Short QT
2007; Lippincott Williams & Wilkins; Volume: 116; Issue: 7 Linguagem: Albanês
10.1161/circulationaha.107.720896
ISSN1524-4539
AutoresMohan Viswanathan, Richard L. Page,
Tópico(s)ECG Monitoring and Analysis
ResumoHomeCirculationVol. 116, No. 7Short QT Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBShort QTWhen Does It Matter? Mohan N. Viswanathan and Richard L. Page Mohan N. ViswanathanMohan N. Viswanathan From the Division of Cardiology, Department of Medicine, University of Washington School of Medicine, Seattle. and Richard L. PageRichard L. Page From the Division of Cardiology, Department of Medicine, University of Washington School of Medicine, Seattle. Originally published14 Aug 2007https://doi.org/10.1161/CIRCULATIONAHA.107.720896Circulation. 2007;116:686–688For half a century, the relationship between the QT interval and cardiac arrhythmias has been recognized,1 although attention has focused primarily on prolongation of the QT. The congenital long-QT syndrome (LQTS) was first identified in patients with syncope, aborted sudden death, or family history of cardiac arrest as an association between a prolonged QT interval and development of potentially fatal polymorphic ventricular tachycardia (torsade de pointes).2,3 Further research has resulted in the identification of a number of etiologic inherited ion channelopathies, and criteria have been defined to allow diagnosis and evaluation of risk based on the QT interval.4 Only in recent years has attention been paid to short QT intervals with the recent discovery of a familial syndrome characterized by short QT interval and sudden death (the short QT syndrome [SQTS]). In this issue of Circulation, Anttonen et al5 add to our understanding of the frequency of a short QT interval and prognosis in a general population.Article p 714A connection between short QT and sudden cardiac arrest was identified as early as 1993 with an association of increased mortality in patients with both QTc≥440 ms and QTc<400 ms.6 Since that time, the SQTS has been defined,7,8 and 4 ion channel mutations have been associated with a rapid repolarization phase of the cardiac action potential, abbreviated QT interval on 12-lead ECG, and predilection to sudden cardiac death.9–12It may be that formerly "idiopathic" ventricular fibrillation relates to a shortened QT. In 1 study, 35% of men with idiopathic ventricular fibrillation were noted to have short QTc intervals (defined as QTc 12 000 ECGs, recorded for occupational health reasons, defined short QTc as the lowest 0.5%; the shortest QTc observed was 335 ms, and over nearly 8 years there were no deaths in the group with the shortest QTc (although follow-up was available on only 35 of the 65 patients in this cohort).14Anttonen and colleagues5 explore the prevalence of short QT in the general population. They report a retrospective analysis of ECGs from 10 822 randomly selected middle-aged men and women with a mean age of 44 years in which they used the Bazett's, Fridericia, and nomogram methods to compute the QTc. They found, at most (depending on method of correction), a frequency of 0.1% for QTc <320 ms, and 0.4% for QTc <340 ms. There was no difference in the all-cause or cardiovascular mortality between subjects with a very short QTc (<320 ms) or short QTc (<340 ms) and those subjects with a normal QT interval (QTc 360 to 450 ms). In fact, cardiovascular mortality was lower for subjects with a short QT interval (adjusted hazard ratio, 0.71; 95% CI, 0.43 to 1.15) compared with those with a QTc of 360 to 449 ms. However, the event rate was extremely low with only 5 cardiovascular deaths (and no sudden deaths) among those with a QTc 450 ms for adult men and >470 ms for adult women.4 As opposed to a prolonged QT interval, there is no uniformly accepted value for the lower limit of the QTc. However, Viskin et al13 used a value of QTc <360 ms in men and QTc 340 ms.The present study contributes significantly to the literature regarding SQTS. The authors took great care to measure the QT and adjust for heart rate with relevant methodology. The patient population was large (n=10 822) and follow-up was both long (29±10 years) and remarkably complete in Finland's Social Insurance Institution's Coronary Heart Disease Study.20 Limitations persist, however. This is a retrospective study of ECGs obtained on the participating subjects; therefore, conclusions based on these data need to be put into the correct context. Furthermore, generalization of the results is limited because only middle-aged subjects were included (ages 30 to 59 years); reports of familial SQTS include a number of individuals <30 years old, so perhaps some younger patients with short QT did not survive to allow enrollment in the study. Generalization to a more ethnically heterogeneous population may also be difficult because this study included a homogeneous Finnish population from 1966 to 1972. Finally, the small number of subjects with a short QT interval in this population renders the study underpowered to assign prognostic value to an incidental ECG finding of a short QT. For example, there were only 11 subjects with QTc <320 ms, and no sudden death events were reported. This provides little reassurance because the 95% confidence intervals around an incidence of 0 out of 11 would include frequencies that might even allow for prophylactic implantable cardioverter defibrillator implantation.How should we put the findings of the study by Anttonen et al into the context of patient care? The present report5 and earlier literature suggest that a short QT interval on 12-lead ECG does not by itself predict risk of life-threatening arrhythmias but rather should be taken in context of each individual patient. On the other hand, because the present finding is rare, one should consider SQTS in a patient with QT <340 ms and other factors suggestive of arrhythmia (such as syncope or family history of sudden death). As further genetic etiologies for SQTS are identified (with their prevalence evaluated in asymptomatic populations with shorter QT intervals), and testing becomes more uniformly accessible, we can look to a day when we will be able to either easily identify the presence of a high-risk mutation or reassure the patient that the risk is indeed low.The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.DisclosuresDr Viswanathan has no disclosures. Dr Page is a consultant to sanofi-aventis and has been a consultant to Berlex Laboratories and Reliant Pharmaceuticals. He has been a consultant to and received grant support from Procter & Gamble Pharmaceuticals.FootnotesCorrespondence to Dr Richard L. Page, Division of Cardiology, Department of Medicine, Robert A. Bruce Endowed Chair in Cardiovascular Research, University of Washington School of Medicine, 1959 NE Pacific St, Room AA510, HSC, Box 356422, Seattle, WA 98195-6422. E-mail [email protected] References 1 Jervell A, Lange-Nielsen F. Congenital deaf-mutism, functional heart disease with prolongation of the Q-T interval, and sudden death. Am Heart J. 1957; 54: 59–68.CrossrefMedlineGoogle Scholar2 Schwartz PJ. The congenital long QT syndromes from genotype to phenotype: clinical implications. J Intern Med. 2006; 259: 39–47.CrossrefMedlineGoogle Scholar3 Vincent GM, Timothy KW, Leppert M, Keating M. The spectrum of symptoms and QT intervals in carriers of the gene for long QT syndrome. N Engl J Med. 1992; 327: 846–852.CrossrefMedlineGoogle Scholar4 Goldenberg I, Moss AJ, Zareba W. QT interval: how to measure it and what is "normal." 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Acta Med Scand Suppl. 1983; 673: 1–120.MedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Heikhmakhtiar A, Lee C, Song K and Lim K (2020) Computational prediction of the effect of D172N KCNJ2 mutation on ventricular pumping during sinus rhythm and reentry, Medical & Biological Engineering & Computing, 10.1007/s11517-020-02124-w, 58:5, (977-990), Online publication date: 1-May-2020. Kline J and Costantini O (2019) Inherited Cardiac Arrhythmias and Channelopathies, Medical Clinics of North America, 10.1016/j.mcna.2019.05.001, 103:5, (809-820), Online publication date: 1-Sep-2019. 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Hattori T, Makiyama T, Akao M, Ehara E, Ohno S, Iguchi M, Nishio Y, Sasaki K, Itoh H, Yokode M, Kita T, Horie M and Kimura T (2011) A novel gain-of-function KCNJ2 mutation associated with short-QT syndrome impairs inward rectification of Kir2.1 currents, Cardiovascular Research, 10.1093/cvr/cvr329, 93:4, (666-673), Online publication date: 15-Mar-2012. Patel C, Yan G and Antzelevitch C (2010) Short QT Syndrome: From Bench to Bedside, Circulation: Arrhythmia and Electrophysiology, 3:4, (401-408), Online publication date: 1-Aug-2010. August 14, 2007Vol 116, Issue 7 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.107.720896PMID: 17698741 Originally publishedAugust 14, 2007 Keywordstorsade de pointesgeneticsfibrillationepidemiologyelectrocardiographyEditorialsPDF download Advertisement SubjectsElectrocardiology (ECG)ElectrophysiologyEpidemiology
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