Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome.

INTRODUCTION: Delta wave morphology correlates with the site of ventricular insertion of accessory AV pathways. Because lesions due to radiofrequency (RF) current are small and well defined, it may allow precise localization of accessory pathways. The purpose of this study was to use RF catheter ablation to develop an ECG algorithm to predict accessory pathway location. METHODS AND RESULTS: An algorithm was developed by correlating a resting 12-lead ECG with the successful RF ablation site in 135 consecutive patients with a single, anterogradely conducting accessory pathway (Retrospective phase). This algorithm was subsequently tested prospectively in 121 consecutive patients (Prospective phase). The ECG findings included the initial 20 msec of the delta wave in leads I, II, aVF, and V1 [classified as positive (+), negative (-), or isoelectric (+/-)] and the ratio of R and S wave amplitudes in leads III and V1 (classified as R > or = S or R < S). When tested prospectively, the ECG algorithm accurately localized the accessory pathway to 1 of 10 sites around the tricuspid and mitral annuli or at subepicardial locations within the venous system of the heart. Overall sensitivity was 90% and specificity was 99%. The algorithm was particularly useful in correctly localizing anteroseptal (sensitivity 75%, specificity 99%), and mid-septal (sensitivity 100%, specificity 98%) accessory pathways as well as pathways requiring ablation from within ventricular venous branches or anomalies of the coronary sinus (sensitivity 100%, specificity 100%). CONCLUSION: A simple ECG algorithm identifies accessory pathway ablation site in Wolff-Parkinson-White syndrome. A truly negative delta wave in lead II predicts ablation within the coronary venous system.

Para-Hisian pacing. A new method for differentiating retrograde conduction over an accessory AV pathway from conduction over the AV node.

BACKGROUND: Differentiation between ventriculoatrial (VA) conduction over an accessory AV pathway (AP) and the AV node (AVN) may be difficult, especially in patients with a septal AP. METHODS AND RESULTS: A new pacing method, para-Hisian pacing, was tested in 149 patients with AP and 53 patients without AP who had AV nodal reentrant tachycardia (AVNRT). Ventricular pacing was performed adjacent to the His bundle and proximal right bundle branch (HB-RB), initially at high output to capture both RV and HB-RB. The output was then decreased to lose HB-RB capture. The change in timing and sequence of retrograde atrial activation between HB-RB capture and noncapture was examined. Loss of HB-RB capture without change in stimulus-atrial (S-A) interval or atrial activation sequence indicated exclusive retrograde AP conduction. An increase in S-A interval without change in His bundle-atrial interval or atrial activation sequence indicated exclusive retrograde AVN conduction. A change in atrial activation sequence indicated the presence of both retrograde AP and AVN conduction. Para-Hisian pacing correctly identified retrograde AP conduction in 132 of 147 AP patients, including all septal and right free wall APs. Retrograde AVN conduction masked AP conduction in 9 of 34 patients with a left free wall AP and 6 of 9 patients with the permanent form of junctional reciprocating tachycardia. Para-Hisian pacing correctly excluded AP conduction in all 53 patients with AVNRT. CONCLUSIONS: Para-Hisian pacing reliably identifies retrograde conduction over septal and right free wall APs, but AVN conduction may mask APs located far from the pacing site or with a long retrograde conduction time.

Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success.

BACKGROUND: Typical atrial flutter (AFL) results from right atrial reentry by propagation through an isthmus between the inferior vena cava (IVC) and tricuspid annulus (TA). We postulated that the eustachian valve and ridge (EVR) forms a line of conduction block between the IVC and coronary sinus (CS) ostium and forms a second isthmus (septal isthmus) between the TA and CS ostium. METHODS AND RESULTS: Endocardial mapping in 30 patients with AFL demonstrated atrial activation around the TA in the counter-clockwise direction (left anterior oblique projection). Double atrial potentials were recorded along the EVR in all patients during AFL. Pacing either side of the EVR during sinus rhythm also produced double potentials, which indicated fixed anatomic block across EVR. Entrainment pacing at the septal isthmus and multiple sites around the TA produced a delta return interval < or = 8 ms in 14 of 15 patients tested. Catheter ablation eliminated AFL in all patients by ablation of the septal isthmus in 26 patients and the posterior isthmus in 4. AFL recurred in 2 of 12 patients (mean follow-up, 33.9 +/- 16.3 months) in whom ablation success was defined by the inability to reinduce AFL, compared with none of 18 patients (mean follow-up, 10.3 +/- 8.3 months) in whom success required formation of a complete line of conduction block between the TA and the EVR, identified by CS pacing that produced atrial activation around the TA only in the counterclockwise direction and by pacing the posterior TA with only clockwise atrial activation. CONCLUSIONS: (1) The EVR forms a line of fixed conduction block between the IVC and the CS; (2) the EVR and the TA provide boundaries for the AFL reentrant circuit; and (3) verification of a complete line of block between the TA and the EVR is a more reliable criterion for long-term ablation success.

Comparison of in vivo tissue temperature profile and lesion geometry for radiofrequency ablation with a saline-irrigated electrode versus temperature control in a canine thigh muscle preparation.

BACKGROUND: It is thought that only a thin layer of tissue adjacent to the electrode is heated directly by electrical current (resistive heating) during radiofrequency ablation. Most of the thermal injury is thought to result from conduction of heat from the surface layer. The purpose of this study was to determine whether lesion depth could be increased by producing direct resistive heating deeper in the tissue with higher radiofrequency power, allowed by cooling the ablation electrode with saline irrigation to prevent the rise in impedance that occurs when the electrode-tissue interface temperature reaches 100 degrees C. METHODS AND RESULTS: In 11 anesthetized dogs, the thigh muscle was exposed and bathed with heparinized canine blood (36 degrees C to 37 degrees C). A 7F catheter, with a central lumen, a 5-mm tip electrode with six irrigation holes, and an internal thermistor, was positioned perpendicular to the thigh muscle and held at a constant contact weight of 10 g. Radiofrequency current was delivered to 145 sites (1) at high constant voltage (66 V) without irrigation (CV group, n = 31), (2) at variable voltage (20 to 66 V) to maintain tip-electrode temperature at 80 degrees C to 90 degrees C without irrigation (temperature-control group, n = 39), and (3) at high CV (66 V) with saline irrigation through the catheter lumen and ablation electrode at 20 mL/min (CV irrigation group, n = 75). Radiofrequency current was applied for 60 seconds but was terminated immediately in the event of an impedance rise > or = 10 omega. Tip-electrode temperature and tissue temperature at depths of 3.5 and 7.0 mm were measured in all three groups (n = 145). In 33 CV irrigation group applications, temperature was also measured with a separate probe at the center (n = 18) or edge (n = 15) of the electrode-tissue interface. In all 31 CV group applications, radiofrequency energy delivery was terminated prematurely (at 11.6 +/- 4.8 seconds) owing to an impedance rise associated with an electrode temperature of 98.8 +/- 2.1 degrees C. All 39 temperature-control applications were delivered for 60 seconds without an impedance rise, but voltage had to be reduced to 38.4 +/- 6.1 V to avoid temperatures > 90 degrees C (mean tip-electrode temperature, 84.5 +/- 1.4 degrees C). In CV irrigation applications, the tip-electrode temperature was not > 48 degrees C (mean, 38.4 +/- 5.1 degrees C) and the electrode-tissue interface temperature was not > 80 degrees C (mean, 69.4 +/- 5.7 degrees C). An abrupt impedance rise with an audible pop and without coagulum occurred in 6 of 75 CV irrigation group applications at 30 to 51 seconds, probably owing to release of steam from below the surface. In the CV and temperature-control group applications, the temperatures at depths of 3.5 (62.1 +/- 15.1 degrees C and 67.9 +/- 7.5 degrees C) and 7.0 mm (40.3 +/- 5.3 degrees C and 48.3 +/- 4.8 degrees C) were always lower than the electrode temperature. Conversely, in CV irrigation group applications, electrode and electrode-tissue interface temperatures were consistently exceeded by the tissue temperature at depths of 3.5 mm (94.7 +/- 9.1 degrees C) and occasionally 7.0 mm (65.1 +/- 9.7 degrees C). Lesion dimensions were smallest in CV group applications (depth, 4.7 +/- 0.6 mm; maximal diameter, 9.8 +/- 0.8 mm; volume, 135 +/- 33 mm3), intermediate in temperature-control group applications (depth, 6.1 +/- 0.5 mm; maximal diameter, 11.3 +/- 0.9 mm; volume, 275 +/- 55 mm3), and largest in CV irrigation group applications (depth, 9.9 +/- 1.1 mm; maximal diameter, 14.3 +/- 1.5 mm; volume, 700 +/- 217 mm3; P < .01, respectively). CONCLUSIONS: Saline irrigation maintains a low electrode-tissue interface temperature during radiofrequency application at high power, which prevents an impedance rise and produces deeper and larger lesions. A higher temperature in the tissue (3.5 mm deep) than at the electrode-tissue interface indicates that direct resistive heating occurred deeper

Radiofrequency catheter ablation of right atriofascicular (Mahaim) accessory pathways guided by accessory pathway activation potentials.

BACKGROUND: Accessory pathways (APs) exhibiting "Mahaim fiber" physiology (antegrade conduction only, long conduction time, and decremental properties) often connect the lateral right atrium to the right bundle branch (right atriofascicular pathways). Potentials from these pathways have not been recorded previously. The purpose of this study was to determine whether AP activation potentials could be recorded from right atriofascicular APs and to determine whether these potentials could be used to localize a site for catheter ablation. METHODS AND RESULTS: Of 26 consecutive patients referred for catheter ablation of an AP producing a preexcited (antidromic) atrioventricular (AV) reentrant tachycardia having a left bundle branch block pattern with short ventriculoatrial and long AV intervals, 23 (88.5%) were found to have a right atriofascicular AP. During antidromic AV reentrant tachycardia, (1) right atrial extrastimuli (that did not penetrant tachycardia, (1) right atrial extrastimuli (that did not penetrate the AV node) advanced the timing of the next QRS complex, indicating that the AP was connected to the right atrium; (2) earliest antegrade ventricular activation was recorded at the apical right ventricular free wall, and (3) ventricular activation was preceded by activation of the distal right bundle branch, indicating a fascicular insertion or a ventricular insertion close to the terminus of the right bundle branch. A single, discrete, high-frequency AP potential was recorded at the lateral, anterolateral, or posterolateral tricuspid annulus in 22 of the 23 patients 63 +/- 12 milliseconds after the local atrial potential and 83 +/- 23 milliseconds before the local ventricular potential during sinus rhythm. The AP potential was also recorded at sites along the right ventricular free wall between the tricuspid annulus and the site of earliest ventricular activation at the apical region. Programmed atrial stimulation and adenosine each produced prolongation of AP conduction time because of an increase in the A-AP interval and Wenckebach block proximal to the AP potential. Radiofrequency current applied at a site recording the AP potential (tricuspid annulus in 19 patients and right ventricular free wall in 3 patients) eliminated AP conduction in all 22 patients. Tachycardia has not recurred in any patient during 18 +/- 13 months of follow-up. AP conduction was absent in all 9 patients who had a follow-up electrophysiological study 3.8 +/- 1.7 months after ablation. CONCLUSIONS: Right atriofascicular APs consist of two components. The proximal component is located at the lateral, anterolateral, or posterolateral tricuspid annulus, does not generate an AP potential recordable by catheter electrodes, and is responsible for the decremental conduction properties. The "distal" component extends from the tricuspid annulus to the distal right bundle branch at the apical right ventricular free wall and generates a large, high-frequency AP potential that accurately identifies a site for ablation.

Late potentials are unaffected by radiofrequency catheter ablation in patients with ventricular tachycardia.

Reentrant ventricular tachycardia is dependent on an area of myofibers, embedded in scar tissue, which exhibit slow conduction. Late potentials recorded by signal-averaged electrocardiography appear to correspond to these zones of slow conduction and frequently are present in patients with VT. We hypothesized that elimination of inducible VT by catheter-mediated ablation of critical areas of slow conduction would alter late potentials. Four patients underwent catheter ablation in which radiofrequency current was delivered to zones of slow conduction exhibiting isolated mid-diastolic potentials that could not be dissociated from the tachycardia. The four patients had developed VT (cycle length 382 +/- 50 msec; mean +/- SEM) 13-180 months after inferior myocardial infarction. Late potentials were present in each patient before catheter ablation was attempted. Although VT was not inducible in any patient immediately after ablation, late potentials were still present in all four patients and there was no significant difference in the QRS duration (136.5 +/- 4.0 msec postablation; 135.7 +/- 4.5 msec preablation), root mean square voltage in the terminal 40 msec of the QRS (10.0 +/- 1.0 microV postablation; 5.9 +/- 0.4 microV preablation), or in the duration of the low amplitude signal (69.2 +/- 2.0 msec postablation; 62.7 +/- 3.4 msec preablation). At follow-up electrophysiology study performed 14 +/- 7 days after ablation, one of the four patients had inducible VT. In conclusion, late potentials persist even after successful radiofrequency catheter ablation and do not appear to be useful for predicting results of follow-up electrophysiology study.

Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential.

BACKGROUND: Verapamil-sensitive, idiopathic left ventricular tachycardia (ILVT) with right bundle branch block configuration and left-axis deviation has been suggested to originate from the left posterior fascicle. The purpose of this study was to determine how frequently potentials generated by the Purkinje fiber network (P potential) can be recorded preceding ventricular activation, and the role of the P potential in guiding radiofrequency catheter ablation. METHODS AND RESULTS: Eight patients (mean age, 26 +/- 10 years) with ILVT (cycle length, 346 +/- 59 milliseconds) were studied. Right and left ventricular endocardial mapping during tachycardia identified earliest ventricular activation at the posteroapical left ventricular septum. In all patients, earliest ventricular activation during tachycardia was preceded by a distinct potential. This potential also preceded ventricular activation during sinus rhythm, consistent with activation of a segment of the left posterior fascicle (P potential). The earliest recorded P potential preceded the QRS during tachycardia by 15 to 42 milliseconds (mean, 27 +/- 9 milliseconds). The application of radiofrequency current at 1 to 4 sites (median, 1) eliminated ILVT in all eight patients. In the seven patients with P potentials recorded at multiple sites within the posteroapical septum, ablation was successful at the site of the earliest P potential and unrelated to the timing of ventricular activation. In the remaining patient, ablation was successful at a site recording a late P potential fusing with earliest ventricular activation. During follow-up (1 to 67 months; median, 10.5) ILVT recurred only in the latter patient. Pace mapping during tachycardia at the successful ablation site in four patients produced a similar QRS with stimulus-QRS interval equal to P-QRS interval during tachycardia. However, a similar QRS was obtained by pacing at nearby sites that recorded a later P potential. CONCLUSIONS: These findings support the hypothesis that ILVT originates from the Purkinje network of the left posterior fascicle. A P potential can be recorded at the posteroapical left ventricular septum during ILVT, and ablation is successful at the site recording the earliest P potential. Pace mapping with similar QRS is not specific due to capture of the Purkinje fiber network at a site remote from the origin of the tachycardia.

A functional approach to the preexcitation syndromes.

Electrophysiologic studies have been used to elicit the mechanisms of the preexcitation syndromes and have become a therapeutic tool over the past decade. A thorough understanding of the physiology and anatomy of accessory pathways that are responsible for preexcitation and the associated arrhythmias is necessary before considering the various forms of intervention. The approach to patients with preexcitation syndromes is discussed, with an emphasis on the functional properties of accessory pathways and the associated arrhythmias.

Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction.

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT), the most common form of supraventricular tachycardia, results from conduction through a reentrant circuit comprising fast and slow atrioventricular nodal pathways. Antiarrhythmic-drug therapy is not consistently successful in controlling this rhythm disturbance. Catheter ablation of the fast pathway with radiofrequency current eliminates AVNRT, but it can produce heart block. We hypothesized that catheter ablation of the site of insertion of the slow pathway into the atrium would eliminate AVNRT while leaving normal (fast-pathway) atrioventricular nodal conduction intact. METHODS AND RESULTS: Eighty patients with symptomatic AVNRT were studied. Retrograde slow-pathway conduction (in which the earliest retrograde atrial potential was recorded at the posterior septum, close to the coronary sinus) was present in 33 patients. The retrograde atrial potential was preceded by a potential consistent with activation of the atrial end of the slow pathway (ASP). In 46 of the 47 patients without retrograde slow-pathway conduction, a potential with the same characteristics as the ASP potential was recorded during sinus rhythm. Radiofrequency current delivered through a catheter to the ASP site (in the posteroseptal right atrium or coronary sinus) abolished or modified slow-pathway conduction in 78 patients, eliminating AVNRT without affecting normal atrioventricular nodal conduction. In the single patient without ASP, the application of radiofrequency current to the proximal coronary sinus ablated the fast pathway and AVNRT: Atrioventricular block occurred in one patient (1.3 percent) with left bundle-branch block, after inadvertent ablation of the right bundle branch. AVNRT has not recurred in any patient during a mean (+/- SD) follow-up of 15.5 +/- 11.3 months. Electrophysiologic study 4.3 +/- 3.3 months after ablation in 32 patients demonstrated normal atrioventricular nodal conduction without AVNRT: CONCLUSIONS: Catheter ablation of the atrial end of the slow pathway using radiofrequency current, guided by ASP potentials, can eliminate AVNRT with very little risk of atrioventricular block.

High and low strength nonsynchronized shocks given during canine ventricular tachycardia.

UNLABELLED: Cardioversion shocks given during ventricular tachycardia may cause ventricular fibrillation or acceleration of ventricular tachycardia, or arrest the tachycardia. A recently proposed theory may explain why the former two phenomena may occur. Briefly, this theory states that potential gradient shock fields of a critical strength delivered to tissue with a critical degree of refractoriness will cause circulating wave fronts of ventricular activation ("rotors") manifest as ventricular arrhythmia. We tested this theory by delivering nonsynchronized shocks 50% higher than defibrillation threshold or 50% lower than defibrillation threshold during 275 episodes of ventricular tachycardia in eight dogs with 5- to 7-day-old myocardial infarcts. Shocks stronger than the defibrillation threshold are likely to create shock fields in the ventricles everywhere stronger than this critical value, and therefore would not generate rotors. Shocks less strong than the defibrillation threshold may create shock fields within the ventricles that include the critical value, and therefore cause rotors if given when critically refractory tissue is present. Nonsynchronized shocks were used to increase the likelihood of encountering tissue with a critical degree of refractoriness. Ventricular fibrillation or acceleration of ventricular tachycardia occurred following 83 of 138 (60%) low strength shocks and following 20 of 137 (14.6%) high strength shocks. The pooled odds ratio for induction of ventricular fibrillation or accelerated ventricular tachycardia after low strength shocks as compared to high strength shocks was 8.9. CONCLUSION: when given during ventricular tachycardia, low strength shocks are much more likely to cause ventricular fibrillation or accelerated ventricular tachycardia than are high strength shocks (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Factors associated with recurrence of accessory pathway conduction after radiofrequency catheter ablation.

Catheter ablation of 215 accessory pathways (APs) using radiofrequency current (RF) was attempted in 204 consecutive patients. Two hundred twelve of the 215 (99%) APs were successfully ablated. After a minimum of follow-up period of 1 month (mean 8.5 +/- 5.4 months), AP conduction had returned in 17 patients (8%). Recurrence of AP conduction was manifest by atrioventricular (AV) reentrant tachycardia in six patients, palpitations suggestive of AV reentrant tachycardia in five patients, ventricular preexcitation on electrocardiogram in five patients, and inducible AV reentrant tachycardia during a follow-up electrophysiological study in one asymptomatic patient. AP conduction returned as early as 12 hours and as late as 4.7 months, but was evident within 2 months of ablation in 15 of 17 (88%) patients. AP conduction recurred in 12%-14% of anteroseptal, right free-wall, and posteroseptal APs, but only 5% of left free-wall APs (P less than 0.01). Retrograde only conducting APs (concealed APs) had recurrence of AP conduction more frequently (16%) than APs that exhibited antegrade conduction (5.5%; P less than 0.01). Failure to record AP potentials from the ablation electrode, reflecting poor AP localization, was a strong predictor for recurrence of AP conduction. AP conduction returned in 19% of 48 APs when AP potentials were not recorded, compared to 5% of 164 APs where AP potentials were recorded from the ablation electrode (P less than 0.01). The time to block of AP conduction from the onset of RF current application was longer in APs with recurrence of conduction (4.9 +/- 6.1 sec vs 2.9 +/- 3.4 sec; P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current.

BACKGROUND: Surgical or catheter ablation of accessory pathways by means of high-energy shocks serves as definitive therapy for patients with Wolff-Parkinson-White syndrome but has substantial associated morbidity and mortality. Radiofrequency current, an alternative energy source for ablation, produces smaller lesions without adverse effects remote from the site where current is delivered. We conducted this study to develop catheter techniques for delivering radiofrequency current to reduce morbidity and mortality associated with accessory-pathway ablation. METHODS: Radiofrequency current (mean power, 30.9 +/- 5.3 W) was applied through a catheter electrode positioned against the mitral or tricuspid annulus or a branch of the coronary sinus; when possible, delivery was guided by catheter recordings of accessory-pathway activation. Ablation was attempted in 166 patients with 177 accessory pathways (106 pathways in the left free wall, 13 in the anteroseptal region, 43 in the posteroseptal region, and 15 in the right free wall). RESULTS: Accessory-pathway conduction was eliminated in 164 of 166 patients (99 percent) by a median of three applications of radiofrequency current. During a mean follow-up (+/- SD) of 8.0 +/- 5.4 months, preexcitation or atrioventricular reentrant tachycardia returned in 15 patients (9 percent). All underwent a second, successful ablation. Electrophysiologic study 3.1 +/- 1.9 months after ablation in 75 patients verified the absence of accessory-pathway conduction in all. Complications of radiofrequency-current application occurred in three patients (1.8 percent): atrioventricular block (one patient), pericarditis (one), and cardiac tamponade (one) after radiofrequency current was applied in a small branch of the coronary sinus. CONCLUSIONS: Radiofrequency current is highly effective in ablating accessory pathways, with low morbidity and no mortality.

Comparison of ventricular arrhythmia induction with use of an indwelling electrode catheter and a newly inserted catheter.

Two methods of serial electrophysiologic testing are in widespread use. Most commonly, the electrode catheter is removed after each study and a new catheter reinserted through the femoral vein for every subsequent test. An alternative method employs an electrode catheter that remains in place during several days of serial testing. Little is known about differences between these two methods with respect to the likelihood of induction of arrhythmia or the frequency of complications. To determine whether inducibility of sustained arrhythmia is altered or if the frequency of complications is unacceptably high with use of an indwelling catheter, a prospective randomized study was conducted in 78 patients. Each patient underwent baseline testing, several days of electropharmacologic testing with an indwelling catheter, a 24 h drug elimination period and placement of a new electrode catheter. Ventricular stimulation studies were then performed in each patient with both the indwelling and new electrode catheters. No differences were found between the indwelling and new catheter tests with respect to induction of arrhythmia, number of extrastimuli required to induce arrhythmia, rate of arrhythmia or requirement for cardioversion. Ventricular pacing thresholds were higher and effective refractory periods were slightly longer when measured with the indwelling catheter. Complications related to the 156 catheter insertions included two that may have been related to the indwelling catheter (one episode of staphylococcal sepsis and one presumed pulmonary embolism) and four that were related to invasive procedures (pneumothorax in all). There were no long-term adverse sequelae of these complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Caffeine and ventricular arrhythmias. An electrophysiological approach.

Little information is known regarding caffeine's effect on the substrate supporting sustained ventricular arrhythmias. This prospective study evaluated the effect of coffee (275 mg of caffeine) on this substrate with programmed ventricular stimulation in 22 patients with a history of symptomatic nonsustained ventricular tachycardia, ventricular tachycardia, or ventricular fibrillation. Patients underwent electrophysiological testing before and 1 hour after coffee ingestion. Mean (+/- SEM) plasma caffeine level achieved after coffee consumption was 6.2 +/- 0.5 mg/L. Mean plasma catecholamine and potassium values were not altered significantly 1 hour following caffeine ingestion. The number of extrastimuli required to induce an arrhythmia was unchanged in 10 patients (46%), increased in six (27%), and decreased in six (27%). Rhythm severity was unchanged in 17 patients (77%), more severe in two (9%), and less severe in three (14%). In those patients with clinical ventricular arrhythmias, caffeine did not significantly alter inducibility or severity of arrhythmias, suggesting little effect on the substrate supporting ventricular arrhythmias.