Atrial defibrillation at the millennium: new challenges for evolving technology.
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Biomedical subjects
Publications and source records attributed to R Boccadamo.
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The effects of oral propafenone therapy on pacing threshold were studied in 36 patients chronically paced for sick sinus syndrome or AV block. The pacemakers, all unipolar models and with noninvasive threshold measurement facilities, were: 9 VVI, 15 AAI, and 12 DDD. Each patient received an initial propafenone dose of 450 mg/day, that in 18 cases was increased to 900 mg/day. Threshold was tested at baseline and at each dosage after 7 days of therapy. With the lower propafenone dosage the threshold, measured at 2.5 V, rose from 0.14 +/- 0.10 to 0.21 +/- 0.16 msec (+55%) in the atrium (P less than 0.0001) and from 0.10 +/- 0.08 to 0.15 +/- 0.09 msec (+63%) in the ventricle (P less than 0.0001). In the 18 patients who received both dosages, the mean atrial and ventricular threshold increased from 0.12 +/- 0.10 to 0.17 +/- 0.14 msec with the lower dose and to 0.27 +/- 0.22 msec (+125%) with the higher dose (P less than 0.0001 for both increments). With the 900 mg/day dose, a threshold increment greater than or equal to 300% was observed in 15% of the stimulated chambers. A good linear correlation (r = 0.76) was found between the ventricular threshold increment and the drug induced QRS widening. In conclusion, treatment with oral propafenone increases atrial and ventricular stimulation threshold in pacemaker patients. Threshold increment is dose dependent and proportional to the drug induced QRS widening. In the majority of the cases the threshold increment is not clinically significant, but caution must be used in prescribing high doses of the drug to patients with high baseline threshold.
A marked increase of chronic atrial pacing threshold resulting in loss of atrial capture, induced by propafenone, is reported in a patient with bradycardia-tachycardia syndrome. After atrial pacemaker implant, the atrial threshold had been measured repeatedly noninvasively and shown to be stable. The threshold rise and loss of atrial capture occurred after 7 days of treatment with propafenone at the dosage of 450 mg daily; drug withdrawal resulted in resumption of atrial capture and a return to prior pacing thresholds.
The efficacy of intravenous propafenone (2 mg/kg) was assessed in 83 consecutive patients: 68 with atrial fibrillation (AF) and 15 with atrial flutter lasting less than 15 days. Conversion to sinus rhythm occurred in 47 patients (57%), including 42 (62%) of those with AF and 5 (33%) of those with atrial flutter (p less than 0.05). The mean time to conversion was 29 +/- 24 minutes. The success rate was strongly affected by arrhythmia duration. Thus, conversion occurred in 40 patients (71%) among the 56 with arrhythmia lasting less than 48 hours but in 7 patients (26%) among the 27 with a longer lasting arrhythmia (p less than 0.0005). Left atrial size (determined echocardiographically in 56 patients) was significantly larger in nonconverters (49 +/- 12 vs 39 +/- 7 mm, p less than 0.0005). In nonconverters the mean ventricular rate decreased from 141 +/- 26 to 104 +/- 22 beats/min (p less than 0.0005). Except for reversible low output state in 3 patients already hemodynamically compromised, no significant side effects were observed. In conclusion, (1) intravenous propafenone allows a quick restoration of sinus rhythm in the majority of patients with AF of recent onset, whereas it seems less effective in atrial flutter; (2) its efficacy is influenced by the duration of the arrhythmia and by left atrial dimensions; (3) the drug allows control of ventricular rate; and (4) its use seems to be safe except in patients with severe cardiac failure.
The efficacy of noninvasive transcutaneous cardiac pacing (TCP) in the treatment of tachyarrhythmic events was tested in 24 patient: 14 with ventricular tachycardia, seven with supraventricular tachycardia and three with atrial flutter. Six (42.9%) ventricular tachycardias were interrupted: in two of the ten patients on whom underdrive pacing was attempted and in all four cases in which overdrive stimulation was possible. Five of the six supraventricular tachycardias utilizing an atrioventricular bypass tract were interrupted, while the TCP was unsuccessful on the only patient with atrioventricular nodal reentrant tachycardia. TCP failed to interrupt the arrhythmia in the three cases of atrial flutter. No clinically significant untoward effects (in particular tachycardia acceleration or ventricular fibrillation) were observed, except for a tolerable thumping sensation on the chest during pacing. In four patients, TCP effects on cardiac activation was evaluated by endocavitary recording: while the mean ventricular threshold was 70 mA, atrial capture was possible on only two patients at a current intensity of 140 and 150 mA. We consider our preliminary experience with TCP in the treatment of tachycardias encouraging. The technique was easily and rapidly usable and it was immediately successful in the majority of atrioventricular reentrant tachycardias and in a relevant percentage of ventricular tachycardias. In this latter setting TCP was mostly effective in the slower tachycardias where overdrive pacing was possible. A further experience with devices provided by higher pacing rates is warranted.
The electrocardiographic and electrophysiologic effects, clinical efficacy and safety of intravenous and oral nadolol therapy were examined in 34 patients with recurrent supraventricular tachyarrhythmias (SVT) undergoing electrophysiologic evaluation. Programmed electrical stimulation was performed in the control (drug-free) state, after infusion of intravenous nadolol (mean dose 0.09 +/- 0.03 mg/kg) and after chronic oral nadolol therapy in patients who responded to intravenous nadolol (mean dose 83 +/- 12 mg for 5 days). Intravenous nadolol administration prolonged mean sinus cycle length (p = 0.009), mean PR interval (p = 0.001) and mean AH interval (p = 0.001), with no significant electrophysiologic effects in the atrium, ventricle or accessory bypass tracts. Oral nadolol had similar electrocardiographic and electrophysiologic effects, but of lesser magnitude. Intravenous nadolol resulted in complete suppression of induced SVT in 78% of patients with sinus and atrioventricular nodal reentrant tachycardia and 11% of patients with atrioventricular (AV) reentrant tachycardia (p less than 0.001). Partial responses were frequent in intraatrial or AV reentrant tachycardia (37%). Oral nadolol suppressed induction of SVT in patients who responded to intravenous nadolol. Adverse reactions to intravenous and oral nadolol were infrequent--6% and 8%, respectively--and usually did not require drug withdrawal. Intravenous nadolol is highly effective in sinus and AV nodal reentrant tachycardia, and a successful electrophysiologic response to it predicts efficacy of long-term oral nadolol therapy. It has limited efficacy alone in AV reentrant tachycardia and should be considered in combination with other antiarrhythmic therapy in this type of SVT.
The safety and efficacy of intravenous Propafenone, in the treatment of atrial fibrillation (a.f.) or flutter (A.F.) of recent onset (15 days), were assessed. Propafenone (2 mg/kg) was administered to 36 consecutive patients (mean age 60.8 years), 28 with a.f. and 8 with A.F. Nineteen patients (52.7%) reverted to sinus rhythm within 85 min (mean 27.2 min): 17 of 28 (60.7%) with a.f. and 2 of 8 (25%) with A.F. The efficacy of the drug was significantly influenced by the time elapsed from the onset of the arrhythmia: 14/21 (66.6%) patients with the arrhythmia lasting less then 48 hours and only 5/15 (33.3%) of those with the arrhythmia lasting more than 48 hours or of unknown onset, were converted (p less than 0.05). 18 patients underwent echocardiographic control: mean left atrial dimensions were 41.4 +/- 11.4 mm in converters and 47.4 +/- 11.2 mm in non converters (p = NS). Mean QRS lengthening observed was 16% (from 89 +/- 35.1 to 103.5 +/- 48.8 msec) (p = NS); QTc interval increased from 390 +/- 64.3 to 403 +/- 36.2 msec (p = NS). Arterial blood pressure showed significant changes only in two patients in whom a serious hypotension developed, needing infusion of adrenergic drugs. Non converters showed a reduction of the ventricular rate from 141.8 +/- 29.4/min to 101.8 +/- 18/min (p less than 0.01) meanwhile the shortest RR interval increased from 359.5 +/- 60.8 to 450 +/- 81.5 msec (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
The efficacy of intracardiac cardioversion was verified in 11 pts suffering from coronary heart disease and recurrent sustained VT. All pts were receiving anti-arrhythmic drugs. Tachycardia cycle length was between 280 and 400 msec. 65 episodes of VT (21 spontaneous and 44 induced) were treated with synchronized shocks of low energy between 0.27 and 2 J using the external cardioverter. Cardioversion was successful in 83% of VT episodes. VT acceleration occurred in one case; transient atrial fibrillation was induced six times. All pts tolerated shocks from 0.27 to 1 J with moderate discomfort; shocks exceeding 1.0 J were less well tolerated. CK levels were not increased. In three pts (VT cycle length of 320, 380 and 400 msec) a permanent Cardioverter (Medtronic Model 7210) was implanted and programmed to operate in non-automatic mode. Every month the pts underwent a follow-up visit to verify the electrophysiological features of VT in non invasively induced VT episodes and the efficacy of transvenous cardioversion. In a mean follow-up period of 9 months, respectively 5, 4 and 3 spontaneous VT episodes occurred. In two pts cardioversion resulted constantly effective, whereas in the third one provoked VT acceleration requiring DC-shock in the last spontaneous episode of VT.
We performed a prospective, randomized crossover study to evaluate the comparative efficacy of transvenous cardioversion and rapid ventricular pacing for termination of induced ventricular tachycardia in patients with spontaneous ventricular tachycardia and organic heart disease. Sixty-two episodes of ventricular tachycardia were induced in 15 patients, mean age 60 +/- 10 years, during electrophysiologic studies. All patients underwent a preselected electrical therapy protocol in a randomized crossover sequence. Transvenous cardioversion was performed by an incremental protocol of three sequential shocks (0.5, 1.1, and 2.7 J). Six asynchronous sequential bursts of rapid ventricular pacing (10 and 15 paced stimuli at 90%, 75%, and 65% of ventricular tachycardia cycle length) were used. Mean cycle length of ventricular tachycardia for the study population was 391 +/- 85 msec. The morphology of the tachycardia was left bundle branch block in 27, right bundle branch block in 32, and indeterminate in three. Characteristics of ventricular tachycardia terminated by the two techniques were comparable. Rate of success for termination of tachycardia with the two methods was also comparable (transvenous cardioversion 83%, rapid ventricular pacing 80%; p greater than .1) and these responses were concordant in 78%. The modes of termination of ventricular tachycardia were similar. The incidence of acceleration of ventricular tachycardia per episode with these preselected protocols was also comparable (transvenous cardioversion 11%, rapid ventricular pacing 6%; p greater than .2). Transient supraventricular tachyarrhythmias were more frequent after transvenous cardioversion (23%) than after rapid ventricular pacing (3%). Significant patient discomfort occurred only after transvenous cardioversion (incidence of 57%).(ABSTRACT TRUNCATED AT 250 WORDS)
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While the technics of cardiac pacing have shown to have a precise role in the diagnosis and treatment of ventricular arrhythmias on a temporary basis, the role of permanent antiarrhythmic devices (PAD) in the treatment of these arrhythmias is still ill defined mainly because of the technological limits concerning the pacemakers and the frequent complications observed during the attempts to interrupt such tachycardias. On the basis of the available data and of theoretical considerations, three groups of pts susceptible of treatment with PAD can be selected: a) pts with brady-dependent arrhythmias where PAD is used as a prophylactic mean; b) pts with recurrent sustained ventricular tachycardia refractory to medical treatment, in whom PAD can be used to interrupt tachycardia; c) pts affected by ventricular fibrillation or rapidly deteriorating ventricular tachycardia (sudden death pts), refractory to conventional treatment, in whom the implantable defibrillator represents the only therapeutic possibility. Even if scanty, the data available seem to confirm that PAD does have a role in the treatment of malignant arrhythmias, although in selected cases and almost always together with drug treatment.
The authors report on two cases of ventricular fibrillation induced by bolus of atropine injected for diagnostic purpose. The electrophysiologic effect of adrenergic stimulation following the parasympathetic blockade, is probably the responsible mechanism rather than myocardial ischemia in the first patient, affected by complete a-v block with narrow QRS. The second patient, affected by coronary heart disease and suspected sick sinus syndrome, had more probably a ventricular fibrillation because of a worsening of the underlying myocardial ischemia due to the increase of the cardiac rate. the reported observations, together with those of other Authors, suggest that atropine, at least when used for diagnostic purpose, should be employed cautiously and preferably having available all the equipment for emergency treatment of cardiorespiratory arrest.
The Authors refer on the methods and the results of permanent electrical treatment with atrial demand pacemakers and radio-frequency systems in 6 cases of brady-tachy syndrome and in 2 cases of recurrent supraventricular tachycardia refractory to drug therapy. In the 6 patients with brady-tachy syndrome atrial demand pacemakers with incorporated radiofrequency receiver were employed; in the 2 patients with supraventricular tachycardia a subcutaneous receiver for radiofrequency stimulation was implanted. The catheters employed were: in 3 patients screw-in leads placed in the right atrial appendage and in 5 unipolar sinus coronary leads. The patient-activated transmitter is been realized in two models: the first one can emit short bursts of eight impulses at the rates of 150-220-260 b/m, each one is selectable by the patient; the number and the period of the beats of the second transmitter can be programmed only by one of us; the stimulator is then given to the patient with a personalized fixed program accordingly to the electrophysiological and clinical observations. During a mean follow up of 7.7 months the safety of the leads both for the stability and the electrical behaviour was noticed in all patients but one with a coronary sinus lead in which a stimulation failure was noticed after the eighth month of stimulation because of high threshold requiring the implantation of a ventricular pacemaker. In the brady-tachy syndrome cases the treatment had a considerable antiarrhythmic efficacy, each patient showing a reduction of hyperkinetic episodes and the ability to interrupt them. In the two cases of refractory supraventricular tachycardia a complete control of the episodes by overdrive stimulation was obtained.
It is described a patient with sick sinus syndrome (atrial bradycardia and reciprocating junctional tachycardia) treated by a permanent ventricular inhibited pacemaker. The catheter is been also connected with a radiofrequency device implanted in order to interrupt the reciprocating tachyarrhythmia with programmed ventricular stimulation.
The criteria commonly followed for the choice of a cardiac pacemaker to be used in the treatment of AV blocks and sick sinus syndrome are described. In case of AV block, the AA, believe that at first implant a ventricular inhibited pacemaker is to be preferred, while for the replacements the choice will be based on clinical grounds (mainly from the data obtained during the periodic controls, such as persistence of spontaneous activity, failure of sensing, etc.). In case of sick sinus syndrome, ventricular inhibited pacemakers are generally to be preferred firstly to secure stimulation even in case of AV block, secondly for the advantage of a greater stability of the endoventricular catheter. Atrial pacemakers (asynchronous, on demand, or bifocal) will be preferred when the atrial contribution is believed to be important from an haemodynamic point of view. Lastly, in single cases, its is possible to implant radiofrequency devices connected with the electrocatheter for the control of the tachyarrhythmic phases.
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