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S O'Nunain

Publications and source records attributed to S O'Nunain.

17 recordsLinked to original sources
PubMed1999

Double-blind placebo-controlled trial of digoxin in symptomatic paroxysmal atrial fibrillation.

BACKGROUND: Digoxin is commonly prescribed in symptomatic paroxysmal atrial fibrillation (AF) but has never been evaluated in this condition. METHODS AND RESULTS: From a multicenter registry, 43 representative patients with frequent symptomatic AF episodes were recruited into a randomized, double-blind crossover comparison of digoxin (serum concentration, 1.29+/-0.35 nmol/L) and placebo. The study end point was the occurrence of 2 AF episodes (documented by patient-activated monitors), censored at 61 days. The median time to 2 episodes was 13.5 days on placebo and 18.7 days on digoxin (P<0. 05). The relative risk (95% CI) of 2 episodes (placebo:digoxin) was 2.19 (1.07 to 4.50). A similar effect was seen on the median time to 1 episode: increased from 3.5 to 5.4 days (P<0.05), relative risk 1. 69 (0.88 to 3.24). The mean+/-SD ventricular rates during AF recordings during placebo and digoxin treatment were 138+/-32 and 125+/-35 bpm, respectively (P<0.01). Twenty-four-hour ambulatory ECG recordings did not show significant differences in the frequency or duration of AF or in ventricular rate. CONCLUSIONS: Digoxin reduces the frequency of symptomatic AF episodes. However, the estimated effect is small and may be due to a reduction in the ventricular rate or irregularity rather than an antiarrhythmic action.

Ambulatory Care↗
PubMed1997

The treatment of patients with infected implantable cardioverter-defibrillator systems.

OBJECTIVE: The purpose of this study was to evaluate the treatment of patients with infected implantable cardioverter-defibrillator systems. METHODS: Retrospective analysis was done of the cases of 21 patients treated for implantable cardioverter-defibrillator infection during an 11-year period. RESULTS: Of 723 cardioverter-defibrillator implantations (550 primary implants, 173 replacements), nine (1.2%) were complicated by early postoperative device-related infections. Late infections developed in two patients 19 and 22 months, respectively, after implantation. Ten other patients were transferred to our institution for treatment of cardioverter-defibrillator infection. The time from implantation to overt infection was 2.2 +/- 1.3 months, excluding the two late infections. The responsible organisms were Staphylococcus aureus (9), Staphylococcus epidermidis (6), Streptococcus hemolyticus (1), gram-negative bacteria (3), Candida albicans (1), and Corynebacterium (1). All patients were treated with intravenous antibiotic drugs. Total system removal was done in 15 patients and partial removal in 2; in 4, the cardioverter-defibrillator system was not explanted. There were no perioperative deaths. A new implantable cardioverter-defibrillator system was reimplanted in 7 patients after 2 to 6 weeks of antibiotic therapy. Ten patients were treated without reimplantation (2 arrhythmia operation, 8 antiarrhythmic drugs). Four patients (3 patients without explantation and 1 with partial system removal) were treated with maintenance long-term antibiotic therapy. During a mean follow-up of 21 +/- 2.8 months, no patient had clinical recurrence of infection. One patient treated with antiarrhythmic drugs without system reimplantation died suddenly. CONCLUSIONS: Infections that involve implantable cardioverter-defibrillator systems can be safely managed by removing the entire system with reimplantation after intravenous antibiotic therapy. In selected patients in whom the risk for system explantation is high and anticipated life expectancy is short, long-term antibiotic therapy to suppress low-virulence infections may represent an acceptable alternative.

Adult↗
PubMed1995

Effect of flecainide on atrial and ventricular refractoriness and conduction in patients with normal left ventricle. Implications for possible antiarrhythmic and proarrhythmic mechanisms.

We studied the effects of intravenous flecainide (2 mg.kg-1) on atrial and ventricular refractoriness and conduction during sinus rhythm, induced atrial fibrillation and atrial pacing at rates of 100, 120 and 150 ppm, in 14 patients with normal left ventricle. Flecainide caused a significant increase in QRS duration during sinus rhythm (mean +/- SD: 87.2 +/- 8.4 ms vs 102.8 +/- 9.1 ms, P < 0.001), atrial fibrillation (87.8 +/- 10.0 ms vs 108.8 +/- 13.7 ms, P < 0.001) and at all paced rates. The duration of the atrial electrogram was significantly increased during sinus rhythm (54.9 +/- 13.2 ms vs 64.8 +/- 16.6 ms, P = 0.003) and at all pacing rates. The PA interval was also significantly prolonged, as was the pacing stimulus-to-atrial-electrogram interval at all pacing rates. There was increased QRS duration and atrial electrogram prolongation at higher pacing rates. Atrial refractoriness was prolonged during sinus rhythm (216.4 +/- 28.2 vs 228.6 +/- 36.1, P = 0.02), but not during atrial pacing at any rate. The QT interval, but not the JT interval or ventricular refractoriness, was significantly prolonged during sinus rhythm and at all pacing rates. Flecainide slows atrial conduction in a use dependent manner and increases atrial refractoriness during sinus rhythm but not during faster atrial pacing, thus not displaying a use-dependent effect. QRS duration is prolonged in a use-dependent manner without a commensurate increase in ventricular refractoriness. In the presence of rapidly conducted atrial fibrillation, which was not found to be slowed by flecainide, this effect may constitute a proarrhythmic mechanism even in patients with no apparent myocardial abnormality.

Adult↗
PubMed1995

Ventricular pacing induced ventricular tachycardia in patients with implantable cardioverter defibrillators.

Appropriately timed noncompetitive ventricular pacing potentially may initiate ventricular tachycardia in patients prone to these arrhythmias. The combination of bradycardia pacing and stored electrograms in a currently available cardioverter defibrillator provides an opportunity to evaluate the occurrence of such pacing induced ventricular tachycardia. During a surveillance period of 18.7 +/- 11.4 months, stored electrograms documented 302 episodes of ventricular tachycardia in 77 patients. Five patients (6.5%) demonstrated 25 episodes (1-16 per patient) of ventricular tachycardia that were immediately preceded by an appropriately paced ventricular beat (8.3% of all episodes of ventricular tachycardia). All five patients had prior myocardial infarctions and a history of monomorphic ventricular tachycardia occurring both spontaneously and in response to programmed electrical stimulation. Antitachycardia pacing terminated pacing induced ventricular tachycardia in 22 episodes; in one episode antitachycardia pacing accelerated ventricular tachycardia. In two cases shock therapy was aborted for nonsustained ventricular tachycardia. We conclude that, in selected nonsustained ventricular tachycardia. We conclude that, in selected postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter defibrillators, appropriately timed ventricular pacing may induce ventricular tachycardia.

Aged↗
PubMed1993

Cardiac arrest.

Explore the source record for details and available documents.

Anti-Arrhythmia Agents↗
PubMed1993

Radiofrequency current delivery by way of a bipolar tricuspid annulus-mitral annulus electrode configuration for ablation of posteroseptal accessory pathways.

OBJECTIVES: This report describes a novel technique for ablation of "difficult" posteroseptal pathways. BACKGROUND: Although radiofrequency ablation of accessory atrioventricular (AV) pathways is successful in > or = 90% of cases, particular difficulty may be encountered with some bypass tracts in the posteroseptal region. METHODS: In eight patients with posteroseptal accessory pathways (two concealed), radiofrequency catheter ablation using conventional unipolar current applications from favorable sites along the tricuspid or mitral annulus, or both, was unsuccessful. Subsequently, a bipolar technique was adopted, with current application between the distal electrodes of two catheters positioned against the septal region at sites of early activation along both mitral and tricuspid annuli. RESULTS: The bipolar configuration proved effective in all cases. The number of bipolar lesions required for success was one (five patients), five (two patients) and nine (one patient). In five patients, bipolar current application abolished pathway conduction using positions at which delivery of unipolar lesions had been ineffective or caused transient block. The AV or ventriculoatrial interval at successful sites varied from 20 to 65 ms, and the time from delta wave onset to local ventricular activation was zero or negative. There were no complications attributable to the bipolar technique. During follow-up of 8 to 36 weeks, pathway conduction has not recurred in any patient. CONCLUSIONS: Bipolar radiofrequency current delivery across the septal region using a tricuspid annulus-mitral annulus electrode configuration may abolish accessory pathway conduction when conventional unipolar applications have proved ineffective. The technique may reduce procedure duration, radiation exposure and overall failure rate in these problematic cases.

Adolescent↗
PubMed1993

Pseudo-pacemaker syndrome following inadvertent fast pathway ablation for atrioventricular nodal reentrant tachycardia.

Atrioventricular nodal reentrant tachycardia that is refractory to drug treatment has recently been treated with radiofrequency catheter ablation. In this case report we describe a patient with atrioventricular nodal reentrant tachycardia in whom radiofrequency ablation of slow pathway was attempted, with inadvertent damage to the fast pathway. The patient developed marked first-degree atrioventricular block associated with symptoms mimicking pacemaker syndrome.

Cardiac Pacing, Artificial↗
PubMed1992

The value of transesophageal atrial pacing in predicting the efficacy of antiarrhythmic drugs in patients with paroxysmal narrow QRS complex tachycardia.

Transesophageal atrial pacing (TAP) is used in the diagnosis and treatment of paroxysmal narrow QRS complex tachycardia (NQT). The aim of this study was to assess the value of this technique in predicting the efficacy of antiarrhythmic therapy. The study group consisted of 30 consecutive patients with spontaneous NQT whose clinical tachycardia was inducible by TAP. Baseline TAP was performed off all antiarrhythmic medication and repeated during oral antiarrhythmic drug therapy. The pacing protocol consisted of three stages: a single extrastimulus introduced at progressively shorter coupling intervals during sinus rhythm, pacing at incremental rates to the point of second-degree AV block, and bursts of rapid pacing. On repeat stimulation while on oral antiarrhythmic therapy (37 pacing studies) NQT was still inducible in 12 cases. During the follow-up period ten patients developed a recurrence of NQT:nine cases out of 12 (75%), in whom NQT was inducible while on antiarrhythmic therapy, and one case out of 25 (4%), in whom NQT was not inducible (P less than 0.001). The sensitivity of TAP in predicting the outcome of the patients with NQT was 90%, and the specificity 89%. The negative predictive value of TAP (prediction of no recurrence of NQT) was 96%, and the positive predictive value (prediction of recurrence of NQT) was 75%. We conclude that TAP is a simple and accurate method for predicting the efficacy of antiarrhythmic treatment in patients with NQT.

Adult↗
PubMed1992

Comparative electrophysiological effects of captopril or hydralazine combined with nitrate in patients with left ventricular dysfunction and inducible ventricular tachycardia.

OBJECTIVE: To assess the electrophysiological and antiarrhythmic effects of pharmacological load manipulation by an angiotensin converting enzyme (ACE) inhibitor (captopril) and a direct vasodilator (hydralazine plus isosorbide mononitrate) in patients with inducible ventricular tachycardia and impaired left ventricular function. DESIGN: Randomised open label cross-over comparison of three regimens. SETTING: Tertiary arrhythmia referral centre. SUBJECTS: Eight patients with reduced left ventricular function and sustained ventricular tachycardia inducible by programmed stimulation. INTERVENTIONS: Three treatment regimens each of 48 hours duration: captopril, hydralazine plus isosorbide mononitrate, and control (no vasodilator). MAIN OUTCOME MEASURES: Changes in central haemodynamics, electrophysiological parameters, and induction of ventricular tachycardia during treatment with captopril, or hydralazine combined with nitrate, compared with a control period. RESULTS: Both vasodilator treatments produced similar balanced reductions in peak systolic pressures and filling pressures compared with controls. Captopril had no effect on sinus cycle length, atrial refractoriness, or intraventricular conduction, but prolonged ventricular effective and functional refractory periods and QT interval during constant rate atrial pacing. Hydralazine combined with nitrate did not significantly alter any electrophysiological variable. Ventricular tachycardia was similarly inducible during all three periods. CONCLUSIONS: Load manipulation by captopril but not hydralazine combined with nitrate prolonged ventricular refractoriness and repolarisation, possibly reflecting a combination of mechano-electrical effect with the restraining influence of ACE inhibitors on reflex sympathetic stimulation.

Aged↗
PubMed1991

The electrophysiological effects of flosequinan.

We have evaluated the acute electrophysiological effects of flosequinan in 18 patients with normal ventricular function. Following intravenous infusion of flosequinan 100 mg over 1 h, mean (SD) systolic blood pressure fell from 131 +/- 19 to 120 +/- 22 mmHg (P less than 0.02) and there was significant shortening of sinus cycle length (732 +/- 151 to 575 +/- 93 ms, P less than 0.001), AH interval (110 +/- 45 to 71 +/- 19 ms, P less than 0.01), QRS duration (98 +/- 28 to 91 +/- 26 ms, P less than 0.02) and QT interval (373 +/- 47 to 337 +/- 35 ms, P less than 0.001), but no change in sinus node recovery time, intra-atrial conduction time, HV interval or the corrected QTc interval. There was a reduction in both anterograde atrioventricular Wenckebach cycle length (299 +/- 53 to 259 +/- 52 ms, P less than 0.01) and retrograde ventriculoatrial Wenckebach cycle length (375 +/- 77 to 300 +/- 56 ms, P less than 0.01). There was no change in atrial or ventricular effective refractory period (ERP) but atrial functional refractory period (FRP) shortened (233 +/- 31 to 212 +/- 24 ms, P = 0.07) as did ventricular FRP (249 +/- 24 to 234 +/- 21 ms, P less than 0.01). Patients received an oral dose of flosequinan 50 mg 12 h later. By 24 h, sinus cycle length, QRS duration and the QT interval had all returned towards baseline values, but ventricular ERP had lengthened (199 +/- 22 to 215 +/- 26 ms, P less than 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Transcoronary atrioventricular nodal modification using microvascular collagen.

Surgical and catheter based techniques for atrioventricular (AV) nodal modification have recently been described. Similarly, transcoronary embolization for the treatment of arrhythmias has recently emerged as a potentially useful approach. This report reviews our experience of a novel technique using embolization of the AV node with an inert agent, cross-linked collagen, for the treatment of AV nodal reentrant tachycardia. Three patients with refractory nodal tachycardia received 0.1-0.5 mL cross-linked collagen (2 mg/mL) delivered via a catheter placed within the nodal artery. All developed transient complete AV block with subsequent recovery of conduction. Two patients have had no further tachycardia and were noninducible at restudy. One patient required electrical modification because of recurrent symptoms. One patient sustained a limited posterior infarct due to back-spill of collagen into the distal right coronary artery. This novel technique provides an alternative approach to a cure for AV nodal tachycardia without producing long-term heart block.

Atrioventricular Node↗
PubMed1991

A comparison of intravenous propafenone and flecainide in the treatment of tachycardias associated with the Wolff-Parkinson-White syndrome.

UNLABELLED: We compared the electrophysiological effects of intravenous propafenone and flecainide on accessory pathway conduction by a randomized crossover study in 16 patients with Wolff-Parkinson-White syndrome. The antegrade refractory period of the pathway increased from 256 +/- 18 msec at baseline to 288 +/- 13 msec on propafenone (P less than 0.05) and to 296 +/- 27 msec on flecainide (P = 0.075). The minimum preexcited RR interval during atrial fibrillation or incremental atrial pacing was prolonged from 225 +/- 37 msec to 262 +/- 22 msec by propafenone (P less than 0.05) and to 301 +/- 31 msec by flecainide (P less than 0.005). The prolongation was significantly greater with flecainide than propafenone (P less than 0.05). Both drugs increased tachycardia cycle length (TCL) from 310 +/- 35 msec to 354 +/- 37 msec (propafenone P less than 0.005) and to 352 +/- 37 msec (flecainide P less than 0.01). Both propafenone and flecainide blocked antegrade conduction in the pathway in five patients. Both drugs rendered atrial fibrillation noninducible in seven patients and orthodromic tachycardia noninducible in five patients. CONCLUSIONS: (1) Flecainide causes a greater prolongation of minimum preexcited RR interval than propafenone; (2) There is no significant difference between propafenone and flecainide on the inducibility of arrhythmias, TCL, or incidence of antegrade conduction block.

Adult↗
PubMed1991

Effects of intravenous adenosine on antegrade refractoriness of accessory atrioventricular connections.

BACKGROUND: Several groups have suggested the use of intravenous adenosine or adenosine triphosphate in the diagnosis of regular broad complex tachycardias. However, the short half-life of these agents has precluded assessment of their effects on refractoriness of accessory connections, and their safety in preexcited arrhythmias has not been demonstrated. METHODS AND RESULTS: We examined the effects of intravenous adenosine on accessory atrioventricular (AV) connections in 30 patients with the Wolff-Parkinson-White syndrome. Intravenous adenosine (12 mg, rapid bolus) was administered to 14 patients (group 1) during continuous atrial pacing at a cycle length 20 msec below that required to cause 2:1 conduction block in the accessory connection (mean pacing cycle length 261 +/- 41 msec). After adenosine, transient 1:1 conduction occurred via the accessory connection in 12 of 14 patients, indicating a shortening of antegrade refractoriness. In three of seven patients, this effect was abolished after intravenous propranolol (0.2 mg/kg). Nineteen patients (group 2) received adenosine (0.17 +/- 0.04 mg/kg) during induced, preexcited atrial arrhythmias. The minimum RR interval during preexcited atrial fibrillation transiently decreased (252 +/- 44 msec to 224 +/- 35 msec, p less than 0.01) after adenosine, but no change in average RR interval was observed (360 +/- 59 msec to 357 +/- 60 msec, NS). The preexcited ventricular response to atrial flutter was transiently accelerated in five of eight patients (415 +/- 21 msec to 360 +/- 49 msec, p less than 0.05) due to shortening of flutter cycle length (207 +/- 10 msec to 180 +/- 24 msec, p less than 0.05). However, 2:1 accessory connection conduction was maintained in all eight patients. All effects were short lived, with the decrease in RR interval during atrial fibrillation occurring for a maximum of two RR intervals only. No patient suffered ventricular arrhythmias or hemodynamic deterioration. CONCLUSIONS: Adenosine shortens antegrade refractoriness of accessory AV connections, and in some patients this action is mediated by beta-adrenergic stimulation. Adenosine may cause acceleration of preexcited atrial arrhythmias, but these effects are transient and should not discourage the use of adenosine as a diagnostic agent in broad complex, regular tachycardias of uncertain origin.

Adenosine↗
PubMed1990

Temporal electrogram analysis: algorithm development.

The automatic discrimination of physiological from pathological tachycardias by rate criteria alone lacks adequate specificity. Tachycardia detection algorithms based upon morphological analysis of the endocardial electrogram have been attributed high specificity although their specificity has not been proven. A previous study had shown temporal electrogram analysis (TEA) to be an algorithm of high sensitivity in the detection of ventricular arrhythmias despite low computational demands. In this study, the specificity and potential for automatic implementation have been assessed. Manual adjustment of thresholds for individual patients gave a maximum potential sensitivity of 97% (26/27 arrhythmias correctly recognized as non-sinus). The use of automatic setting of thresholds reduced sensitivity to 81%. The specificity of the algorithm, as assessed by exercise testing, was only 60%.

Adult↗