Circadian Variation of Beat‐to‐Beat QT Interval Variability in Patients with Prior Myocardial Infarction and the Effect of β‐Blocker Therapy

Furukawa, Yoichi; Shimizu, Hiroki; Hiromoto, Kenji; Kanemori, Tetsuzou; Masuyama, Tohru; Ohyanagi, Mitsumasa

doi:10.1111/j.1540-8159.2006.00379.x

Cited by 24 publications

(16 citation statements)

References 24 publications

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“…For example, no effect at rest (Piccirillo et al, 2001; Nayyar et al, 2013); a reduction during atrial pacing in normal subjects (Mine et al, 2008); no effect on head up tilt increase in QTV in heart failure patients (Nayyar et al, 2013); and reduction of QTV increase during anger recall in post MI patients (Magrí et al, 2012). Circadian variation of QTV is abolished by beta blockade (Furukawa et al, 2006). …”

Section: Discussionmentioning

confidence: 99%

Autonomic Modulation in Patients with Heart Failure Increases Beat-to-Beat Variability of Ventricular Action Potential Duration

et al. 2017

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Background: Exaggerated beat-to-beat variability of ventricular action potential duration (APD) is linked to arrhythmogenesis. Sympathetic stimulation has been shown to increase QT interval variability, but its effect on ventricular APD in humans has not been determined.Methods and Results: Eleven heart failure patients with implanted bi-ventricular pacing devices had activation–recovery intervals (ARI, surrogate for APD) recorded from LV epicardial electrodes under constant RV pacing. Sympathetic activity was increased using a standard autonomic challenge (Valsalva) and baroreceptor indices were applied to determine changes in sympathetic stimulation. Two Valsalvas were performed for each study and were repeated, both off and on bisoprolol. In addition sympathetic nerve activity (SNA) was measured from skin electrodes on the thorax using a novel validated method. Autonomic modulation significantly increased mean short-term variability in ARI; off bisoprolol mean STV increased from 3.73 ± 1.3 to 5.27 ± 1.04 ms (p = 0.01), on bisoprolol mean STV of ARI increased from 4.15 ± 1.14 to 4.62 ± 1 ms (p = 0.14). Adrenergic indices of the Valsalva demonstrated significantly reduced beta-adrenergic function when on bisoprolol (Δ pressure recovery time, p = 0.04; Δ systolic overshoot in Phase IV, p = 0.05). Corresponding increases in SNA from rest both off (1.4 uV, p < 0.01) and on (0.7 uV, p < 0.01) bisoprolol were also seen.Conclusions: Beat-to-beat variability of ventricular APD increases during brief periods of increased sympathetic activity in patients with heart failure. Bisoprolol reduces, but does not eliminate, these effects. This may be important in the genesis of ventricular arrhythmias in heart failure patients.

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Section: Discussionmentioning

confidence: 99%

Autonomic Modulation in Patients with Heart Failure Increases Beat-to-Beat Variability of Ventricular Action Potential Duration

et al. 2017

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“…In addition, digoxin may suppress QTV [42] . A rise in QTV during daytime, probably owing to sympathetic activation in patients with myocardial infarction, was attenuated by ␤ -blocker administration [43] . According to our study, diltiazem boosts QTV and propranolol suppresses QTV, whereas zatebradine does not show any appreciable effects on QTV.…”

Section: Discussionmentioning

confidence: 99%

Three Different Bradycardic Agents, Zatebradine, Diltiazem and Propranolol, Distinctly Modify Heart Rate Variability and QT-Interval Variability

Yamabe

Sanyal²,

Miyamoto³

et al. 2007

Pharmacology

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Zatebradine, diltiazem and propranolol are all antiarrhythmic agents, and all induce bradycardia, but each is known to have a different initial molecular mechanism: zatebradine is a channel blocker of the hyperpolarization-activated inward current (I_f ); diltiazem is a blocker of the L-type Ca²⁺ channel (I_CaL), and propranolol is a β-blocker. To further investigate the mechanisms underlying their clinical effects, we studied their effects on heart rate variability (HRV) and QT-interval variability (QTV). To this end, guinea pigs were treated with either zatebradine (1.5 mg/kg, i.p.), diltiazem (40 mg/kg, i.p.) or propranolol (20 mg/kg, i.p.). A dose of each agent that decreased HR by 20–22% was used in this study. HRV and QTV were analyzed by a fast Fourier and/or a wavelet transform algorithm. Zatebradine, an I_f channel blocker, had no significant effect on HRV and QTV. Diltiazem, a non-dihydropyridine I_CaL blocker, increased high frequency (HF) power and decreased the power ratio of the low frequency (LF) range to the HF range (L/H) in HRV, and increased QTV. Propranolol, a non-selective β-antagonist, decreased LF power and L/H ratios in HRV, and appreciably reduced QTV. These differences in pharmacological action may help us better understand the antiarrhythmic and/or proarrhythmic actions of these agents when they are used clinically for reducing HR.

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“…The QT Interval represents ventricular depolarization, and repolarization and is the measurement from the onset of the QRS complex to the end deflection of the T wave (Furukawa, Shimizu, Hiromoto, Kanemori, Masuyama, & Ohyanagi, 2006;Hunt, 2005). The QT Interval normally ranges from 0.2-0.4 sec and is often corrected to be independent of heart rate.…”

Section: Qt Intervalmentioning

confidence: 99%

“…It is modulated by both sympathetic and parasympathetic activity (Bilchick & Berger, 2006). The QT Interval is the measurement from the onset of the QRS complex to the end deflection of the T wave and represents ventricular depolarization and repolarization (Furukawa et al, 2006;Hunt, 2005). It is also modulated by autonomic function (Viitasalo et al, 1998).…”

Section: Autonomic Nervous System Functionmentioning

confidence: 99%

“…The QT Interval, measured from the onset of the QRS complex to the end of the T wave, represents ventricular depolarization and repolarization (Furukawa et al, 2006;Hunt, 2005) and is modulated by autonomic nervous system function (Viitasalo et al, 1998). The autonomic nervous system influences both cardiac repolarization and QT length directly through its effect on heart rate.…”

Section: Qt Interval Durationmentioning

confidence: 99%

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The Effects of Glucose Tolerance, Hypertension, and Race on Heart Rate Variability, QT Interval Duration, and Left Ventricular Hypertrophy in Overweight-Obese Adolescents

Lee¹

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Circadian Variation of Beat‐to‐Beat QT Interval Variability in Patients with Prior Myocardial Infarction and the Effect of β‐Blocker Therapy

Cited by 24 publications

References 24 publications

Autonomic Modulation in Patients with Heart Failure Increases Beat-to-Beat Variability of Ventricular Action Potential Duration

Autonomic Modulation in Patients with Heart Failure Increases Beat-to-Beat Variability of Ventricular Action Potential Duration

Three Different Bradycardic Agents, Zatebradine, Diltiazem and Propranolol, Distinctly Modify Heart Rate Variability and QT-Interval Variability

The Effects of Glucose Tolerance, Hypertension, and Race on Heart Rate Variability, QT Interval Duration, and Left Ventricular Hypertrophy in Overweight-Obese Adolescents

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