An exponential formula for heart rate dependence of QT interval during exercise and cardiac pacing in humans: Reevaluation of Bazett's formula

Sarma, J. S. M.; Sarma, Radha J.; BILITCH, MICHAEL; Katz, Darryl; Song, Siyu

doi:10.1016/0002-9149(84)90312-6

Cited by 148 publications

(45 citation statements)

References 18 publications

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“…Based on linear regression analysis of the corrected MAP 90 against the RR interval, the present exponential equation dissociated the RR influence better than Bazett's or Fridericia's with less slope and the lowest CV for the linear regression. As with the present isolated heart, an exponential model was also found to be most suitable for QT rate-correction in dogs and human (Matsunaga et al, 1997;Sarma et al, 1984). This is the first report to demonstrate that the exponential rate-correction method corrected the QT/ MAP 90 against RR more effectively than the widely-used generic formulae in isolated guinea pig heart.…”

Section: Discussionsupporting

confidence: 60%

Accurate detection of drug-induced delayed ventricular repolarization with a suitable correction formula in Langendorff guinea pig heart

et al. 2010

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-The aims of this study were to determine a suitable method to correct the ventricular repolarization period against the RR interval in isolated perfused Langendorff guinea pig heart and to clarify the reliability of this model using several drugs. QT and RR intervals from an electrocardiogram and the epicardial monophasic action potential duration (MAP 90 ) were measured. Two drugs clinically known to be QT-prolonging (E-4031, moxifloxacin) and two known to be non-QT-prolonging (verapamil, zatebradine) were used for the study. To determine a method of correcting the ventricular repolarization period against RR interval, heart rates were slowed with 0.3 µM zatebradine, a specific bradycardiac agent, and then accelerated with atrial pacing to obtain a wide range of MAP 90 /RR relationships. An exponential rate-correction model elicited the most appropriate algorithm for the relationship among the four models tested. Based on linear regression analysis, the exponential showed superior dissociation of corrected MAP 90 s against RR intervals than generic Bazett's and Fridericia's formulae. E-4031 and moxifloxacin prolonged the corrected QT (QTc) intervals and MAP 90 under atrial pacing at a cycle length of 0.25 sec (MAP 90(pacing) ) dose-dependently; verapamil and zatebradine failed to prolong them, indicating that the reliability of this model was excellent. MAP 90(pacing) prolongation by moxifloxacin, the positive compound in the clinical "Thorough QT/QTc Study", was seen at around QTc-prolonging concentrations in clinic, suggesting that the sensitivity would be appropriate for QT evaluation. We therefore concluded that the isolated guinea pig heart model is sufficiently sensitive and useful for assessing the potential QT prolongation of drugs.

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Section: Discussionsupporting

confidence: 60%

Accurate detection of drug-induced delayed ventricular repolarization with a suitable correction formula in Langendorff guinea pig heart

et al. 2010

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“…Many workers have investigated the relationship of the QT/RR relationship during exercise [4,6,[13][14][15]. As with all of these studies, we have also shown a linear relationship between the QT and RR interval, even though different mathematical models across the studies have been used.…”

Section: Figuresupporting

confidence: 56%

“…In this subject population, logarithmic transformation of the data resulted in an approximately linear relationship between the QT and RR intervals for all individuals across the range of heart rates obtained. Other workers have demonstrated that different mathematical models such as exponential models describe the relationship between QT and RR interval data [3,4]. Recently it has been demonstrated that not only is the relationship between the QT interval and heart rate unique for a given individual but that the mathematical formula describing this relationship is also unique [8].…”

Section: Evaluation Of a Sscf From Exercise And Resting Ecgsmentioning

confidence: 99%

“…As with all of these studies, we have also shown a linear relationship between the QT and RR interval, even though different mathematical models across the studies have been used. This linear relationship during exercise is suggested to be conserved within an individual even when different exercise methods are used [4]. However, none of these studies has proposed deriving a relationship for each individual to correct QT for rate when investigating potential effects on QT interval for a drug that also increases heart rate although some studies have suggested using the QT interval at nominal heart rates (e.g.…”

Section: Figurementioning

confidence: 99%

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Lack of correlation between exercise and sibenadet‐induced changes in heart rate corrected measurement of the QT interval

Newbold¹,

Sanders

Reele

2006

Brit J Clinical Pharma

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What is already known about this subject• When this study was conducted it was already known that the 'standard' methods of correcting the QT interval for hear t rate were not optimal and that bias could result in their use in certain circumstances, in particular when drugs or conditions also induced wide fluctuations in heart rate.• The use of subject specific correction methods had been advocated and whilst these had been shown to apparently correct QT interval over usual physiological heart rates, they had not been tested under conditions where drugs could potentially increase heart rate and 'standard' correction methods gave apparent increases in QT interval. Furthermore, subject specific correction methods had usually been generated over a normal physiological heart rate range and made the assumption that the relationship remained linear outside of this usual range. What this study adds• A subject specific correction factor for QT correction can be calculated from a wide range of heart rates using exercise testing and the relationships between QT and RR are unique for a given individual.• The generation of subject specific correction factors from ECGs collected under resting conditions is not a robust method.• That subject specific correction factors derived from exercise testing are not appropriate to apply to drugs (with no evidence to suggest effects on the QT interval) that induce increases in heart rate and that the relationship between the QT and RR interval during exercise is clearly different to the QT/RR relationship of a drug that increases heart rate. AimsWe sought to investigate subject specific QT interval correction factors (SSCF) determined at rest and after exercise and to determine the validity of these factors after the administration of a probe drug known to increase hear t rate without directly affecting cardiac repolarization. MethodsThirty-two healthy volunteers underwent graded exercise, multiple recordings of electrocardiogram during rest over a day and a treatment phase administering inhaled placebo or sibenadet (a β 2 -adrenoceptor/dopamine D 2 -receptor agonist) at 250, 500 or one of 750 or 1000 µ g. SSCF were determined from linear regression of plots of log RR interval vs. log QT after exercise (QTcX), rest (QTcR), and combined data (QTcC). The SSCFs along with Bazett & Fridericia corrections were applied to the ECGs after inhalation of sibenadet. ResultsSSCFs obtained from the combination of the exercise and resting day (mean QTcC = 0.41) and exercise alone (mean QTcX = 0.40) were similar with a good fit to the data (mean r 2 = 0.92 and 0.93, respectively) while data at rest resulted in a less pronounced slope (mean QTcR = 0.27) and poorer fit (mean r 2 = 0.52). After the administration of sibenadet, none of the SSCFs, Bazett or Fridericia corrections adequately corrected QT for heart rate induced changes. ConclusionsNeither a SSCF from exercise, Bazett's or Fridericia's correction factors, adequately corrected the QT interval after the administration of a sympathomimetic agoni...

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“…13,14) Power spectral analysis of HRV: After the recordings were scanned by computer (SCM280, Fukuda Denshi), digitized RR intervals were transferred to a personal computer using commercially available Holter data-process-Vol 41 No 6 ing software (Version 1.033, Fukuda Denshi). Consecutive series of RR intervals obtained during the day were subjected to a "coarse-graining" spectral analysis 15) which allows elimination of the 1 / f component 16,17) from the HRV autopower spectra while leaving the harmonic component intact.…”

Section: Methodsmentioning

confidence: 99%

Is the QT Interval an Indicator of Autonomic State?

et al. 2000

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SUMMARYProlonged QT interval is suggested to indicate an increased risk of sudden cardiac death in certain clinical conditions such as diabetes mellitus. We investigated whether the individual QT interval is an indicator of an autonomic state. An ambulatory 24-hour ECG was recorded in 53 subjects from different clinical backgrounds. Power spectral components of heart rate variability (HRV) and the QT interval were regressively obtained at a heart rate of 60, 70, 80, 90, or 100 beats per minutes (bpm). Log values of the high-frequency component of HRV (HF: 0.15-0.50 Hz, a scale of cardiac parasympathetic tone) failed to show a relationship with the QT interval. In contrast, the QT interval at a heart rate of 90 bpm and 100 bpm showed a significant correlation with the log values of the low-frequency component (LF: 0.04-0.15 Hz) and the log[LF / HF], i.e., a putative scale of sympathetic tone (100 bpm: QT vs logLF: r = 0.414, p < 0.005, QT vs log[LF / HF]: r = 0.416, p < 0.002). Also, attenuated rate-dependent QT shortening was associated with greater logLF and log[LF / HF] values at a heart rate of 80, 90, or 100 bpm. These results suggest that the QT interval at a moderate heart rate (approximately 90-100 / min) and the degree of rate-dependent QT shortening are related to individual sympathetic tone. (Jpn Heart J 2000; 41: 713-721) Key words: Diabetes mellitus, Coronary artery disease, Ambulatory ECG monitoring, Heart rate variability, Sympathetic nerve, Parasympathetic nerve PPROLONGED QT intervals have been shown to be related to an increased risk of sudden cardiac death in apparently healthy subjects 1) in addition to patients with coronary artery disease (CAD)2) or diabetes mellitus (DM).3) To clarify the underlying pathogenic mechanism of these clinical observations, it appears important to understand whether the QT interval is associated with a particular cardiac autonomic state or not. However, the response of the QT interval to pharmacological autonomic modifications is often conflicting.4-10) Also, an intricate sympathovagal interaction 11) blurs the respective contribution of each limb of the autonomic nerve system to the QT interval. Thus, it is not readily predictable how the autonomic state is reflected on the QT interval in conditions without specific

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An exponential formula for heart rate dependence of QT interval during exercise and cardiac pacing in humans: Reevaluation of Bazett's formula

Cited by 148 publications

References 18 publications

Accurate detection of drug-induced delayed ventricular repolarization with a suitable correction formula in Langendorff guinea pig heart

Accurate detection of drug-induced delayed ventricular repolarization with a suitable correction formula in Langendorff guinea pig heart

Lack of correlation between exercise and sibenadet‐induced changes in heart rate corrected measurement of the QT interval

Is the QT Interval an Indicator of Autonomic State?

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