Risk stratification for sudden cardiac death: current status and challenges for the future

Wellens, Hein J.J.; Schwartz, Peter J.; Lindemans, Fred W.; Buxton, Alfred E.; Goldberger, Jeffrey J.; Hohnloser, Stefan H.; Huikuri, Heikki V.; Kääb, Stefan; Rovere, Maria Teresa La; Malik, Marek; Myerburg, Robert J.; Simoons, Maarten L.; Swedberg, Karl; Tijssen, Jan; Voors, Adriaan A.; Wilde, Arthur A.M.

doi:10.1093/eurheartj/ehu176

Cited by 358 publications

(325 citation statements)

References 117 publications

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“…Finally, left ventricular ejection fraction, which is the mainstay of assessing sudden cardiac death risk from a clinical perspective, was not included in the current analysis. However, most sudden cardiac deaths occur among those without known heart disease,29 as was the case with our study cohort at baseline.…”

Section: Discussionsupporting

confidence: 52%

The Metabolic Syndrome and Risk of Sudden Cardiac Death: The Atherosclerosis Risk in Communities Study

Hess

Al‐Khalidi

Friedman

et al. 2017

JAHA

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BackgroundPrior studies have demonstrated a link between the metabolic syndrome and increased risk of cardiovascular mortality. Whether the metabolic syndrome is associated with sudden cardiac death is uncertain.Methods and ResultsWe characterized the relationship between sudden cardiac death and metabolic syndrome status among participants of the ARIC (Atherosclerosis Risk in Communities) Study (1987–2012) free of prevalent coronary heart disease or heart failure. Among 13 168 participants, 357 (2.7%) sudden cardiac deaths occurred during a median follow‐up of 23.6 years. Participants with the metabolic syndrome (n=4444) had a higher cumulative incidence of sudden cardiac death than those without it (n=8724) (4.1% versus 2.3%, P<0.001). After adjustment for participant demographics and clinical factors other than components of the metabolic syndrome, the metabolic syndrome was independently associated with sudden cardiac death (hazard ratio, 1.70, 95% confidence interval, 1.37–2.12, P<0.001). This relationship was not modified by sex (interaction P=0.10) or race (interaction P=0.62) and was mediated by the metabolic syndrome criteria components. The risk of sudden cardiac death varied according to the number of metabolic syndrome components (hazard ratio 1.31 per additional component of the metabolic syndrome, 95% confidence interval, 1.19–1.44, P<0.001). Of the 5 components, elevated blood pressure, impaired fasting glucose, and low high‐density lipoprotein were independently associated with sudden cardiac death.ConclusionsWe observed that the metabolic syndrome was associated with a significantly increased risk of sudden cardiac death irrespective of sex or race. The risk of sudden cardiac death was proportional to the number of metabolic syndrome components.

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Section: Discussionsupporting

confidence: 52%

The Metabolic Syndrome and Risk of Sudden Cardiac Death: The Atherosclerosis Risk in Communities Study

Hess

Al‐Khalidi

Friedman

et al. 2017

JAHA

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“…Considering that between 45-50% of SCD occur in the general population (without known heart disease) [132] one important challenge is to identify non-invasive markers that can be measured in routine tests such as 10-s ECG or standard Holter recordings. Taking into account the different etiology and complexity of factors involved in SCD, it is also important to consider the combination of different markers that have been proved to be associated with risk separately (possibly including also chemical and genetic biomarkers).…”

Section: Challenges and Future Perspectivesmentioning

confidence: 99%

Techniques for Ventricular Repolarization Instability Assessment From the ECG

2016

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Abstract-Instabilities in ventricular repolarization have been documented to be tightly linked to arrhythmia vulnerability. Translation of the information contained in the repolarization phase of the ECG into valuable clinical decision-making tools remains challenging. This work aims at providing an overview of the last advances in the proposal and quantification of ECG-derived indices that describe repolarization properties and whose alterations are related with threatening arrhythmogenic conditions. A review of the state-of-the-art is provided, spanning from the electrophysiological basis of ventricular repolarization to its characterization on the surface ECG through a set of temporal and spatial risk markers.Index Terms-Electrophysiological basis of the ECG, ECG waves, ECG intervals, repolarization instabilities, spatial and temporal ventricular repolarization dispersion, cardiac arrhythmias, biophysical modeling of the ECG, ECG signal processing, repolarization risk markers, T wave alternans, QT variability.

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“…Currently, there is no cure for VF, with only rudimentary treatment options available; thus, sudden cardiac death from VF remains a major worldwide health problem 3, 4. The Purkinje system is implicated in the genesis of primary VF,5, 6, 7 with radiofrequency ablation successfully treating this lethal arrhythmia by targeting triggers, such as a premature ventricular beat emanating from Purkinje tissue 7, 8, 9, 10.…”

mentioning

confidence: 99%

Elimination of Purkinje Fibers by Electroporation Reduces Ventricular Fibrillation Vulnerability

Livia

Sugrue

Witt

et al. 2018

JAHA

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BackgroundThe Purkinje network appears to play a pivotal role in the triggering as well as maintenance of ventricular fibrillation. Irreversible electroporation (IRE) using direct current has shown promise as a nonthermal ablation modality in the heart, but its ability to target and ablate the Purkinje tissue is undefined. Our aim was to investigate the potential for selective ablation of Purkinje/fascicular fibers using IRE.Methods and ResultsIn an ex vivo Langendorff model of canine heart (n=8), direct current was delivered in a unipolar manner at various dosages from 750 to 2500 V, in 10 pulses with a 90‐μs duration at a frequency of 1 Hz. The window of ventricular fibrillation vulnerability was assessed before and after delivery of electroporation energy using a shock on T‐wave method. IRE consistently eradicated all Purkinje potentials at voltages between 750 and 2500 V (minimum field strength of 250–833 V/cm). The ventricular electrogram amplitude was only minimally reduced by ablation: 0.6±2.3 mV (P=0.03). In 4 hearts after IRE delivery, ventricular fibrillation could not be reinduced. At baseline, the lower limit of vulnerability to ventricular fibrillation was 1.8±0.4 J, and the upper limit of vulnerability was 19.5±3.0 J. The window of vulnerability was 17.8±2.9 J. Delivery of electroporation energy significantly reduced the window of vulnerability to 5.7±2.9 J (P=0.0003), with a postablation lower limit of vulnerability=7.3±2.63 J, and the upper limit of vulnerability=18.8±5.2 J.ConclusionsOur study highlights that Purkinje tissue can be ablated with IRE without any evidence of underlying myocardial damage.

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Risk stratification for sudden cardiac death: current status and challenges for the future

Cited by 358 publications

References 117 publications

The Metabolic Syndrome and Risk of Sudden Cardiac Death: The Atherosclerosis Risk in Communities Study

The Metabolic Syndrome and Risk of Sudden Cardiac Death: The Atherosclerosis Risk in Communities Study

Techniques for Ventricular Repolarization Instability Assessment From the ECG

Elimination of Purkinje Fibers by Electroporation Reduces Ventricular Fibrillation Vulnerability

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