ArticleHeart rhythm2012
Torsades de pointes following acute myocardial infarction: evidence for a deadly link with a common genetic variant.
Article in Heart rhythm, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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17 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Variability in reported midpoints of (in)activation of cardiac INa.The Journal of general physiology · 2025Pooled it
- Factors associated with clinically diagnosed long QT syndrome in Korean adults: a nationwide case-control study.Frontiers in pharmacology · 2026Article
- Genetic Background and Clinical Phenotype in an Italian Cohort with Inherited Arrhythmia Syndromes and Arrhythmogenic Cardiomyopathy (ACM): A Whole-Exome Sequencing Study.International journal of molecular sciences · 2025Article
- Acquired Long QT Syndrome after Acute Myocardial Infarction: A Rare but Potentially Fatal Entity.Texas Heart Institute journal · 2020Article
- Modifier genes for sudden cardiac death.European heart journal · 2018Review
- Classification and Reporting of Potentially Proarrhythmic Common Genetic Variation in Long QT Syndrome Genetic Testing.Circulation · 2018Review
- Medico-legal perspectives on sudden cardiac death in young athletes.International journal of legal medicine · 2017Review
- Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction.Journal of geriatric cardiology : JGC · 2016Review
- Management of survivors of cardiac arrest - the importance of genetic investigation.Nature reviews. Cardiology · 2016Review
- Post-mortem whole-exome sequencing (WES) with a focus on cardiac disease-associated genes in five young sudden unexplained death (SUD) cases.International journal of legal medicine · 2016Article
- A Clinical Perspective on Sudden Cardiac Death.Arrhythmia & electrophysiology review · 2016Article
- Control of cardiac repolarization by phosphoinositide 3-kinase signaling to ion channels.Circulation research · 2015Review
- Genetics of sudden cardiac death caused by ventricular arrhythmias.Nature reviews. Cardiology · 2014Review
- Nav 1.5 mutations linked to dilated cardiomyopathy phenotypes: Is the gating pore current the missing link?Channels (Austin, Tex.) · 2014Article
- Methadone, QTc interval prolongation and torsade de pointes: Case reports offer the best understanding of this problem.Therapeutic advances in psychopharmacology · 2013Article
- Molecular and genetic basis of sudden cardiac death.The Journal of clinical investigation · 2013Review
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13 authors at 5 institutions in 6 countries.
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Abstract
backgroundAlthough QT prolongation following myocardial infarction (MI) is generally moderate, cases with marked QT prolongation leading to life-threatening torsades de pointes (TdP) have been described.
objectiveTo investigate the genetic substrate of this phenomenon.
methodsWe studied 13 patients who developed TdP in the subacute phase of MI (2-11 days) and a group of 133 ethnically matched controls with uncomplicated MI. Long QT syndrome genes and the KCNH2-K897T polymorphism were screened by using denaturing high-performance liquid chromatography plus direct sequencing and a specific TaqMan assay, respectively.
resultsTwo of the 13 patients (15%) who presented with QT prolongation and TdP were found to carry long QT syndrome mutations (KCNH2-R744X and SCN5A-E446K). Nine of the remaining 11 patients (82%) carried the KCNH2-K897T polymorphism, which was present in 35% of the controls (P = .0035). Thus, patients with an acute MI carrying the KCNH2-K897T polymorphism had an 8-fold greater risk of experiencing TdP compared with controls (95% confidence interval = 2-40).
conclusionsOur data suggest that the common K897T polymorphism is associated with an increased risk of TdP developing in the subacute phase of MI. Our findings support the concept that the electrical remodeling associated with this healing phase of MI may unmask a genetic substrate predisposing to a time-limited development of life-threatening arrhythmias. They also provide the first line of evidence in support of the hypothesis that a common polymorphism, previously described as a modifier of the severity of LQTS, may increase the risk of life-threatening arrhythmias in a much more prevalent cardiac disease such as myocardial infarction.
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