Author + information
- Rahul Jain, MD, MPH and
- John M. Miller, MD∗ ()
- Department of Medicine, Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana
- ↵∗Reprint requests and correspondence:
Dr. John M. Miller, Krannert Institute of Cardiology, Indiana University School of Medicine, 1800 North Capitol Avenue, E-488 Indianapolis, Indiana 46202.
Atrioventricular nodal re-entrant tachycardia (AVNRT) is the most common form of paroxysmal supraventricular tachycardia (SVT). In this issue of JACC: Clinical Electrophysiology, Kawamura et al. (1) report an interesting small series of patients with incessant AVNRT, comparing features of these patients with those of a larger group of patients with more typical paroxysmal AVNRT. The topic is noteworthy because these uncommon patients present diagnostic and therapeutic challenges to the electrophysiologist. The authors do an admirable job of going through the standard diagnostic maneuvers that are universally taught, but sadly not universally applied in practice, and thereby obtain a definitive diagnosis in their cases, which then leads to correct and successful therapy.
In the scientific literature, there are only 3 prior case reports of true incessant AVNRT (2–4), and interestingly, all were of the fast-slow type. Given this paucity of data, the current report adds important pieces of information. In this study, the only significant difference in electrophysiological properties between the paroxysmal and incessant AVNRT groups was the HV interval (longer in the group with incessant AVNRT). Although this finding should not have any bearing on whether tachycardia is incessant or paroxysmal, the authors also found that all the patients with incessant tachycardia with long HV intervals had tachycardia-induced cardiomyopathy. Although they do not specifically note this, their data show a striking inverse relationship between HV interval and ejection fraction (EF); that is, the longer the HV interval, the lower the EF. Cruz et al. (5) reported similar long HV intervals in patients with tachycardia-induced cardiomyopathy involving an AV accessory pathway (AP). It is not clear whether a mild myopathy with concomitant His-Purkinje disease that was worsened by incessant relatively slow tachycardia came first or whether the deterioration in left ventricular function led to the increase in HV interval. In the current series, patients with incessant SVT also tended to have lower EF than those with paroxysmal SVT (49% vs. 60%). It is known that patients who have successful treatment of the arrhythmia responsible for tachycardia-induced myopathy have recovery of some measures of systolic function but still have enlarged chambers, which signifies incomplete recovery (6), and that these patients are at risk for repeat worsening of systolic function if tachycardia recurs (7). Post-ablation normalization of an HV interval that had been prolonged during tachycardia-medicated heart failure has been reported (2), but it is not known what generally happens to HV intervals with recovery and subsequent worsening of systolic function if it occurs. Of note, there has been no clear association of prolonged HV interval with some other forms of tachycardia-related myopathy, such as that seen with premature ventricular complexes.
Perhaps the most intriguing question in this group of patients is why some of them have incessant tachycardia and others do not. The authors hypothesize that differences in anterograde versus retrograde pathway refractoriness play a critical role, using the so-called permanent form of junctional reciprocating tachycardia as a model. In that disorder, all 4 requirements for re-entry are satisfied: 1) a potential circuit is present (composed of atrium, AV node-His, ventricle, and AP); 2) unidirectional block is present (no anterograde conduction in the AP); 3) enough slow conduction is present (in the AV node and AP) to allow all portions of the circuit to recover refractoriness in time for the next cycle; and 4) an initiator is present (typically a premature atrial or ventricular complex, but in the permanent form of junctional reciprocating tachycardia, a sinus complex suffices). Thus, patients with incessant atypical AVNRT might be expected to have permanent anterograde slow pathway block, such that sinus rhythm would propagate over the fast pathway to the His, then back up the slow pathway, and tachycardia could begin as in Figure 1 in the report by Kawamura et al. (1). Although the authors’ findings were not as tidy as one might have hoped (i.e., patients with atypical AVNRT did not all have fixed anterograde slow pathway block, nor did patients with typical AVNRT always have retrograde slow pathway block), the principle seems clear. Modifiers of refractoriness such as rate and autonomic tone have yet to be fully explored. Curiously, a disproportionate number of patients with fast-slow AVNRT had incessant tachycardia (63% of incessant cases); viewed differently, 10% of patients with fast-slow AVNRT (5 of 52 patients) had incessant SVT compared with 1% of patients with slow-fast AVNRT (3 of 290 patients, p < 0.001). Why this marked imbalance occurs is unclear; Kawamura et al. (1) propose that the magnitude of difference between refractory periods of fast and slow pathways is a key, but their limited data make this difficult to prove. Other studies have likewise shown that long-RP tachycardias predominate among cases of tachycardia-mediated cardiomyopathy (2–5).
Kawamura et al. (1) have added to our knowledge of these interesting arrhythmias, which raises further questions. It is humbling that as common as these arrhythmias are, our understanding of them is far from complete.
↵∗ Editorials published in JACC: Clinical Electrophysiology reflect the views of the authors and do not necessarily represent the views of JACC: Clinical Electrophysiology or the American College of Cardiology.
Dr. Jain has received speaking honoraria from Biosense-Webster. Dr. Miller has received support from Medtronic, Inc., Boston Scientific Corp. (training support; lecturer), Biosense-Webster, Inc. (training support; lecturer; consultant), St. Jude Medical, Biotronik, Inc. (lecturer), and Topera, Inc. (advisor).
- American College of Cardiology Foundation
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- Scheinman M.M.,
- Vedantham V.,
- Marcus G.M.,
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- Badhwar N.
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- Cheriex E.C.,
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