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PubMed1999

ST segment elevation in the right precordial leads induced with class IC antiarrhythmic drugs: insight into the mechanism of Brugada syndrome.

We evaluated two patients without previous episodes of syncope who showed characteristic ECG changes similar to Brugada syndrome following administration of Class IC drugs, flecainide and pilsicainide, but not following Class IA drugs. Patient 1 had frequent episodes of paroxysmal atrial fibrillation resistant to Class IA drugs. After treatment with flecainide, the ECG showed a marked ST elevation in leads V2 and V3, and the coved-type configuration of ST segment in lead V2. A signal-averaged ECG showed late potentials that became more prominent after flecainide. Pilsicainide, a Class IC drug, induced the same ST segment elevation as flecainide, but procainamide did not. Patient 2 also had frequent episodes of paroxysmal atrial fibrillation. Pilsicainide changed atrial fibrillation to atrial flutter with 2:1 ventricular response, and the ECG showed right bundle branch block and a marked coved-type ST elevation in leads V1 and V2. After termination of atrial flutter, ST segment elevation in leads V1 and V2 continued. In this patient, procainamide and quinidine did not induce this type of ECG change. In conclusion, strong Na channel blocking drugs induce ST segment elevation similar to Brugada syndrome even in patients without any history of syncope or ventricular fibrillation.

Anti-Arrhythmia Agents↗
PubMed1996

Atrial flutter: a newly recognized complication of pediatric lung transplantation.

BACKGROUND AND METHODS: Atrial flutter after pediatric lung transplantation has not previously been reported. We reviewed the records of 78 children who underwent lung transplantation at our institution to characterize the incidence and clinical course of postoperative atrial flutter. The diagnosis was based on either a surface or transesophageal electrocardiogram that demonstrated a fixed cycle length atrial tachycardia that did not require ventricular participation. RESULTS: Atrial flutter occurred in seven of 62 (11.3%) patients who underwent bilateral sequential lung transplantation, zero of 10 patients after single lung transplantation, and zero of six patients after heart-lung transplantation. Ages of the patients with atrial flutter ranged from 2.5 months to 14 years. Electrocardiographic findings among patients varied with respect to p-wave morphology and atrioventricular conduction. No patient had a prior atrial arrhythmia or coexisting structural cardiac disease. None had atrial flutter in relation to a rejection episode. Two patients had atrial flutter transiently during the first postoperative day, but it resolved spontaneously. Five patients had recurrent atrial flutter that began 13 +/- 7 days after the operation. The mean cycle length of atrial flutter was 196 +/- 65 msec. The arrhythmia was unresponsive to digoxin in four patients to whom it was administered. It was controlled with procainamide in four patients and with flecainide in one. At 1 and 6 months after lung transplantation, procainamide was discontinued in two patients without recurrence. One patient died of bronchiolitis obliterans 6 months after the operation while still receiving flecainide. Two patients continue to receive procainamide 4 and 7 months after transplantation. CONCLUSIONS: (1) Atrial flutter commonly occurs after bilateral lung transplantation in children. (2) Electrocardiographic manifestations are variable. (3) Type 1 antiarrhythmic agents provide satisfactory control.

Adolescent↗
PubMed2003

Electrocardiographic effects of intravenous cocaine: an experimental study in a canine model.

Cocaine abuse causes cardiac dysfunction. Acute intravenous administration of cocaine may lead to development of severe arrhythmias, conduction abnormalities, ST-T changes, and sudden death. Understanding arrhythmogenesis due to cocaine may provide a therapeutic approach to reduce morbidity and mortality. We studied the arrhythmogenic activity and other electrocardiographic abnormalities resulting from an intravenous bolus of cocaine. Baseline and postanesthetic electrocardiographic findings were compared with those after administration of intravenous bolus of various doses of cocaine hydrochloride in 20 dogs. The study was done in three phases (phase I: low dose of cocaine [1 mg/kg, 15 experiments]; phase II: medium dose [2 mg/kg, 30 experiments]; and phase III: high dose [5-7 mg/kg, 10 experiments]). Plasma levels of cocaine were estimated. The low dose induced sinus bradycardia, sinus arrhythmia, atrial ectopic, wandering pacemaker, unifocal ventricular premature contractions, and ventricular couplets. The medium dose generated moderately severe arrhythmias that were of supraventricular origin. Atrial flutter and atrial fibrillation were observed in two experiments each. Ventricular arrhythmias were manifested as unifocal, multifocal, interpolated ventricular premature contractions as well as bigeminy, trigeminy, couplets, and salvos. The high dose of 5-7 mg/kg increased electrocardiographic intervals and caused ST-segment elevation as well as serious life-threatening arrhythmias. Three of the dogs developed sustained ventricular tachycardia followed by ventricular flutter-fibrillation and death.

Animals↗
PubMed1987

Frequency, diagnosis and clinical characteristics of patients with multiple accessory atrioventricular pathways.

Multiple accessory atrioventricular (AV) pathways were documented in 52 of 388 patients (13%) who underwent detailed electrophysiologic evaluation. Multiple AV pathways were identified during intraoperative mapping or electrophysiologic study by different patterns of ventricular preexcitation during atrial fibrillation, flutter or atrial pacing with different delta-wave morphologic and ventricular activation patterns; different sites of atrial activation during right ventricular pacing or orthodromic reciprocating tachycardia; or preexcited reciprocating tachycardia using a second pathway as the retrograde limb of the tachycardia. A logistic model was used to determine which clinical, electrocardiographic and electrophysiologic variables were associated with multiple AV pathways. Right free-wall and posteroseptal accessory AV pathways were more common in patients with multiple AV pathways and were frequently associated. Multivariate logistic regression identified Ebstein's anomaly, and a history of preexcited reciprocating tachycardia as significant variables (p less than 0.0001). Pathway location was not subjected to statistical analysis because of confounding variables.

Adolescent↗
PubMed1995

A prospective study of electrical cardioversion for sustained tachycardias by emergency unit personnel.

Acute symptomatic tachyarrhythmias are commonly seen by emergency unit personnel. Electrical cardioversion is often used at Groote Schuur Hospital to treat such patients because of concerns about the safety and efficacy of intravenous anti-arrhythmic agents. All patients presenting with acute symptomatic tachyarrhythmias who were managed only by the staff of the Emergency Unit were entered into the study to assess the efficacy and safety of direct current (DC) cardioversion. Those with sinus tachycardia or atrial fibrillation of more than 24 hours' duration were excluded. Staff, on joining the unit, were instructed in the use and technique of DC cardioversion, and given simple guidelines for the management of acute tachyarrhythmias. Fifty-three patient events were seen over a period of 16 months: 7 patients had ventricular tachycardia, 21 had atrial flutter, 20 had paroxysmal junctional re-entry tachycardia, 4 had atrial fibrillation and 1 had multifocal atrial tachycardia. Fifty-two were successfully converted to sinus rhythm. One patient with atrial flutter and 9 with paroxysmal junctional re-entry tachycardia reverted after undergoing vagal manoeuvres or receiving intravenous verapamil. Of the remaining 43 patients, 42 (98%) were cardioverted with synchronised DC shock under midazolam sedation (7/7 ventricular tachycardia, 20/20 atrial flutter, 11/11 paroxysmal junctional re-entry tachycardia, 4/4 atrial fibrillation, 0/1 multifocal atrial tachycardia). Four patients had their sedation electively reversed with flumazenil. No complications occurred. DC cardioversion was only considered inappropriate in the 1 patient with multifocal atrial tachycardia. This study shows that if simple guidelines are followed, non-cardiologist junior medical personnel can safely and effectively manage sustained, acute, symptomatic tachyarrhythmias by employing DC cardioversion as and when appropriate.

Atrial Fibrillation↗
PubMed1989

[Atrial flutter with 1:1 AV conduction during intravenous flecainide treatment].

Acute drug treatment of recent onset atrial flutter may reduce the ventricular rate by increasing block in the A-V node (digitalis/verapamil) or act by directly affecting the atria by reducing the atrial rate or converting flutter to sinus rhythm (1a and 1c antiarrthythmic drugs). Treatment that reduces the atrial rate may cause 1:1 A-V conduction. Quinidine and disopyramide are well known for increasing A-V conduction to 1:1 in some patients, because of their anticholinergic effect on the A-V node. Flecainide, a 1c antiarrhythmic drug, slows down atrial conduction, reducing flutter rate by 1/3. Clinical studies have shown flecainide to be effective in converting atrial fibrillation, atrial tachycardia, A-V reentry and A-V nodal reentry tachycardias to sinus rhythm. The effect on atrial flutter has been less impressive. Flecainide prolongs A-V conduction and increases Wenckebach cycle length. In spite of this, 1:1 A-V conduction may occur during treatment with intravenous flecainide for atrial flutter. We present a case where this is demonstrated and review the literature.

Aged↗
PubMedDate not supplied

Comparison of intravenous diltiazem and verapamil for the acute treatment of atrial fibrillation and atrial flutter.

STUDY OBJECTIVES: To compare the efficacy and safety of intravenous diltiazem and verapamil in controlling ventricular rate in patients with atrial fibrillation or flutter, and to evaluate the effects of these agents on left ventricular systolic function. DESIGN: Prospective, randomized, double-blind, crossover study. SETTING: University-affiliated hospital and Veterans Administration hospital. PATIENTS: Seventeen men with atrial fibrillation or flutter with a ventricular rate of 120 beats/minute or higher and a systolic blood pressure of 100 mm Hg or greater. INTERVENTIONS: Patients received up to two intravenous boluses of either diltiazem or verapamil, followed by an 8-hour continuous infusion if a therapeutic response was achieved (phase I). After a washout period, patients who responded were crossed over to receive the other drug in a similar fashion (phase II). MEASUREMENTS AND MAIN RESULTS: At the end of each infusion, the patient's ejection fraction was assessed by gated angiography. Of the 17 men initially randomized, 8 successfully completed both phases I and II. In these patients, baseline mean (+/- SD) ventricular rates before treatment with intravenous diltiazem and verapamil were 138 +/- 15 and 132 +/- 9 beats/minute, respectively (NS). At 2 minutes after the initial bolus dose, the mean ventricular rate decreased to 100 +/- 13 beats/minute in the diltiazem group compared with 114 +/- 17 beats/minute in those receiving verapamil (p < 0.05). Mean ventricular rates of 96 +/- 11 and 97 +/- 9 beats/minute were maintained during the 8-hour continuous infusion of diltiazem and verapamil, respectively (NS). On completion of the bolus dose(s) and during continuous infusions, there were no significant differences in blood pressures between the groups. Mean ejection fractions were 35.6 +/- 13.6% and 35.5 +/- 15.4% in the diltiazem and verapamil groups, respectively (NS). For the 17 patients, the mean maximum percentage decreases in blood pressure were not significantly different between groups. However, three patients developed symptomatic hypotension, all of whom were randomized to receive verapamil initially. CONCLUSION: Intravenous diltiazem and verapamil are comparable in terms of efficacy and effect on systolic function in patients with rapid atrial fibrillation and flutter. However, hypotension may limit therapy with verapamil in some patients.

Aged↗
PubMed2001

Initial clinical experience with a new arrhythmia detection algorithm in dual chamber implantable cardioverter defibrillators.

AIM: Inappropriate therapy, due to poor discrimination of supraventricular tachycardia (SVT) from ventricular tachycardia (VT) remains a major problem in patients with an implantable cardioverter defibrillator (ICD). Theoretically, the addition of atrial sensing in discrimination algorithms should improve this differentiation. The aim of the study is to evaluate the performance of a new tachycardia discrimination algorithm, SMART Detection. METHODS AND RESULTS: Twenty-six patients received a non-thoracotomy ICD system (Phylax AV, Biotronik, Germany). All documented spontaneous arrhythmia episodes were analyzed. During a mean follow-up of 8 months, a total number of 139 events with stored electrograms were recorded in 12 patients. The final diagnosis was ventricular fibrillation (VF) or polymorphic VT (n=20), monomorphic VT (n=69), SVT (n=26), other ventricular arrhythmia (n=3) and T wave oversensing (n=21). In 6 episodes a dual tachycardia was present. Considering SVT episodes, inappropriate therapy occurred in 2 cases of atrial flutter due to stable ventricular rate (<30 ms), 1 case of atrial tachycardia and 2 cases of sinus tachycardia due to a sudden onset (> 10%). CONCLUSION: With the SMART Detection algorithm, discrimination of VT from SVT achieved a sensitivity of 100%, with an accuracy of 95.6% for all ventricular arrhythmias. In the case of SVT, the algorithm appropriately detected and inhibited therapy in 88% of atrial fibrillation.

Adult↗
PubMed1982

[Drug treatment of a trial fibrillation in patients with Wolff-Parkinson-White syndrome].

In 10 patients with ventricular preexcitation (Kent bundle), in whom atrial fibrillation (A.F.) was present, the effect of some common antiarrhythmic drugs on the conduction through the anomalous pathway, and on the ventricular rate was estimated. Procainamide caused transient complete block in the accessory pathway (disappearance of the aberrant QRS) and marked reduction of the average ventricular rate in all instances. Lidocaine caused incomplete block in the accessory pathway (reduction of the number of the aberrant QRS) and significant reduction of the average ventricular rate in all tested subjects. Amiodarone slowed the ventricular rate (increase of the average and minimum R-R intervals between wide QRS complexes) in two patients, but it did not block the anomalous pathway (all QRS complexes remained aberrant); whereas in 1 patient the ventricular rate became faster and regular and the patient had syncope, while the QRS remained always aberrant. This response was probably due to the change of A.F. into atrial flutter with atrio-ventricular conduction through the anomalous pathway only. Digitalis increased the average ventricular rate and shortened the minimum R-R interval between aberrant QRS complexes 3 out of 3 times. On the basis of our experience and of the data in the literature, we conclude that, in the management of A.F. in patients with W.P.W. syndrome:--the most effective drugs are those of the 1st group of Singh and Hauswirth classification (especially Procainamide and Ajmaline);--Lidocaine is less effective, but not ineffective and its utilization may be recommended whenever the previous drugs may be hazardous;--Amiodarone, although capable of modifying the electrophysiologic properties both of the anomalous pathway and of the A-V node, seems to be less reliable;--the drugs which influence only the A-V node (Verapamil, beta-Blockers, etc.) are quite ineffective;--finally, the Digitalis is not suitable because this drug increases the ventricular rate by decreasing the effective refractory period (ERP) of the anomalous pathway.

Adolescent↗
PubMed1998

Resolution of cardiomyopathy after ablation of atrial flutter.

OBJECTIVES: We sought to serially assess left ventricular (LV) function before and after catheter ablation of atrial flutter (AFI). BACKGROUND: The relation of tachycardia-induced cardiomyopathy to AFI and its response to direct catheter ablation are unknown. METHODS: LV function was assessed in a series of 59 consecutive patients with successful radiofrequency ablation (RFA) of AFI before and after the procedure. Eleven patients had dilated cardiomyopathy (LV ejection fraction [LVEF] <50%) and congestive heart failure (CHF) symptoms and are the subject of this report. LV function was assessed by LVEF on two-dimensional echocardiography and functional status by New York Heart Association (NYHA) CHF classification. RESULTS: Patients were 59 +/- 8 years old, and were all male. Five patients had a preablation diagnosis of idiopathic cardiomyopathy. The preablation LVEF was 30.9 +/- 11.0% and improved to 41.3 +/- 16% (p = 0.005) when measured 7 months after successful ablation. NYHA CHF class improved from 2.6 +/- 0.5 to 1.6 +/- 0.9 (p = 0.002). Six (55%) of 11 patients had normalization of the LVEF, with complete resolution of CHF symptoms. A lower preablation LVEF and functional class predicted nonresolution of dilated cardiomyopathy (p = 0.002 and 0.001, respectively). CONCLUSIONS: Restoration of normal sinus rhythm by RFA in patients with chronic AFI and cardiomyopathy substantially improved LV function. Resolution of dilated cardiomyopathy occurred in the majority of patients. Tachycardia-induced cardiomyopathy may be a more common mechanism of LV dysfunction in patients with AFI than expected, and aggressive treatment of this arrhythmia should be considered.

Adult↗
PubMed2001

[Atrial flutter: a possible early sign of acute rejection in heart transplantation. A case report].

The authors report the case of a cardiac transplant patient with a recurrence of atrial flutter two months after electrical cardioversion and despite long-term preventive treatment with amiodarone. Early investigation for signs of rejection with 4 endomyocardial biopsies was negative. Aggravation of the haemodynamic status due to flutter with a rapid ventricular response led to an attempted radio-frequency ablation. Endocavitary mapping confirmed persistence of sinus activity in the native atrium and the presence of a circuit of type I isthmic flutter (anticlockwise circuit) in the donor atrium. Ablation by radio-frequency in the same procedure was successful. A fifth myocardial biopsy the same day finally confirmed stage 3A acute rejection. No signs of recurrent rejection or arrhythmia have been observed after 24 months' follow-up in this patient. This preliminary experience confirms the need to look for graft rejection by repeated myocardial biopsies in cardiac transplant, patients with atrial flutter and the efficacy of radio-frequency ablation in cases of resistance to conventional therapy.

Atrial Flutter↗
PubMed1982

Verapamil in cardiac arrhythmias: an overview.

1. Verapamil remains the most widely used calcium antagonist for the treatment of cardiac arrhythmias. It is the most potent and effective drug for the acute treatment of paroxysmal supraventricular tachycardia particularly, circus movement tachycardia with or without pre-excitation. 2. As it is a powerful depressant of atrioventricular nodal conduction it reduces the ventricular rate in atrial flutter and fibrillation with reversion to sinus rhythm in a proportion of patients with these arrhythmias. Because verapamil does not increase airways resistance it can be used in patients with obstructive airways disease. The drug is also effective in supraventricular tachyarrhythmias following open-heart surgery and myocardial infarction. 3. It is not an effective drug against ventricular arrhythmias unless due to coronary artery spasm. The use of verapamil should be avoided in the presence of sick sinus node syndrome, clinical cardiac failure and treatment with other negative inotropic drugs.

Administration, Oral↗
PubMedDate not supplied

[The effectiveness and safety of d,l-sotalol in the ambulatory treatment of atrial fibrillation and flutter].

Data on short and long term efficacy and safety of d,l sotalol in patients with atrial fibrillation or atrial flutter is limited. The aims of this study were to (1) assess the antiarrhythmic efficacy of d,l sotalol maintaining normal sinus rhythm in patients with refractory atrial fibrillation or flutter, (2) evaluate the efficacy of d,l sotalol in preventing recurrences of paroxysmal atrial fibrillation or flutter, (3) evaluate the control of ventricular rate in patients with paroxysmal or refractory atrial fibrillation or flutter unsuccessfully treated with other antiarrhythmic agents, (4) determine predictors of efficacy (5) assess the safety of d,l sotalol in this setting. Two hundred patients with chronic or paroxysmal atrial fibrillation or atrial flutter or both, who had failed one to six previous antiarrhythmic drug trials were treated with d,l sotalol 80 to 440 mg/day orally. Fifty four percent was female, age 47 +/- 16 years (range 7-79), follow up period 7 +/- 7 months (range 1 to 14 months), 79% of patients had the arrhythmia for more than one year. The atrial fibrillation in 37.5% of patients was chronic and paroxysmal in 23.5. The atrial flutter was chronic in 31% of patients and paroxysmal in 8%. Eighty two percent of patients was in functional class I (NYHA) and 82% had cardiac heart disease: left atrial (LA) size 44 +/- 10 mm, right atrial (RA) size 37 +/- 7 mm and left ventricular ejection fraction (LVEF) 58 +/- 8%. Total success was achieved in 58% of patients (atrial fibrillation 40% and 18% in atrial flutter), partial success in 38% (atrial fibrillation in 18% and 20% in atrial flutter) and 4% of patients failure. It was p < 0.07 when compared total success vs partial success among atrial fibrillation and atrial flutter groups. Patients with cardiac heart disease responded worst (p = 0.10) to the drug than those without it, specially if the heart was dilated. We concluded that d,l sotalol has moderate efficacy to convert and maintain normal sinus rhythm, as well as it acts controlling paroxysmal relapses and ventricular heart rate.

Adolescent↗
PubMed2001

Disturbed atrioventricular electromechanical function long after Mustard operation for transposition of great arteries: a potential contributing factor to atrial flutter.

OBJECTIVE: The objectives were to study atrial and ventricular electromechanical function in patients long after Mustard repair for transposition of great arteries and to identify possible causes and physiologic disturbances in those with recurrent atrial flutter. METHODS: Electromechanical atrial and ventricular function was assessed in 22 patients (11 women) aged 27 +/- 5 years, 10 to 29 (mean 24) years after initial Mustard operation with electrocardiography and echocardiography. The study subjects involved 12 patients with documented atrial flutter and the remaining 10 without history of atrial arrhythmia served as controls. All patients were studied while in sinus rhythm. RESULTS: There was no difference in age, gender, or age at original Mustard surgery between the 2 patient groups. The P wave and QRS duration were significantly broader in patients compared with controls (128 +/- 14 ms vs 100 +/- 10 ms, P <.05 and 120 +/- 20 ms vs 93 +/- 6 ms, P <.01). Right ventricular end diastolic dimension was not different, whereas left ventricular fraction shortening was less (20% +/- 10% vs 35% +/- 12%, P <.01) in the patient group. Left and septal total ventricular long axes amplitude were significantly lower in patients compared with controls (1.4 +/- 0.4 cm vs 1.7 +/- 0.3 cm, P <.05 and 0.6 +/- 0.2 cm vs 1.0 +/- 0.3 cm, P <.01). Right-sided total long axis excursion was equally reduced in the 2 groups (1.0 +/- 0.3 cm). Septal and right-sided but not left-sided "a" wave was smaller in the patients (1.2 +/- 1 mm vs 3 +/- 1.2 mm, P <.001 and 1 +/- 1.3 mm vs 3 +/- 0.9 mm, P <.01). Right atrial electromechanical delay was significantly longer in patients with respect to controls (110 +/- 14 ms vs 84 +/- 25 ms, P <.001), but on the left there was no difference. The P wave duration correlated closely with right atrial electromechanical delay, r = 0.79, P <.003. Significant tricuspid regurgitation was found in 9 of 12 patients but none of the controls. CONCLUSION: Right ventricular dysfunction is present long after Mustard operation for transposition of great arteries whether flutter occurs. However, in patients with history of atrial flutter, evidence of left ventricular dysfunction, significant tricuspid regurgitation, impaired right atrial electrical and mechanical function, and reversed onset of atrial systole is also present. The consistent association of the disturbed atrial and ventricular electromechanical behavior suggests a multifactorial etiology for atrial arrhythmia.

Adult↗
PubMed2004

[Specific complications in the treatment with implantable cardioverter-defibrillators].

BACKGROUND: Using implantable cardioverter-defibrillators in treatment of malignant ventricular arrhythmias revealed new complications specific to this therapy. Inappropriate therapy, arrhythmic storm and device related proarrhythmia belong to the most significant complications. The authors describe specific complications in a group of ICD patients, analyze their etiology and prognostic value. There are some recommendations for the management of specific complications. METHODS AND RESULTS: 138 consecutive patients underwent ICD implantation between 1994-2001. Median follow-up was 47,35 months. Average left ventricular ejection fraction was 38 +/- 14% and 71% of patients suffered from coronary artery disease. From the total of 2490 arrhythmic episodes 1490 were evaluated in detail. 253 episodes (17%) were classified as inappropriate therapy. The most common etiology of inappropriate therapy was atrial fibrillation with rapid ventricular response (68%), atrial flutter (13%) and sinus tachycardia (11%). After the therapeutic intervention, 65% of them remained free of inappropriate therapy. There were 38 arrhythmic storms in 19 patients as another serious complication. CONCLUSIONS: All the observed arrhythmic episodes were ventricular tachycardias (p<0.04). Patients with arrhythmic storm in history had significantly lower survival (p<0.05). The risk factors of cardiac nonsudden death were: age >66 years, left ventricular ejection fraction <35% and arrhythmic storm history. The authors present recommendations for the treatment of the most common specific ICD complications.

Adult↗
PubMed1994

Automated analysis of spontaneously occurring arrhythmias by implantable devices. Limitations of using rate and timing features alone.

Real-time automated systems for arrhythmia analysis by implantable antitachycardia devices have been designed to incorporate two-channel rate criteria with intracavitary atrial and ventricular electrogram morphology. Because the power requirements for morphologic analysis substantially limit antitachycardia device longevity, the authors sought to develop an alternative algorithm that relies solely on rate and three newly developed timing features: onset (median ventricular rate filtering to detect abrupt onset), loss of atrioventricular (AV) sequency (premature ventricular depolarizations), and regularity-multiplicity (minimal median cycle length variation concurrent with integral [n:1] AV periodicity). This system was assessed using spontaneously occurring arrhythmias in patients undergoing electrophysiology studies. Electrograms were captured on FM tape (1-500 Hz) using biopolar catheters in the high right atrium and the left ventricular apex. In 11 patients, 25 distinct arrhythmias were analyzed, which included sinus tachycardia (ST) (1 passage), supraventricular tachycardia (SVT) (6 passages), ventricular tachycardia (VT) with concurrent sinus rhythm (16 passages), VT with concurrent atrial flutter (VT/AFl) (2 passages), and ventricular fibrillation (VF) (1 passage). The algorithm correctly diagnosed 1 of 1 episode of ST, 4 of 6 episodes of SVT, 15 of 16 episodes of VT with concurrent sinus rhythm, 0 of 2 episodes of VT/AFl, and 1 of 1 episode of VF. Ventricular tachycardia episodes were misdiagnosed as SVT because of absence of loss of AV sequency in VT onset (1 episode), presence of multiplicity between VT and AFl (1 episode), and absence of VT regularity during AFl (1 episode).(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗