Josephson Clinical Cardiac Electrophysiology


Ectopic Rhythms and Premature Depolarizations

Ectopic depolarizations can arise from many areas of the heart, but the surface electrocardiogram (ECG) is markedly limited in its ability to define the origin of such ectopic activity, even on a “macroscopic” level, that is, distinguishing supraven tricular from ventricular activation. Recording intracardiac electrograms is the most reliable method of defining the ori gin of ectopic activity. Such recordings have thus provided the most accurate method of localizing and characterizing ectopic activity and have made us aware of the many limitations of the surface ECG in the evaluation of these arrhythmias. In a more mechanistic era of our field, investigators were interested in using intracardiac recordings not only for localization but also to infer mechanism. Hariman et al 1-4 demonstrated that the use of high gain specially filtered electrograms (0.1 and 25-50 Hz) can be used to detect automaticity in ectopic foci of the ventricle, atrium, and atrioventricular (A-V) junction. The frequency with which such signals can be obtained was not evaluated. However, it is logical that, analogous to sinus node electrograms, automaticity could be detected in very well-localized areas. Another potential method to localize and postulate mechanisms of arrhythmias is through the use of re cording monophasic action potentials (MAP) to record after depolarizations. 5-9 While many accept MAP recordings, much concern exists in my mind as to whether what is recorded is truly responsible for the arrhythmia it is being used to localize. In my opinion, further validation of these techniques demonstrating a causal relationship to arrhythmogenesis is needed before this technique is applied clinically. The mechanism of ectopic rhythms may include normal automaticity, abnormal automaticity, and triggered activity. The responses to alterations in autonomic tone, specific anti arrhythmic drugs (adenosine, Na + channel blockade, etc), and overdrive stimulation vary not only by underlying mechanism but also by the site of origin. Wit and colleagues provide an excellent review of these characteristics. 10 ATRIAL DEPOLARIZATIONS Although several P-wave algorithms have been proposed to localize atrial depolarizations or atrial tachycardia, 11-13 limita tions of ECG localization must be recognized. Atrial anatomy, prior surgery, fibrosis, drugs, and atrial position in the thorax

can influence the propagation of atrial activity and, therefore, P-wave morphology. Thus, the predictive accuracy of P-wave morphology for sites of ectopic atrial impulses is limited in the presence of these factors. Although a P wave in the surface ECG is the manifestation of atrial activation, even the absence of P waves cannot prove the absence of atrial activity. In an occasional patient, the surface ECG demonstrates the absence of P waves, a normal QRS complex, and a regular ( Figure 6.1 ) or an irregular rhythm ( Figure 6.2 ), suggesting either a junc tional (His bundle) rhythm with atrial quiescence or atrial fi brillation (AF). In such cases, atrial electrograms frequently can be recorded in either the left or right atrium, and in some cases, they may be localized to a discrete site within one or both atria ( Figure 6.2 ). 14-16 This situation occurs not uncom monly in the setting of chronic heart disease (particularly rheumatic heart disease), with dilated, diseased atria. 16 More over, in our experience, during the so-called sinoventricular conduction that is due to hyperkalemia, atrial electrograms have always been recorded. Thus, because atrial activity may be present without representation on the ECG, intracardiac recordings may be the only method of assessing unexplained supraventricular rhythms. Endocardial mapping of the atria is a tool with which the site of origin of atrial premature depolarizations (APDs) can be ascertained. 17 Because P-wave morphology on the surface ECG is determined by the patterns of interatrial and intra-atrial conduction, which can be markedly affected by disease and/or drugs, the ECG cannot always be used accu rately before the site of origin of APDs. 15,18-20 Figure 6.3 demonstrates an APD that originates in the left atrium. Other frequent sites of APDs and atrial tachycardias are the atrial appendages, crista terminalis, coronary sinus, ligament of Marshall, superior vena cava, and fibers around the mitral and tricuspid valves. The relative frequency of these sites, and their electrocardiographic features, in a large series of atrial tachycardias was reported by Kistler et al ( Figure 6.4 ). 12 The pulmonary veins are an important source of APDs. Hais saguerre and colleagues 21,22 have shown that APDs originating in the pulmonary veins can initiate AF. A study of nonpulmo nary vein triggers of AF by the Santangeli and coworkers dem onstrated that the distribution of these sites was quite similar to the frequent sites of atrial tachycardia described by Kistler and

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