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Pulmonary Vein Arrhythmias. Introduction: Recent studies demonstrated that atrial arrhythmias may be generated within pulmonary veins. The purpose of this study was to compare the endocardial activation times at effective and ineffective ablation sites during radiofrequency catheter ablation of arrhythmias initiated or generated within pulmonary veins. Methods and Results: Twenty-one of 28 patients without structural heart disease underwent successful ablation of 23 arrhythmogenic foci within a pulmonary vein. Electrograms were recorded at 75 pulmonary venous sites and categorized into three groups: 23 successful ablation sites; 28 unsuccessful target sites within an arrhythmogenic pulmonary vein; and 24 sites within nonarrhythmogenic pulmonary veins. The endocardial activation time of premature depolarizations arising at successful target sites was significantly earlier than at other sites. During premature depolarizations, an endocardial activation time of -75 msec or earlier had a sensitivity of 83% and a specificity of 79% for identification of a successful ablation site. Endocardial activation times earlier than -100 msec were recorded only at successful ablation sites, and endocardial activation times later than -30 msec were recorded only at sites within nonarrhythmogenic pulmonary veins. The presence of a split potential during sinus rhythm or premature depolarizations was not a specific indicator of a successful ablation site. Conclusion: The endocardial activation times of premature depolarizations that arise within pulmonary veins and initiate atrial tachycardia/fibrillation are useful in identifying successful ablation sites.

Prior studies have demonstrated that sympathetic tone may influence the effects of adenosine on His-Purkinje automaticity, and that enhanced vagal tone may influence its effects on the sinus node. However, the interaction between autonomic tone and the effects of adenosine on the sinus node in humans remains unknown. Therefore, this study was designed to investigate the interaction between different states of autonomic tone and the bradycardiac response of the sinus node to adenosine. In 11 patients without structural heart disease who underwent a clinically indicated electrophysiology procedure, the sinus cycle length was measured before and after a 12-mg bolus of adenosine in the baseline state, during an infusion of 2 mcg/min of isoproterenol, after the administration of 0.2 mg/kg of propranolol, and again after the administration of 0.04 mg/kg of atropine. Adenosine significantly lengthened the sinus cycle length in the baseline state (760 +/- 165 vs 909 +/- 188 ms, P < 0.05), during isoproterenol infusion (516 +/- 67 vs 766 +/- 146 ms, P < 0.05), after propranolol (850 +/- 153 vs 914 +/- 143 ms, P < 0.05) and after the combination of propranolol and atropine (662 +/- 76 vs 801 +/- 121 ms, P < 0.05). The degree of lengthening in sinus cycle length was significantly greater (P < 0.05) during isoproterenol infusion (253 +/- 157 ms, or 51% +/- 40%) than in the baseline state (149 +/- 85 ms, or 20% +/- 12%), after propranolol (68 +/- 53 ms, or 8% +/- 8%), and after propranolol and atropine (140 +/- 110 ms, or 21% +/- 18%). The negative chronotropic effect of adenosine is influenced by autonomic tone. The effect of adenosine on the sinus node is accentuated by beta-adrenergic stimulation and unaffected by beta-adrenergic blockade or combined beta-adrenergic and cholinergic blockade.

The Accufix (Telectronics Pacing Systems, Englewood, Colo.) atrial active fixation pacemaker lead has a preformed J stiff retention wire than can fracture and erode through the atrium. We screened 85 patients with digital fluoroscopy and detected 18 (21%) lead fractures. Fourteen (16%) leads were successfully extracted by percutaneous techniques. The mean time for extraction and placement of a new atrial lead was 109 ± 53 min, and a lead > 1 year old but not in the presence of a fracture was associated with a significantly longer extraction time. There were two extraction complications. One patient had a fever following the extraction, and one patient had a focal sensory deficit 1 week after the extraction probably caused by a paradoxical embolus. Standard percutaneous extraction tools can be used for successful and safe removal of a fractured Accufix lead.

Previous studies have reported a significant morbidity and mortality associated with coronary artery bypass graft (CABG) surgery in conjunction with the placement of an implantable cardioverter defibrillator (ICD) with an epicardial lead system. In the absence of a control group, how significantly the component of concomitant placement of the ICD system contributes to these untoward outcomes remains unknown. The purpose of this study was to assess the short- and long-term complications in patients undergoing CABG surgery in conjunction with the placement of an ICD with epicardial leads and to compare these complications with those of patients who had only CABG surgery (control group). The study group (group A) consisted of 56 patients who underwent CABG surgery and placement of an ICD pulse generator with epicardial leads. A control group (group B) consisted of 56 patients who underwent CABG surgery only during the same time period. The two groups were matched for age, sex distribution, left ventricular function, surgical approach, number of bypass grafts per patient, bypass pump time, and length of follow-up period. The early mortality for group A was 7.1% versus 1.8% for group B (p > 0.05). The incidence of early morbidity (congestive heart failure, infection, supraventricular and ventricular arrhythmias) for groups A and B was similar (26.8% vs 25.0%, p > 0.05). The incidence of late mortality and morbidity (progression of congestive heart failure, recurrence of coronary events, chronic atrial fibrillation) for groups A and group B were 7.7% versus 5.5% (p > 0.05) and 23.1% versus 21.8% (p > 0.05), respectively. However, death caused by cardiopulmonary difficulties was more frequent in group A than group B (12.5% vs 1.8%, p < 0.05). With the availability of the nonthoracotomy lead system and the pulse generator capable of delivering biphasic shock waveform, to place such an ICD system at a later time after the CABG surgery appears to be the preferred approach to treat patients who need both surgical coronary revascularization and ICD.

Coronary revascularization has been suggested as sole therapy for secondary prevention of sudden cardiac arrest associated with ischemia. The use of implantable defibrillators (ICD) in combination with coronary revascularization for this patient population is unclear. Among 412 consecutive patients receiving an ICD, 23 (6%) were identified as sudden cardiac arrest survivors who were noninducible with programmed stimulation and had unstable angina or ischemia on a functional study; they underwent successful coronary revascularization. During a follow-up of 34 ± 18 months, 10 (43%) of the 23 patients received ICD shocks (8 ± 8 per patient, range 1 to 22 shocks), and nine of the 10 patients had syncope/presyncope associated with at least one ICD discharge. Patients with ICD discharges were compared with those without ICD discharges, and no clinical characteristics were statistically different between the two groups. In conclusion, revascularization alone may be inadequate therapy for survivors of sudden cardiac arrest associated with ischemia who are noninducible with programmed stimulation, and clinical variables cannot predict which patients are likely to have recurrent malignant ventricular arrhythmias.

No prospective studies have compared sotalol and amiodarone during electropharmacologic testing. The purpose of this prospective, randomized study was to compare the electrophysiologic effects of sotalol and amiodarone in patients with coronary artery disease and sustained monomorphic ventricular tachycardia (VT). Patients with coronary artery disease and sustained monomorphic VT inducible by programmed stimulation were randomly assigned to receive either sotalol (n = 17) or amiodarone (n = 17). The sotalol dose was titrated to 240 mg twice daily over 7 days. Amiodarone dosing consisted of 600 mg 3 times daily for 10 days. An electrophysiologic test was performed in the baseline state and at the end of the loading regimen. An adequate response was defined as the inability to induce VT or the ability to induce only relatively slow hemodynamically stable VT. During the follow-up electrophysiologic test, 24% of patients taking sotalol and 41% of those taking amiodarone had an adequate response to therapy (p = 0.30). Amiodarone lengthened the mean VT cycle length to a greater degree than sotalol (28% vs 12%, p < 0.01). There were no significant differences in the effects of sotalol and amiodarone on the ventricular effective refractory period. In patients with coronary artery disease, amiodarone and sotalol are similar in efficacy in the treatment of VT as assessed by electropharmacologic testing. The effects of the 2 drugs on ventricular refractoriness are similar, but amiodarone slows VT to a greater extent than sotalol.

Iodixanol, a new ratio 6 nonionic iodinated contrast agent with an osmolality equal to serum, was compared with iohexol in a randomized, double-blind, parallel study. Two hundred patients undergoing elective diagnostic cardiac angiography were randomized to iodixanol (n = 101) or iohexol (n = 99). There were no differences noted between the 2 agents in the mean changes in systolic or diastolic blood pressure or heart rate during or immediately after any angiography. However, significantly more patients had a decrease in diastolic blood pressure of20 mm Hg during left coronary angiography with iodixanol. The only significant differences in any electrophysiologic parameter were slightly more PR prolongation during left coronary angiography with iodixanol and more ST-segment depression with iohexol during coronary angiography. Neither was clinically significant. Injection-associated discomfort occurred with both agents, but more patients experienced moderate to severe discomfort with iohexol (52%) than with iodixanol (17%) (p0.001). Only 1 potentially serious adverse event, ventricular fibrillation with iohexol, was considered related to contrast, and there were no differences noted between the agents. Overall, angiographic quality was equal with all angiograms being assessed as good or excellent in both groups (p = 0.885). In this low-risk population undergoing cardiac angiography, iodixanol is safe and effective without clinically important differences from iohexol. Additional studies in patients at high risk for complications should help further define the role of iodixanol in cardiac angiography.

Typical atrioventricular (AV) nodal reentry tachycardia (AVNRT) is characterized by anterograde activation over a slowly conducting pathway and by retrograde activation through a rapidly conducting pathway. Preliminary reports suggest that radiofrequency catheter modification can eliminate typical AVNRT while preserving anterograde conduction. Radiofrequency catheter modification was used to treat 88 patients with typical AVNRT. After baseline electrophysiologic evaluation, the ablation catheter was positioned proximal and superior to the site of maximal His deflection. Radiofrequency energy was applied until there was significant attenuation of retrograde conduction, and elimination of AVNRT inducibility. Eighty-one patients were successfully treated and form the basis of this report. A new paroxysmal supraventricular tachycardia with RP greater than PR interval was induced at electrophysiologic testing after successful ablation in 9 patients (11%). Mean atrial-His activation time was 140 +/- 31 ms, and the ventriculoatrial activation time was 170 +/- 46 ms. This arrhythmia was induced only with ventricular pacing during isoproterenol infusion and appeared to be mediated by AV nodal reentry. New retrograde dual AV nodal physiology after modification was more frequent in patients with atypical tachycardia than in those without (4 of 9 vs 2 of 72; p less than 0.0001). Although none of the patients were treated, only 1 of 9 had an episode of spontaneous atypical tachycardia during a mean follow-up of 12 months. Results of this study confirm that typical AVNRT can be rendered noninducible without the complete destruction of reentrant pathways. Because induction of "atypical" AVNRT was not predictive of spontaneous arrhythmia recurrence, it should not be an indication for additional ablation sessions or long-term drug therapy.

The natural history of patients with ischemic cardiomyopathy, asymptomatic nonsustained ventricular tachycardia, and negative electrophysiologic studies was assessed in a retrospective analysis of 55 consecutive patients. The results suggest that the prognosis for arrhythmic death in these patients is not necessarily benign.

The cost of definitive therapy was compared in 25 patients who underwent radiofrequency catheter ablation of accessory pathways in 1990 and 25 patients who underwent surgical ablation of accessory pathways in 1989. In the radiofrequency group, 23 of 25 patients had a single accessory pathway and the remaining 2 patients each had 2 accessory pathways. In the surgical group, 20 patients had a single accessory pathway and 5 patients each had 2 accessory pathways. The success rate was 96% in each group. The mean duration of hospitalization was 3 +/- 1 days in the radiofrequency group and 9 +/- 4 days in the surgical group (p less than 0.0001). All the cost data are expressed in fiscal year 1990/1991 dollar values. The total cost of therapy in the radiofrequency group was $14,919 +/- $6,740 compared with $53,265 +/- $12,755 in the surgical group (p less than 0.0001). The cost of radiofrequency ablation consisted of a hospital charge of $7,753 +/- $3,472 and physician fees of $7,166 +/- $3,439. The hospital charge included charges for use of the electrophysiology laboratory, hospital stay, electrocardiograms, echocardiograms and blood studies. The cost of surgery consisted of a hospital charge of $37,708 +/- $10,179 and physician fees of $15,557 +/- $3,149. The hospital charge in the surgical group included the costs of a baseline electrophysiology study, in-hospital care and a follow-up office visit. In conclusion, radiofrequency catheter ablation of accessory pathways results in a dramatic reduction in the cost of definitive therapy in patients with the Wolff-Parkinson-White syndrome.

Seventy-four patients (16 women, 58 men, age 58 ± 21 years, mean ± standard deviation) who received an implantable Cardioverter de/ibrillator (ICD) after experiencing a single episode of ventricular tachycardia or ventricular fibrillation were followed to determine if antiarrhythmic drug therapy affects the incidence of ICD discharges. Thirty-three patients (group A) were treated with an antiarrhythmic drug that was either untested or previously demonstrated during electropharmacological testing to be ineffective in suppressing the induction of ventricular tachycardia. Forty-one patients (group B) were not treated with an antiarrhythmic drug. There were no significant differences between the two groups in regards to age, sex, incidence of coronary artery disease, left ventricular function or the type of ICD pulse generator used. During a mean follow-up of 14 months for the entire cohort, 15 patients (46%) in group A and 18 patients (44%) in group B experienced at least one ICD shock. The time to the first appropriate shock (5 ± 5 months in both groups) and the frequency of ICD shocks (0.3 ± 0.2/month in group A vs 0.4 ± 0.5/month in group B) were similar in both groups. The incidence of syncope at the time of ICD discharge was higher in group A than group B patients (31% vs 5%, P < 0.05). In conclusion, antiarrhythmic drugs that are untested or have failed electropharmacological testing do not appear to reduce the probability of ICD discharge over a short-term (mean 14 months) follow-up in patients who have had only one clinical episode of VT/VF and may increase the risk of syncope during ICD discharge. Studies with a larger sample size and longer follow-up period will be needed to confirm these findings.

Ten consecutive patients with recurrent episodes of symptomatic, idiopathic, sustained monomorphic ventricular tachycardia (VT) originating in the right ventricle underwent an attempt at catheter ablation of the ventricular tachycardia. There were seven women and three men, with a mean age of 39 +/- 14 years (+/- SD). None of the patients had any evidence of structural heart disease. The VT had a left bundle branch block configuration and an inferior axis in each patient, and the mean cycle length was 313 +/- 75 msec. Based on the methods of induction of the VT and the response of the VT to verapamil, the VT mechanism was presumed to be reentry in six patients, triggered activity in three patients, and catecholamine-sensitive automaticity in one patient. Sites for ablation were guided by pace mapping, and an appropriate target site was identified in the right ventricular outflow tract in each patient. From one to three shocks of 100-360 J (mean total, 336 +/- 195 J) were delivered from a defibrillator between the tip of the ablation catheter (cathode) and a patch electrode on the anterior chest (anode). An electrophysiology test 7-9 days after ablation demonstrated that VT was still inducible in only one patient, who was treated with amiodarone. One other patient had a recurrence of VT 3 weeks after ablation and was treated with verapamil. Eight of 10 patients were not treated with antiarrhythmic medications and have had no episodes of symptomatic VT during 15-68 months of follow-up (mean follow-up, 33 +/- 18 months). There were no acute or long-term complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Right ventricular refractory periods obtained using atrial and ventricular pacing with an atrioventricular (AV) interval of 160 ms were compared with those obtained with an AV interval of 0 ms in a group of 53 patients. The mean right ventricular effective refractory periods were longer at an AV interval of 160 ms than at an AV interval of 0 ms at pacing cycle lengths of 600 (mean 2.5 +/- 1.8 ms difference) and 400 ms (mean 3.8 +/- 2.4 ms difference; P less than 0.01). In a subset of 10 patients, left ventricular volumes measured by two-dimensional echocardiography demonstrated that pacing with an AV interval of 160 ms was associated with a higher end-diastolic volume and stroke volume than pacing with an AV interval of 0 ms (P less than 0.001). Autonomic blockade did not alter the relationship between AV interval and ventricular refractoriness. We conclude that 1) right ventricular refractory periods are shorter at an AV interval of 0 ms than at an AV interval of 160 ms; 2) these differences are not caused by changes in autonomic tone but are associated with differences in ventricular volumes; and 3) if precise determinations of ventricular refractoriness are desired, then the timing of atrial systole should be controlled by atrial pacing.

TOIVONEN, L.K., ET AL.: The Ventricular Excitability-Interval Relationship in Early Diastole in Humans: The Influence of the Electrode Configuration During Bipolar Stimulation. The purpose of this sludy was to determine (he relationship belween ventricular excitability and the extrastimuJus (S2) coupling interval in early diastole in humans. The influence of the electrode configuration during bipolar stimulation was examined. Ventricular strength-interval curves were constructed using an eight beat drive train at a cycle length 0/ 600 msec, 2-msec decrements in the S2 coupling interval, and 0.2-mA increments in the current intensity 0/ S2 at each coupling interval. A transient dip in ihe excitation threshold was observed in early diastole during bipolar pacing when the distal electrode was the anode in six of 17 patients {35%}. In contrast, this type of dip was not observed when the distal electrode was the cathode. The excitation threshold at the trough of the dip ranged from 1.0 to 2.2 mA. Unipolar strength-interval curves indicated that a dip occurred with anodal but not cathodal pacing. We postulated that the dip might inter/ere with the accurate determination of the ventricular ejfective refractory period hy resulting in transient loss of ventricular capture during decremental scanning of diastole with S2. A gap in ventricular capture was produced in all six patients who demonstrated a dip in the bipolar strength-interval curve by selecting an S2 current intensity that fell within the dip. In conclusion, the bipolar strength-interval curve may display an early diastolic dip in the excitation threshold, depending on the electrode conjiguration. During determination of the ventricular effective refractory period, if the stimulus intensity falls within the range of current intensities encompassed by the dip, a transient early diastolic gap in ventricular capture will he observed as diastole is scanned with S2. If this type of gap is not recognized, the ventricular effective refractory period may be overestimated. (PACE. Vol. 13, July 1990}

The yield of sustained, monomorphic ventricular tachycardia (VT) induced by programmed ventricular stimulation was compared, using basic drive trains of 400 ms, 600 ms and sinus rhythm, to identify the most efficient sequence of basic drive trains to use during programmed stimulation. Fifty-five patients with coronary artery disease and inducible sustained monomorphic VT not requiring countershock to terminate underwent 81 electrophysiology tests in which 1 to 3 extrastimuli were introduced during sinus rhythm and after basic drive trains of 600 and 400 ms. In 72 electrophysiology tests, sustained, monomorphic VT was induced at the right ventricular apex. The yield of VT using a drive cycle length of 400 ms was 63 of 72 (88%), compared to 46 of 72 (64%) when the drive cycle length was 600 ms, and 23 of 72 (32%) when the extrastimuli were introduced during sinus rhythm (p less than 0.001 for all pairwise comparisons). In 14 electrophysiology tests in which VT was not induced using a 400 ms basic drive cycle length at the apex, the yield of VT was higher using a 400 ms drive cycle length at a second right ventricular site (12 of 14) than with a 600 ms drive cycle length (3 of 12) or sinus rhythm (4 of 12) at the apex (p less than 0.05). The yield of sustained, monomorphic VT induced by 1 to 3 extrastimuli increases as the basic drive cycle length shortens. Whereas programmed stimulation is conventionally started during sinus rhythm or with a drive cycle length of 600 ms, the present results suggest that starting with a drive cycle length of 400 ms may be more efficient.

OBJECTIVES Using data from the Multicenter UnSustained Tachycardia Trial (MUSTT), we examined the factors used to select antiarrhythmic drug therapy and their impact on outcomes. BACKGROUND The MUSTT examined the use of programmed ventricular stimulation (PVS) to guide antiarrhythmic therapy in patients with coronary arteriosclerosis, left ventricular dysfunction and asymptomatic, unsustained ventricular tachycardia (VT). Trial outcomes may reflect factors used to select antiarrhythmic drug therapy. METHODS We compared subgroups of patients with inducible sustained VT randomized to PVS-guided antiarrhythmic therapy (n = 351), in particular those receiving PVS-guided antiarrhythmic drug therapy (n = 142) versus no antiarrhythmic therapy (controls, n = 353). RESULTS “Effective” antiarrhythmic drug therapy (i.e., the term “effective” was used to denote therapy that resulted in noninducible VT or hemodynamically stable induced VT) was found for 142 of the 351 patients (43%), most often at the first or second PVS session (125/142, 88%). Mortality among the 142 patients did not differ from that among control patients. Of these 142 patients, the PVS end point was noninducibility in 91 patients and stable VT in 51 patients. Mortality did not differ between these two groups either, but arrhythmia was numerically more frequent in the PVS-induced stable VT group. Mortality was greatest in the few patients receiving propafenone (unadjusted p = 0.07, adjusted p = 0.14 vs. controls), but mortality with all agents did not differ from that of controls, even after adjustment. CONCLUSIONS Even when presenting the results as favorably as possible, we found no benefit with PVS-guided drug therapy in patients with clinical unsustained VT who had inducible sustained VT. These findings are unaltered by using different end points for PVS or considering the response to individual drugs.

We studied the immediate reproducibility of the results of the head-up tilt-table test in elderly patients (age > or =60 years). Twenty-seven consecutive men underwent 51 tests. The overall reproducibility was 98%, including 92% of a positive test and 100% of a negative test. The finding of this study validates the use of intravenous pharmacologic intervention in the elderly population.

A 53-year-old female visited our out-patient department complaining of right flank pain. Ultrasonography revealed a solid mass lesion in the lower pole of the right kidney and further evaluation was scheduled. A few days later, she suddenly felt pain at the abdominal enlarged mass. Computed tomographic (CT) scan revealed a huge retroperitoneal mass with heterogenous density. Spontaneous rupture of renal tumor was suspected and emergency nephrectomy was performed. The ruptured tumor was pale, elastic firm and invaded directly to the duodenum. Histopathological findings revealed fibrous cells with frequent nuclear mitosis. Smooth muscle actin was identified immunohistochemically. Therefore, the tumor was diagnosed as leiomyosarcoma. The patient died 2 months after operation due to perforation of the intestine.

Recognition of tachyarrhythmia by an implantable cardioverter-defibrillator (ICD) requires an intact rate-sensing lead. We retrospectively examined 266 consecutive patients requiring an ICD to characterize the incidence, clinical presentation, diagnosis, and management of a defective rate-sensing lead. To identify clinical parameters that may contribute to lead complications, we also assessed the effects of age, gender, type of rate-sensing lead, manufacturer of the lead, and surgeon. Over a follow-up period of 30 +/- 22 months (mean +/- standard deviation), a defective lead was found in 9 (3.4%) patients, in 9 (1.7%) of 514 leads over a period of 2 to 39 (mean 17 +/- 15) months after implantation. Except for 1 patient, in whom a lead fracture was incidently found during ICD generator replacement, these patients had multiple inappropriate shocks of recent onset. Clinical parameters were not helpful in identifying patients at risk for lead complication. An abnormal beeping signal obtained while the patients performed various maneuvers was helpful in confirming a defect. All of the defective leads were epicardial. These cases were managed by placement of a transvenous endocardial lead.

Nineteen patients with ischemic heart disease were studied to determine plasma levels of isosorbide dinitrate (ISDN) and its metabolites, isosorbide-2-mononitrate (2-ISMN) and isosorbide-5-mononitrate (5-ISMN) for 6 hrs during intravenous administration of ISDN, using gas chromatography. Differences in plasma levels of these substances were also evaluated in patients with or without preanesthetic medication of ISDN. These patients ranging in ages from 42 to 80 years were administered ISDN intravenously at a rate of 1 micrograms.kg-1 x min-1 during anesthesia and surgery. Preanesthetic administration of ISDN consisted of transdermal application of 40 mg dose. Surgery included gastrectomy, pneumonectomy, extended cholecystectomy, radical mastectomy and so on under either enflurane anesthesia or neuroleptanesthesia. Plasma ISDN levels increased and reached a plateau 3 hrs after the start of intravenous infusion of ISDN in patients of both groups. Plasma 2-ISMN levels increased gradually and reached a plateau 5 hrs after the commencement of intravenous administration of ISDN in patients of both groups. Plasma 5-ISMN levels increased gradually reaching the peak 6 hrs after the start of intravenous infusion of ISDN in both groups. Plasma ISDN, 2-ISMN and 5-ISMN levels were slightly higher in patients who received preanesthetic ISDN than in those who did not receive preanesthetic ISDN. However, there were no statistical differences in plasma ISDN or 2-ISMN levels between the groups except prior to the infusion. On the contrary, plasma 5-ISMN levels were significantly higher in patients who received preanesthetic ISDN than in those who did not receive preanesthetic ISDN for 3 hrs after the start of the infusion.

BACKGROUND Delivery of shocks within the right atrium has been reported to be more effective than conventional external shocks in converting atrial fibrillation (AF), but these two cardioversion techniques have never been compared prospectively. The purpose of this study was to compare the efficacies of external and internal cardioversion in patients with chronic AF unresponsive to prior attempts at electrical and/or pharmacological cardioversion. Low-dose amiodarone was used in all patients after cardioversion to suppress recurrences of AF. METHODS AND RESULTS One hundred twelve patients with AF of at least 1 month in duration were randomly assigned to undergo external cardioversion with 300-360-J shocks or internal cardioversion with 200-300-J shocks delivered through a standard electrode catheter within the right atrium. The patients were treated with amiodarone (200 mg/day 5-7 days/week) for 1 month before electrical cardioversion and afterward if the cardioversion was successful. The patients were evaluated at regular intervals during 1 year of follow-up. The efficacy of internal cardioversion was significantly greater than that of external cardioversion (91% versus 67%, p = 0.002). The only variable that was associated with the outcome of cardioversion was body weight. Among patients in whom sinus rhythm was restored, AF recurred as often after internal and external cardioversion; at 1 year of follow-up, 37% of patients in whom external or internal cardioversion had been effective were still in sinus rhythm. Patients who had undergone an attempt at electrical cardioversion before entry into this study were less likely to remain in sinus rhythm after cardioversion. The only complications of cardioversion were one instance of cerebral thromboembolism after external cardioversion and one instance of transient pulmonary edema after internal cardioversion. Therapy with amiodarone was discontinued because of an adverse drug effect in only three patients. CONCLUSIONS Internal cardioversion is more effective than external cardioversion in restoring sinus rhythm and is as safe as external cardioversion in patients with chronic AF. The recurrence rate of AF is the same after both types of cardioversion. If conventional electrical cardioversion is ineffective, internal cardioversion should be attempted. The combination of low-dose amiodarone and external or internal cardioversion may result in maintaining sinus rhythm long-term in patients with refractory AF.

Effect of pirenzepine, famotidine or a combination of both agents on gastric secretion during anesthesia and surgery was evaluated in 42 surgical patients ranged in age from 17 y to 70 y. They underwent orthopedic, ophthalmic, ENT, plastic, oral or non-abdominal surgery under either neuroleptanesthesia or enflurane anesthesia. They received either pirenzepine 10 mg, famotidine 20 mg or the combination of both agents intravenously just before the induction of anesthesia. Volume and acidity of gastric juice were measured during 3 hours after the administration of these agents. A continued decrease in volume and acidity of gastric juice was observed 3 hrs after the administration of the agents both in the pirenzepine group and in the famotidine group. Efficacy of the combination of pirenzepine and famotidine on gastric secretion tended to be more prominent than that of either pirenzepine or famotidine alone.

To evaluate the effect of sympathetic activation on the efficacy of the implantable cardioverter-defibrillator (ICD) in converting ventricular tachycardia (VT) or ventricular fibrillation (VF), 32 patients who received an ICD because of life-threatening VT/VF underwent 1 week postimplant ICD testing both before and after infusion of 25 (16 patients) or 50 (16 patients) ng/kg/min of epinephrine for greater than or equal to 12 minutes. These infusion rates are known to result in plasma epinephrine concentrations comparable to mild-moderate stress. The patients' mean age was 63 +/- 10 years; 26 had coronary artery disease, 2 had dilated cardiomyopathy and 4 had no evidence of structural heart disease. VT and VF were induced in 16 patients each by programmed stimulation or alternating current. Among the 16 patients with VT, the first ICD discharge (26 to 30 J) was effective in 15 patients in the baseline state and in all 16 patients during epinephrine infusion. Among patients with VF, the first ICD discharge (26 to 30 J) terminated VF in all patients in the baseline state, compared with 12 of 16 patients during epinephrine infusion (p less than 0.05). In 4 patients, VF was terminated during epinephrine infusion only by the second or third ICD discharge (30 J). In conclusion, physiologic increases in the plasma epinephrine concentration may increase the number and energy of shocks needed to terminate VF.

Fifteen consecutive patients with drug-refractory, recurrent, sustained, monomorphic ventricular tachycardia and a history of remote myocardial infarction underwent catheter ablation of ventricular tachycardia. Shocks of 100 to 300 J were delivered to sites at which pacing during ventricular tachycardia resulted in concealed entrainment, in which the ventricular tachycardia accelerated to the pacing rate, there was a long stimulus to QRS interval and there was no change in the configuration of the QRS complex during pacing at several rates compared with the configuration during ventricular tachycardia, thus identifying a zone of slow conduction in the reentrant circuit. Concealed entrainment was demonstrated in nine (60%) of 15 patients, and the stimulus to QRS intervals were 90 to 400 ms. At sites of concealed entrainment, the endocardial activation time relative to the QRS complex during ventricular tachycardia ranged from -125 to +50 ms, the timing of the local electrogram relative to the QRS complex was the same during entrainment as during ventricular tachycardia and the pace map during sinus rhythm was discordant with that of the ventricular tachycardia in seven patients. In the six patients in whom a site of concealed entrainment could not be identified, the target site for ablation was selected on the basis of identification of an isolated mid-diastolic potential, activation mapping and pace mapping. The mean (+/- SD) cumulative number of joules delivered to the target site was 306 +/- 140. A successful long-term clinical outcome was achieved in 9 of the 15 patients (mean follow-up 20 +/- 7 months). The clinical success rate was the same whether the target site was selected on the basis of concealed entrainment (five of nine, 56%) or on the basis of the other mapping techniques (four of six, 67%). In conclusion, the responses to pacing suggest that sites at which there is concealed entrainment may be located within a zone of slow conduction in the ventricular tachycardia reentry circuit, although not necessarily in an area critical for the maintenance of reentry. The long-term clinical efficacy of catheter ablation targeted to sites of concealed entrainment is about 60%, similar to the results achieved when conventional mapping techniques are used.

BACKGROUND This study compared the sensitivity, specificity, and efficiency of a "conventional" and "accelerated" programmed stimulation protocol in 293 patients with coronary artery disease who had a history of sustained or nonsustained monomorphic ventricular tachycardia (VT). METHODS AND RESULTS In the conventional protocol, one and two extrastimuli were introduced during sinus rhythm and during basic drive trains at cycle lengths of 600 and 400 msec at the right ventricular apex and then at the outflow tract or septum. In the accelerated protocol, one, two, and then three extrastimuli were introduced at each of three basic drive train cycle lengths (350, 400, and 600 msec) at the right ventricular apex; the procedure was repeated at a second right ventricular site. Six hundred thirty-four electrophysiological tests were performed using one of these two protocols either in the baseline state (293 tests) or during drug testing (341 tests). The yield of sustained, monomorphic VT was 89% with the conventional protocol and 92% with the accelerated protocol during baseline tests in patients who had a history of sustained VT (p = 0.05); 20% and 34%, respectively, during baseline tests in patients with a history of nonsustained VT (p = 0.06); and 70% and 77%, respectively, during drug testing (p = 0.2). To induce sustained, monomorphic VT, 10.1 +/- 5.0 (mean +/- SD) protocol steps and 14.4 +/- 8.7 minutes were required with the conventional protocol, compared with 4.0 +/- 3.7 steps and 5.6 +/- 6.1 minutes with the accelerated protocol (p less than 0.001 for each comparison). Among the tests in which sustained, monomorphic VT was induced, sustained polymorphic VT or ventricular fibrillation was induced more often with the conventional protocol (3.6%) than with the accelerated protocol (0.9%, p = 0.05). CONCLUSIONS The efficiency of programmed stimulation can be improved by the early use of a basic drive train cycle length of 350 msec and three extrastimuli. Compared with a conventional stimulation protocol, the accelerated protocol used in this study reduces the number of protocol steps and duration of time required to induce monomorphic VT by an average of more than 50% and improves the specificity of programmed stimulation without impairing the yield of monomorphic VT.

We studied the influence of prolonged anesthesia and surgery on total body water (TBW) with tetrapolar bioelectrical impedance analysis (BIA). Eight patients who underwent prolonged anesthesia were selected as the subjects of the study and were compared with nine patients who underwent surgery of less than 3 hours. Plasma hormone concentrations were also examined. In the prolonged anesthesia patients, TBW increased significantly as compared with those of the patients who underwent short surgery (P less than 0.05). TBW showed the most remarkable increase on the first post operative day. Plasma ADH and aldosterone concentrations increased in the patients of both groups. However, we could not find a significant relationship between TBW and plasma hormone concentrations. BIA seems to be a useful method to estimate TBW during perioperative periods. However, further detailed investigation would be necessary to obtain a reliable technique in such an unstable condition.

OBJECTIVE: To determine the incidence of loss of consciousness occurring in association with shocks delivered by automatic implantable cardioverter-defibrillators (AICD) in patients who had undergone implantation as treatment for ventricular tachycardia or ventricular fibrillation. DESIGN: Cohort study. SETTING: Two major tertiary medical care facilities. PATIENTS: A total of 180 patients who had undergone implantation of an AICD for treatment of ventricular tachycardia or ventricular fibrillation. INTERVENTION: Implantation of an AICD that delivered only high-energy shock. MEASUREMENTS: During a mean (+/- SD) follow-up period of 16 +/- 12 months, the incidence of loss of consciousness occurring in association with spontaneous AICD shocks was determined. Various clinical factors were analyzed to identify predictors of loss of consciousness that occurred during AICD shocks. MAIN RESULTS: Of the 180 patients who received an AICD, 106 patients (59%) experienced AICD shocks during follow-up. Sixteen of the 180 patients (9%) experienced loss of consciousness; 13 of these 16 patients had syncope and 3 died suddenly, in association with AICD shocks. The absence of syncope during one AICD shock did not always predict the absence of syncope during subsequent shocks. Syncope could not be predicted by age, sex, history of syncope, left ventricular function, type of underlying heart disease, electrophysiologic findings, rate of ventricular tachycardia, antiarrhythmic medications, and type of pulse generator implanted. CONCLUSIONS: Patients with sustained ventricular tachycardia or ventricular fibrillation who receive an AICD that delivers only high-energy shock therapy are at moderate risk for experiencing loss of consciousness during AICD shocks. No clinical variables were found to be predictors of syncope. Therefore, driving and other activities that require patients to be extra vigilant should not be assumed to be safe after implantation of an AICD that delivers only high-energy shock. Language: en

Evidence of an atriofascicular accessory pathway has not been reported previously. In the patient presented in this case report, an electrophysiology study demonstrated a constant left bundle branch block QRS configuration despite varying degrees of ventricular preexcitation, in association with a constant artrioventricular interval during incremental atrial pacing and programmed atrial stimulation. The presence of an atrioventricular, nodoventricular, nodofascicular, and atrial-His accessory pathway was ruled out. The findings are best explained by the presence of an underlying left bundle branch block and an atriofascicular accessory pathway connecting the atrium and right bundle. The atriofascicular accessory pathway was a passive bystander during an atrial tachycardia and was not directly involved in the generation of the tachycardia. To our knowledge, this is the first report of an atriofascicular accessory pathway.

The electrophysiologic effects of circulating epinephrine in humans were examined in four study groups of 10 subjects each. In 10 subjects without structural heart disease (Group 1) and in 10 patients with coronary disease or dilated cardiomyopathy (Group 2) epinephrine infusion at 25 and 50 ng/kg body weight per min for 14 min resulted in an elevation of the plasma epinephrine concentration in the physiologic range. In both groups it produced a dose-dependent decrease in the effective refractory period of the atrium, atrioventricular (AV) node and ventricle and improvement in AV node conduction. Epinephrine facilitated the induction of sustained ventricular tachycardia in 3 of the 20 subjects. In Group 3, a beta-adrenergic blocking dose of propranolol was added to the infusion of 50 ng/kg per min of epinephrine. Propranolol not only reversed the effects of epinephrine, but also lengthened these variables compared with baseline values. In Group 4, propranolol was administered first, followed by 50 ng/kg per min of epinephrine. Propranolol alone slowed AV node conduction and mildly prolonged the refractory periods. In the presence of betablockade, epinephrine had no effect on AV node properties but resulted in a lengthening of the atrial and ventricular effective refractory periods. In conclusion, epinephrine in physiologic doses shortens the effective refractory period of the atrium, AV node and ventricle, improves AV node conduction and may facilitate the induction of sustained ventricular tachycardia. The overall electrophysiologic effects of epinephrine result from stimulation of beta-receptors. Stimulation of alpha-receptors by epinephrine has no effect on the AV node but prolongs the effective refractory period of the atrium and ventricle, partially offsetting the shortening of refractory periods mediated by beta-receptor stimulation.

The results of 206 programmed ventricular stimulation studies performed in 130 patients (100 men and 30 women, mean age 62 +/- 12 years, +/- standard deviation) were examined prospectively to determine the sequelae of nonsustained polymorphic ventricular tachycardia (VT) induced during programmed ventricular stimulation. The clinical indication for the electrophysiologic study was either documented monomorphic VT or unexplained syncope. The pacing protocol included 2 right ventricular pacing sites, 2 basic drive cycle lengths and up to 3 extrastimuli. In 111 studies, nonsustained polymorphic VT was induced and with continuation of the programmed stimulation protocol, sustained monomorphic VT was induced in 48 studies (43%) and polymorphic VT was induced in 13 studies (12%). Overall, sustained monomorphic VT was induced in 110 studies and sustained polymorphic VT in 18 studies. The incidence of nonsustained polymorphic VT preceding the induction of sustained polymorphic VT was significantly greater than the incidence of nonsustained polymorphic VT preceding the induction of sustained monomorphic VT (72 vs 44%, p less than 0.05). Nonsustained polymorphic VT is not a useful predictor of the outcome of programmed ventricular stimulation. The use of nonsustained polymorphic VT as an endpoint for stimulation would be likely to improve the specificity of programmed ventricular stimulation by limiting the induction of sustained nonclinical arrhythmias that require countershock, but at the cost of significantly impairing the yield of monomorphic VT.

This prospective study compared the yield of programmed ventricular stimulation with single and double extrastimuli during an infusion of isoproterenol with that of programmed stimulation with triple extrastimuli. The subjects of this study were 58 patients who underwent programmed stimulation and did not have inducible ventricular tachycardia (VT) with single or double extrastimuli at two basic drive cycle lengths and at two right ventricular sites; 17 patients had a history of uniform VT unrelated to exercise, and 41 had no history of documented or suspected VT or ventricular fibrillation (VF). Programmed stimulation was performed with triple extrastimuli at both right ventricular sites. Isoproterenol was infused as a dose titrated to increase the sinus rate by 25% or to a rate of 100 beats/min, whichever was greater, and stimulation then was repeated with single and double extrastimuli. Among the 17 patients with a history of uniform VT, the clinical VT was induced by three extrastimuli in five patients (29%) and by two extrastimuli during isoproterenol infusion in six patients (35%, p greater than 0.05). Among the total study population of 58 patients, nonclinical multiform VT or VF was induced by three extrastimuli in 29 patients (50%), and by two extrastimuli during isoproterenol infusion in 15 patients (26%, p less than 0.05). Therefore stimulation with two extrastimuli during isoproterenol infusion has the same probability of inducing a clinical form of VT as does stimulation with extrastimuli, but the former has a significantly lower probability of inducing nonclinical multiform VT and VF.

Thirty-three patients with recurrent ventricular tachycardia (VT) underwent catheter ablation with direct-current shocks. One to four shocks of 100-300 joules were delivered to the presumed VT exit sites as identified by endocardial mapping and pace mapping. Fifteen patients (45%) had no recurrence of symptomatic VT during a follow-up interval of 15.5 +/- 10 months (mean +/- standard deviation). Five patients experienced six nonfatal complications (new VT or ventricular fibrillation, transient neurological deficit, atrioventricular block, brachial artery thrombosis). In conclusion, catheter ablation in selected patients with recurrent VT has the potential for preventing recurrences of VT over the long-term and is relatively safe.

Pirmenol is an investigational type 1A antiarrhythmic drug the long-term efficacy of which has not been fully determined. Therefore the long-term efficacy of oral pirmenol in suppressing ventricular premature depolarizations (VPDs) was assessed in an open-label, dose-titration study. Twelve patients (eight men and four women; mean age 57 +/- 12 years) were treated for 24 to 36 months (mean 33 +/- 4). Seven had structural heart disease (three valvular heart disease, two ischemic heart disease, and two hypertensive heart disease) and five did not. The mean left ventricular ejection fraction was 0.63 +/- 0.13. Exclusion criteria included less than 30 VPDs/hr, greater than 15 beats of ventricular tachycardia (VT), or prior failure of more than two antiarrhythmic drugs. Drug efficacy was assessed by 24-hour ambulatory ECG monitoring performed every 3 months during the first year, every 4 months during the second year, and at 6-month intervals during the third year. The mean hourly frequency of VPDs during the placebo phase was 732 +/- 608. Seven patients (58%) were treated successfully with effective (greater than 75%) long-term suppression of VPDs. Two patients (17%) had a partial response with effective suppression of VPDs for the first 16 months and 5 months of treatment, respectively. Three patients failed to show consistent suppression of VPDs while receiving pirmenol. The daily dose of pirmenol ranged from 200 to 500 mg (mean 317 +/- 94 mg at the beginning of the study and 375 +/- 97 mg at the end). No proarrhythmic effects were identified during long-term treatment, and none of the patients withdrew from the study prematurely.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of our study was to determine whether an infusion of epinephrine reverses the electrophysiologic effects of verapamil and whether reversal of verapamil's effects on the induction of paroxysmal supraventricular tachycardia (PSVT) by epinephrine during electropharmacologic testing is predictive of stress-related recurrences of PSVT during long-term treatment with verapamil. The infusion rates of epinephrine used in this study were 25 and 50 ng/kg/min, which previously have been demonstrated to result in plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. The subjects of this study were 17 patients with recurrent PSVT who underwent an electrophysiologic study in the control state and after at least 2 days of treatment with 240-480 mg/day verapamil. After assessing the response to verapamil, epinephrine was infused and testing was repeated. Verapamil significantly slowed atrioventricular conduction and prolonged refractoriness in the atrium and atrioventricular node. The effects of the two infusion rates of epinephrine were generally similar in magnitude and, therefore, the results were pooled. Epinephrine partially or completely reversed all of verapamil's electrophysiologic effects. Verapamil suppressed the induction of sustained PSVT in 15 patients. Epinephrine facilitated the induction of PSVT in seven of these 15 patients. All 15 patients were treated on a long-term basis with verapamil. The eight patients in whom epinephrine did not facilitate the induction of PSVT had no recurrences of PSVT during 9-18 months of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was to determine whether there is accentuated antagonism between sympathetic and vagal effects on ventricular refractory periods (VRPs) in humans. The effects of 0.04 mg/kg of atropine on the right ventricular effective and functional refractory periods were determined in the setting of beta-adrenergic blockade by propranolol (0.15 mg/kg loading dose, then 0.1 mg/min continuous infusion, group 1) and in the setting of beta-adrenergic stimulation by 25 or 50 ng/kg/min isoproterenol (groups 2 and 3, respectively). Groups 4 to 6 served as control groups. In group 4, VRPs were determined on three occasions separated by 10 min each in the absence of drug. VRPs also were determined on two occasions after infusion of propranolol (group 5) or 25 ng/kg/min of isoproterenol (group 6). Groups 1 to 4 consisted of 10 subjects each, and groups 5 and 6 consisted of five subjects each. VRPs were determined with the use of basic drive cycle lengths of 600, 500, 400, and 350 msec. Because of sinus tachycardia, sufficient data for comparison of groups 1 to 3 were available only at drive cycle lengths of 400 and 350 msec. Atropine significantly shortened the VRPs in groups 1 to 3, but the magnitude of atropine's effects in group 3 (5.3% to 5.8% shortening at drive cycle length of 350 msec) was significantly greater than in group 1 (2.6% to 3.0% shortening, p less than .05) Data from the control groups demonstrated that there was no effect of time on measurement of VRPs either in the drug-free state or in the presence of propranolol or isoproterenol. The results of this study indicate that cholinergic tone lengthens VRPs in the absence of background sympathetic activity and that this lengthening of VRPs may become accentuated during beta-adrenergic stimulation.

Three patients who had incessant ventricular tachycardia and in whom a zone of slow conduction was identified are presented. Each patient's tachycardia was refractory to multiple antiarrhythmic drugs and was being treated with amlodarone at the time of the electrophysiologic study. The ventricular tachycardia cycle length was 500 to 580 ms. In Patients 1 and 2, a single site at the posterolateral wall or low septum in the left ventricle was identified at which overdrive pacing during ventricular tachycardia resulted in ventricular capture with a stimulus to QRS interval of 280 to 400 ms and with little or no change in the configuration of the QRS complexes during pacing as compared with during ventricular tachycardia. In Patient 3, the same phenomenon was observed at two areas in the left ventricle: at the inferior wall, overdrive pacing during ventricular tachycardia resulted in a stimulus to QRS interval of 440 to 470 ms, whereas at the posterolateral wall, the stimulus to QRS interval was 320 to 360 ms. Transcatheter shocks of 100 to 240 J delivered at the pacing sites have been successful in preventing recurrences of ventricular tachycardia over a follow-up period of 10 to 11 months.These observations may be explained by the pacing site being located within a reentrant circuit in a zone of slow conduction bounded by inexcitable tissue between the pacing site and the exit site of the reentrant circuit. In Patient 3, the variable stimulus to QRS intervals are explained by variable proximity of the pacing sites within the slow conduction zone to the exit site of the reentrant circuit. The findings of this report demonstrate that it may be possible to identify a zone of slow conduction that is a critical component of the reentrant circuit of ventricular tachycardia. Initial results suggest that this slow conduction zone may be an ideal location to deliver transcatheter shocks for the purpose of ventricular tachycardia ablation.

This study determines the results of programmed stimulation in patients with syncope or near-syncope presumed to have the carotid sinus Syndrome based on the finding of carotid sinus hypersensitivity and the absence of any other apparent cause for syncope or near-syncope after clinical evaluation. Fourteen patients had coronary artery disease, 1 had dilated cardiomyopathy and 18 patients did not have structural heart disease. Programmed simulation was performed at 2 basic drive cycle lengths and 2 right ventricular sites with 1 to 3 extrastimuli. Sustained unimorphic ventricular tachycardia (VT) was induced in 5 of 15 patients tiho had.structural heart disease, and in none of the 18 patients who did not (p 0.05). Patients who had inducible unimorphic VT were treated with antiarrhythmic drugs that suppressed the induction of VT, and 4 of 5 patients also received a pacemaker; no patient had a recurrence of syncope during fofiowup. Patients who had inducible polymorphii VT and VF (n = 10) or no inducible VT (n = 18) received treatment directed at only carotid sinus syndrome. Two patients with inducible VT or VF and 1 patient without inducible VT had recurrent syncope during follow-up, but none had cardiac arrest or died sriddeniy. it is concluded that programmed stimulation should be performed in patients presumed to have carotid sinus syndrome who have structural heart disease; unimorphic VT may be induced in one-third of these patients, raising the possibility that VT fs the cause of syncope. Antiarrhythmic drug therapy may be unnecessary if pdymorphic VT or VP is induced. in patients without heart disease, programmed stimulation is highly unlikely to yield a clinically significant arrhythmia.

Objectives. The purpose of this study was to determine whether the polarity of a monophasic shock used with a transvenous lead system affects the defibrillation threshold. Background. The ability to implant an automatic defibrillator depends on achieving an adequate defibriilation threshold. Methods. A transvenous defibrillation lead with distal and proximal shocking electrodes was used in this study. In 29 consecutive patients, the defibrillation threshold, using a step-down protocol was determined twice in random order: 1) with the distal coil as the anode, and 2) with the polarity reversed. Only the 20 patients in whom an adequate defibrillation threshold could be obtained with the transvenous lead alone were included in this study. These patients were 61 ± 14 years old (mean ± SD) and had a mean ejection fraction of 28 ± 12%. Results. The mean defibrillation threshold was 11.5 ± 5.0 J with the distal coil as the anode versus 16.9 ± 7.7 J with the distal coil as the cathode (p = 0.04). The defibrillation threshold was lower by a mean of 9 ± 7 J with the former configuration in 14 patients and was lower by a mean of 7 ± 6 J with the latter configuration in 3 patients; in 3 patients it was the same with both configurations. Use of a subcutaneous patch was avoided in five patients by utilizing the distal electrode as the anode. Conclusions. Defibrillation thresholds with monophasic shocks are ~30% lower with the distal electrode as the anode. The use of anodal shocks may obviate the need for a subcutaneous patch and allow more frequent implantation of a transvenous lead system.

The purpose of this study was to determine whether pharmacologically induced elevations in the plasma epinephrine concentration within reported physiologic limits alter the response to quinidine during electropharmacologic testing. Twenty-one patients with coronary artery disease and a history of unimorphic ventricular tachycardia were found to have inducible sustained unimorphic ventricular tachycardia that was suppressed by treatment with oral quinidine gluconate. Epinephrine was then infused at a rate of either 25 or 50 ng/kg per min and testing was repeated. These infusion rates of epinephrine were previously demonstrated to result in elevations of the plasma epinephrine concentration in the range of concentrations that occur during a variety of stresses. Quinidine significantly lengthened the ventricular refractory periods and the QRS duration at a ventricular pacing cycle length of 350 ms, which was used as an index of intraventricular conduction. Epinephrine partially or completely reversed the effects of quinidine on ventricular refractory periods, but had no effect on QRS duration. During electropharmacologic testing of quinidine, no ventricular tachycardia was inducible in 12 patients, and only nonsustained ventricular tachycardia, 8 to 48 beats in duration, was inducible in 9 patients. Retesting during infusion of epinephrine demonstrated inducible sustained unimorphic ventricular tachycardia in 2 of the 12 patients in whom quinidine had completely suppressed the induction of ventricular tachycardia and in 8 of the 9 patients in whom only nonsustained ventricular tachycardia had been inducible during testing of quinidine. In conclusion, physiologic elevations in the plasma epinephrine concentration may reverse quinidine-induced prolongation of ventricular refractoriness but not intraventricular conduction. Epinephrine may facilitate the induction of sustained ventricular tachycardia in patients in whom quinidine has suppressed this arrhythmia. Patients in whom nonsustained ventricular tachycardia is inducible during electropharmacologic testing may be particularly susceptible to antagonism by epinephrine of quinidine's therapeutic effects.

Determinants of the ventricular cycle length during atrial fibrillation were examined in 52 patients. Thirty-three patients had structural heart disease and none had an accessory atrioventricular (AV) connection. The AV node effective and functional refractory periods, the shortest atrial pacing cycle length associated with 1:1 conduction, the AV node conduction time and indexes of concealed conduction in the AV node were measured in the baseline state (36 patients) and after modification of sympathetic tone by infusion of isoproterenol or propranolol (8 patients each). Atrial fibrillation was then induced with rapid atrial pacing, and the mean, shortest and longest ventricular cycle lengths were measured. Variables that correlated most strongly with the mean RR interval during atrial fibrillation were the AV node effective refractory period (r = 0.93; p less than 0.001), AV node functional refractory period (r = 0.87; p less than 0.001) and shortest atrial pacing cycle length associated with 1:1 conduction (r = 0.91; p less than 0.001). The AH interval during sinus rhythm (r = 0.74; p less than 0.001) and during atrial pacing at the shortest cycle length with 1:1 conduction (r = 0.52; p less than 0.001) had weaker correlations. Measures of concealed conduction did not improve the prediction of the mean or longest ventricular cycle length during atrial fibrillation. In conclusion, the refractory periods and conductivity of the AV node are the best indicators of the potential of the node to transmit atrial impulses to the ventricles during atrial fibrillation. The degree of concealed conduction in the AV node is a less important determinant of the mean ventricular rate during atrial fibrillation.

The purpose of this study was to define the natural history of 99 patients with unexplained syncope who underwent an electrophysiologic test that either was entirely normal or demonstrated nonspecific abnormalities that were nondiagnostic (inducible polymorphic ventricular tachycardia or ventricular fibrillation, a mildly prolonged sinus node recovery time of less than 2 s, a His-ventricular interval of 55 to 99 ms or supraventricular tachycardia not associated with hypotension). The mean age (+/- SD) of the patients was 56 +/- 19 years; structural heart disease was present in 47 patients and absent in 52. Complete follow-up was available in 95 patients. During 20 +/- 11 months of follow-up, 2 patients (2%) died suddenly, 19 patients (20%) had recurrent syncope and 74 patients (78%) had no further episodes of syncope. Among the 19 patients who continued to have syncope after the electrophysiologic testing, the cause of syncope was established clinically in 4 and was found to be high degree atrioventricular (AV) block (2 patients) or sinus node dysfunction (2 patients). No clinical or laboratory findings distinguished patients who had sudden death or syncope during follow-up from patients who did not. In conclusion, in patients with unexplained syncope who undergo an electrophysiologic test that is nondiagnostic 1) the incidence of sudden death is low (2%); 2) the remission rate of syncope is high (80%); 3) the electrophysiologic test may be documented to have been falsely negative in greater than or equal to 20% of patients who continue to have syncope, syncope in these patients being caused by AV block or sinus node dysfunction; and 4) patients at risk of sudden death or recurrent syncope, or both, cannot be readily identified prospectively.

No previous studies have determined the pharmaco-dynamics of intravenous procainamide when administered in a dose of 15 mg/kg and at a rate of 50 mg/min, as is common practice during electropharmacologic testing. In this study, 30 patients received procainamide in this fashion; the right ventricular effective refractory period and the QRS duration at a ventricular pacing rate of 120/minute were then determined every minute for 20 minutes. Ten patients received no maintenance infusion of procainamide (group A), 10 received a 4 mg/min maintenance infusion (group B) and 10 received an 8 mg/min maintenance infusion (group C). Ten additional patients received no procainamide and served as control subjects (group D). The plasma procainamide concentration was measured at 1, 5, 10, 15 and 20 minutes after the loading dose was administered. A stable plasma procainamide concentration was not present in group A, B, or C until 15 minutes after infusion of the loading dose. The effective refractory period and QRS duration increased compared with baseline at 1 minute, decreased between 1 and 10 minutes and then remained essentially unchanged between 10 and 20 minutes in all 3 treatment groups. Concentration-effect relation was linear in each treatment group. The plasma procainamide concentrations in group C were significantly greater than in group A; however, the effects on refractoriness and QRS duration were similar in both groups. These findings indicate that with a procainamide dosing method commonly used during electropharmacologic testing, the plasma procainamide concentration decreases significantly during the first 15 minutes after the loading dose is administered.(ABSTRACT TRUNCATED AT 250 WORDS)

The short-term effects of incremental doses of procainamide (7.5, 15, 22.5, and 30 mg/kg) on right ventricular effective refractory period, intraventricular conduction, and induction of ventricular tachycardia were determined in 31 patients who had a history of sustained, unimorphic ventricular tachycardia. QRS duration during incremental ventricular pacing was used as an index of rate-dependent changes in intraventricular conduction. The mean plasma procainamide concentrations corresponding to the incremental doses were 5.5 +/- 1.2 (+/- SD), 9.0 +/- 1.6, 12.6 +/- 2.2, and 16.3 +/- 3.2 mg/liter. Each incremental dose of procainamide up to a dose of 30 mg/kg resulted in a significant increment in right ventricular effective refractory period and each dose up to 22.5 mg/kg potentiated a rate-dependent prolongation of QRS duration. After the 7.5 mg/kg dose of procainamide, induction of ventricular tachycardia was suppressed in eight of 31 patients. After higher doses of procainamide, induction of ventricular tachycardia was suppressed in two additional patients. In three of 10 patients in whom the induction of ventricular tachycardia was suppressed by 7.5, 15, or 22.5 mg/kg of procainamide, sustained unimorphic ventricular tachycardia was again inducible after a higher dose of procainamide. In three of 31 patients, only nonsustained ventricular tachycardia was inducible after a 7.5 to 22.5 mg/kg dose of procainamide; however, in two of these three patients, sustained ventricular tachycardia was again inducible after administration of a higher dose of procainamide. In conclusion, during electropharmacologic testing with procainamide, it is worthwhile to test a dose of 7.5 mg/kg, because this dose is often effective in patients who respond to this drug. However, the results of this study indicate that procainamide may be effective in suppressing the induction of sustained ventricular tachycardia at a relatively low plasma concentration, but not at a higher plasma concentration. Therefore, during long-term therapy with procainamide it may be important to avoid plasma procainamide concentrations not only lower, but also higher than the concentration that results in the suppression of induction of tachycardia.

During paroxysmal supraventricular tachycardia, patients frequently experience chest pain and marked ST segment depression suggesting acute myocardial ischemia. The purpose of this study was to assess whether ST depression during supraventricular tachycardia is caused by myocardial ischemia as reflected by net myocardial lactate production. Twenty-five patients (14 men, 11 women) who had a history of paroxysmal supraventricular tachycardia and a mean age (± SD) of 38 ± 14 years underwent electrophysiologic testing. Twenty-four of these patients had no evidence of coronary disease, whereas one patient had undergone previous coronary bypass surgery. Nineteen patients had orthodromic and six patients had atrioventricular node reentrant tachycardias.A 12 lead electrocardiogram and simultaneous femoral artery and coronary sinus blood samples for lactate determinations were obtained at baseline and at 5 and 10 min of supraventricular tachycardia. Mean baseline heart rate of 83 ± 12 beats/min increased to 180 ± 25 beats/min during supraventricular tachycardia. All patients had 1 to 8 mm of ST segment depression in 1 to 9 of the 12 leads. Chest pain occurred in 64% of patients during supraventricular tachycardia. Baseline myocardial lactate extraction was 28 ± 13% with no significant change at 5 or 10 min of tachycardia. In contrast, in a comparison group of seven patients with known coronary artery disease, atrial pacing at 168 ± 26 beats/min in five patients resulted in ≥ 1 mm ST depression in 2 to 7 of the 12 leads and a change in lactate extraction from a baseline of 29 ± 13% to −27 ± 20% (p < 0.05) indicating net myocardial lactate production.In conclusion, in patients with coronary artery disease, supraventricular tachycardia may be associated with chest pain or marked ST segment depression, or both, in the absence of acute myocardial ischemia.