently, and some patients with LQTS mutations may have no manifest baseline phenotype. The question of whether the latter situation is one of high risk for administration of QT prolonging drugs or during myocardial ischemia is under active investigation. More generally, the identification of LQTS genes has provided tremendous new insights for our understanding of normal cardiac electrophysiology and its perturbation in a wide range of conditions associated with sudden death. It seems likely that the approach of applying information from the genetics of uncommon congenital syndromes to the study of common acquired diseases will be an increasingly important one in the next millennium.

Impact of transisthmus linear ablation of typical atrial flutter on coronary sinus activation time.

Complete or incomplete bidirectional isthmus conduction block after linear ablation of atrial flutter is difficult to interpret without detailed multiple electrodes mapping along the tricuspid annulus and the low right atrial isthmus area. The influence of isthmus block on the intraatrial septal and coronary sinus activation has not been assessed by endocardial mapping. This study was designed to analyze the intraartial and interatrial activation times in a retrospective fashion to investigate (1) whether isthmus conduction block can change the coronary sinus activation sequence during low lateral right atrial pacing, and (2) the correlation between change of coronary sinus activation time and isthmus conduction block. Sixty-five consecutive patients (mean age, 57 +/- 18 years) with clinically documented typical atrial flutter were studied. A 20-pole "Halo" catheter was placed around the tricuspid annulus including the entire low right atrial isthmus to verify complete bidirectional isthmus block. Activation time from ostium to distal coronary sinus (OCS-->DCS), and interatrial septum and isthmus activation times during right atrial pacing were analyzed and compared before and after incomplete or complete isthmus block. Complete bidirectional isthmus block was achieved in 50 (77%) patients. During low lateral right atrial pacing, linear ablation at low right atrial isthmus results in a significant delay of activation in all coronary sinus recording sites with greater extent at the ostium area without influence on interatrial septum activation in complete and incomplete isthmus conduction block. The difference of the OCS-->DCS interval before and after ablation, delta (OCS-->DCS), was well correlated with results of isthmus conduction block and significantly longer in patients with complete than those with incomplete isthmus block (34 +/- 11 vs 11 +/- 8 ms, P < 0.001), thereby allowing a value of 20 ms as a discriminative parameter to differentiate incomplete (< 20 ms) from complete (> or = 20 ms) isthmus counterclockwise conduction block with a sensitivity of 96% and a specificity of 88%. In conclusion, creation of a line of block at the inferior vena cava-tricuspid annulus isthmus could change coronary sinus activation sequence during low lateral right atrial pacing in sinus rhythm. The change of coronary sinus activation time after linear ablation, delta (OCS-->DCS), was well correlated with isthmus conduction block by using a value > or = 20 ms to discern complete counterclockwise isthmus block.

Persistent atrial flutter in patients treated for atrial fibrillation with amiodarone and propafenone: electrophysiologic characteristics, radiofrequency catheter ablation, and risk prediction.

INTRODUCTION: Antiarrhythmic drugs have been reported to promote the conversion of atrial fibrillation to atrial flutter in patients with paroxysmal atrial fibrillation. However, information about the electrophysiologic mechanism and response to radiofrequency ablation of these drug-induced atrial flutters is limited. Furthermore, the determinants of the development of persistent atrial flutter in patients treated for atrial fibrillation with antiarrhythmic drugs are still unknown. METHODS AND RESULTS: Among the 136 patients treated for atrial fibrillation with amiodarone (n = 96) or propafenone (n = 40), 15 (11%, mean age 65.5 +/- 12.3 years) were identified to have subsequent development of persistent atrial flutter based on surface ECG characteristics during antiarrhythmic drug treatment. The mean interval between the beginning of drug treatment and the onset of atrial flutter was 5.0 +/- 5.5 months. Intracardiac mapping and entrainment studies revealed that 11 patients had counterclockwise typical atrial flutter, and 4 had clockwise typical atrial flutter. All 15 patients underwent successful ablation with creation of complete bidirectional isthmus conduction block. After a mean follow-up of 12.3 +/- 4.2 months, 14 (93%) of 15 patients who underwent successful ablation and continued taking antiarrhythmic drugs have remained in sinus rhythm. Univariate analysis of clinical variables demonstrated that only atrial enlargement was significantly related to the occurrence of persistent atrial flutter. CONCLUSION: In patients with atrial fibrillation, persistent typical atrial flutter might occur during antiarrhythmic drug treatment, and atrial enlargement was a risk factor for the development of such an arrhythmia. Radiofrequency ablation and continuation of pharmacologic therapy offered a safe and effective means of achieving and maintaining sinus rhythm.

Is 8-mm more effective than 4-mm tip electrode catheter for ablation of typical atrial flutter?

BACKGROUND: The prospective, randomized study comparing 4- with 8-mm tip electrodes for radiofrequency linear ablation of typical atrial flutter is not available. METHODS AND RESULTS: A total of 104 consecutive patients with typical atrial flutter were randomly assigned to undergo radiofrequency linear ablation using a 4- (Group I, n=54) or 8-mm tip electrode (Group II, n=50) catheter (temperature-control model, preset 70 degrees C). If complete bidirectional isthmus block could not be achieved after 5 pulses, the ablation catheter was changed to the other type; the maximal radiofrequency pulse number was limited to <10 pulses. Complete or incomplete isthmus conduction block was assessed by activation sequence in a multielectrode Halo catheter during low lateral right atrial and proximal coronary sinus pacing. Before shifting to the other catheter type, the 8-mm electrode catheter achieved higher complete isthmus block rate (92% versus 67%, P<0.05) with fewer pulses (2+/-1 versus 3+/-1, P<0.05), shorter procedure time (24+/-15 versus 31+/-12 minutes, P<0.05), and shorter fluoroscopic time (14+/-10 versus 23+/-15 minutes, P<0.05). After 5 failed ablation pulses, 12 (67%) of 18 patients in group I attained complete isthmus block by using an 8-mm tip catheter, but none of 4 patients in group II achieved complete block by changing to a 4-mm tip catheter. CONCLUSIONS: The 8-mm tip electrodes are more effective than the standard 4-mm length electrodes in linear ablation for typical atrial flutter. This clinical benefit may be of particular value for some patients with broad and/or thick isthmus.

Characteristics and radiofrequency catheter ablation of septal accessory atrioventricular pathways.

Septal accessory AV pathways are located in the complex AV septal space that also contains the specialized conduction system. They have unique electrocardiographical and electrophysiological characteristics to be differentiated from free-wall accessory pathways. Some of the septal pathways have AV nodelike conduction properties and produce a similar activation sequence in the retrograde conduction. Several methods have been developed to distinguish them from AV nodal pathways. Radiofrequency catheter ablation using the titration method and endocardial approach without entrance into the coronary sinus is effective in eliminating most of the septal accessory pathways without impairment of AV conduction. However, some posteroseptal accessory pathways may require energy application inside the coronary sinus, thus information of the coronary sinus anatomy is important for preventing complication.

Electrophysiological mechanisms and determinants of vagal maneuvers for termination of paroxysmal supraventricular tachycardia.

BACKGROUND: The vagal maneuvers used for termination of paroxysmal supraventricular reentrant tachycardia (PSVT) appear to involve more complex mechanisms than we have known, and further study should be done to explore the possible mechanisms. METHODS AND RESULTS: In this study, 133 patients with PSVT and 30 age- and sex-matched control subjects were included. We assessed the effects of different vagal maneuvers on termination of PSVT and compared baroreflex sensitivity and beta-adrenergic sensitivity between the patients with PSVT and control subjects. Out of 85 patients with atrioventricular reciprocating tachycardia (AVRT), vagal maneuvers terminated in 45 (53%). Of these, 28 (33%) terminated in the antegrade limb and 17 (20%) terminated in the retrograde limb. Out of 48 patients with atrioventricular nodal reentrant tachycardia (AVNRT), vagal maneuvers terminated the tachycardia in the antegrade slow pathway (14%) or in the retrograde fast pathway (19%). Baroreflex sensitivity was poorer but isoproterenol sensitivity test better in patients with AVNRT. Poorer antegrade atrioventricular node conduction properties and better vagal response determined successful antegrade termination of AVRT by vagal maneuvers. Poorer retrograde accessory pathway conduction property but better vagal response determined successful retrograde termination of AVRT. Better sympathetic and vagal response associated with poorer retrograde atrioventricular node conduction determined retrograde termination of AVNRT by the Valsalva maneuver. CONCLUSIONS: Both the vagal response and conduction properties of the reentrant circuit determine the tachycardia termination by vagal maneuvers. Improved understanding of the interaction of autonomic and electrophysiological mechanisms in maintaining or terminating PSVT may provide important insight into the pathophysiology of these two tachycardias.

Electrophysiologic characteristics of different ectopic rhythms during slow pathway ablation in patients with atrioventricular nodal reentrant tachycardia.

The presence of ectopic rhythm has been considered to be the most important marker for successful slow pathway ablation, but the details of different ectopic rhythms have not been well described. This study included 83 consecutive patients with typical AV node reentrant tachycardia who underwent slow pathway ablation. The interval between the atrial signals of the His bundle electrogram and the distal ablation catheter [A(H)-A(Ab)], and the interval between the atrial components of the distal ablation catheter and the ostium of coronary sinus catheter [A(Ab)-A(CSos)] were measured. One hundred episodes of ectopic rhythm occurred with 81 (81%) successful applications. There are two different origins and three activation sequences of ectopic rhythms, including HIS rhythm (78 applications, the earliest atrial activation in the His bundle electrogram), CSos rhythm (6 applications, the earliest atrial signal in the coronary sinus ostium electrogram) and CSos preceding HIS (CSos-->HIS) rhythm (16 applications, the atrial activation sequences changing from CSos to HIS rhythm). The CSos rhythm had a shorter mean cycle length (445 +/- 81 vs. 511 +/- 132 vs. 579 +/- 140 ms, p < 0.05), a shorter [A(Ab)-A(CSos)] interval (-2.5 +/- 9.8 vs. 14.1 +/- 11.2 vs. 12.8 +/- 8.4 ms, p < 0.05) and a lower success rate (33% vs. 84% vs. 94% p < 0.05) than HIS rhythm and CSos-->HIS rhythm. Otherwise, the mean cycle length of ectopic rhythm was significant shorter in successful than in failed ablation (506 +/- 135 vs. 559 +/- 118 ms, p = 0.04). In conclusion, we found two different origins and three activation sequences of ectopic rhythms. CSos rhythm had a lower success rate in ablation of slow pathway, thus it was a poor marker for successful ablation.

Radiofrequency ablation of idiopathic left ventricular tachycardia with changing ECG morphology.

Idiopathic left ventricular tachycardia is a distinct clinical entity with a typical ECG of right bundle branch block and left axis deviation. We presented a 39-year-old man with idiopathic left ventricular tachycardia, which demonstrated change in the configuration of QRS complex during successive radiofrequency catheter ablation. We proposed that this idiopathic left ventricular tachycardia may have alternative pathways within the reentrant circuit leading to different exits.

Effects of antiarrhythmic drugs on variability of ventricular rate and exercise performance in chronic atrial fibrillation complicated with ventricular arrhythmias.

For conversion of atrial fibrillation to sinus rhythm and management of ventricular arrhythmias, antiarrhythmic drugs were frequently used. However, the effects of antiarrhythmic drugs on exercise performance and on the variability of ventricular rate were not available. This study included 37 patients who had chronic atrial fibrillation complicated with symptomatic ventricular arrhythmias. The patients were divided into three groups and received sotalol, propafenone, and procainamide, respectively. Before and after taking the drugs for 14 days, these patients received treadmill exercise test, 24 h Holter electrocardiogram, and tilt table test for evaluation of the exercise performance and the variability of ventricular rate (including the mean RR intervals, mRR, the standard deviation of RR intervals, SDRR, and the root mean square of the difference in successive RR intervals, rMSSD). All these antiarrhythmic drugs could suppress ventricular arrhythmia but only sotalol could significantly increase the exercise duration (374+/-50 to 476+/-55 s, P=0.02), and reduce the maximal heart rate (186+/-23 to 136+/-16 beats/min, P=0.01) during exercise test. Furthermore, only sotalol increased the mRR (777+/-60 to 885+/-66 ms, P=0.02), SDRR (190+/-40 to 216+/-48 ms, P=0.04) and rMSSD (223+/-48 to 253+/-40 ms, P=0.03) during 24 h Holter electrocardiogram. With head-up tilt, the mRR, SDRR and rMSSD all decreased significantly before drug therapy, and these changes were still present only after propafenone therapy. Therefore, comparisons among sotalol, propafenone and procainamide showed that sotalol increased the exercise performance and the variability of ventricular rate in patients who had chronic atrial fibrillation complicated with symptomatic ventricular arrhythmias.

Idiopathic ventricular fibrillation: clinical, electrophysiologic characteristics and long-term outcomes.

The long-term prognosis, including risks of arrhythmic recurrence of idiopathic ventricular fibrillation (VF), is uncertain; moreover, the role of electrophysiologic study in the diagnosis and guiding of antiarrhythmic drugs therapy for idiopathic VF remains controversial. The purpose of this study was to study the clinical features, electrophysiologic characteristics and long-term clinical outcomes of six consecutive patients (five males) who had at least one episode of aborted cardiac arrest (5 patients) or syncope (1 patients) with documentation of ventricular fibrillation (VF) in the absence of apparent heart disease. Idiopathic VF was diagnosed by exclusion. All patients underwent the electrophysiologic study including intravenous antiarrhythmic drug testing. Recurrences of VF after therapy and the long-term outcomes were assessed. The mean age at the first episode was 43+/-19 years (range from 16 to 63 years). All patients had sustained VF induced by double (3 patients) or triple (3 patients) ventricular extrastimuli at a paced cycle length of 400 or 500 ms from the right ventricular apex. Intravenous procainamide and/or mexiletine could suppress the reinduction of sustained VF in 4 (67%) of 6 patients. Recurrence of VF (documented VF attack, sudden cardiac arrest or syncope) was observed in 3 (100%) of 3 patients who received procainamide or mexiletine alone. Four patients (including 3 patients who experienced recurrence) received amiodarone alone or in combination with mexiletine, and these drugs could effectively prevent recurrence of VF. One patient with exercise-induced VF remained asymptomatic without any treatment during a follow-up period of 95 months. Another patient received an implantable cardioverter-defibrillator without concomitant antiarrhythmic drug therapy and had no discharge of electrical shock during 28 months of follow-up. During a mean follow-up period of 64+/-40 months (range from 28 to 128 months), all the patients were alive except patient No. 2 who died of acute hepatic failure. In conclusion, electrophysiologic study is a reliable diagnostic method, but it was of limited value in guiding antiarrhythmic drug therapy for preventing recurrence of idiopathic VF. Class I drug alone was associated with a high recurrence rate (100%) despite predictions that it would be effective by the electrophysiologic study. Amiodarone alone or in combination with mexiletine effectively prevented the recurrence of VF during the long-term follow-up along with a favourable outcome.