Josephson Clinical Cardiac Electrophysiology


Chapter 6: Ectopic Rhythms and Premature Depolarizations ■

only method of localizing the origin of such P waves. More over, if P-wave morphologies of APDs appear similar to sinus P waves, the only method of differentiating those premature impulses from sinus arrhythmia, sinus node reentry, or ecto pic impulses in the region of the sinus node is mapping the sequence of atrial activation of the early complexes. An atrial activation sequence, which is different from that during sinus rhythm, confirms the premature complexes as ectopic, despite a surface P-wave morphology similar to sinus. Automaticity (suggested by recording Phase 4 activity) and triggered activ ity (suggested by recording delayed afterdepolarizations) have been postulated as the mechanism of APDs 2,3 based on ex perimental studies. 25-28 How valid these conclusions are and, if they are, how frequent such mechanisms are operative remain speculative. Certainly, many of the atrial tachycardias that are catecholamine sensitive are likely to be due to these mecha nisms. The morphology of the electrogram at the site of origin (ie, fractionated, split, etc) does not determine the mechanism of the APD. It is only a reflection of propagation of the atrial impulse. The site of origin of an atrial impulse can affect the P-R interval. 29-31 Such an apparent alteration in A-V conduction (ie, changing P-R interval) may result from a different input into the A-V node, either qualitatively or in relationship to the activation of the remainder of the atrium. An example of that phenomenon is depicted in Figure 6.6 ; different atrial rhythms are associated with different P-R intervals despite identical A-H intervals. This situation is a result of an earlier input into the A-V node relative to atrial activation during the rhythm shown on the left. Shorter A-H intervals than sinus are more often observed, with ectopic atrial activation origi nating in the coronary sinus or inferoposterior left atrium

RA 75%

LA 25%

RAA < 1%

PV 20% LAA < 1%

CT 30%

Roof < 1%

Perinodal 10%

Septum < 1%

CS body 2% Septum < 1%

CS os 10%

TA 20%

Sup. MA 4%


FIGURE 6.4 Sites of origin of atrial tachycardias. The sites of mapped atrial tachycardias are shown on a schema of the heart. P waves characterizing these sites are possible, with limitations. CS, coronary sinus; CT, crista terminalis; LA, left atrium; LAA, left atrial appendage; MA, mitral annulus; PV, pulmonary vein; RA, right atrium; RAA, right atrial appendage. (Modified from Kistler PM, Haqqani HM, Fynn SP, et al. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol . 2006;48:1010-1017, with permission from Elsevier.) coworkers ( Figure 6.5 ). 23,24 APDs that initiate AF are typically very early (on the T wave of the preceding complex), adding another limitation to ECG localization, and the P-wave mor phology is difficult to characterize when superimposed on the T wave. Because superiorly directed P waves can be observed with APDs that originate low in the right atrium, as well as in the left atrium or coronary sinus, intracardiac recording is the

RAA = right atrial appendage TV = tricuspid valve CT = crista terminalis ER = eustacian ridge SVC = superior vena cava AVNRT = AV node reentrant tachycardia

LAA = left atrial appendage MV = mitral valve CS = coronary sinus LOM = ligament of Marshall LLAP = left lateral accessory pathway PW = posterior wall


























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PAF ( N = 1531) PERS ( N = 496) LS PERS ( N = 141)

*2 patients with longstanding persistent AF

FIGURE 6.5 The location and frequency of nonpulmonary vein triggers in 2,168 patients with paroxysmal (PAF), persistent (PERS), and long-standing persistent (LS PERS) atrial fibrillation (AF). Common AF trigger sites have a similar distribution to the common sites of organized atrial tachycardia. (Reprinted from Santangeli P, Zado ES, Hutchinson MD, et al. Prevalence and distribution of focal triggers in persistent and long standing persistent atrial fibrillation. Heart Rhythm . 2016;13:374-382. Figure 4, with permission from Elsevier.)

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