LETTER TO THE EDITOR
Papillary muscle hypothesis of idiopathic left ventricular tachycardia
Peng-Sheng Chen, MD, FACCa,
Hrayr S. Karagueuzian, PhD, FACC and
Young-Hoon Kim, MD, FACC
a Cedars-Sinai Medical Center, Room 5342, 8700 Beverly Boulevard, Los Angeles, California, USA 90048-1865
chenp{at}csmc.edu
Nogami et al. (1) recently demonstrated that diastolic (P1) and presystolic (P2) Purkinje potentials are critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia. The authors posit that P1 represents the activation potential in the distal portion of the specialized Purkinje tissue and P2 represents the activation potential of the left posterior fascicle. There was no mentioning of the papillary muscle as a possible source of these potentials.
In most parts of the ventricular endocardium, Purkinje potentials and myocardial potentials are nonseparable. This is not true at the papillary muscle, where Purkinje potentials and ventricular muscle potentials are widely separated (2,3). Joyner et al. (2) reported that pacing from a Purkinje strand inserting into the apex of the papillary muscle results in apex to base Purkinje activation. The activation then excites the ventricular muscle via the Purkinje ventricular muscle junction at the base of the papillary muscle, and propagates from base of the papillary muscle to the apex of the papillary muscle. The resulting activation sequence shown in Figure 1B of that article is identical to the sequence of activation shown in Figure 2 of the study of Nogami et al. (1). The Purkinje strands (fibromuscular band or false tendon), which are often seen in dogs, are also found commonly in humans, especially among patients with idiopathic left ventricular tachycardia (4).
The safety factor of propagation from Purkinje to ventricular muscle is lower than that from the ventricular muscle to the Purkinje fibers (2,5). This asymmetrical safety factor of propagation may contribute to the occurrence of unidirectional block and reentry. The papillary muscle may serve as an anchor to reentrant wavefronts (3), resulting in sustained ventricular tachycardia. These two mechanisms may be important in the generation and maintenance of sustained ventricular tachycardia near the papillary muscle.
Clearly separated Purkinje potentials are characteristic findings for endocardial recordings near the papillary muscle (2,3). Successful radiofrequency ablation at these sites (1) suggests that the reentrant wavefronts responsible for idiopathic left ventricular tachycardia are adjacent to or are located within the papillary muscle.
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References
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1. Nogami A, Naito S, Tada H, et al. Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia. J Am Coll Cardiol. 2000;36:811–823[Abstract/Free Full Text]
2. Joyner RW, Ramza BM, Tan RC. Effects of stimulation frequency on Purkinje-ventricular conduction. Ann NY Acad Sci. 1990;591:38–50[Medline]
3. Kim Y-H, Xie F, Yashima M, et al. Role of papillary muscle in the generation and maintenance of reentry during ventricular tachycardia and fibrillation in isolated swine right ventricle. Circulation. 1999;100:1450–1459[Abstract/Free Full Text]
4. Thakur R, Klein GJ, Sivaram CA, et al. Anatomic substrate for idiopathic left ventricular tachycardia. Circulation. 1996;93:497–501[Abstract/Free Full Text]
5. Berenfeld O, Jalife J. Purkinje-muscle reentry as a mechanism of polymorphic ventricular arrhythmias in a 3-dimensional model of the ventricles. Circ Res. 1998;82:1063–1077[Abstract/Free Full Text]
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