(Circulation. 2006;113:e855.)
© 2006 American Heart Association, Inc.
Correspondence |
EPICARE Center, Department of Public Health Sciences, Wake Forest University, Winston-Salem, NC
Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Wash
We appreciate Dr Lehmanns supportive comments on our articles1,2 in Circulation. Dr Lehmann also brings up a relevant question: Why did we not include QRS duration as a covariate in our QT adjustment models?
This question was examined in some detail in previous publications.3,4 Adding the QRS interval as a covariate with the R-R interval did not increase the R2 value in men, and it increased by less than 1% in women.
What is the reason for this seemingly counterintuitive paradox? The QT interval is, without exception, the sum of the excitation time and the action potential duration of the myocardial cells in the region repolarizing last. This region is excited in normal conduction during the initial half of the QRS interval because repolarization sequence is semireverse with respect to depolarization; therefore, its excitation time is perhaps smaller than expected. Excitation times in the so called "incomplete bundle-branch blocks"(QRS <120 ms) vary.5 The significance of the QRS contribution to QT adjustment, if included as a covariate, is again a different question as noted.
In major ventricular conduction defects, repolarization becomes more concordant with respect to the depolarization sequence. QRS duration contributes more heavily to the QT interval, and it must be included as a covariate with the R-R interval in QT adjustment formulas. As an alternative, a univariate formula for JT without the QRS interval can be used. Properly established upper percentile limits for adjusted QT or JT intervals for normal conduction and for bundle-branch blocks must be used in evaluation of prolonged repolarization.3,4,6
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2. Rautaharju PM, Kooperberg C, Larson JC, LaCroix A. Electrocardiographic predictors of incident congestive heart failure and all-cause mortality in postmenopausal women: the Womens Health Initiative. Circulation. 2006; 113: 481489.
3. Rautaharju PM, Zhang ZM, Prineas R, Heiss G. Assessment of prolonged QT and JT intervals in ventricular conduction defects. Am J Cardiol. 2004; 93: 10171021.[CrossRef][Medline] [Order article via Infotrieve]
4. Rautaharju PM, Prineas RJ, Kadish A, Larson J, MSc, Lund B. Normal standards for QT and QT subintervals derived from a large ethnically diverse population of women aged 50 to 79 years (the Womens Health Initiative [WHI]). Am J Cardiol. 2006; 97: 730737.[CrossRef][Medline] [Order article via Infotrieve]
5. Zhou SH, Wong S, Rautaharju PM, Karnik N, Calhoun HP. Should JT rather than QT interval be used to detect prolongation of ventricular repolarization? An assessment in normal conduction and in ventricular conduction defects. J Electrocardiol. 1992; 25: 16.[Medline] [Order article via Infotrieve]
6. Rautaharju PM, Zhang ZM. Linearly scaled, rate-invariant normal limits for QT interval: eight decades of incorrect application of power functions. J Cardiovasc Electrophysiol. 2002; 13: 12111218.[CrossRef][Medline] [Order article via Infotrieve]
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