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Ann Thorac Surg 1995;60:425
© 1995 The Society of Thoracic Surgeons

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Invited Commentary

Invited Commentary

Department of Surgery, University of Colorado Health Sciences Center, 4200 E Ninth Ave, Box C-305, Denver, CO 80262

See also page 422.

All cardiac dysrhythmias are due to (1) enhanced automaticity, (2) reentry, or (3) both. Automaticity is the inherent capacity of cardiac conduction tissue to depolarize spontaneously (phase IV depolarization) until it reaches ``threshold'' and then ``fires.'' Hypokalemia, digitoxicity, and local myocardial ischemia are the usual suspects when a surgeon confronts a surgical intensive care unit patient with multifocal ventricular ectopy. Intuitively, muscle distal to a total coronary occlusion should die. It typically does. A very narrow ``border zone'' surrounding an infarct, however, remains alive but unhappy.

This slim rim of periischemic myocardium harbors energy-starved membrane ion pumps that leak sodium and calcium ions long after the QRS complex is gone. The resultant ``late potentials'' have been recognized in single cells, but in 1983 Simson and associates [1] reported that they could detect them by summating these tiny potentials with signal-averaged surface electrocardiography. Simson and associates also incriminated these ``late potentials'' as bad actors by proving that they vanished when we successfully surgically resected periischemic endocardium in patients with ventricular tachycardia [1].

Conceptually, ``late potentials'' derived from periischemic borderzone tissue create electrically unstable microzones that can initiate depolarization, causing a premature ventricular contraction [2]. These random premature ventricular contractions are potentially risky in that they could land on a T wave and degenerate into ventricular fibrillation [3].

Multiple myocardial infarction trials now have been published. To everyone's surprise, documentation of a patent vessel (due either to spontaneous thrombolysis or to therapeutic intervention) feeding a myocardial infarction has consistently conferred a favorable prognosis. Why should blood flow to scar make any difference? This article by Terada and colleagues suggests that surgical revascularization of a completely occluded vessel may eliminate these potentially life threatening ``late potentials.'' Although revascularization of the scar does not make it beat, reperfusion of the angry, adjacent periischemic border zone might electrically pacify this arrhythmogenic rim of tissue.

Terada and co-workers note that even long after a myocardial infarction, antegrade blood flow provided by a surgical bypass graft influences dangerous ``late potentials.'' The long-term patency of catheter-based techniques in opening completely occluded coronary arteries has been disappointing. This study provides persuasive additional evidence supporting durable surgical revascularization of totally occluded coronary arteries.

References

1. Simson MB, Untereker WJ, Spielman SR, Harken AH, Josephson MJ. Relation between late potentials on the body surface and directly recorded fragmented electrograms in patients with ventricular tachycardia. Am J Cardiol 1983;51:105–12.[Medline]
2. Harken AH. Surgical treatment of cardiac arrhythmias. Sci Am 1993;269:68–74.[Medline]
3. Harken AH. Cardiac arrhythmias. In: Wilmore D, Cheung L, Harken A, Holcroft J, Meakins J, eds. Scientific American surgery. New York: Scientific American Publishing, 1994.

This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Alden H. Harken Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Harken, A. H. Search for Related Content PubMed Articles by Harken, A. H. Related Collections Related Article