Indexes of Temporal Myocardial Repolarization Dispersion and Sudden Cardiac Death in Heart Failure: Any Difference?

Piccirillo, Gianfranco; Rossi, Pietro; Mitra, M; Quaglione, Raffaele; Dell’Armi, A.; Barba, Daniele Di; Maisto, Damiana; Lizio, Andrea; Barillà, Francesco; Magrì, Damiano

doi:10.1111/anec.12005

Cited by 32 publications

(57 citation statements)

References 40 publications

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“…42 Experimental and clinical evidence show that this repolarization phase is closely linked to sympathetic activity. 14,15,43,44 The small, though significant, positive relation we found between T e VI and the SGNA/VNA ratio could therefore support its usefulness, since we showed that after MI, notwithstanding a preserved left ventricular ejection fraction, this terminal repolarization phase worsens owing to the increased sympathetic and reduced vagal activity or to both events. Conversely, the same terminal repolarization phase, under baseline conditions, seems unrelated to dispersion owing to the increased SGNA/VNA ratio.…”

Section: Discussionmentioning

confidence: 56%

Myocardial repolarization dispersion and autonomic nerve activity in a canine experimental acute myocardial infarction model

Piccirillo¹,

Moscucci²,

D'Alessandro³

et al. 2014

Heart Rhythm

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Background Evidence from a canine experimental acute myocardial infarction (MI) model shows that until the seventh week after MI the relationship between stellate ganglionic nerve and vagal nerve activities (SGNA/VNA) progressively increases. Objective We evaluated how autonomic nervous system activity influences temporal myocardial repolarization dispersion at this period. Methods We analyzed autonomic nerve activity as well as QT and RR variability from recordings previously obtained in 9 dogs. From a total 48 short-term electrocardiographic segments, 24 recorded before and 24 seven weeks after experimentally-induced MI, we obtained three indices of temporal myocardial repolarization dispersion: QTe (from q wave T to wave end), QTp (from q wave to T wave peak) and Te (from T wave peak to T wave end) variability index (QTeVI, QTpVI, TeVI). We also performed a heart rate variability power spectral analysis on the same segments. Results After MI, all the QT variables increased QTeVI (median [interquartile range]) (from - 1.76[0.82] to −1.32[0.68]), QTeVI (from −1.90[1.01] to −1.45[0.78]) and TeVI (from −0.72[0.67] to −0.22[1.00]), whereas all RR spectral indexes decreased (p<0.001 for all). Distinct circadian rhythms in QTeVI (p<0.05,) QTpVI (p<0.001) and TeVI (p<0.05) appeared after MI with circadian variations resembling that of SGNA/VNA. The morning QTpVI and TeVI acrophases approached the SGNA/VNA acrophase. Conversely, the evening QTeVI acrophase coincided with another SGNA/VNA peak. After MI, regression analysis detected a positive relationship between SGNA/VNA and TeVI (R2: 0.077; β: 0.278; p< 0.001). Conclusion Temporal myocardial repolarization dispersion shows a circadian variation after MI reaching its peak at a time when sympathetic is highest and vagal activity lowest.

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Section: Discussionmentioning

confidence: 56%

Myocardial repolarization dispersion and autonomic nerve activity in a canine experimental acute myocardial infarction model

Piccirillo¹,

Moscucci²,

D'Alessandro³

et al. 2014

Heart Rhythm

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“…While various metrics [e.g., SDQT (27), normalized QTV (24), QTV index (10), short-term variability ratio (37), peakto-end of T wave interval variability (44)] have been proposed to quantify beat-to-beat repolarization variability, the association of individual measures with future adverse events has been inconsistent among studies (24,41,50). Nevertheless, SDQT has been shown to correlate significantly with normalized QTV and the QTV index in HF patients (41).…”

Section: Study Limitationsmentioning

confidence: 99%

Autonomic modulation of repolarization instability in patients with heart failure prone to ventricular tachycardia

Nayyar

Roberts‐Thomson

Hasan

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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QT variability (QTV) signifies repolarization lability, and increased QTV is a risk predictor for sudden cardiac death. The aim of the present study was to investigate the role of autonomic nervous system activity on QTV. This study was performed in 29 subjects: 10 heart failure (HF) patients with spontaneous ventricular tachycardia [HFVT(+)], 10 HF patients without spontaneous VT [HFVT(-)], and 9 subjects with structurally normal hearts (HNorm). The beat-to-beat QT interval was measured on 3-min records of surface ECGs at baseline and during interventions (atrial pacing and esmolol, isoprenaline, and atropine infusion). Variability in QT intervals was expressed as the SD of all QT intervals (SDQT). The ratio of the SDQT to SD of RR intervals (SDRR) was calculated as an index of QTV normalized to heart rate variability. There was a trend toward a higher baseline SDQT-to-SDRR ratio in the HFVT(+) group compared with the HFVT(-) and HNorm groups (P = 0.09). SDQT increased significantly in the HFVT(+) and HFVT(-) groups compared with the HNorm group during fixed-rate atrial pacing (P = 0.008). Compared with baseline, isoprenaline infusion increased SDQT in HNorm subjects (P = 0.02) but not in HF patients. SDQT remained elevated in the HFVT(+) group relative to the HNorm group despite acute β-adrenoceptor blockade with esmolol (P = 0.02). In conclusion, patients with HF and spontaneous VT have larger fluctuations in beat-to-beat QT intervals. This appears to be a genuine effect that is not solely a consequence of heart rate variation. The effect of acute autonomic nervous system modulation on QTV appears to be limited in HF patients.

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“…Albeit controversial [17,27,28,29,30], an increase in both spatial and temporal QT subsegment dispersion is thought to represent a useful noninvasive marker of arrhythmic risk in patients with congestive heart failure and in other disease settings [9,12,13,22,23,31,32]. Conversely, whether the QT dispersion might be an additive marker in identifying HCM patients with an increased arrhythmia propensity represents a matter of debate.…”

Section: Discussionmentioning

confidence: 99%

“…However, a number of clinical variables, such as distribution and magnitude of ventricular hypertrophy and fibrosis, as well as LV dysfunction, might potentially alter this ECG-derived parameter, thus limiting its use in routine clinical practice [7,8,9,10,11]. Recently, it has been suggested that the T peak -T end interval (T p T e ) may be a surrogate for transmural dispersion of repolarization and T p T e may be a more sensitive index of the dispersion of ventricular repolarization than the whole QT e or the Q-T peak interval (QT p ), given it closely reflects the termination of repolarization in the 3 myocardial cell layers [16,17,18]. In this context, the relationship between each of the QT segment dispersions and ventricular arrhythmias is an aspect not yet systematically investigated in HCM.…”

Section: Introductionmentioning

confidence: 99%

Spatial QT Dispersion Predicts Nonsustained Ventricular Tachycardia and Correlates with Confined Systodiastolic Dysfunction in Hypertrophic Cardiomyopathy

Magrì

Piccirillo²,

Ricotta

et al. 2015

Cardiology

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Objectives: An increased dispersion of myocardial repolarization represents one of the mechanisms underlying the arrhythmic risk in hypertrophic cardiomyopathy (HCM). We investigated spatial myocardial repolarization dispersion indices in HCM patients with nonsustained ventricular tachycardia (NSVT) and, contextually, their main clinical determinants. Methods: Fifty-two well-matched HCM outpatients were categorized into two groups according to the presence or the absence of NSVT at 24-hour Holter electrocardiogram (ECG) monitoring. Each patient underwent a clinical examination, including Doppler echocardiogram integrated with tissue Doppler imaging, cardiac magnetic resonance, and 12-lead surface ECG to calculate the dispersion for the following intervals: QRS, Q-T_end (QT_e), Q-T_peak, T_peak-T_end (T_pT_e), J-T_peak, and J-T_end. Results: The NSVT group showed only QT_e dispersion and T_pT_e dispersion values to be significantly higher than their counterparts. NSVT occurrence was independently predicted by late gadolinium enhancement presence (p = 0.021) and QT_e Bazett dispersion (p = 0.030), the latter strongly associated with the myocardial performance index (MPI) obtained at the basal segment of the interventricular septum (p = 0.0004). Conclusion: Our data support QT_e dispersion as an easy and noninvasive tool for identifying HCM patients with NSVT propensity. The strong relationship between QT_e dispersion and MPI allows us to hypothesize an intriguing link between electrical instability and confined myocardial areas of systodiastolic dysfunction.

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Indexes of Temporal Myocardial Repolarization Dispersion and Sudden Cardiac Death in Heart Failure: Any Difference?

Cited by 32 publications

References 40 publications

Myocardial repolarization dispersion and autonomic nerve activity in a canine experimental acute myocardial infarction model

Myocardial repolarization dispersion and autonomic nerve activity in a canine experimental acute myocardial infarction model

Autonomic modulation of repolarization instability in patients with heart failure prone to ventricular tachycardia

Spatial QT Dispersion Predicts Nonsustained Ventricular Tachycardia and Correlates with Confined Systodiastolic Dysfunction in Hypertrophic Cardiomyopathy

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