Effect of β-adrenergic stimulation on QT interval accommodation

Seethala, Srikanth; Shusterman, Vladimir; Saba, Samir; Mularski, Susan; Němec, Jan

doi:10.1016/j.hrthm.2010.10.012

Cited by 32 publications

(39 citation statements)

References 33 publications

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“…APD 80 adaptation curves exhibited monoexponential time courses with significantly different time constants in going from BHR to SHR ( f¡s ϭ 48 Ϯ 9.2 s) compared with from SHR to BHR ( s¡f ϭ 30.4 Ϯ 4.7 s; P Ͻ 0.05, n ϭ 5 hearts). A similar trend was reported for QT adaptation in patients upon sudden HR changes (49).…”

Section: Bradycardia-induced Changes In Catsupporting

confidence: 84%

Bradycardia alters Ca²⁺dynamics enhancing dispersion of repolarization and arrhythmia risk

Kim

Němec

Papp

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Kim JJ, Němec J, Papp R, Strongin R, Abramson JJ, Salama G. Bradycardia alters Ca 2ϩ dynamics enhancing dispersion of repolarization and arrhythmia risk. Am J Physiol Heart Circ Physiol 304: H848 -H860, 2013. First published January 11, 2013; doi:10.1152/ajpheart.00787.2012.-Bradycardia prolongs action potential (AP) durations (APD adaptation), enhances dispersion of repolarization (DOR), and promotes tachyarrhythmias. Yet, the mechanisms responsible for enhanced DOR and tachyarrhythmias remain largely unexplored. Ca 2ϩ transients and APs were measured optically from Langendorff rabbit hearts at high (150 ϫ 150 m 2 ) or low (1.5 ϫ 1.5 cm 2 ) magnification while pacing at a physiological (120 beats/min) or a slow heart rate (SHR ϭ 50 beats/min). Western blots and pharmacological interventions were used to elucidate the regional effects of bradycardia. As a result, bradycardia (SHR 50 beats/min) increased APDs gradually (time constant f¡s ϭ 48 Ϯ 9.2 s) and caused a secondary Ca 2ϩ release (SCR) from the sarcoplasmic reticulum during AP plateaus, occurring at the base on average of 184.4 Ϯ 9.7 ms after the Ca 2ϩ transient upstroke. In subcellular imaging, SCRs were temporally synchronous and spatially homogeneous within myocytes. In diastole, SHR elicited variable asynchronous sarcoplasmic reticulum Ca 2ϩ release events leading to subcellular Ca 2ϩ waves, detectable only at high magnification. SCR was regionally heterogeneous, correlated with APD prolongation (P Ͻ 0.01, n ϭ 5), enhanced DOR (r ϭ 0.9277 Ϯ 0.03, n ϭ 7), and was gradually reversed by pacing at 120 beats/min along with APD shortening (P Ͻ 0.05, n ϭ 5). A stabilizer of leaky ryanodine receptors (RyR2), 3-(4-benzylcyclohexyl)-1-(7-methoxy-2,3-dihydrobenzo[f][1,4]thiazepin-4(5H)-yl)propan-1-one (K201; 1 M), suppressed SCR and reduced APD at the base, thereby reducing DOR (P Ͻ 0.02, n ϭ 5). Ventricular ectopy induced by bradycardia (n ϭ 5/15) was suppressed by K201. Western blot analysis revealed spatial differences of voltage-gated L-type Ca 2ϩ channel protein (Cav1.2␣), Na ϩ -Ca 2ϩ exchange (NCX1), voltage-gated Na ϩ channel (Nav1.5), and rabbit ether-a-go-go-related (rERG) protein [but not RyR2 or sarcoplasmic reticulum Ca 2ϩ ATPase 2a] that correlate with the SCR distribution and explain the molecular basis for SCR heterogeneities. In conclusion, acute bradycardia elicits synchronized subcellular SCRs of sufficient magnitude to overcome the source-sink mismatch and to promote afterdepolarizations. action potential adaptation; arrhythmia; bradycardia; optical mapping; secondary Ca 2ϩ release BRADYCARDIA, DEFINED AS heart rate (HR) Ͻ 60 beats/min in adult humans (12), is usually a normal adaptive response to conditions of low metabolic demand, such as rest and sleep. Bradycardia due to pathological conditions, e.g., sick sinus syndrome, atrioventricular (AV) nodal disease, or conduction system disease, is common in clinical practice and frequently causes symptoms because of inappropriately low cardiac output. Less frequently, profound bradycardia, usuall...

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Section: Bradycardia-induced Changes In Catsupporting

confidence: 84%

Bradycardia alters Ca²⁺dynamics enhancing dispersion of repolarization and arrhythmia risk

Kim

Němec

Papp

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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“…This study elucidates the differences of opinion on the effects of dobutamine on QTc in the very few studies that have previously commented on this question [9][10][11]. The present study showed no significant effect of dobument of the change in QT with change in heart rate for each individual.…”

Section: Discussionsupporting

confidence: 78%

“…Dobutamine is a relatively infrequently used method to induce myocardial stress for imaging so that such cases are infrequent. Second, the effects of dobutamine entails considerations of its kinetics in the circulation (pharmacokinetics) and binding to relevant cardiac receptors which are manifested as immediate responses as well as a mono-exponential response to a new steadystate value [11,15]. Third, evaluation of a new QT correction formulae confront the challenge of the absence of a true (gold) standard against which a new formula can be judged.…”

Section: Limitationsmentioning

confidence: 99%

Value of a New QT Interval Correction Formula in Adjusting for Increases in Heart Rate

Rabkin¹

2017

Int J Clin Cardiol

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identification of individuals with genetic mutations that carry a high risk of sudden death [5]. A new QT-heart rate correction formula (QTc) has been developed based on ECGs from about 13,600 individuals in the NHANES US population study [6]. This QTc was shown to be was superior to other formulae [6,7]. The value of this approach, however, has not been tested in the same individual under different conditions of heart rate stress.A critical aspect of the evaluation of the QT interval is its adjustment for heart rate because of the recognized inverse relationship between QT interval and heart rate. Studies that established QTc formulae including the most recent one, utilized data on different individuals who have different heart rates. While there is considerable power in the large numbers of individuals from population based studies, they do not address between individual variability. Specifically these studies are not able to take into consideration variables that produce different resting heart rates that might in turn influence the QT interval. The importance of the individual responses to test the robustness of the QT-heart rate correction formulae is well recognized [8]. The new QT-heart rate adjustment formula has not been subject to protocol driven changes in heart rate to determine whether QTc is stable when heart rate is increased. The objective of this study was to examine the new QT correction formula for its ability to remain stable in the same individual across a range of heart rates. Methods PopulationThe patient population were individuals who reAbstract Background and objective: QT interval correction for heart rate (QTc) is essential for clinical usage. A new QTc formula has been developed based on a data agnostic mathematical approach in a large population ECG data base. The formula requires testing on a within individual basis under conditions of intervention to increase heart rate. The objective of this study was to examine the stability and reliability the new QTc formulae within individuals when Heart Rate (HR) is increased by dobutamine.

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“…Reference [6] points out that the dependence relationship is more sensitive to sympathetic activity. The results of this human experiment indicate that dobutamine can increase the fast adaption (i.e , linear correlation of the two signals) of QTI to RRI change.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to the dependence on RRI, QTI is determined by the factors independent of RRI such as the regulation of ANS itself [3,4]. Moreover, the accommodation of QTI to RRI is very complicated, including not only an immediate response to the current RRI but also a chronic response in which the time constant is about 1~2 min [5,6]. Heart period and ventricular repolarization exhibit rhythmical fluctuations and remarkable correlation both in the low frequency (0.04~0.15 Hz, LF) band and high frequency (0.15~0.…”

Section: Introductionmentioning

confidence: 99%

Reflection of Autonomic Regulation Behaviour Using Short:Term Cross:Spectral Analysis on RR and QT Intervals

Zhan

Liu

et al. 2016

2016 Computing in Cardiology Conference (CinC)

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Effect of β-adrenergic stimulation on QT interval accommodation

Cited by 32 publications

References 33 publications

Bradycardia alters Ca²⁺dynamics enhancing dispersion of repolarization and arrhythmia risk

Bradycardia alters Ca²⁺dynamics enhancing dispersion of repolarization and arrhythmia risk

Value of a New QT Interval Correction Formula in Adjusting for Increases in Heart Rate

Reflection of Autonomic Regulation Behaviour Using Short:Term Cross:Spectral Analysis on RR and QT Intervals

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Effect of β-adrenergic stimulation on QT interval accommodation

Cited by 32 publications

References 33 publications

Bradycardia alters Ca2+dynamics enhancing dispersion of repolarization and arrhythmia risk

Bradycardia alters Ca2+dynamics enhancing dispersion of repolarization and arrhythmia risk

Value of a New QT Interval Correction Formula in Adjusting for Increases in Heart Rate

Reflection of Autonomic Regulation Behaviour Using Short:Term Cross:Spectral Analysis on RR and QT Intervals

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Bradycardia alters Ca²⁺dynamics enhancing dispersion of repolarization and arrhythmia risk

Bradycardia alters Ca²⁺dynamics enhancing dispersion of repolarization and arrhythmia risk