Noncapturing stimuli during the basic drive shorten ventricular refractoriness.
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Biomedical subjects
Publications and source records attributed to J Sousa.
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BACKGROUND: We conducted this study to determine the feasibility of an abbreviated therapeutic approach to the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardia, in which the diagnosis is established and radiofrequency ablation carried out during a single electrophysiologic test. METHODS: One hundred six consecutive patients were referred for the management of documented, symptomatic paroxysmal supraventricular tachycardias (66 patients) or the Wolff-Parkinson-White syndrome (40 patients). All agreed to undergo a diagnostic electrophysiologic test and catheter ablation with radiofrequency current. No patient had had such a test previously. RESULTS: Among the 66 patients with paroxysmal supraventricular tachycardias, the mechanism was found to be atrioventricular nodal reentry in 46 (70 percent) (typical in 44 and atypical in 2), atrioventricular reciprocating tachycardia involving a concealed accessory pathway in 16 (24 percent), atrial tachycardia in 2 (3 percent), and noninducible paroxysmal supraventricular tachycardia in 2 (3 percent). A successful long-term outcome was achieved in 57 of 62 patients (92 percent) with paroxysmal supraventricular tachycardia in whom ablation was attempted and in 37 of 40 patients (93 percent) with the Wolff-Parkinson-White syndrome. The only complications were one instance of occlusion of the left circumflex coronary artery, leading to acute myocardial infarction, and one instance of complete atrioventricular block. The mean (+/- SD) duration of the electrophysiologic procedures was 114 +/- 55 minutes. CONCLUSIONS: The diagnosis and cure of paroxysmal supraventricular tachycardia or the Wolff-Parkinson-White syndrome during a single electrophysiologic test are feasible and practical and have a favorable risk-benefit ratio. This abbreviated therapeutic approach may eliminate the need for serial electropharmacologic testing, long-term drug therapy, antitachycardia pacemakers, and surgical ablation.
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.
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The results of electrophysiologic testing after short-term and long-term treatment with amiodarone were compared in 71 patients with ventricular tachycardia. Electrophysiologic testing was performed in the baseline state after 11 +/- 3 days of treatment with 1.2 to 2.4 gm/day of amiodarone, and after 13 +/- 4 weeks of therapy with a daily amiodarone dose of 400 mg. After short-term therapy, 62% of the patients had an adequate response to amiodarone. In 27 patients who were hemodynamically unstable, ventricular tachycardia was induced and became noninducible or hemodynamically stable after combination therapy with a class I agent. Among 18 patients who did not have inducible ventricular tachycardia after short-term therapy, eight (44%) had inducible, hemodynamically unstable ventricular tachycardia after long-term treatment with amiodarone. On the other hand, six of the 27 patients who had hemodynamically unstable ventricular tachycardia after short-term therapy had an adequate response after long-term treatment with amiodarone. Therefore an adequate electrophysiologic response after short-term therapy does not guarantee a similar response after long-term treatment, and an inadequate response after short-term therapy does not always predict a similar response after long-term therapy.
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The purpose of this study was to evaluate the results of electrophysiologic testing and the long-term prognosis of 56 patients with coronary artery disease who presented with aborted sudden death unrelated to acute myocardial infarction. The mean age of the patients was 62 +/- 8 years (+/- standard deviation) and 48 were men. The mean left ventricular ejection fraction was 0.34 +/- 0.16. During the baseline electrophysiology test, sustained monomorphic ventricular tachycardia (VT) was inducible in 22 patients who then underwent electropharmacologic testing: 11 patients were treated with antiarrhythmic drugs that suppressed the induction of VT or resulted in the VT becoming hemodynamically stable; 10 patients who failed drug testing received an automatic implantable cardioverter/defibrillator (AICD); one patient underwent endocardial resection. Among 34 patients who did not have inducible sustained VT, a precipitant of cardiac arrest (severe ischemia, proarrhythmia) was identified and was corrected in 9 of 34. An AICD was recommended in the remaining 25 patients; however, nine patients refused and were treated empirically with antiarrhythmic drugs. The mean follow-up was 22 +/- 12 months. The 2-year actuarial incidence of sudden death was 31% in patients who were treated with drugs based on the results of electropharmacologic testing, 26% in patients who were treated with antiarrhythmic drugs on an empiric basis, 0% among patients in whom a correctable etiology for the cardiac arrest was identified, and 9% among patients who underwent implantation of an AICD. The 3-year actuarial incidence of sudden death among the 20 patients treated with antiarrhythmic drugs was 53%, compared with 9% among the 26 patients who underwent AICD implantation (p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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The purpose of this study was to evaluate the serial changes in T wave configuration in patients undergoing successful radiofrequency catheter ablation of accessory atrioventricular (AV) connections. Twenty-nine consecutive patients with overt preexcitation and 16 patients with a concealed accessory atrioventricular (AV) connection were included. An electrocardiogram (ECG) was recorded before ablation and 15 min, 1 or 2 days and 1 and 3 months after ablation. Postablation T wave abnormalities occurred in 22 (76%) of the 29 patients who had overt pre-excitation but in none of the 16 patients with a concealed accessory AV connection. The T wave abnormalities were not related to myocardial necrosis or echocardiographic abnormalities. The ECG location and severity of T wave changes were dependent on the accessory AV connection location and degree of baseline pre-excitation, respectively. Fourteen of 19 patients with a posteriorly located AV connection (left, right or septal) had T wave inversion or flattening in the inferior leads and 3 patients had precordial T wave peaking. Two patients with an anteroseptal AV accessory connection had both inferior T wave inversion or flattening and precordial T wave peaking. Among seven patients with a manifest left lateral accessory AV connection, two had lateral T wave inversion or flattening and two had precordial T wave peaking. There was 95% concordance between the directional change of the T wave after ablation and the direction of the delta wave on the baseline ECG.(ABSTRACT TRUNCATED AT 250 WORDS)
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.
BACKGROUND: The strength-interval relation between the intensity of premature stimulus and the ventricular effective refractory period (VERP) has been well characterized. The effects of variation in the intensity of the basic drive train stimuli (S1) on VERP are not as well defined. This relation was studied in 44 patients undergoing clinically indicated electrophysiological study. METHODS AND RESULTS: The outputs of two stimulus isolation units were connected in parallel, allowing the intensity of S1 to be varied independently of intensity of the extrastimulus (S2). To prevent confounding effects from cycle length change, continuous overdrive pacing was performed for 3 minutes before each measurement of VERP. The effect of S1 intensity on VERP was assessed in 24 patients with S2 intensity kept constant at twice threshold. VERP shortened from 232 +/- 19 msec at an S1 intensity of 1.5 times threshold to 219 +/- 20 msec at 5 mA and 211 +/- 19 msec at 10 mA (p less than 0.0001 for baseline versus 5 mA and for 5 mA versus 10 mA). Autonomic blockade with atropine and propranolol blunted but did not completely eliminate this effect. To assess whether the effect of S1 intensity on VERP was independent of S2 intensity, S2 strength-interval curves were generated in 10 patients at low (1.5 times threshold) and high (10 mA) S1 intensities. All portions of the strength-interval curve were shifted to the left by an increase in S1 intensity. The time course of change in VERP after an abrupt increase in S1 intensity was assessed in an additional 10 patients. VERP changed slowly, requiring 18 +/- 28 seconds to shorten by 2 msec and 64 +/- 46 seconds to decrease by 10 msec after a change in S1 intensity from 1.5 times threshold to 10 mA. In a final group of 10 patients, VERP was measured using an eight-beat drive train and a 4-second intertrain interval. With this more conventional protocol, VERP shortened by 14 +/- 8 msec with an increase in S1 intensity from 1.5 times threshold to 10 mA. CONCLUSIONS: Increasing S1 intensity results in clinically significant, progressive shortening of VERP in man. This effect is independent of S2 intensity. The prolonged time course of the change in VERP after an increase in S1 intensity and the attenuation of this effect by autonomic blockade are consistent with stimulation of sympathetic nerve terminals and catecholamine release as a result of intense stimulation.
BACKGROUND: The purpose of this study was to describe a new technique for catheter ablation of the atrioventricular junction using radiofrequency energy delivered in the left ventricle. METHODS AND RESULTS: Catheter ablation of the atrioventricular (AV) junction using a catheter positioned across the tricuspid annulus was unsuccessful in eight patients with a mean +/- SD age of 51 +/- 19 years who had AV nodal reentry tachycardia (three patients), orthodromic tachycardia using a concealed midseptal accessory pathway, atrial tachycardia, atrial flutter (two patients), or atrial fibrillation. Before attempts at catheter ablation of the AV junction, each patient had been refractory to pharmacological therapy, and four had failed attempts at either catheter modification of the AV node using radiofrequency energy or surgical and catheter ablation of the accessory pathway. Conventional right-sided catheter ablation of the AV junction using radiofrequency energy in six patients and both radiofrequency energy and direct current shocks in two patients was ineffective. The mean amplitude of the His bundle potential recorded at the tricuspid annulus at the sites of unsuccessful AV junction ablation was 0.1 +/- 0.08 mV, with a maximum His amplitude of 0.03-0.28 mV. A 7F deflectable-tip quadripolar electrode catheter with a 4-mm distal electrode was positioned against the upper left ventricular septum using a retrograde aortic approach from the femoral artery. Third-degree AV block was induced in each of the eight patients with 20-36 W applied for 15-30 seconds. The His bundle potential at the sites of successful AV junction ablation ranged from 0.06 to 0.99 mV, with a mean of 0.27 +/- 0.32 mV. There was no rise in the creatine kinase-MB fraction and no complications occurred. An intrinsic escape rhythm of 30-60 beats/min was present in seven of the eight patients. Each patient received a permanent pacemaker and has been asymptomatic during 3-13 months of follow-up. CONCLUSIONS: Catheter ablation of the AV junction can be achieved effectively and safely using radiofrequency energy delivered in the left ventricle when the conventional right-sided approach is unsuccessful.
BACKGROUND: Catheter ablation of accessory atrioventricular (AV) connections has been demonstrated to be effective in more than 85% of patients. One of the risks of this procedure is radiation exposure during the fluoroscopic imaging necessary to guide catheter manipulation. The objective of the present study was to measure the radiation received by patients and physicians during radiofrequency catheter ablation and to estimate the resultant somatic and genetic risks. METHODS AND RESULTS: Radiation exposure to patients and physicians was measured during attempts at radiofrequency catheter ablation of accessory AV connections in 31 consecutive patients. Radiation exposure was measured using thermoluminescent sensors placed on the patient and on the physician. Somatic and genetic risks were estimated based on the radiation levels recorded using these sensors. The durations of fluoroscopy and of the catheter ablation procedure were recorded for each patient. Catheter ablation was successful in 28 of 31 patients (90%). Mean +/- SD duration of fluoroscopy was 44 +/- 40 minutes. The largest patient radiation dose was measured over the ninth vertebral body posteriorly (median, 7.26 rem [roentgen equivalents man]; range, 0.31-135.7 rem). Median radiation dose to the thyroid was 0.46 rem (range, 0.06-7.26 rem), and median radiation dose to the posterior iliac crest was 2.43 rem (range, 0.01-8.3 rem). The greatest radiation dose to the operator was recorded at the left hand (99 mrem). Mean radiation dose to the operator's eyes was 28 mrem. CONCLUSIONS: Radiofrequency catheter ablation of accessory AV connections may result in significant radiation exposure to the patient and to the physician. Each hour of fluoroscopic imaging is associated with a lifetime risk of developing a fatal malignancy of 0.1% and a risk of a genetic defect of 20 per 1 million births. Although these risks must be recognized, they are relatively small compared with the risks associated with alternate approaches to management, including no therapy, antiarrhythmic drug therapy, and surgery.
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In this study, the rate dependent effect of quinidine on the ventricular effective refractory period (VERP) was evaluated in 30 patients undergoing electropharmacological testing with quinidine. The VERPs were measured in the baseline state and after at least 2 days of treatment with 1,458-2,044 mg/day of quinidine gluconate (mean plasma quinidine concentration 2.2 +/- 0.7 mcg/mL). In 20 patients, the VERP was measured using conventional basic drive trains of 8 beats and basic drive cycle lengths of 600, 500, 400, and 350 msec. In another 10 patients, the VERP was measured after 3 minutes of continuous ventricular pacing at cycle lengths of 600 and 400 msec, and compared to the VERPs measured at the same basic drive cycle lengths using basic drive train durations of 2 and 8 beats. In the baseline state and after treatment with quinidine, the VERP shortened progressively as the basic drive train cycle length decreased and as the drive train duration increased to 3 minutes (P less than 0.001). Quinidine consistently prolonged the VERP by 9%-11% (P less than 0.001), regardless of the basic drive train cycle length. Quinidine's effect was also not affected by the basic drive train duration. In conclusion, the effect of quinidine on VERP in humans is independent of the rate of the basic drive train, both when measured using conventional 8-beat basic drive trains and when a three minute drive train duration is used in order to attain the maximum effect of the basic drive train cycle length on the VERP.(ABSTRACT TRUNCATED AT 250 WORDS)
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)
Studies have been conducted to determine whether the mutagens in fried beef ingested by human subjects are excreted in the urine. Urine samples were collected from individuals on liquid or regular diets before and after a fried beef meal. The mutagenic activity of the samples was tested in the Ames Salmonella/microsome assay system. The results showed that in individuals on liquid diets, most of the urinary mutagenic activity is recovered within 2-6 h after consuming a fried beef meal. In one individual tested, mutagenic activity was found in urine samples obtained 6-15 h after the fried beef meal. No mutagenic activity was detected in any of the urine samples obtained 15-24 h following the meal. In individuals on a regular diet, however, mutagenic activity was frequently observed in urine samples obtained 16-24 h following the fried beef meal, although the mutagenic activity was not as great as that in the preceding 16 h. It appears that the mutagenic agents generated by the frying of beef are ingested, absorbed, and excreted by the human body in biologically detectable quantities. These results suggest that subjects should abstain from fried beef at least one day prior to and during urine mutagenicity screening.
The mutagenic activity of urine samples from nonsmoking individuals before and after the consumption of either red wine or grape juice was determined. Urine samples collected from individuals on liquid or regular diets were concentrated using XAD-2 resin. No mutagenic activity of urine concentrates was detected with Salmonella tester strains TA98 or TA100 with or without microsomal activation. The addition of 1000 units of beta-glucuronidase into the agar overlay did not show any mutagenic activity. The mutagens in red wine and grape juice, however, were extracted using the XAD-2 column. Concentrates of urine samples spiked with either of the two extracts exhibited mutagenic activity.