The role of silent ischemia, the arrhythmic substrate and the short-long sequence in the genesis of sudden cardiac death

Gomes, J. Anthony; Alexopoulos, Dimitrios; Winters, Stephen L.; Deshmukh, Pramod; Fuster, Valentín; Suh, K

doi:10.1016/0735-1097(89)90005-3

Cited by 77 publications

(6 citation statements)

References 40 publications

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“…This observation suggests that either the re-entrant circuit or site of ectopic activity is the same for every PoVT-episode in case of respectively re-entry or focal activity as the underlying mechanism. Rhythms prior to VT’s were most often SLS-sequences or SR comparable to observations made by Gomes et al in patients with silent ischemia [ 14 ]. However, the multiple types of VT-initiation in this study reflect involvement of different underlying mechanisms in PoVT-onset [ 14 ].…”

Section: Discussionsupporting

confidence: 79%

“…In patients with preserved systolic function, the majority of the VT’s had a SO [ 8 – 10 ]. Analysis with 24-h Holter in patients silent ischemia demonstrated that recurrent monomorphic VT’s were often preceded by SLS-sequences and subsequently induced by VPBs [ 14 ]. Several studies reported on the occurrence of VT early after Heartmate II implantation but the onset of these PoVT has not yet been examined [ 15 – 19 ].…”

Section: Introductionmentioning

confidence: 99%

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Hemodynamic deterioration precedes onset of ventricular tachyarrhythmia after Heartmate II implantation

Yaksh

Kik

Knops

et al. 2016

J Cardiothorac Surg

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BackgroundEarly postoperative ventricular tachyarrhythmia (PoVT) after left ventricular assist device (LVAD) implantation are common and associated with higher mortality-rates. At present, there is no data on initiation of these PoVT and the role of alterations in cardiac hemodynamics. Case PresentationA LVAD was implanted in a patient with end-stage heart failure due to a ischemic cardiomyopathy. Alterations in cardiac rhythm and hemodynamics preceding PoVT-episodes during the first five postoperative days were examined by using continuous recordings of cardiac rhythm and various hemodynamic parameters. All PoVT (N=120) were monomorphic, most often preceded by short-long-short-sequences or regular SR and initiated by ventricular runs. Prior to PoVT, mean arterial pressure decreased; heart rate and ST-segments deviations increased. ConclusionsPoVT are caused by different underlying electrophysiological mechanisms. Yet, they are all monomorphic and preceded by hemodynamic deterioration due to myocardial ischemia.

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Section: Discussionsupporting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Hemodynamic deterioration precedes onset of ventricular tachyarrhythmia after Heartmate II implantation

Yaksh

Kik

Knops

et al. 2016

J Cardiothorac Surg

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“…33 Therefore, part of the arrhythmogenesis may be explained by the PES-SB DOR 34 (after the short CI PVC) and another by the CI of the subsequent PVC. PES-SB dispersion was globally higher following PVC (versus same CI PAC) because of their non-uniform local CI across the heart.…”

Section: Discussionmentioning

confidence: 99%

Premature Ventricular Contraction Coupling Interval Variability Destabilizes Cardiac Neuronal and Electrophysiological Control

Hamon¹,

Rajendran²,

Chui³

et al. 2017

Circ: Arrhythmia and Electrophysiology

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Background Variability in premature ventricular contraction (PVC) coupling interval (CI) increases the risk of cardiomyopathy and sudden death. The autonomic nervous system regulates cardiac electrical and mechanical indices, and its dysregulation plays an important role in cardiac disease pathogenesis. The impact of PVCs on the intrinsic cardiac nervous system (ICNS), a neural network on the heart, remains unknown. The objective was to determine the effect of PVCs and CI on ICNS function in generating cardiac neuronal and electrical instability using a novel cardio-neural mapping approach. Methods and Results In a porcine model (n=8) neuronal activity was recorded from a ventricular ganglion using a microelectrode array, and cardiac electrophysiological mapping was performed. Neurons were functionally classified based on their response to afferent and efferent cardiovascular stimuli, with neurons that responded to both defined as convergent (local reflex processors). Dynamic changes in neuronal activity were then evaluated in response to right ventricular outflow tract PVCs with fixed short, fixed long, and variable CI. PVC delivery elicited a greater neuronal response than all other stimuli (P<0.001). Compared to fixed short and long CI, PVCs with variable CI had a greater impact on neuronal response (P<0.05 versus short CI), particularly on convergent neurons (P<0.05), as well as neurons receiving sympathetic (P<0.05) and parasympathetic input (P<0.05). The greatest cardiac electrical instability was also observed following variable (short) CI PVCs. Conclusions Variable CI PVCs affect critical populations of ICNS neurons and alter cardiac repolarization. These changes may be critical for arrhythmogenesis and remodeling leading to cardiomyopathy.

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“…As described by Gelzer et al27 and outlined in Figure 1, it is hypothesized that specific sequences of premature stimulus intervals (including SLSS and similar sequences) can, through the influence of APD and CV restitution, cause enhanced spatial dispersion of repolarization, leading to spatially discordant APD alternans, conduction block, reentry, and VF. This sequence of events provides an explanation for the observation that certain patterns of premature complexes, including short‐long‐short,5 long‐short3 and short‐long,4 promote reentry, VT, and VF. In this study, we confirmed that the coupled maps model, when supplied with APD restitution data from canine right ventricles, predicted the presence of discordant alternans, in the form of beat‐to‐beat patterns of sign changes in spatial gradients of APD and DI, when compared with observations from optical mapping data.…”

Section: Discussionmentioning

confidence: 86%

“…A substantial proportion of sudden cardiac arrests, approximately half in a recent study,2 are associated with ventricular tachycardia (VT) or ventricular fibrillation (VF). It has been observed clinically that sustained VT and VF are often preceded by several irregularly timed premature complexes,3, 4 and studies conducted to explore this phenomenon have shown that specific coupling interval patterns of premature complexes, such as short‐long‐short5 and short‐short‐short,6 tend to lead to reentry and VT. Various researchers have examined the mechanism by which premature complexes or pacing history can interact with electrical restitution properties, including the dependence of action potential duration (APD) and conduction velocity (CV) on the preceding diastolic interval (DI) to produce dynamical heterogeneity of refractoriness, wave break, reentry, and VF7, 8, 9, 10, 11 (see elsewhere12, 13 for reviews).…”

Section: Introductionmentioning

confidence: 99%

Discordant Alternans as a Mechanism for Initiation of Ventricular Fibrillation In Vitro

Muñoz

Gelzer

Fenton

et al. 2018

JAHA

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BackgroundVentricular tachyarrhythmias are often preceded by short sequences of premature ventricular complexes. In a previous study, a restitution‐based computational model predicted which sequences of stimulated premature complexes were most likely to induce ventricular fibrillation in canines in vivo. However, the underlying mechanism, based on discordant‐alternans dynamics, could not be verified in that study. The current study seeks to elucidate the mechanism by determining whether the spatiotemporal evolution of action potentials and initiation of ventricular fibrillation in in vitro experiments are consistent with model predictions.Methods and ResultsOptical mapping voltage signals from canine right‐ventricular tissue (n=9) were obtained simultaneously from the entire epicardium and endocardium during and after premature stimulus sequences. Model predictions of action potential propagation along a 1‐dimensional cable were developed using action potential duration versus diastolic interval data. The model predicted sign‐change patterns in action potential duration and diastolic interval spatial gradients with posterior probabilities of 91.1%, and 82.1%, respectively. The model predicted conduction block with 64% sensitivity and 100% specificity. A generalized estimating equation logistic‐regression approach showed that model‐prediction effects were significant for both conduction block (P<1×10−15, coefficient 44.36) and sustained ventricular fibrillation (P=0.0046, coefficient, 1.63) events.ConclusionsThe observed sign‐change patterns favored discordant alternans, and the model successfully identified sequences of premature stimuli that induced conduction block. This suggests that the relatively simple discordant‐alternans‐based process that led to block in the model may often be responsible for ventricular fibrillation onset when preceded by premature beats. These observations may aid in developing improved methods for anticipating block and ventricular fibrillation.

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The role of silent ischemia, the arrhythmic substrate and the short-long sequence in the genesis of sudden cardiac death

Cited by 77 publications

References 40 publications

Hemodynamic deterioration precedes onset of ventricular tachyarrhythmia after Heartmate II implantation

Hemodynamic deterioration precedes onset of ventricular tachyarrhythmia after Heartmate II implantation

Premature Ventricular Contraction Coupling Interval Variability Destabilizes Cardiac Neuronal and Electrophysiological Control

Discordant Alternans as a Mechanism for Initiation of Ventricular Fibrillation In Vitro

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