Sinus nodal echoes. Clinical case report and canine studies

Sinus nodal echoes are illustrated in (1) a case report, and (2) a study of the effects of atrial premature beats after atrial drive in dogs. When atrial premature beats confront the sinus node while it is still refractory, 3 types of response may be seen: (1) Complete interpolation—the subsequent sinus beat (or escape) comes precisely at the expected time; (2) incomplete interpolation—the subsequent sinus beat is delayed; and (3) sinus echoes—the sinus beat appears earlier than expected. In all 3 instances the node is entered, but the pacemaker fails to be reset. Although the echo has the form of a sinus beat, it is followed by a pause, presumably as a result of repenetration of the sinus node through pathways unused during exit. The curves characterizing the expansion by vagal stimulation of the nodal refractory period and total echo circuit time are defined, together with the latency of cholinergic effect on nodal refractoriness, sinus automaticity and exit conduction of the echo. The secondary concealment zone of a completely interpolated atrial premature beat is established. Atrial preexcitation (before the echo) sometimes evokes a second echo. The limiting factor on sustained sinoatrial reciprocation thus appears to be total echo circuit time rather than refractoriness of atrium or echo entrance pathways. The repetitive echoes seen in this study may be the basis for some clinical cases of sinus or atrial tachycardia.     

肌袖性房性心律失常的动态心电图特征分析

目的探讨肌袖性房性心律失常的动态心电图(DEC)特征。方法对比8例肌袖性房性心律失常与10例非肌袖性房性心律失常患者的临床和DEC特点。结果肌袖性房性心律失常有频发房性期前收缩,短阵房性心动过速,心房扑动,均发生短阵心房颤动,发作时间为2~15min不等,诱发心房颤动的房性期前收缩联律间期(0.24±0.03)s,明显短于对照组房性期前收缩联律间期(0.34±0.05)s(P<0.01)。结论肌袖性房性心律失常的DEC中窦性心律、房性心动过速、心房扑动、心房颤动交替转换,诱发心房颤动发作的房性期前收缩联律间期短,几乎均呈“P-on-T”现象。     

Atrial rhythms in response to an early atrial premature depolarization in man

The effect of an early atrial premature depolarization (APD) on spontaneous atrial rate was assessed in 16 patients in sinus rhythm. At close coupling intervals (range 27 to 48 per cent of the preceding sinus cycle), atrial acceleration was observed for several beats following the APD in 13 patients. On the basis of P wave configuration and the intra-atrial activation sequence, the accelerated beats appeared to originate from the sinus node. Furthermore, this “sinus” acceleration appeared regardless of the site at which the APD was introduced and was unrelated to latency or current strength. The findings are consistent with APD-induced sinus node re-entry, although sinus node pacemaker acceleration and shift is an alternative mechanism. Sinus node re-entry may explain certain instances of “interpolated” APD's and atrial tachyarrhythmias seen clinically.     

An Unusual Narrow QRS Complex Tachycardia: What Is the Mechanism?

The electrocardiogram of a 72‐year‐old woman showed episodes of nonsustained narrow QRS complex tachycardia. Tracing analysis suggested that the arrhythmia was due to interpolated atrial extrasystoles occurring in bigeminal rhythm. Interpolation of atrial extrasystoles is a rare phenomenon. In this condition, a premature atrial beat is “sandwiched” between 2 normal sinus beats, and sinus PP interval containing the extrasystole is often longer than unaffected sinus cycles. Alternative mechanisms for the arrhythmia are discussed, such as: (1) sinus node reentry; (2) 1:2 response to atrial ectopy over the fast and the slow atrioventricular nodal pathways; and (3) couplets of atrial extrasystoles.     

The postponed compensatory pause as a manifestation of positive feedback in atrioventricular conduction.

A patient with hypertensive cardiovascular disease was found to have unusual varieties of premature atrial and ventricular contractions. If the premature atrial contraction resulted in a greatly prolonged P-R interval, such that the increment in P-R exceeded the decrement in the preceding R-P, the next sinus P wave, occurring after a normal P-P interval, was found to be blocked. Also, numerous interpolated ventricular extrasystoles were observed in which the postextrasystolic P-R intervals were markedly prolonged and in which the compensatory pauses were postponed for one or two beats. We also present data from one dog in which a premature atrial activation produced a chain reaction such that complete A-V block occurred three beats later. We propose that the chain reaction which evoked the delayed block in the dog and the postponed compensatory pauses in the patient reflects the operation of a positive feedback mechanism in A-V conduction. Positive feedback is initiated by an extremely long P-R, which results in a very short R-P before the next cycle. This then leads to a still longer P-R, which then elicits a still shorter R-P. Block ultimately supervenes when the atrial activation wave arrives at the A-V junction during its effective refractory period.     

Atrial stimulation and intranodal migration of sinus pacemaker in man (author's transl)

In order to demonstrate, in man, sinus node pacemaker shift following atrial stimulation, we compared, in 26 patients, the curve of sinus node function obtained with Strauss' method with that resulting by the scanning with premature atrial stimulation of the first returning cycle following either a single premature atrial induced beat (140 ms shorter than the basic cycle) (group A), or a train of 8 consecutive atrial beats induced with a rate slightly faster (10 beats/m) than the control sinus rhythm (group B). Assuming that no changes in sinus pacemaker automaticity or in sinoatrial conduction occur owing to atrial stimulation, curves with the same shape should be observed if the site of the dominant pacemaker remains unchanged: whereas, different lengths of the compensatory phase (zone I) should be expected if an intranodal pacemaker shift occurs. For evaluating the length of the compensatory zone (zone I), we calculate, on the curve of the sinus node function, the mean value of the relation points included in the first third of the reset zone (zone II). According to our results, the length of the compensatory phase (zone I) evaluated on the curve resulting by the scanning of the first returning cycle following either a single premature atrial induced beat (group A), or eight consecutive atrial beats (group B) was shorter than that observed with the original Strauss' method (10% and 18% respectively). However, only in the group B, this difference was statistically significant. In addition, a significant inverse relationship between the shortening of the compensatory zone and the sinoatrial conduction index was also observed. Considering that our results have been corrected in such way as to repeal eventual changes in sinus pacemaker automaticity or sinoatrial conduction following atrial stimulation, the shortening of the compensatory zone, we have observed in our patients, strongly suggests an intranodal sinus pacemaker shift. If we assume that this result could represent an indirect evidence of this phenomenon, some clinical implications may follow: 1) another limitation, in addition to others known (intraatrial conduction delay, sinus arrhythmia, changes in sinus node automaticity, difference between retrograde and antegrade conduction time) could decrease the accuracy of atrial stimulation techniques in the estimation of the sinoatrial conduction time; 2) sinus pacemaker shift following atrial stimulation, may induce an understimulation of the true sinoatrial conduction time; however, according to our results, the error is generally small, so that it does no preclude the usefulness of atrial stimulation techniques in the evaluation of sinoatrial conduction; 3) the more evident and significant shortenings of the compensatory phase occurred with atrial pacing technique: this finding could explain why shorter sinoatrial conduction times are generally observed with Narula's method in comparison with Strauss' method.     

Thresholds, refractory periods, and conduction times of the normal and diseased human atrium

In order to better understand the electrophysiology of the diseased human atrium, we measured high right atrial refractory periods, threshold, and conduction times of 61 patients undergoing routine electrophysiologic study. Refractory periods and conduction times of patients with apparently normal atria were compared to those of patients with a history of persistent sinus bradycardia, atrial fibrillation, or other forms of primary atrial tachyarrhythmia. Refractory periods and thresholds were derived from strength-interval curves. Conduction times were measured for all premature beats induced. Threshold, refractory periods, and conduction times of premature beats induced late in the cardiac cycle did not distinguish patients with normal atria from patients with bradycardia or tachycardia. In contrast, increases in conduction time of early cycle premature beats separated patients with these abnormalities from patients with normal atria. The increases in interatrial and intraatrial conduction time of early cycle premature beats were the strongest correlates of primary atrial tachyarrhythmia (r = 0.52, p = 0.0065 and r = 0.274, p = 0.041, respectively) and induction of repetitive atrial firing (r = 0.65, p = 0.002, and r = 0.59, p = 0.0001, respectively). This increase in conduction time of early cycle premature beats may predispose these patients to primary atrial tachyarrhythmias.     

起源于肺静脉的房性心律失常体表心电图和心内电生理特点

目的:分析起源于肺静脉的房性心律失常体表心电图和心内电生理特点,识别触发心房纤颤(房颤)的房性期前收缩(房早)和房性心动过速(房速)。方法:回顾性分析房性心律失常并阵发性房颤84例体表心电图(房颤组),非房颤组84例体表心电图为频发房早(800次/24 h)。房颤组结合心内电生理检查及Lasso环状电极标测,行导管射频消融(RFCA)肺静脉隔离(PVI)。结果:房颤组电隔离肺静脉286支,均达即刻成功标准,无并发症发生。房颤组体表心电图呈房早、房速、心房扑动(房扑)和阵发性房颤(房颤)频繁发作和交替转换,并常伴长间歇,房早联律间期470～280(420±57)ms明显短于非房颤组的房早联律间期660～350(610±86)ms,P0.05,房颤多由短联律间期房早触发。心内电生理改变为Lasso环状电极标测到起源于肺静脉的连续、快速、有序或无序的较P波提前,时限短、峰锐利的尖峰电位(Spike电位),同步心电图显示该Spike电位常是阵发性房颤的触发因素。经导管射频消融消除肺静脉内电位或隔离肺静脉与心房间的电或组织连接,可终止房性心律失常,维持窦性心律。结论:起源于肺静脉的房性心律失常的特点是短联律间期房早,也是阵发性房颤的触发因素。     

Observations in patients showing A-V junctional echoes with a shorter P-R than R-P interval: Distinction between intranodal reentry or reentry using an accessory pathway with a long conduction time

Single test stimulation of the ventricle revealed initiation of echoes with a supraventricular QRS complex with a shorter P-R than R-P interval in 28 of 300 patients consecutively studied with programmed electrical stimulation of the heart because of documented or suspected tachycardias. In all 28 the initiation of echoes was related to a discontinuity in the retrograde conduction curve. In 10 patients a different atrial activation sequence in the endocavitary leads was present before and after the discontinuity in the retrograde conduction curve. In five of these a sustained tachycardia with a shorter P-R than R-P interval could be initiated, and in all five patients an accessory pathway with a long conduction time as the retrograde arm of the tachycardia circuit could be demonstrated. In these five patients spontaneous initiation of tachycardia was observed during sinus rhythm or after atrial premature beats. Tachycardia accelerated after the administration of atropine. In the remaining 23 patients the initiation of echoes showing a shorter P-R than R-P interval was nonsustained. In these patients spontaneous initiation of such echoes during sinus rhythm or initiation by atrial premature beats was not observed, and echoes with this relation of the P-R and R-P intervals systematically disappeared after administration of atropine.It is postulated that in these patients a slow atrioventricular (A-V) nodal pathway is used in the retrograde direction during echoes showing a shorter P-R than R-P interval. Sustained A-V junctional tachycardia showing this relation between P-R and R-P intervals favors incorporation of an accessory pathway with slow retrograde conduction in the tachycardia circuit.     

Gaps in anterograde conduction in patients with the short PR interval, normal QRS complex syndrome.

Of 8 patients with the short PR interval, normal QRS complex syndrome studied recently, 3 reported here displayed gaps in anterograde conduction. Atrial premature beats at decreasing coupling intervals conducted with minimal AH prolongation until a zone within the cardiac cycle was reached where conduction failed at a supra-Hisian level. Conduction resumed at earlier atrial coupling intervals and was associated with a sudden increase in the AH interval and the appearance of atrial echo beats with earliest atrial activation on the proximal coronary sinus electrogram. It is suggested that the failure of anterograde conduction at relatively late atrial coupling intervals was caused by a short AH functional refractoriness produced by the pre-excitation of the lower AV junction by a partial AV nodal bypass. Conduction resumed only when early atrial premature beats found the extranodal pathway refractory and were transmitted with decremental delay through the AV node.     

Right atrial versus left atrial echo zones: A proposed new criterion for determining the atrial site of retrograde preexcitation

In a patient whose electrocardiogram (ECG) initially (1966) showed a Type A Wolff-Parkinson-White pattern, recurrent supraventricular tachycardia (SVT) developed but never subsequently showed antegrade bypass conduction. Intracardiac pacing studies (1975) revealed that premature high right atrial (induced 250–450 msec after atrial depolarization) or coronary sinus depolarization (250–550 msec) resulted in SVT. Late coronary sinus depolarization resulted in SVT without A-H prolongation. During SVT, P wave morphology changed and the coronary sinus atrial electrogram preceded that from the low right atrium; retrograde ventriculoatrial conduction time was 240 msec. Neither pacing the high right atrium or coronary sinus up to rates of 200 beats/min nor progressive atrial premature depolarizations from the high right atrium or coronary sinus resulted in antegrade bypass conduction. Failure of antegrade bypass conduction does not preclude SVT due to retrograde pre-excitation and must be distinguished from atrioventricular (A-V) nodal reentry. Atrial effective refractory period (200 msec) was shorter than the minimal time required for an atrial impulse to return to the atrium (380 msec), suggesting concealed antegrade bypass conduction. Stimulation of the atrium linked to the A-V bypass results in earlier bypass activation and recovery and explains the differing high right atrial vs coronary sinus echo zones.     

Ventricular Extrasystoles with Interpolation or Postponed Compensatory Pause during Atrial Fibrillation: Fact or Fiction?

A Holter recording obtained from a patient with atrial fibrillation showed ventricular extrasystoles often in bigeminal rhythm. Most extrasystoles were followed by a long return cycle, and only in a few instances the postextrasystolic interval was short. The latter phenomenon was interpreted as a manifestation of poor retrograde concealed penetration of the ventricular impulse into the atrioventricular (A‐V) junction: accordingly, an ensuing relatively early fibrillation impulse reached the ventricular chamber, since it did not find the A‐V node refractory. These events are similar to what happens in interpolated ventricular extrasystoles occurring during sinus rhythm, the absent or minimal concealed retrograde penetration of the ectopic impulse into the A‐V node being necessary to permit anterograde conduction of the ensuing sinus impulse. Analysis of the recording also revealed that a very long (>2 second) interval between two consecutive narrow beats only occurred after an “interpolated” extrasystole. This was interpreted with the same mechanism underlying the “postponed compensatory pause” observed at times after interpolated ventricular extrasystoles during sinus rhythm: the minimal or nil penetration of the ventricular ectopic impulse into the A‐V junction, followed by conduction of an ensuing early atrial impulse, “shifts to the right” the A‐V nodal refractory period, preventing conduction of several further supraventricular impulses and generating a pause. Both interpolated ventricular extrasystoles and the phenomenon of “postponed compensatory pause” are, thus, conceivable during atrial fibrillation, although no definite demonstration is possible.     

Ventricular ectopic activity after premature atrial beats in acute myocardial infarction.

Ventricular ectopic activity occurred only after premature atrial beats in a patient with an acute inferior wall myocardial infarction. The ventricular ectopic activity occurred only when the coupling interval between the premature atrial beats and preceding sinus beat was less than or equal to 0-44 s. The sinus cycle length, however, appeared to influence the form of expression of ventricular ectopic activity independent of coupling intervals, with single premature ventricular contractions occurring at cycle lengths greater than or equal to 0-72 s, couplets at cycle lengths of 0-68 to 0-71 s, and ventricular tachycardia at cycle lengths less than or equal to 0-67 s.     

Intra-atrial conduction delay and fragmented atrial activity in patients with paroxysmal atrial fibrillation

To examine the electrophysiologic characteristics of paroxysmal atrial fibrillation (PAF), we studied intra-atrial conduction delay and fragmented atrial activity during premature stimulation of high right atrium in the following four groups: Group I (n = 25), patients without PAF and without sick sinus syndrome (SSS); Group II (n = 22), patients with PAF but without SSS; Group III (n = 10), patients without PAF and with SSS; Group IV (n = 6), patients with PAF and SSS. Intra-atrial conduction delay was the increase in the interval (from the stimuli to the coronary sinus electrogram) observed with early premature beats greater than or equal to 20 ms compared with that of basic rhythm. Fragmented atrial activity was defined as disorganized atrial activity greater than or equal to 150% of the duration of high atrial activity of basic beats recorded. The conduction delay zone (CDZ) and fragmented atrial activity zone (FAZ) were significantly wider in Groups II, III and IV than in Group I. There were no significant differences in either CDZs or FAZs among Groups II, III and IV. Thus, the widening of CDZs and/or FAZs are characteristic of PAF and SSS. CDZ and FAZ may be good indices of development of PAF in patients without SSS.     

Atrial premature beats coupling interval determines lone paroxysmal atrial fibrillation onset.

In 20 patients with recurrent episodes of lone paroxysmal atrial fibrillation we assessed the onset pattern of each episode of either atrial fibrillation or of atrial flutter during a 24-h Holter monitoring. We evaluated 24 twenty-four-hour Holter tape recordings and our data are related to 168 episodes of paroxysmal atrial fibrillation and 27 episodes of paroxysmal atrial flutter. Eighty-five percent of atrial fibrillations and 67% of atrial flutters were of short duration (less than 5 min). The majority of patients (80%) had either nocturnal or daily episodes of arrhythmia and PP intervals immediately before onset of arrhythmia did not show significant variations in 77% of cases. The coupling interval of the supraventricular premature beats eliciting atrial fibrillation was significantly shorter than the coupling intervals of the spontaneous isolated supraventricular premature beats (p less than 0.0001); again, in 6 patients with either atrial fibrillation or flutter, the coupling interval at onset of fibrillation was significantly shorter in comparison to flutter (p less than 0.0001). In conclusion, vagal or sympathetic prevalence does not seem to influence significantly the beginning of the arrhythmia, while the coupling interval of the atrial premature beats plays a critical role in the inducibility of atrial flutter or fibrillation.     

三磷酸腺苷静脉注射诱发快速性心律失常

本研究选择79例阵发性室上性心动过速患者,在窦性心律或诱发的室上性心动过速发作时分级递增静脉注射三磷酸腺苷332次,诱发出窦性心动过速194例次(58.43%)、房性反复搏动34例次(10.24%)、室上性心动过速13例次(3.92%)、偶发房性早搏8例次(2.41%)、阵发性心房颤动3例次(0.9%)和偶发室性早搏2例次(0.6%)。除室上性心动过速外,均为一过性。未引起血液动力学障碍。     

Mechanism of escape, extrasystolic, and parasystolic arrhythmias. Study on an electrical analogue.

A simple analogue of the heart consisting of a system of neon relaxation oscillators is presented. The analogue may display rhythm patterns similar to sinus rhythm, escape rhythm, isorrhythmic dissociation with synchronization, atrial extrasystoles, ventricular extrasystoles, and parasystole. The strict rules followed by these arrhythmias, as well as the deviations from the rules commonly followed by the equivalent heart arrhythmias, may be easily reproduced on the analogue. Such features are the Treppe phenomenon and captured beats in escape rhythm, fixed coupling intervals in extrasystoles, partial or complete atrioventricular block in very premature atrial extrasystoles, prolongation of the period following an atrial extrasystole, interpolated premature beats, complete compensatory pause and the rule of bigeminy in ventricular extrasystoles, slight instability of the parasystolic period, multiple length parasystolic periods slightly different from the exact multiples of the parasystolic idioperiod, preference of the parasystoles for certain phase in the sinus cycle, synchronization at a phase difference and fluctuation repeatedly and without interruption from a parasystolic to an extrasystolic rhythm and synchronization in escape rhythm with isorrhythmic dissociation. The mechanisms involved in these phenomena are discussed in detail. The striking similarity between the properties of the cardiac pacemakers and those of the relaxation oscillators on the one hand and betwen the rhythm patterns of the heart and those of the analogue on the other may permit the hypothesis that the mechanisms operating in the analogue may be used in analyzing and understanding heart arrhythmias.     

Arrhythmias documented by 24 hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease.

Results are reported of portable 24 hour dynamic electrocardiographic monitoring in 50 male medical students without cardiovascular disease, as defined by normal clinical and noninvasive cardiovascular examination. During waking periods, maximal sinus rates ranged from 107 to 180 beats/min (mean +/- 5). Twenty-five subjects (50 percent) had episodes of marked sinus arrhythmia as defined by spontaneous changes in adjacent cycle lengths of 100 percent or more. Fourteen subjects (28 percent) had sinus pauses of more than 1.75 seconds, usually during sinus arrhythmia. Transient nocturnal type I second degree atrioventricular (A-V) block was noted in three subjects (6 percent). Of 28 patients (56 percent) having atrial premature beats, only 1 (2 percent) had more than 100 such beats (141) in 24 hours. Of 25 patients (50 percent) having premature ventricular contractions, only 1 (2 percent) had more than 50 such contractions (86) in 24 hours. In conclusion, frequent atrial and ventricular premature beats are unusual in a young adult male population. In contrast, bradyarrhythmias (including marked sinus arrhythmia with sinus pauses, sinus bradycardia and nocturnal A-V block) are common. These findings are useful in evaluating the clinical significance of arrhythmias detected with portable monitoring.     

The origins of the sinus node pacemaker complex in man: demonstration of dominant and subsidiary foci

To test the hypothesis that the human sinus node is capable of demonstrating multiple sites of impulse generation, we assessed spontaneous shifts in the sinus node pacemaker complex, and shifts after overdrive atrial pacing, premature atrial stimulation and carotid sinus massage. A total of 24 patients aged 59 +/- 15 years (mean +/- SD) in whom stable sinus node electrograms were obtained were selected for the study. Ten of the 24 patients had sick sinus syndrome, whereas 14 had no sinus node dysfunction. All 24 patients had atrial pacing at cycle lengths of 1,000 to 300 ms; 9 patients had premature atrial stimulation and 12 had carotid sinus massage. Shifts in the sinus node pacemaker complex occurred spontaneously in 4 (17%) of the 24 patients; after atrial pacing at cycle lengths of 800 to 300 ms (mean 387 +/- 92) in 15 (63%) of 24 patients; after premature atrial stimulation at one or more coupling intervals in 5 (56%) of 9 patients and during carotid sinus massage in 9 (75%) of 12 patients. Shifts in the sinus node pacemaker complex lasted one to six beats and returned to the original site within two to seven beats. Spontaneous shifts in the sinus node pacemaker complex occurred in 3 of 14 patients without sick sinus syndrome and were induced in 6 (60%) of 10 patients with sick sinus syndrome and 11 (79%) of 14 patients without sick sinus syndrome. Shifts in sinus node pacemaker complex were characterized by loss of primary negativity, change in P wave morphology, significant (p less than 0.001) prolongation of sinoatrial interval and sinus cycle length.     

Electrocardiographic analysis of ectopic atrial activity obscured by ventricular repolarization: P wave isolation using an automatic 62-lead QRST subtraction algorithm

INTRODUCTION: Atrial activity on the surface ECG during premature beats and supraventricular arrhythmias frequently is obscured by the superimposed QRST complex of the previous cardiac cycle. This study examines the performance of a newly developed automatic QRST subtraction algorithm to isolate ectopic P waves from the preceding T-U wave. METHODS AND RESULTS: The 62-lead ECG recordings were obtained during (1) sinus rhythm and programmed right atrial stimulation in 12 patients (group A); and (2) sinus rhythm and atrial premature beats, atrial tachycardia, or paroxysmal atrial fibrillation in 5 patients (group B). Pacing in group A patients was conducted at a slow drive cycle length to generate an ectopic P wave not obscured by the previous QRST complex and by delivering single premature extrastimuli at progressively shorter coupling intervals to produce an ectopic P wave obscured by the upsloping (early T-U wave), peak (middle T-U wave), and downsloping component of the T-U wave (late T-U wave). All ectopic P waves in group B patients were concealed by the preceding T-U wave. Automatic QRST subtraction was attained using an adaptive template constructed from averaged QRST complexes (mean 83 +/- 25 complexes) obtained during sinus rhythm (groups A and B) or atrial overdrive pacing (group A). P wave integral maps subsequently were computed, visually compared, and mathematically correlated. A high correspondence in spatial map pattern was observed between integral maps of "nonobscured" and previously "obscured" paced P waves obtained in group A patients (mean r = 0.88 +/- 0.07) as well as between integral maps of two to three previously obscured P waves with the same atrial arrhythmia morphology obtained in group B patients (mean r = 0.94 +/- 0.05). Improved morphologic P wave replication in group A patients was acquired when concealment occurred in the early (mean r = 0.90 +/- 0.08) or late part of the T-U wave (mean r = 0.90 +/- 0.06) as opposed to the middle T-U wave (mean r = 0.85 +/- 0.07) (P = NS and P < 0.05 for early vs middle and late vs middle T-U wave, respectively). CONCLUSION: This novel automatic 62-lead QRST subtraction algorithm enables discrete isolation of T-U wave obscured ectopic atrial activity on the surface ECG while retaining the intricate spatial detail in P wave morphology. Future clinical application of the algorithm may enable improved ECG localization of focal triggers of paroxysmal atrial fibrillation, atrial tachycardia, and the atrial insertion of accessory pathways.