Biomedical subjects
Publications and source records attributed to W M Miles.
Spontaneous echo contrast has never been described in association with cardiac defibrillation. In this report, we present a patient who developed dense echo contrast as a result of a shock delivered from a transvenous defibrillator system.
The permanent form of junctional reciprocating tachycardia (PJRT) has been successfully eliminated by ablation of the accessory pathway responsible for the tachycardia. The coexistence of multiple accessory pathways responsible for different, long RP-interval tachycardias was not documented previously. Five patients with PJRT underwent radiofrequency catheter ablation of accessory pathways. Three of 5 patients had 2 accessory pathways each: 1 had 2 left free wall accessory pathways, another had a right posterior free wall and right posteroseptal pathway, whereas the third had 2 right posteroseptal pathways approximately 1 cm apart. The remaining 2 patients each had 1 right posteroseptal accessory pathway. Seven of 8 pathways were successfully ablated with a median of 3 radiofrequency pulses. No patient developed complications. Peak serum creatine kinase ranged from 131 to 311 IU/liter, with peak MB fraction 7 to 17 IU/liter, or 5 to 11%. Follow-up electrophysiologic study, 29 to 70 days after ablation, revealed no inducible tachycardia and no evidence of accessory pathway conduction, except for the 1 pathway not ablated. All patients remained asymptomatic 17 to 29 months after ablation. Thus, patients with PJRT can have several accessory pathways that can be safely and effectively eliminated with radiofrequency catheter ablation.
AV nodal reentry capable of VA block during tachycardia was successfully eliminated using a posteroseptal ablation pulse delivered well away from the site of earliest atrial activation during tachycardia. A possible explanation is that the arrhythmia represented typical AV nodal reentrant tachycardia with transient intra-atrial conduction block during tachycardia.
OBJECTIVES: The aim of this study was to determine whether patients with ventricular arrhythmias in the absence of coronary artery disease also have abnormalities in sympathetic innervation. BACKGROUND: We have previously shown by cardiac sympathetic scintigraphy using iodine-123-metaiodobenzylguanidine (I-123-MIBG) that patients with ventricular tachycardia after myocardial infarction have regional cardiac sympathetic denervation. It is not known whether patients with ventricular tachycardia in the absence of coronary artery disease also have regional cardiac sympathetic denervation. METHODS: We performed cardiac I-123-MIBG and thallium-201 single-photon emission computed tomographic (SPECT) scans at rest in 18 patients (mean age 47 +/- 18 years) with cardiomyopathy (n = 6), left ventricular hypertrophy (n = 1), valvular disease (n = 2) or a structurally normal heart (n = 9) who presented with monomorphic (n = 15) or polymorphic (n = 3) ventricular tachycardia. These scans were compared with scans in 12 control patients without ventricular tachycardia (mean age 30 +/- 17 years) who had cardiomyopathy (n = 3) or a structurally normal heart (n = 9). Cardiac sympathetic denervation was defined as myocardial areas having thallium uptake with reduced or absent I-123-MIBG uptake. RESULTS: Twelve (67%) of 18 patients with ventricular tachycardia had regional cardiac sympathetic denervation compared with 1 (8%) of 12 patients who did not have ventricular tachycardia (p = 0.002). In the nine patients with a structurally normal heart and ventricular tachycardia, five (55%) patients had regional cardiac sympathetic denervation compared with zero of nine control patients with a structurally normal heart (p = 0.029). Five patients underwent right ventricular radiofrequency ablation for ventricular tachycardia, and sympathetic denervation was adjacent to the ablation site in one of these patients. CONCLUSIONS: Patients with ventricular tachycardia in the absence of coronary artery disease have abnormal cardiac sympathetic innervation detectable by cardiac sympathetic scintigraphy. The role of regional cardiac sympathetic denervation in arrhythmogenesis remains to be determined.
Between 1977 and 1986, 589 patients (age, 57 +/- 13 years; 464 men and 125 women) received amiodarone for ventricular fibrillation (VF; 147 patients), sustained (VT-S; 242 patients) or nonsustained (VT-NS; 80 patients) ventricular tachycardia, or supraventricular tachycardia (SVT; 120 patients). Mean left ventricular ejection fraction was 36 +/- 17%, with 23% in New York Heart Association functional class I, 49% in class II, 25% in class III, and 3% in class IV. Sixty-two percent had ischemic heart disease. Follow-up was 32 +/- 27 months (mean +/- SD). Life table analysis revealed that patients with VF, VT-S, and VT-NS had a cumulative incidence of sudden death of 9% at 1 year, increasing by about 3% per year. By years 2 and 5, the cumulative incidence of sudden death, VF, or VT-S recurrence was 26% and 38% and the percent of patients still taking amiodarone was 54% and 32%. For patients with SVT at years 2 and 5, the cumulative incidence of sudden death was 1% and 3%, and of sudden death or SVT recurrence the cumulative incidence was 20% and 29%. The percent of patients still taking amiodarone was 67% and 43%. Of 14 clinical variables assessed, New York Heart Association functional class was the best predictor of sudden death and arrhythmic failure and no other variable added independent predictive power. Older age and lower left ventricular ejection fraction were independent predictors of drug failure (sudden death or arrhythmic failure or need to discontinue amiodarone because of side effects). We conclude that despite its side effect profile, amiodarone is an effective and reasonably well-tolerated antiarrhythmic drug.
Early afterdepolarizations (EADs), possibly caused by reduced K+ conductance, have been hypothesized to cause the long QTU interval and ventricular tachyarrhythmias (VT) in patients with the long QT syndrome (LQTS). In a 26-year-old woman with aborted sudden death as a consequence of the idiopathic LQTS, we recorded with a contact electrode left ventricular endocardial EADs that were enhanced by epinephrine and phenylephrine. Because of uncertain efficacy and side effects achieved with beta-adrenoceptor blockade, the patient underwent left-sided cardiac sympathectomy, at which time we obtained left ventricular biopsy tissue. Crude membrane vesicles were prepared from this tissue and single-channel activity was studied after incorporation of the vesicles in an artificial lipid bilayer (phosphatidylserine, phosphatidylethanolamine, 4:5 weight ratio in decane) in the tip of a patch clamp pipette. Bath and pipette contained 100 mmol/L KCI and 25 mmol/L N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) at pH 7.4. We recorded K+ conducting channels with a mean slope conductance of 49.9 +/- 4.7 picosiemens (pS) (n = 5). Channel open probability was increased by the addition of 1 to 10 mumol/L Ca2+ to the experimental chamber. Addition of charybdotoxin (1-3 nmol/L), a known specific inhibitor of Ca(2+)-activated K+ channels, blocked channel activity. These results are the first to demonstrate Ca(2+)-activated K+ channels from a patient with idiopathic LQTS. These channels appear to show normal characteristics when studied in an artificial planar lipid bilayer.
OBJECTIVES: We compared the electrophysiologic effects on atrioventricular (AV) node physiology of selective "fast" versus selective "slow" pathway radiofrequency ablation in 42 patients with drug-resistant AV node reentrant tachycardia who underwent 51 ablation attempts to prevent tachycardia recurrence while preserving AV conduction. BACKGROUND: The recent introduction of radiofrequency ablation to treat AV node reentrant tachycardia allows the opportunity to study the effects of selective elimination of the different limbs involved in AV node reentrant tachycardia. METHODS: Selective fast pathway ablation was attempted in 13 patients by delivering radiofrequency energy anteriorly across the tricuspid valve anulus. Selective slow pathway ablation was attempted in 29 patients by delivering radiofrequency energy posteriorly across the tricuspid valve anulus at sites where putative slow pathway potentials were recorded. RESULTS: Selective fast pathway ablation eliminated AV node reentrant tachycardia without AV block in 6 (46%) of 13 patients after one ablation session and in an additional 3 patients (69% of total) after repeat ablation sessions. Slow pathway ablation eliminated AV node reentrant tachycardia without AV block in 26 (90%) of 29 patients after one radiofrequency ablation session and in an additional 2 patients (97% of total) after repeat ablation sessions. Selective fast pathway ablation increased the PR interval (140 to 220 ms, p = 0.0001) and AH interval (66 to 153 ms, p = 0.0001), whereas slow pathway ablation did not change these intervals. Fast pathway radiofrequency ablation caused retrograde block in 7 (64%) of 11 patients, whereas no patients undergoing slow pathway ablation developed selective retrograde block. Single AV node echo beats were commonly induced after slow but not fast pathway ablation (17 of 29 patients vs. 1 of 11 patients, respectively, p = 0.01) and did not predict recurrence of AV node reentrant tachycardia. CONCLUSIONS: Successful selective radiofrequency ablation of fast or slow pathways in patients with AV node reentrant tachycardia resulted in different electrophysiologic properties after ablation. Slow pathway ablation produced more successful outcomes, with a decreased prevalence of recurrent AV node reentrant tachycardia or AV block.
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BACKGROUND: The purpose of this study was to test the feasibility of radiofrequency catheter ablation of Mahaim fibers at the tricuspid annulus. METHODS AND RESULTS: Four patients who fulfilled criteria for having Mahaim fibers and preexcited reciprocating tachycardia underwent radiofrequency catheter ablation. Three patients had atriofascicular connections, and one patient had an atrioventricular connection. The mean age was 27 years (age range, 11-48 years). All patients had highly symptomatic tachycardias, producing syncope in one patient and presyncope in the remaining three patients. Symptoms were present for a mean of 13 years (range, 4-23 years). All pathways conducted only anterogradely, and preexcitation resulted in a left bundle branch block QRS morphology. Adenosine caused block in the accessory pathway in the three patients in whom it was tested. The stimulus to delta interval increased by 75 msec (range, 35-90 msec) during rapid atrial pacing. The atrial insertion of the Mahaim fiber was in the right lateral atrium in one patient, right posterolateral atrium in two patients, and right posterior atrium in one patient. The ventricular insertion was in the distal right bundle branch in three patients and in the posterolateral right ventricle near the tricuspid annulus in the patient with an atrioventricular connection. Stimulus to delta wave mapping was used to help localize the atrial insertion of the atriofascicular connections. A mean of 15 radiofrequency pulses (range, 10-19 pulses) delivered to the tricuspid annulus in the posterior to lateral regions eliminated accessory pathway conduction in all patients. No complications occurred. Tachycardia did not recur during a mean follow-up of 8 months (range, 2-15 months). CONCLUSIONS: Radiofrequency current applied to the tricuspid annulus can safely eliminate tachycardia in patients with Mahaim fibers.
BACKGROUND: Autonomic modulation, especially increased sympathetic activity may play a role in the genesis of ventricular arrhythmias. The purpose of this study was to determine whether beta-sympathetic stimulation with isoproterenol would alter sustained ventricular tachycardia (VT) circuits similarly during the drug-free and antiarrhythmic drug-treated states. METHODS AND RESULTS: Twenty-five patients with repeatedly inducible, hemodynamically stable, sustained VT were evaluated by programmed ventricular stimulation. In the antiarrhythmic drug-free state, isoproterenol (0.03 microgram/kg per minute) shortened the following intervals (in milliseconds; mean +/- SEM; 25 patients; paired t test): sinus cycle length (792 +/- 37 to 568 +/- 18; (p < 0.001), ventricular paced QT interval (386 +/- 8 to 348 +/- 6; p < 0.001), ventricular paced QRS duration (185 +/- 4 to 182 +/- 4; p = 0.014), ventricular effective (238 +/- 5 to 208 +/- 4; p < 0.001) and functional (261 +/- 6 to 227 +/- 5; p < 0.001) refractory periods, and the VT cycle length (VTCL) (311 +/- 9 to 291 +/- 9; p < 0.001). Isoproterenol (0.03 microgram/kg per minute) was administered during 31 antiarrhythmic drug trials (procainamide, n = 18; quinidine, n = 13) in 22 patients. Isoproterenol shortened the sinus cycle length, QT interval during ventricular pacing, and ventricular effective and functional refractory periods before and during procainamide and quinidine therapy (ANOVA; isoproterenol effect, p < or = 0.0002 for all). The amount of decrease in these intervals with isoproterenol was the same before and during procainamide and quinidine therapy (ANOVA interaction, p = NS for all). The QRS duration during ventricular pacing and VTCL were also shortened by isoproterenol before and during procainamide (baseline, n = 17; QRS, 182 +/- 4 to 178 +/- 4 msec; VTCL, n = 18, 314 +/- 11 to 291 +/- 11 msec; during procainamide, QRS, 218 +/- 7 to 197 +/- 6 msec; VTCL, 422 +/- 15 to 359 +/- 11 msec) and quinidine (baseline, n = 13; QRS, 190 +/- 6 to 185 +/- 5 msec; VTCL, n = 12, 298 +/- 10 to 280 +/- 9 msec; during quinidine, QRS, 223 +/- 9 to 208 +/- 8 msec; VTCL, 415 +/- 14 to 355 +/- 10 msec) (isoproterenol effect p < or = 0.0003 for all). However, the amount of decrease in QRS duration and VTCL with isoproterenol was greater during procainamide and quinidine than in the drug-free state (ANOVA interaction, p < or = 0.02 for all). These changes continued to be significant when normalized for the initial QRS duration and VTCL (p < or = 0.03 for all). CONCLUSIONS: Isoproterenol affects presumed reentrant sustained VT circuits less in the absence of antiarrhythmic drugs but markedly attenuates the antiarrhythmic drug-induced slowing of sustained VT. To the extent that the change in QRS duration reflects a change in conduction within the VT circuit, these data imply that the attenuation of drug-induced slowing of VT by isoproterenol is due to a greater change in conduction rather than refractoriness.
BACKGROUND: Radiofrequency energy has been used safely and successfully to eliminate accessory pathways in patients with the Wolff-Parkinson-White syndrome and the substrate for atrioventricular nodal reentrant tachycardia. However, this form of ablation has had only limited success in eliminating ventricular tachycardia in patients with structural heart disease. In contrast, direct-current catheter ablation has been used successfully to eliminate ventricular tachycardia in patients with and without structural heart disease. The purpose of this study was to test whether radiofrequency energy can safely and effectively ablate ventricular tachycardia in patients without structural heart disease. METHODS AND RESULTS: Sixteen patients (nine women and seven men; mean age, 38 years; range, 18-55 years) without structural heart disease who had ventricular tachycardia underwent radiofrequency catheter ablation to eliminate the ventricular tachycardia. Two patients presented with syncope, nine with presyncope, and five with palpitations only. Mean duration of symptoms was 6.7 years (range, 0.5-20 years). Radiofrequency catheter ablation successfully eliminated ventricular tachycardia in 15 of 16 patients (94%). Sites of ventricular tachycardia origin included the high right ventricular outflow tract (12 patients), the right ventricular septum near the tricuspid valve (three patients), and the left ventricular septum (one patient). The only ablation failure was in a patient whose ventricular tachycardia arose from a region near the His bundle. An accurate pace map, early local endocardial activation, and firm catheter contact with endocardium were associated with successful ablation. Radiofrequency ablation did not cause arrhythmias, produced minimal cardiac enzyme rise, and resulted in no detectable change in cardiac function by Doppler echocardiography. CONCLUSIONS: Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart disease is effective and safe and may be considered as early therapy in these patients.
Surgical treatment options for interruption of atrioventricular node reentrant tachycardia include (1) skeletonization of the atrioventricular node by dissecting it from most of its atrial inputs and (2) discrete cryosurgery of the perinodal tissues by applying a series of sequential cryolesions to the atrial tissues immediately adjacent to the atrioventricular node. Both these techniques attempt to interrupt one of the dual atrioventricular node conduction pathways while preserving the other. This report describes 17 consecutive patients who underwent surgical treatment, 10 patients with skeletonization of the atrioventricular node and seven patients with discrete perinodal cryosurgery. There were 10 female and seven male patients and their ages ranged from 28 to 56 years (mean 38). Two of the 17 patients had Wolff-Parkinson-White syndrome and their accessory pathways were interrupted before the atrioventricular nodal reentrant tachycardia was ablated. All the procedures were performed in a normothermic beating heart while atrioventricular conduction was monitored closely. In the skeletonization technique, the right atrial septum was mobilized and the atrioventricular node exposed anterior to the tendon of the Todaro. The perinodal cryosurgical procedure was also performed through a right atriotomy and a series of sequential 3 mm cryolesions were placed around the borders of the triangle of Koch on the inferior right atrial septum. There were no operative deaths. Two patients who underwent the skeletonization operation had heart block necessitating pacemaker therapy. At postoperative electrophysiologic study, no echoes or atrioventricular nodal reentrant tachycardia were inducible in any of the 17 patients. All patients have remained free of arrhythmia recurrence and have required no antiarrhythmic therapy after a follow-up of 5 to 28 months (mean 14). In conclusion, both atrioventricular node skeletonization and perinodal cryosurgery successfully ablate atrioventricular nodal reentrant tachycardia; however, perinodal cryosurgery appears to be safer in avoiding heart block, is more easily performed, and is our procedure of choice for the management of medically refractory atrioventricular nodal reentrant tachycardia.
It has been previously demonstrated that radiofrequency (RF) energy can be safely applied to successfully eliminate accessory pathways in patients with the Wolff-Parkinson-White syndrome. This technique may also be used to successfully eliminate atrioventricular (AV) nodal reentrant tachycardia by elimination of either the fast or slow AV nodal pathways. However, RF energy has achieved only limited success in eliminating ventricular tachycardia (VT) in patients with structural heart disease, such as coronary artery disease and dilated cardiomyopathy. Direct-current catheter techniques have successfully eliminated VT in patients with and without structural heart disease, but this technique is limited by the risk of barotrauma and proarrhythmia. We used RF catheter ablation techniques to eliminate VT in patients without structural heart disease. Our results from the basis of this report. 16 patients (nine women and seven men; mean age 38; range 18 to 55 years) who did not have any identifiable structural heart disease by echocardiography where included in this study. These patients underwent RF catheter ablation to eliminate VT. Two patients had presented with syncope, nine with presyncope and five with palpitations only. The mean duration of symptoms was 6.7 years (range 0.5 to 20 years). VT was successfully eliminated by RF catheter techniques in 15 of the 16 patients (a 94% success rate). Importantly, successful ablation sites included regions other than the right ventricular outflow tract. Areas of VT origin therefore included the high right ventricular outflow tract (twelve patients), right ventricular septum near the tricuspid valve (three patients), and the left ventricular septum (one patient). The only ablation failure was in a patient whose VT arose from a region near the His bundle. Successful ablation occurred in patients in whom an accurate pace map could be obtained and early local endocardial activation was obtainable. Further, firm catheter contact with endocardium was required for successful elimination of VT. RF ablation did not cause any identifiable arrhythmia and produced a minimal cardiac enzyme rise. It also resulted in no detectable change in cardiac function by Doppler echocardiography. Based on these findings, we conclude that RF catheter ablation of VT in patients without structural heart disease was highly effective and safe. It may therefore be considered as early therapy in these patients.
Nonpharmacologic therapy for ventricular arrhythmias has gained growing attention with the development of the implantable cardioverter-defibrillator. In addition, the reports of adverse effects of drug therapy from several studies, including the Cardiac Arrhythmia Suppression Trial (CAST), have supported the need for these devices. The development of new implantable cardioverter-defibrillators that have the capability of antitachycardia pacing, bradycardia pacing, cardioversion and defibrillation has enhanced their clinical utility. The currently available implantable cardioverter-defibrillators have been shown to significantly improve survival after sudden cardiac arrest in patients with life-threatening ventricular arrhythmias. Newer devices with expanded capabilities may reduce mortality even further. In this report the features of currently available antitachycardia devices and implantable cardioverter-defibrillators are reviewed and the features and current implant data on newer antitachycardia devices are discussed.
The site of ventricular stimulation is an important variable in the initiation of ventricular tachycardia (VT) by programmed ventricular stimulation. Among 169 patients studied consecutively, 17 (10%) had ventricular tachycardia induced by programmed electrical stimulation from the right ventricular outflow tract but not from the apex. Fourteen of these 17 patients had had prior myocardial infarction (12 had inferior, and two had both inferior and anterior myocardial infarction), two had a dilated cardiomyopathy, and one had a localized cardiomyopathy. Fourteen patients had echocardiograms suitable for analysis. Of these, 12 had posterior/inferior ventricular wall motion abnormalities located at the base of the heart. The ventricular effective refractory periods from the right ventricular outflow tract and right ventricular apex were 237 +/- 4 and 244 +/- 5 msec, respectively (p less than 0.05, mean +/- SEM). Induced VT had a cycle length of 229 +/- 4 msec and had the morphology of right bundle branch block in 12 patients, of left bundle branch block in three patients, and had both morphologies in two patients. In 14 patients the axis was superior. VT was initiated with two extrastimuli in 15 patients and with burst right ventricular pacing in two patients. Similar pacing techniques with identical pacing intervals did not induce VT at the right ventricular apex in 14 of these 17 patients. Further, among the 15 patients whose VT was induced at the right ventricular outflow tract with two extrastimuli, neither burst pacing (n = 13) nor two extrastimuli introduced at faster paced rates (n = 12) induced VT at the right ventricular apex.(ABSTRACT TRUNCATED AT 250 WORDS)
The incidence and clinical predictors of amiodarone pulmonary toxicity were examined in 573 patients treated with amiodarone for recurrent ventricular (456 patients) or supraventricular (117 patients) tachyarrhythmias. Amiodarone pulmonary toxicity was diagnosed in 33 of the 573 patients (5.8%), based on symptoms and new chest radiographic abnormalities (32 of 33 patients) and supported by abnormal pulmonary biopsy (13 of 14 patients), low pulmonary diffusion capacity (DLCO) (nine of 13 patients), and/or abnormal gallium lung scan (11 of 16 patients). Toxicity occurred between 6 days and 60 months of treatment for a cumulative risk of 9.1%, with the highest incidence occurring during the first 12 months (18 of 33 patients). Older patients developed it more frequently (62.7 +/- 1.7 versus 57.4 +/- 0.5 years, p = 0.018), with no cases diagnosed in patients who started therapy at less than 40 years of age. Gender, underlying heart disease, arrhythmia, and pretreatment chest radiographic, spirometric, or lung volume abnormalities did not predict development of amiodarone pulmonary toxicity, whereas pretreatment DLCO was lower in the group developing it (76.0 +/- 5.5% versus 90.4 +/- 1.4%, p = 0.01). There was a higher mean daily amiodarone maintenance dose in the pulmonary toxicity group (517 +/- 25 versus 409 +/- 6 mg, p less than 0.001) but no difference in loading dose. No patient receiving a mean daily maintenance dose less than 305 mg developed pulmonary toxicity. Patients who developed toxicity had higher plasma desethylamiodarone (2.34 +/- 0.18 versus 1.92 +/- 0.04 micrograms/ml, p = 0.009) but not amiodarone concentrations during maintenance therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
To determine whether a contraction-excitation feedback mechanism exists in human atrium, we investigated the effects of varying the atrioventricular (AV) interval from 0 to 360 msec during AV pacing at a cycle length of 400 msec on atrial pressure, size, and refractoriness in 10 patients (group 1, without supraventricular tachycardia). The same parameters were determined in another 10 patients (group 2, with different spontaneous AV relations) during AV reciprocating tachycardia or AV nodal reciprocating tachycardia and during high right atrial (RA) pacing at the tachycardia cycle length. In group 1 patients, peak and mean RA pressure, RA effective refractory period (RA-ERP), and left atrial (LA) size all decreased to minimal values at an AV interval of 120 msec and remained low as the AV interval was increased and approached 400 msec. The increase in each of the variables from its lowest to greatest value was as follows: Mean systemic blood pressure, 20.9 +/- 3.1 mm Hg; LA size, 0.55 +/- 0.05 cm; RA peak pressure, 10.4 +/- 1.8 mm Hg; RA mean pressure, 3.5 +/- 0.6 mm Hg; and RA-ERP, 22.5 +/- 3.0 msec, p less than 0.001 for each. The weighted mean correlation coefficient with RA-ERP was significant for RA peak pressure and LA size (p less than 0.001 for each). These same relations were investigated in five patients with the Wolff-Parkinson-White syndrome and AV reciprocating tachycardia and five patients with AV nodal reciprocating tachycardia (group 2).(ABSTRACT TRUNCATED AT 250 WORDS)
Transmural myocardial infarction in dogs produces denervation of sympathetic nerves in viable myocardium apical to the infarct that may be arrhythmogenic. It is unknown whether sympathetic denervation occurs in humans. The purpose of this study was to use iodine-123-metaiodobenzylguanidine (MIBG), a radiolabeled guanethidine analog that is actively taken up by sympathetic nerve terminals, to image noninvasively the cardiac sympathetic nerves in patients with and without ventricular arrhythmias after myocardial infarction. Results showed that 10 of 12 patients with spontaneous ventricular tachyarrhythmias after myocardial infarction exhibited regions of thallium-201 uptake indicating viable perfused myocardium, with no MIBG uptake. Such a finding is consistent with sympathetic denervation. One patient had frequent episodes of nonsustained ventricular tachycardia induced at exercise testing that was eliminated by beta-adrenoceptor blockade. Eleven of the 12 patients had ventricular tachycardia induced at electrophysiologic study and metoprolol never prevented induction. Sympathetic denervation was also detected in two of seven postinfarction patients without ventricular arrhythmias. Normal control subjects had no regions lacking MIBG uptake. This study provides evidence that regional sympathetic denervation occurs in humans after myocardial infarction and can be detected noninvasively by comparing MIBG and thallium-201 images. Although the presence of sympathetic denervation may be related to the onset of spontaneous ventricular tachyarrhythmias in some patients, it does not appear to be related to sustained ventricular tachycardia induced at electrophysiologic study.