CLINICAL STUDY: ELECTROPHYSIOLOGY
Sympathetic stimulation produces a greater increase in both transmural and spatial dispersion of repolarization in LQT1 than LQT2 forms of congenital long QT syndrome
Yasuko Tanabe, MD*,
Masashi Inagaki, MD ,
Takashi Kurita, MD*,
Noritoshi Nagaya, MD*,
Atsushi Taguchi, MD*,
Kazuhiro Suyama, MD, PhD*,
Naohiko Aihara, MD*,
Shiro Kamakura, MD, PhD*,
Kenji Sunagawa, MD, PhD ,
Kazufumi Nakamura, MD, PhD ,
Tohru Ohe, MD, PhD, FACC ,
Jeffrey A. Towbin, MD ,
Silvia G. Priori, MD, PhD|| and
Wataru Shimizu, MD, PhD*
* Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, Suita, Japan
Department of Cardiovascular Dynamics, National Cardiovascular Center, Suita, Japan
Department of Cardiovascular Medicine, Okayama University Medical School, Okayama, Japan
Department of Pediatrics (Cardiology), Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA
|| Molecular Cardiology, Salvatore Maugeri Foundation, Pavia, Italy
Manuscript received June 14, 2000;
revised manuscript received October 24, 2000,
accepted November 29, 2000.
Reprint requests and correspondence: Dr. Wataru Shimizu, Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita, Osaka, 565-8565 Japan wshimizu{at}hsp.ncvc.go.jp
OBJECTIVES
The study compared the influence of sympathetic stimulation on transmural and spatial dispersion of repolarization between LQT1 and LQT2 forms of congenital long QT syndrome (LQTS).
BACKGROUND
Cardiac events are more associated with sympathetic stimulation in LQT1 than in LQT2 or LQT3 syndrome. Experimental studies have suggested that the interval between Tpeak and Tend (Tp-e) in the electrocardiogram (ECG) reflects transmural dispersion of repolarization across the ventricular wall.
METHODS
We recorded 87-lead body-surface ECGs before and after epinephrine infusion (0.1 µg/kg/min) in 13 LQT1, 6 LQT2, and 7 control patients. The Q-Tend (QT-e), Q-Tpeak (QT-p), and Tp-e were measured automatically from 87-lead ECGs, corrected by Bazetts method (QTc-e, QTc-p, Tcp-e), and averaged among all 87-leads and among 24-leads, which reflect the potential from the left ventricular free wall. As an index of spatial dispersion of repolarization, the dispersion of QTc-e (QTc-eD) and QTc-p (QTc-pD) were obtained among 87-leads and among 24-leads, and were defined as the interval between the maximum and the minimum of the QTc-e and the QTc-p, respectively.
RESULTS
Epinephrine significantly increased the mean QTc-e but not the mean QTc-p, resulting in a significant increase in the mean Tcp-e in both LQT1 and LQT2, but not in control patients. The epinephrine-induced increases in the mean QTc-e and Tcp-e were larger in LQT1 than in LQT2, and were more pronounced when the averaged data were obtained from 24-leads than from 87-leads. Epinephrine increased the maximum QTc-e but not the minimum QTc-e, producing a significant increase in the QTc-eD in both LQT1 and LQT2 patients, but not in control patients. The increase in the QTc-eD was larger in LQT1 than in LQT2 patients.
CONCLUSIONS
Our data suggest that sympathetic stimulation produces a greater increase in both transmural and spatial dispersion of repolarization in LQT1 than in LQT2 syndrome, and this may explain why LQT1 patients are more sensitive to sympathetic stimulation.
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Abbreviations and Acronyms
| | APD | = action potential duration | | ECG | = electrocardiogram | | LQTS | = long QT syndrome | | QTc-e | = corrected Q-Tend interval | | QTc-p | = corrected Q-Tpeak interval | | QTc-eD | = dispersion of QTc-e | | QTc-pD | = dispersion of QTc-p | | QT-e | = Q-Tend interval | | Tcp-e | = corrected interval between Tpeak and Tend | | TdP | = torsade de pointes | | TDR | = transmural dispersion of repolarization |
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