Beat‐to‐Beat Repolarization Lability Identifies Patients at Risk for Sudden Cardiac Death

Atiga, Walter L.; Calkins, Hugh; Lawrence, John H.; Tomaselli, Gordon F.; Smith, Joseph M.; Berger, Ronald D.

doi:10.1111/j.1540-8167.1998.tb00130.x

Cited by 267 publications

(218 citation statements)

References 31 publications

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“…Specific variability analyses included: the standard deviation of normal‐to‐normal RR and QT intervals (SDNN_RR and SDNN_QT in all ECG leads, respectively);several other time and frequency domain indices of RR interval variability, including the very low (0.0–0.04 Hz), low (0.04–0.15 Hz), high (0.15–0.40 Hz), and total (0.0–0.40 Hz) frequency powers of RR interval variability in natural log‐transformed units (ln ms2/Hz) calculated using autoregression (lnAR) and the Lomb periodogram method (lnLo) (Schlegel et al., 2010);the QT variability index (QTVI) (Atiga et al., 1998), using the means and variances of the RR interval (Piccirillo et al., 2007) rather than those of the heart rate (Berger et al., 1997) in the denominator of the QTVI equation; andthe “unexplained” part of QTV (Solaimanzadeh et al, 2008; Starc & Schlegel, 2008), wherein the QTV signal is decomposed into two parts, one being described by the concomitant RR interval HRV and/or by the concomitant variability of the QRS‐T angle and the other representing the “unexplained” part of QTV. Decomposition is performed according to a model (Solaimanzadeh et al, 2008; Starc & Schlegel, 2008) that takes into account the hysteresis‐like properties of QT interval dynamics (Lang, Flapan, & Nielsen, 2001) as also the fact that while changes in QT intervals are predominantly driven by changes in RR intervals (Almeida et al, 2006), they can also occur in response to changes in QT wavefront direction descriptors, such as in the QRS‐T angle or equivalent (Acar, Yi, Hnatkova, & Malik, 1999; Kors, van Herpen, & Bemmel, 1999).…”

Section: Methodsmentioning

confidence: 99%

“…the QT variability index (QTVI) (Atiga et al., 1998), using the means and variances of the RR interval (Piccirillo et al., 2007) rather than those of the heart rate (Berger et al., 1997) in the denominator of the QTVI equation; and…”

Section: Methodsmentioning

confidence: 99%

“…Besides the measurement of HRV, which has been used predominantly for the assessment of sympathovagal balance, these techniques include indices of the electrical remodeling of the ventricles (e.g., the QRS‐T angle [Kardys et al., 2003]), ventricular depolarization (e.g., high‐frequency QRS [HFQRS] ECG [Abboud, Berenfeld, & Sadeh, 1991; Schlegel et al., 2004]), and ventricular repolarization. The indices of ventricular repolarization comprise various indices of QT interval variability (QTV), such as the QT variability index (QTVI) (Atiga et al., 1998; Berger et al., 1997; Starc & Schlegel, 2006) and the unexplained part of QTV (unexplained QTV), which represents an intrinsic part of QTV independent of simultaneous heart rate variability, the influence of the heart rate on QTV having been eliminated (Starc & Schlegel, 2008). …”

Section: Introductionmentioning

confidence: 99%

“…(2003), an increased spatial QRS‐T angle had more prognostic value for fatal endpoints than any classic cardiovascular risk factor, including diabetes. Finally, a number of studies show that the index of QT interval variability QTVI (Berger et al., 1997) can identify patients at risk for sudden cardiac death (Atiga et al., 1998; Haigney et al., 2004; Piccirillo et al., 2007), possibly even more than both left ventricular ejection fraction (as assessed by ultracardiography) and T‐wave alternans (Atiga et al., 1998; Berger et al., 1997). …”

Section: Introductionmentioning

confidence: 99%

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Evidence of cardiac electrical remodeling in patients with Huntington disease

et al. 2018

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ObjectiveAlthough Huntington's disease (HD) is a disease of the central nervous system, HD mortality surveys indicate heart disease as a major cause of death. Cardiac dysfunction in HD might be a primary consequence of peripherally expressed mutant huntingtin or secondary to either a general decline in health or the onset of neurological dysfunction. The aim of the study was to clarify the heart muscle involvement.Materials and MethodsWe measured conventional and advanced resting ECG indices. Thirtyone subjects with a confirmed huntingtin gene mutation and 31 age‐ and gender‐matched controls were included. The HD subjects were divided into four groups based on their Unified Huntington Disease Rating Scale (UHDRS) motor score.ResultsWe detected changes in advanced ECG variables connected with electrical ventricular remodeling (t test, p < 0.01). The increase in the unexplained part of both QT variability and the standard deviation of normal‐to‐normal QT intervals, presumably reflecting beat‐to‐beat changes in repolarization, was most pronounced. Further, both variables correlated with the product of the cytosine–adenine–guanine (CAG) triplets’ repeat length and the subjects’ age (CAP), the former R = 0.423 (p = 0.018) and the latter R = 0.499 (p = 0.004). There was no correlation between the CAP score and any of variables representing autonomic nervous system activity.ConclusionsBoth autonomic nervous system dysfunction and cardiac electrical remodeling are present in patients with HD. The changes in advanced ECG variables observed in the study evolve with HD progression. The increased values of QT unexplained variability may be a marker of temporal inhomogeneity in ventricular repolarization associated with malignant ventricular arrhythmias.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Evidence of cardiac electrical remodeling in patients with Huntington disease

et al. 2018

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“…In damaged myocardium, the QT interval does not adapt appropriately to RR interval variation (33) and carries a prospective risk for an adverse outcome. In the present study, both MQT and ΔMQT intervals correlated significantly to the NN and ΔNN intervals, respectively.…”

Section: Discussionmentioning

confidence: 99%

Circadian cardiac autonomic function in perinatally HIV-infected preschool children

Benchimol-Barbosa

2009

Braz J Med Biol Res

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The 24-h heart rate variability and QT-interval adaptation was investigated in perinatally HIV-infected preschool children classified according to immunological status in order to assess autonomic function at early stages of infection. Thirty-five perinatally HIV-infected and clinically stable children (4.8 ± 0.3 years) were enrolled after approval of the study by the University Hospital Pedro Ernesto Ethics Committee and written informed parental consent was obtained. The children were classified according to peripheral CD4+ count (cells/µL) as follows: group 1, N = 11 (≥1000); group 2, N = 7 (≥500 and <1000); group 3, N = 17 (<500). Left ventricular ejection fraction (>55%), 24-h RR interval variability (RRV) indexes (NN, SDANN, SDNN index, r-MSSD) and 24-h QT and Bazett-corrected QT (QTc) were determined, and groups were matched for age, body surface area, and left ventricular ejection fraction, reducing biases in RRV. The peak differences (∆) between the highest and lowest RRV and QT indexes were extracted from nocturnal (1 am-6 am) and daytime (1 pm-6 pm) hourly assessed segments, respectively. Pearson’s correlation (r) and Kruskal-Wallis ANOVA were used to compare groups. CD4+ count correlated positively with ∆NN (r = 0.45; P = 0.003). There were no significant differences in daytime NN among groups. Nighttime SDNN index (P = 0.01), nighttime r-MSSD (P = 0.003), ∆NN (P = 0.01), ∆SDNN index (P = 0.03) and ∆r-MSSD (P = 0.004) were significantly lower in group 3 than in the other groups. Expected nighttime QTc-interval lengthening was not observed in all groups. In perinatally HIV-infected preschool children with preserved left ventricular systolic function, parasympathetic-mediated autonomic dysfunction parallels immune status, impairing both RRV and circadian QTc interval adaptation

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Effects of nortriptyline and paroxetine on QT variability in patients with panic disorder

Yeragani¹,

Pohl²,

Jampala³

et al. 2000

Depress. Anxiety

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This study investigated beat‐to‐beat QT variability in patients with panic disorder before and after treatment with nortriptyline (n = 13) and paroxetine (n = 16), using an automated algorithm to compute QT intervals. An increase in QT variability appears to be associated with symptomatic patients with dilated cardiomyopathy and also with an increased risk for sudden cardiac death. QTvi (QT variability index: a log ratio of QT variance normalized for mean QT over heart rate variability normalized for mean heart rate) was significantly higher in supine posture in patients with panic disorder treated with nortriptyline (P> = 0.006) but not paroxetine. Thus paroxetine may be a better drug of choice especially in patients with coexisting cardiac disease. These findings are important especially in view of the recent reports of increased risk for cardiovascular mortality and sudden death in patients with anxiety and depression. QTvi can be a valuable noninvasive measure of temporal repolarization lability, especially to study the side effects of medications which affect cardiac autonomic function. Depression and Anxiety 11:126–130, 2000. © 2000 Wiley‐Liss, Inc.

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Beat‐to‐Beat Repolarization Lability Identifies Patients at Risk for Sudden Cardiac Death

Abstract: (1) This noninvasive measure of temporal repolarization lability identified patients with SCD and predicted arrhythmia-free survival. (2) Further studies are needed to determine the mechanisms that mediate beat-to-beat QT interval variability.

Cited by 267 publications

References 31 publications

Evidence of cardiac electrical remodeling in patients with Huntington disease

Evidence of cardiac electrical remodeling in patients with Huntington disease

Circadian cardiac autonomic function in perinatally HIV-infected preschool children

Effects of nortriptyline and paroxetine on QT variability in patients with panic disorder

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