I once wrote, paraphrasing Churchill's description of Stalin, that "The AV node is an enigma in an island of whimsy surrounded by a sea of uncertainty." I could easily substitute the T wave for the AV node in that statement. Despite intense study for 100 years, unanswered questions about the T wave abound. Some of these important questions are relatively pedestrian and include how to accurately measure the QT interval when the end of the T wave is blurred or merged with the U wave, or the T wave contour is distorted; how to correct for rate changes (Bazett's formula is most commonly used despite its under correction at slow rates and over correction at fast rates and the fact that Bazett applied it only in normal, relatively young, drug-free individuals); the relation of the T wave to the U wave, what causes the U wave, and what the importance of the QU interval is; the meaning of T wave lability (for the clinician: just what does "nonspecific T wave change" really mean?); the mechanism of broad negative T waves in non-Q-wave myocardial infarction and CNS injury; how to measure T wave dispersion accurately and what does it mean; the impact of autonomic and hormonal alterations; and the true upper limit of normal for the QT and QTc intervals for men and women.

Then, probing deeper, what is the relationship of the long QT syndrome (LQTS) to the sudden infant death syndrome; do all patients who develop drug-induced LQTS start with a congenital abnormality; do early after-depolarizations precipitate or maintain torsades de pointes; can torsades de pointes occur in the atria; and do patients who prolong ventricular repolarization after cardiac remodeling from heart failure or ventricular hypertrophy really die from torsades de pointes?

And then, at a basic level, how relevant are data from models such as the left ventricular wedge, isolated myocytes and membrane patches, and computer simulations? What is the role of M cells in repolarization, the U wave, and torsades de pointes? How do the intracellular Ca2+/calmodulin-dependent processes regulate the development of torsades de pointes?

While it seems we have more questions than answers—and indeed the questions I have asked are only a partial list—Cardiac Repolarization: Bridging Basic and Clinical Science attempts to answer some of those questions. From basic electrophysiology, pharmacology, and molecular biology to clinical physiology and pathophysiology and a consideration of specific electrocardiographic phenomena and syndromes, world-class experts give their views on these and related topics.

The study of cardiac repolarization is an area of intense interest, but an evolving field. As new knowledge accumulates, our concepts are certain to change, but that is the challenge and fun of what we do. Hopefully, in several years, we will be reading a much updated second edition.

Douglas P. Zipes, md

Indianapolis, IN

Douglas P. Zipes, md Indiana University School of Medicine, Indianapolis, IN

Was this article helpful?

0 0

Post a comment