Familial Sudden Death Is an Important Risk Factor for Primary Ventricular Fibrillation

Dekker, Lukas; Bezzina, Connie R.; Henriques, José P.S.; Tanck, Michael W.T.; Koch, Karel T.; Alings, Marco; Arnold, Alfred; Boer, Menko‐Jan de; Gorgels, Anton P.M.; Michels, H. R.; Verkerk, Agnes; Verheugt, Freek W.A.; Zijlstra, Felix; Wilde, Arthur A.M.

doi:10.1161/circulationaha.105.606145

Cited by 255 publications

(175 citation statements)

References 21 publications

Supporting

Mentioning

160

Contrasting

Unclassified

Order By: Relevance

“…34 Several studies have also demonstrated a familial predisposition to SCD that may or may not be related to genetic channelopathies. [35][36][37] Coronary spasm is also a cause of cardiac arrest, particularly in male smokers with minimal or no pre-existing CAD. 38 Mitral valve prolapse in female patients with ECG repolarisation abnormalities, and frequent complex ventricular ectopy, has also been associated with out-of-hospital cardiac arrest.…”

Section: Department Of Defense Cardiovascular Death Registry In the Umentioning

confidence: 99%

A Clinical Perspective on Sudden Cardiac Death

2016

Arrhythmia &Amp; Electrophysiology Review

View full text Add to dashboard Cite

This article presents the epidemiology, aetiology and pathophysiology of sudden cardiac death. The modern management of survivors as well as of family members of victims is discussed, as are the relevant recommendations of guidelines prepared by learned societies. KeywordsOut-of-hospital cardiac arrest, sports-related sudden death, sudden cardiac death, sudden unexplained death syndrome Disclosure: The authors have no conflicts of interest to declare.

show abstract

Section: Department Of Defense Cardiovascular Death Registry In the Umentioning

confidence: 99%

A Clinical Perspective on Sudden Cardiac Death

2016

Arrhythmia &Amp; Electrophysiology Review

View full text Add to dashboard Cite

show abstract

“…Furthermore, patients with similar risk factors for CAD may suffer from SCD or nonfatal ischemic events. Although the explanation for this difference is far from clear, data from a recent case-control strongly suggest that there is a genetic predisposition to primary VF in the setting of an acute MI [49]. Furthermore, there is new understanding of the cascade that relates the distal events of atherosclerosis to the proximal event of SCD.…”

Section: Atherosclerosis and Thrombosis Cascadementioning

confidence: 99%

Genomics, heart failure and sudden cardiac death

Darbar

2008

Heart Fail Rev

View full text Add to dashboard Cite

Sudden cardiac death (SCD) is among the most common causes of death in developed countries throughout the world. Despite decreased overall cardiac mortality, SCD vrates appear to be increasing in concert with escalating global prevalence of coronary disease and heart failure, the two major conditions predisposing to SCD. This unfavorable trend is a consequence of our inability to identify those who will die suddenly from lethal ventricular arrhythmias and to develop effective therapies for all populations at risk. The known risk factors for SCD lack the predictive power needed to generate preventive strategies for the large number of fatal arrhythmic events that occur among lowerrisk subsets of the population. Even among recognized high-risk subsets, prediction of SCD remains challenging. With the exception of the implantable cardioverter defibrillator (ICD) there are few effective strategies for the prevention and treatment of SCD. This article discusses the prospect of genomic science as an approach to the identification of patients at high-risk for SCD. While the final common pathway for SCD is malignant ventricular arrhythmias, there are many potential contributors, pathways, and mechanisms by which common genetic variants (polymorphisms) could affect initiation and propagation of life-threatening cardiac arrhythmias. Recent advances in genomic medicine now provide us with novel approaches to both identify candidate genes/pathways and relatively common polymorphisms which may predispose patients to increased risk for SCD. Improved understanding of the relationship between common polymorphisms and SCD will not only improve risk stratification such that ICDs can be targeted to those patients most likely to benefit from them but also provide new insight into the pathophysiology of SCD. KeywordsSudden cardiac death; Genomics; Heart failure; Single nucleotide polymorphisms Heart failure and SCD Heart failure (HF) afflicts approximately 5 million people in the United States, with 550,000 new cases reported annually, but as the population ages both the incidence and prevalence is expected to rise [1]. HF is associated with high mortality and is reportedly responsible for 300,000 deaths annually in the US [1]. Prior to advent of neuro-hormonal antagonists, the mean duration of survival after onset of HF was 1.7 years for men and 3.2 years for women, with only half of patients still alive after 5 years of onset [2]. The two modes of death in patients with HF are circulatory failure due to progressive left ventricular (LV) dysfunction associated with gradual worsening of symptoms, or sudden cardiac death (SCD) in relatively clinically stable patients [3].Although the proportion of sudden deaths in published trials varies significantly, probably due to varying interpretations of reported modes of death, clinical trials data suggests that SCD accounts for approximately one-third of all HF deaths [4]. Epidemiologic evidence from the Framingham heart study suggests that about one-half of all deaths due to HF occur...

show abstract

“…4 Genetic susceptibility to SCD in the setting of CAD is supported by several epidemiologic studies demonstrating that a family history of SCD is an independent risk factor for SCD and primary VF. 5,6,7 Sympathetic activation, mediated by the β adrenergic receptors β1AR and β2AR, favors the development of ventricular arrhythmias (VA) and SCD. 2,[8][9][10][11][12] Two common nonsynonymous single nucleotide polymorphisms (SNPs) in each of the single-exon β1AR and β2AR genes are observed: β1AR Ser49Gly and Arg389Gly, and β2AR Gly16Arg and Gln27Glu, the latter two of which are in linkage disequilibrium (LD).…”

Section: Introductionmentioning

confidence: 99%