Letter to the Editor What is a monophasic action potential recorded by the Franz contact electrode

After over 20 years of successful use of the Franzcontact electrode technique by many others and myself(over 1000 publications to date), the recent paper byKondo et al. [1] claims that it is not the tip electrode, butrather the distant-from-tip or bindifferentQ electrode thatrecords the monophasic action potential (MAP). Theintroduction starts out by staging a contradiction betweenthe classical MAP theory and the one stated by Franz [2]when in fact there is none really stated. The wording isconfusing throughout their text and, in my view, of littlehelp to foster the understanding of the complex issue ofMAP genesis and recording. More important, the study byKondo et al. [1] contains a plethora of methodologicalflaws of which only some can be addressed here.The isolated canine wedge preparation used by theauthors is small compared to the BARD catheter used inthis study. Despite the authors’ assertion, the BARDcatheter is not bFranz-likeQ. It also is not drawn to properscale in their figures. In reality, the BARD electrode shaftwould look more like a btowerQ sitting on the small isolatedwedge preparation. The Franz catheter was designed forhuman and large animal hearts and in those has providedhigh-resolution recordings of spatial heterogeneities inmyocardial repolarisation. For smaller hearts or prepara-tions we have developed greatly miniaturized MAPelectrodes [3].The study by Kondo et al. reports on a multitude ofinterventions (KCl application, local cooling, ATX-IIapplication, multiple micro-electrode impalements whichare time-consuming and often unstable, and intramuralplunge electrodes). All data sets are n=1 with little if anystatistics provided on spatial confinement of the effectsof KCl, ATX-II, or cooling. Clearly, diffusion must occurand blur the distinction between sites only 2–5 mmapart.It has long been recognized that KCl depolarizesmyocardium, and when an electrode is placed onto theKCl site an MAP is obtained [4]. We thus maintain thatthe KCL site in the study by Kondo et al. [1] is theMAP-generating site. The KCl electrode and the intra-mural needle electrode were fed into the same amplifier.As the authors stated, the intramural needle electrode(after initial injury and subsequent healing-over) recordedan electrogram. An electrogram recorded at one inputand an MAP recorded at another (the KCl site), whensuperimposed and of similar amplitude, still looks like anMAP. However, this is an MAP generated at the KClsite—with an intramural electrogram superimposed. Thefact that the MAP is upright when the KCl electrode isconnected to the positive amplifier input (as was the casein their study) further supports this contention [2].To pick one of the illustrations that are used to re-interpret the role of the MAP electrodes, Fig. 2 inKondo et al. [1] at first glance produces convincingevidence of their alternative hypothesis because both theMAP signal and the transmembrane action potentialprolong in concert in response to a decrease in temper-ature. However, it should be realized that the KClelectrode was coupled against the needle electrode at thecooled site. Naturally, this would produce a prolongedelectrogram (QT) that by superimposition onto the KCL-MAP template makes the MAP appear longer. Another