Figure 8A.1.1 A rhythm strip with a persistent sinus tachycardia.

Figure 8A.1.2 A 24-hour heart rate histogram. Heart rate is indicated on the ordinate and time of the day on the abscissa. Note the absence of without diurnal heart rate changes, yet there is more variability than would be expected with a nonsinus atrial tachycardia.

Initial treatment with a beta-blocker and calcium-channel blocker was ineffective (ivabradine was not yet available),^2,3 and radiofrequency sinus node modification was undertaken with a decrease in mean HR to 80 bpm. The drugs were continued, and the patient felt better for 2 years but symptoms recurred. On repeat AECG monitoring, her mean HR was approximately 100 bpm. Repeat sinus node modification decreased her mean HR to 75 bpm. Beta-blocker and calcium-channel blocker were continued.³ At 2-year follow-up, her exercise tolerance improved and mean HR was approximately 80 bpm.

This work was supported in part by a grant from the Dr. Earl E. Bakken Family in support of heart-brain research.

References

1. Olshansky B, Sullivan RM. Inappropriate sinus tachycardia. J. Am. Coll. Cardiol. 2013;61(8):793–801.

2. Raj SR. Highlights in clinical autonomic neurosciences: Treatment insights for postural tachycardia syndrome and inappropriate sinus tachycardia. Auton. Neurosci. 2013;177(2):72–73.

3. Ptaszynski P, Kaczmarek K, Ruta J, et al. Metoprolol succinate vs. ivabradine in the treatment of inappropriate sinus tachycardia in patients unresponsive to previous pharmacological therapy. Europace. 2013;15(1):116–121.

Figure 8B.1.1

Patient History

Supraventricular tachycardia in a 68-year-old male with coronary artery disease who presented with episodes of palpitations. An intravenous bolus of adenosine terminates the tachycardia.

Question

What is the most likely diagnosis of this case?

Interpretation

P waves are similar during tachycardia that is terminated by adenosine following prolongation of the PR interval. This response and the similarity of P waves during tachycardia with those during sinus rhythm suggest sinus nodal reentry. A cardioselective beta-blocker is the appropriate therapy.

Patient History

A 79-year-old male presented to the emergency department with a 16-hour history of irregular palpitations.

Discussion

This ECG (Figure 8C.1.1) demonstrates a regular atrial tachyarrhythmia consistent with atrial flutter (low-amplitude F waves are seen in the inferior leads) at a cycle length of 240 ms (arrow). Conduction to the ventricle is regularly irregular, alternating between a fusion of the atrioventricular node and accessory pathway (*), and exclusive accessory pathway conduction (#). This tracing requires differentiation between intermittent preexcitation versus frequent premature ventricular contractions. Note that couplets of wide complex beats occur in fixed relationship to the flutter interval, i.e., two flutter cycles.

Figure 8C.1.1

Patient History

A 50-year-old male presented to hospital with a 72-hour history of recurrent rapid palpitations and presyncope.

Discussion

This ECG (Figure 8C.2.1) demonstrates incessant focal atrial tachycardia. At the beginning of the tracing, a long R-P narrow complex supraventricular tachyarrhythmia at a rate of approximately 110 bpm is noted. After the eighth QRS complex, the tachyarrhythmia spontaneously terminates (last atrial impulse is conducted to the ventricle). Following a brief pause, there is a spontaneous sinus impulse (*) followed by tachyarrhythmia resumption at an atrial rate of approximately 200 bpm for two impulses (arrows). Following a second pause, there is again a sinus impulse (second *) followed by tachycardia resumption (note the stable coupling interval between the first beat of tachyarrhythmia and the preceding sinus beat). In this latter case, the atrial rate is intermediate (approximately 160 bpm); however, the origin of the tachyarrhythmia is stable; that is, there is unchanged tachyarrhythmia P-wave morphology, which compared to the sinus P wave is relatively narrow and prominent (high amplitude), suggesting a high septal or cristae origin.

Figure 8C.2.1

Patient History

A 55-year-old female with incessant tachycardia arrived at the hospital after three failed attempts at treatment by another institution.

Figure 8C.3.1

Discussion

Ablation of this focal atrial tachycardia was successfully carried out in the base of the left atrial appendage. The P-wave morphology is broad, upright, and notched in lead V₁ and in inferior leads, consistent with a left superior pulmonary vein tachycardia origin. However, the deeply inverted P wave in lead I strongly indicates a left atrial appendage origin. When tachycardia is incessant, the left and right atrial appendages are a classic site of origin.

Patient History

A 31-year-old male with incessant atrial tachycardia (AT) with variable conduction to the ventricle.

Figure 8C.4.1

Discussion

The AT cycle length is 360 ms.

The P-wave morphology is broad, upright, and notched in lead V₁ (red arrows) and in inferior leads, suggesting a left superior pulmonary vein (LSPV) origin. The low-amplitude P wave in lead I is also consistent with this site.

This AT was mapped distally within a small branch of the LSPV, where catheter pressure terminated the tachycardia. Ablation was not performed at this distal site. Instead, the PV was isolated in the antral region.

Patient History

An 18-year-old male presented with severe congestive heart failure, incessant tachycardia at 120 bpm, and an ejection fraction of 15%.

Figure 8C.5.1

Discussion

The tachycardia is inverted in lead V₁ with late precordial transition. This suggests either the right atrial appendage (RAA) or the tricuspid annulus. The RAA is a classic site for incessant tachycardias and tachycardia-mediated cardiomyopathy. This focus was ablated in the lateral base of the RAA. Within 4 months, the ejection fraction had returned to normal.

Patient History

A 52-year-old female presented with paroxysmal atrial tachycardia (AT).

Discussion

This ECG (Figure 8C.6.1) shows an AT, which is negative/positive biphasic in lead V₁ and in the inferior leads. This is a nonspecific pattern and has been observed from sites on the right or left side of the septum and in the noncoronary aortic cusp. This tachycardia was successfully ablated in the right perinodal region using cryoablation to avoid AV nodal damage.

Figure 8C.6.1

Patient History

A 28-year-old female presented with AT.

Discussion

This ECG (Figure 8C.6.2) is another AT which is negative positive in lead V₁ and the inferior leads. Note that the spontaneous ventricular ectopics (asterisk) unmask the P-wave morphology (red arrows). During sustained 1:1 tachycardia, the P wave cannot be clearly seen. On this occasion, the focus was mapped to the left septum immediately adjacent to the right perinodal region. Ablation at this site eliminated the tachycardia.

Figure 8C.6.2

When this ECG pattern is observed, careful mapping on both sides of the septum and within the aortic noncoronary cusp (NCC) is necessary.

Figure 8C.6.3 Composite figure of the two preceding figures showing the ECG similarity for tachycardia originating on either side of the septum.

Patient History

A 53-year-old male patient, with a long history of symptomatic paroxysmal atrial fibrillation, underwent radiofrequency ablation in 2010 (isolation of pulmonary veins). A second ablation was performed in February 2014 for persistent atrial fibrillation: reisolation of the two left and the right superior pulmonary veins, extensive defragmentation, roof and mitral isthmus lines. During follow-up the patient still complained of regular palpitations. Repeat ECGs showed the same aspect of atypical atrial flutter.

The ECG (Figure 8C.7.1) shows atrial flutter with an atrial cycle length of 280 ms. The F-wave morphology is negative in leads I, II, and V₄–V₆, positive in leads V₁–V₃, isoelectric in leads III and aVF, and slightly negative in aVL. Note the sharp F waves in leads V₁ and V₂ (red arrows). The ventricular response is irregular (between 2/1 and 5/1). The morphology of the atrial waves is not typical of a right atrial isthmus-dependent flutter but rather that of a left atrial flutter. 3D color mapping (Biosense Webster Carto) and ablation confirmed a clockwise perimitral flutter.

Figure 8C.7.1 Perimitral flutter.

Question

What is the ECG definition of atrial flutter?

Answer

In order to diagnose atrial flutter (right or left) on the standard ECG, a 12-lead ECG recording is required. In atrial flutter we observe, in some derivations, no return of the atrial electrical activity to the isoelectric line. Instead, the atrial electrical activity crosses the isoelectric line in an oblique way (leads II, III, aVF in typical right atrial flutter). In other instances, there may be a return to the isoelectric line (for example in V₁ in typical atrial flutter). When there is a clear return to the isoelectric line in all derivations and discrete P′ waves, we speak about atrial tachycardia which may be focal or sometimes reentrant (in that case, the interval between 2 P′ waves is not electrically silent but is occupied by very low-amplitude potentials, which are too small to be visible on the ECG). These potentials will be recorded intracardially. As mentioned above, some ECG features can help to anticipate the right or left location of the flutter circuit.

Discussion

Left atrial flutter is a frequent complication of atrial fibrillation ablation, particularly ablation including linear lesions (i.e., mitral isthmus and roof lines). Right atrial flutter is also possible when cavotricuspid isthmus has not been previously ablated. It is important to try to predict the location of a flutter circuit, especially when a new radiofrequency ablation procedure is planned. Indeed, the procedure strategy is markedly different between right atrial and left atrial flutter ablations. The ECG pattern of left atrial flutter is very heterogeneous, especially after ablation, since many mechanisms may be encountered: i.e., macroreentrant or microreentrant circuits. However, as shown by Bocheyer et al.,¹ it is sometimes possible to grossly anticipate the location of the circuit. For example, flattened or low amplitude of F waves in inferior leads are in favor of a left atrial flutter, as well as spike F waves in lead V₁. This aspect was seen on the present ECG of a clockwise perimitral flutter.

Reference

1. Bocheyer A, Yang Y, Cheng J, et al. Surface electrocardiographic characteristics of right and left atrial flutter. Circulation. 2003;108:60–68.

Patient History

A 50-year-old male patient suffered from incessant atrial tachycardia associated with severe left ventricular (LV) dysfunction (LV ejection fraction 30%). Coronary angiography was normal. The initial diagnosis was likely an arrhythmic cardiomyopathy. A first radiofrequency ablation of this tachycardia was performed in March 2014 with success. One year later, the patient complained of recurrent palpitations. Repeat ECGs confirmed that the arrhythmia was intermittent.

Figure 8C.8.1 shows a regular wide QRS tachycardia at a rate of 116 bpm with a left bundle branch block (LBBB) morphology (QRS duration 130–140 ms) and left axis deviation. P′ waves are clearly visible and are negative in inferior leads, and have a low amplitude in the other leads either slightly positive or flattened. RP′ interval is long (440 ms), while P′R interval is short (130 ms).

Figure 8C.8.1 RA focus 1.

Figure 8C.8.2 was recorded in sinus rhythm. A blocked atrial premature beat (APB) is seen after every two sinus beats. The morphology of each APB is constant: negative in leads II, III, and aVF, probably positive in leads V₁–V₃ (spike on T waves) and rather negative in leads V₄–V₆.

Figure 8C.8.2 RA focus 2.

Question

Can P-wave morphology predict the location of focal atrial tachycardia?

Answer

It is possible to accurately predict the location of the focus and its inside the atria. Some algorithms have been developed and may help, but they are quite complicated. In any case, they must be seen as indicators.

Discussion

Preexisting LBBB in sinus rhythm immediately rules out ventricular tachycardia with very slow retrograde conduction. The tachycardia is supraventricular, either junctional or atrial. It could be paroxysmal junctional tachycardia with retrograde atrial activation through a slow-conducting accessory pathway in the posteroseptal region or the fast-slow type of AV nodal reentrant tachycardia. Analysis of Figure 8C.8.1 only cannot rule out those possibilities. It could also be an atrial tachycardia originating from the posteroseptal region of the right atrium, with 1/1 AV conduction. Figure 8C.8.2 gives some clues, showing APBs with the same morphology as the tachycardia atrial beats. This strongly suggests an atrial focus giving rise to single premature, nonsustained or sustained runs of tachycardia. A mapping and ablation procedure confirmed the presence of an atrial focus close to the coronary ostium.

Reference

1. Kistler PM, Roberts-Thomson KC, Haqqani HM, 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.

Patient History

A 60-year-old male presented with palpitation and chest pain. ECG upon arriving to the emergency department is shown (Figure 8C.9.1).

Figure 8C.9.1

Note the two P waves (red arrows), followed by QRS 2:1 conduction with an atrial rate of 250 bpm.

Figure 8C.9.2

Figure 8C.9.3

Discussion

Transesophageal echocardiogram was performed to exclude the presence of atrial thrombus.

Intracardiac tracing showed 2:1 atrial flutter, and an ablation by cavotricuspid isthmus (CTI) was performed.

This resulted in normal sinus rhythm (single P wave—red arrow) and the following ECG (Figure 8C.9.4) was recorded.

Figure 8C.9.4

Patient History

A 58-year-old female with a history of hypertrophic cardiomyopathy (HCM) had symptomatic atrial fibrillation and underwent catheter ablation using wide-area antral pulmonary vein isolation. She began to have recurrent palpitations that were found to be due to an organized atrial tachycardia/flutter, for which she underwent another ablation procedure. After successful termination of left atrial tachycardia during ablation, the ECG shown in Figure 8C.10.1A (standard gain) was obtained. On careful inspection, some small deflections were observed that are better seen on the bottom recording (Figure 8C.10.1B) of exactly the same ECG but at 4× normal gain. Here, the small deflections are marked with black circles (or open circles where they probably occur but are obscured by sinus P waves or QRS complexes).

Figure 8C.10.1

Question

What is the nature of these extra waves?

Discussion

The ECG shows sinus rhythm with a very long PR interval, right bundle branch block (RBBB), and right axis deviation. The extra, small deflections highlighted in Figure 8C.10.1B are very narrow and have a superior and leftward axis and are not well seen in the right precordial leads but are inverted in the lateral precordial leads. Though difficult to diagnose as such on the ECG, intracardiac recordings showed that these signals were due to an incessant atrial tachycardia that was present in the previouslyisolated left pulmonary venous antrum. This is unusual in that the isolated portion of the atrium does not usually have an independent rhythm (or only slow, dissociated firing) and generally contains such a small muscle mass that even if it depolarized, it would not have enough size to register on the regular ECG. In this case, an ongoing tachycardia was present in the isolated segment, which had a large enough tissue volume (hypertrophied as part of the patient’s HCM) that evidence of the tachycardia could be seen in Figure 8C.10A.

Lessons

Two dissociated rhythms in the same heart is not unusual, for instance sinus rhythm with complete heart block and a junctional escape rhythm. It is very unusual, however, for two dissociated rhythms to be occurring in the same chambers (both atria, as in this case, or both ventricles). This can occur in transplanted hearts, in which the posterior left atrium with pulmonary vein attachments remains with the donor heart anastomosed to it, or rarely in post-maze surgery patients, and those who have undergone right ventricular disarticulation for treatment of ventricular arrhythmias due to right ventricular cardiomyopathy/dysplasia.

Patient History

A 42-year-old female had a 3-year history of palpitations. Physical examination was normal and noninvasive evaluation showed a structurally normal heart. She had normal exertional capacity, but noted irregular palpitations with increasing frequency when she took vigorous walks. An event monitor was obtained from which a diagnosis of paroxysmal atrial fibrillation (AF) was made. Neither beta- nor calcium-channel blockade were tolerated and when symptoms progressed (50% of the time, associated with fatigue), she was referred for electrophysiologic evaluation. An ECG was obtained at an outpatient consultation visit, as shown (Figure 8C.11.1).

Figure 8C.11.1

Question

What does the ECG show?

Discussion

The ECG (Figure 8C.11.1) shows an organized AT with discrete P waves that are all identical in morphology, but with varying rate (black circles denote clear P waves, open circles indicate where P waves are likely present but obscured by QRS complexes). The patient went on to have successful catheter ablation of a focal tachycardia arising near the ostium of the left superior pulmonary vein; her palpitations ceased entirely thereafter.

Lessons

The initial diagnosis of AF was made based from a monitor recording showing a rapid arrhythmia with irregular RR intervals; perhaps the physician reviewing the monitor merely looked at the irregularly irregular ventricular rate and assumed the fibrillation was the cause. Instead, it is an organized AT with irregular, but otherwise identical P waves. This had therapeutic implications for the patient; drug therapy may not have been different whether the rhythm was AF or AT, but an organized AT is significantly easier to treat with catheter ablation than is AF. Further, the great degree of irregularity strongly suggested a focal mechanism, since reentrant ATs are usually very regular: wavefront propagation around a fixed anatomic circuit typically proceeds as rapidly as it can, within the constraints of local refractoriness, and is rather regular. Significant alterations in conduction velocity that present the wavefront to tissue that is still refractory from the prior AT cycle will often result in tachycardia termination (this is part of the premise of using premature extrastimuli or overdrive pacing to terminate reentrant arrhythmias). Thus, generally speaking, the more irregular a tachycardia, the more likely it has a focal origin.

Patient History

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