Rolando González

Radiofrequency catheter ablation as a cure for idiopathic tachycardia of both left and right ventricular origin.

OBJECTIVES The purpose of this study was 1) to investigate the efficacy and safety of radiofrequency energy catheter ablation as curative treatment for idiopathic tachycardia of both left and right ventricular origin, and 2) to compare the usefulness of different methods used to map the site of origin of idiopathic ventricular tachycardia. BACKGROUND Percutaneous radiofrequency catheter ablation has been used with dramatic success in the treatment of patients with Wolff-Parkinson-White syndrome, atrioventricular node reentrant tachycardia and bundle branch reentrant tachycardia. Limited data are available on the use of radiofrequency energy catheter ablation as curative treatment for idiopathic tachycardia of both left and right ventricular origin. METHODS Twenty-eight consecutive patients (13 to 71 years old) presenting with idiopathic ventricular tachycardia were enrolled in the study. The site of origin of both left and right ventricular tachycardia was mapped using earliest endocardial activation times during tachycardia and by pace mapping. These mapping techniques were compared. RESULTS Radiofrequency ablation was successful in all eight patients (100%) with left ventricular tachycardia. Tachycardia recurred in one patient. The ablation procedure was complicated by mild aortic insufficiency in one patient. Right ventricular outflow tract tachycardia was successfully ablated in 17 (85%) of 20 patients. The success rate at follow-up was 85%. In one patient, the ablation procedure was complicated by acute ventricular perforation and death. Pace maps from successful ablation sites were better than pace maps from unsuccessful sites (p < 0.004). Endocardial activation times at successful ablation sites were not different from unsuccessful sites (p < 0.13). CONCLUSIONS Radiofrequency catheter ablation is an effective treatment for idiopathic ventricular tachycardia. The site of origin of tachycardia is best identified using pace mapping. Significant complications can occur and should be considered in the risk/benefit analysis for each patient.

Sudden cardiac death and polymorphous ventricular tachycardia in pationts with normal QT intervals and normal systolic cardiac function

This study delineates the clinical spectrum of 15 patients with polymorphic ventricular tachycardia and normal QT intervals in the absence of apparent structural heart disease, adverse drug effects, or electrolyte disturbances. Patients presented with either palpitations (n = 2), presyncope (n = 5), syncope (n = 4), no symptoms (n = 1), or aborted sudden death (n = 3). Mean age was 41 years (range 20 to 64), and mean follow-up 38 months (range 4 to 109). Left ventricular function was normal as determined by either echocardiogram (n = 9) or left ventriculography (n = 9). Episodes of polymorphic ventricular tachycardia (VT) were analyzed in terms of the preceding interval, and the relation of the initiating coupling interval to the QT interval (coupling interval/QT interval = polymorphic VT index). The mean QT for the group as a whole was 0.41 +/- 0.02 second. Patients could be separated into 3 distinct groups. Four patients had polymorphic VT reproducibly induced by exercise and initiated by late-coupled beats (mean polymorphic VT index 1.27 +/- 0.21). Isoproterenol induced polymorphic VT in 3 of 4 patients, and all 4 responded to chronic beta blockade. Two patients had polymorphic VT during episodes of coronary artery spasm, and both responded to calcium channel blockade. Polymorphic VT unrelated to exertion or coronary vasospasm occurred in 9 patients. Tachycardia onset was initiated by closely coupled beats (mean polymorphic VT index 0.95 +/- 0.16), and was preceded by a pause in 4 patients, and no pause in 5 patients. Sudden death occurred in 5 of 9 patients with the shortest polymorphic VT indexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical and electrophysiologic features and role of catheter ablation techniques in adult patients with automatic atrioventricular junctional tachycardia

A total of 8 patients with junctional tachycardia (JT) were included for study. Patients with JT had a supraventricular arrhythmia that was initiated by a junctional complex without PR prolongation and episodes of atrioventricular (AV) dissociation. JT could not be initiated by pacing and occurred either spontaneously (3 patients) or with isoproterenol (5 patients). Tachycardia could be consistently terminated by either carotid sinus massage (1 patient), intravenous adenosine (2 patients), or critically timed ventricular premature complexes (3 patients). In 6 of the 8 other patients, tachycardia foci (atrial or ventricular) or mechanisms (AV node reentry) were found. Two patients underwent complete AV junctional ablation and 2 had termination of tachycardia without change in the AV conduction by perinodal application of radiofrequency lesions. AVJT appears to be due to abnormal automaticity and may be successfully ablated by application of radiofrequency energy to perinodal areas.

Usefulness of sotalol for drug-refractory malignant ventricular arrhythmias

Fifty patients with recurrent sustained symptomatic ventricular tachycardia (43 patients) or ventricular fibrillation (7 patients) resistant to a mean of 2.8 + 1.4 antiarrhythmic drugs were treated with sotalol, a beta-adrenergic receptor antagonist, and 45 underwent invasive electrophysiologic testing before and after sotalol therapy. The arrhythmia became noninducible in 10, was slower and hemodynamically well tolerated in 12 and was poorly tolerated in 23. Four patients were empirically treated with long-term administration of oral sotalol as were 21 patients who either had noninducible arrhythmia (10 patients) or had hemodynamically stable ventricular tachycardia (11 patients). In these 25 patients treated with long-term administration of sotalol, there was no recurrence of ventricular tachycardia in the group with noninducible arrhythmia, whereas 37% of patients with inducible ventricular tachycardia had new ventricular tachycardia or sudden death. Programmed ventricular stimulation with up to three extrastimuli proved to be an excellent predictor of drug efficacy and a good predictor of inefficacy. A positive prior response to amiodarone was not a reliable indicator of a positive response to sotalol. Side effects included those attributed to both beta-adrenergic blockade as well as proarrhythmic effects. The latter were observed in two of four patients with a QT interval greater than 600 ms. Sotalol was found to be effective therapy for a subset of patients with ventricular tachycardia unresponsive to type IA drugs.

Closed chest permanent atrioventricular block in dogs

Ten mongrel dogs underwent transcutaneous His bundle ablation by means of pulsed synchronized electrical shocks delivered between an electrode catheter adjacent to the His bundle and a metal plate behind the dogs back. Detailed histologic studies were performed 3 months after induction of stable complete atrioventricular (AV) block in nine dogs. The ventricular response ranged from 35 to 51 beats/min (bpm). Graded increases in overdrive ventricular pacing resulted in graded increases in pacemaker suppression up to a paced cycle length of 450 msec. All dogs showed extensive damage to the approaches to the AV node, the AV node, and the penetrating portion of the common bundle. This technique resulted in complete AV block with typical features of an infranodal pacemaker and correlated with the histologic findings of severe damage to the AV junction. The minimal myocardial damage suggests that this technique may be applicable for control of drug refractory supraventricular arrhythmias in humans.

Reentry confined to the atrioventricular node: Electrophysiologic and anatomic findings

A patient with recurrent disabling, paroxysmal supraventricular tachycardia refractory to drug treatment underwent electrophysiologic studies. The paroxysmal supraventricular tachycardia was found to be due to atrioventricular (A-V) nodal reentry. The patient died shortly after surgical His bundle section and detailed anatomic studies were performed. These showed fatty infiltration of the approaches to the sinoatrial node, atrial preferential pathways, and A-V node and common bundle. The A-V node was mechanically damaged and the common His bundle was completely severed. These abnormalities were clearly delineated and there was no evidence of an atrio-His bundle bypass tract to an accessory A-V node. Specifically, the central fibrous body and pars membranacea were defined and no atrial muscular fibers pierced these structures to joint the A-V bundle. It is concluded that paroxysmal supraventricular tachycardia due to A-V nodal reentry can be confined to the A-V node.

Effects of glucose-insulin-potassium solution on myocardial salvage and left ventricular function after primary angioplasty.

ObjectiveTo evaluate the effects of glucose-insulin-potassium (GIK) therapy on infarct size and left ventricular function when used as an adjuvant therapy to primary angioplasty. DesignProspective, randomized, double-blind, placebo-controlled study. SettingCardiac intensive care unit at a university hospital. PatientsThirty-seven patients with acute myocardial infarction for whom primary angioplasty was indicated. InterventionsEligible patients were randomized by a blinded pharmacist to GIK solution (30% glucose in water with insulin 50 U/L, and KCl 40 mM/L) vs. placebo at 1.5 mL/kg/hr for 24 hrs. Measurements and Main ResultsTc 99m sestamibi myocardial scintigraphy was performed at admission and at 3 months. Primary end points were the changes in left ventricular ejection fraction (LVEF) and the size of salvaged myocardium. Baseline clinical characteristics were similar in both groups. At the 3-month follow-up, a significant overall decrease in infarct size (37 ± 16% vs. 12 ± 10%, p < .005) and an increase in LVEF (34 ± 13% vs. 49 ± 9%, p = .005) were observed. Patients randomized to GIK solution experienced a significant increase in their LVEF at 3 months (39 ± 12 to 51 ± 13, p = .002). Patients who received placebo had no significant differences between baseline and 3-month measurements (44 ± 13 vs. 49 ± 14, p = NS). There was a trend toward an increase in myocardial salvage in the GIK group, which did not reach statistical significance. When patients from both groups were compared directly, differences in LVEF improvement were no longer significant. ConclusionsGIK solution did not improve LVEF or decrease the infarct size among patients undergoing primary angioplasty.

Emergency intracardiac defibrillation for refractory ventricular fibrillation during routine electrophysiologic study

Ventricular fibrillation refractory to cardiopulmonary resuscitation including multiple transthoracic defibrillations occurred in four patients during 1,215 consecutive ventricular tachycardia induction studies. A technique of emergency intracardiac defibrillation for management of refractory ventricular fibrillation is described. In four patients, stable monomorphic ventricular tachycardia (320 to 570 ms cycle length) was induced during the study and overdrive ventricular pacing resulted in ventricular fibrillation. These patients did not respond to prompt transthoracic defibrillations (5 to 15 attempts/patient) and cardiopulmonary resuscitation, including antiarrhythmic therapy. As a last resort, intracardiac defibrillation was performed with use of a previously inserted standard right ventricular quadripolar catheter as cathode and a posterior skin patch as anode. High energy intracardiac defibrillation pulses (100 to 500 J) delivered from a standard defibrillator successfully terminated each arrhythmia. Intracardiac defibrillation is technically simple and appears effective in terminating refractory ventricular fibrillation in the electrophysiology laboratory. However, further research is necessary to determine the safety and efficacy of this technique, as well as potential applications in other emergency settings.

Electrophysiologic Characterization of Surgically Induced His Bundle Rhythm in Man

Seven patients who had His bundle section and permanent ventricular pacemaker insertion for intractable recurrent supraventricular tachycardia underwent electrophysiologic studies 4–6 months postoperatively. The permanent pacemaker was inhibited to assess the His bundle recovery time (HBRT) and spontaneous His bundle rate (SHBR) (tenth postinhibition cycle). In addition, in five of the seven patients, the HBRT and SHBR was also assessed during mild supine exercise and after administration of intravenous atropine followed by lidocaine. There was no significant difference in HBRT or SHBR before exercise (2695 ± 1056 ms; 1435 ± 75 ms), during mild supine exercise (2220 ± 1564 ms; 1379 ± 42 ms), or after atropine (2152 ± 544 ms; 1379 ± 117 ms) or lidocaine (3943 ± 3198; 1487 ± 139 ms, respectively). Only one patient showed consistent lengthening of both HBRT and SHBR after lidocaine. On a separate day, programmed ventricular extrasiimuli were induced during ventricular overdrive pacing. In three of the seven patients, programmed ventricular extrastimuli resulted in typical bundle branch reentrant depolarizations. Four of the seven patients underwent maximal exercise treadmill testing. In none of these four patients did the His bundle rate exceed that of the implanted pacemaker. We conclude that prolonged pauses often follow pacemaker inhibition in these patients; therefore, careful follow‐up of pacemaker function is required. Surgically induced His bundle rhythms in man are characterized by spontaneous rates of 38.7 to 45,5 beats/min and do not increase their rate after vagolysis or during mild exercise. In addition, the atrioventricular node is not required for bundle branch reentry in man.

Emergency simultaneous transthoracic and epicardial defibrillation for refractory ventricular fibrillation during routine implantable cardioverter-defibrillator testing in the operating room

Abstract Ventricular fibrillation (VF) induced during routine implantable cardioverter-defibrillator placement in the operating room almost always responds to the prompt application of direct-current epicardial shocks (≤40 J), and in some cases, high-energy transthoracic shocks or internal paddle defibrillation is needed to terminate VF. In rare cases, VF that is unresponsive to the standard methods occurs. Recently, a method of emergency intracardiac defibrillation was described for treatment of refractory VF during routine electrophysiologic study. 1 This method uses a standard right ventricular pacing catheter and a posterior skin patch. Defibrillation is performed from the distal pole of the right ventricular catheter to the posterior patch. This method has been successful in 9 of 9 patients at our institution in the electrophysiology laboratory. However, no such rescue procedure has been described for refractory VF induced in the operating room. In this report, we describe 2 patients who received emergency simultaneous transthoracic and epicardial defibrillation for the management of refractory VF during implantable cardioverter-defibrillator placement and testing.