Kronik sigara içiciliğinin EKG parametrelerine etkileri

Amaç: Mevcut çalışmada Tp-e/QT, Tp-e/QTc oranları ve Tp-e aralığı, kullanılarak kronik sigara içiciliğinin ventriküler repolarizasyon ve EKG parametreleri üzerine kronik etkisini araştırmayı amaçladık. Yöntem: Kesitsel tanımlayıcı desendeki çalışma hastane kayıtları üzerinden yürütülmüştür. Kronik sigara içen ve hiç sigara içmemiş 60’ar toplam 120 hasta çalışmaya alınmıştır. EKG’ler 25mm/sn kayıt hızı ile çekilmiştir. Tp-e aralığı, T dalgasının tepesinden sonuna kadarki süre, QT aralığı ise Q dalga başlangıcından T dalga sonuna kadar geçen süredir. EKG ölçümleri, ölçüm hatalarını azaltmak için iki araştırmacı tarafından büyüteç kullanılarak manuel olarak yapılmıştır. Ölçümlerde DII derivasyonu kullanılmıştır. Bulgular: Sigara içenlerde Tp-e/QT, Tp-e/QTc değerleri ve Tp-e aralığı daha yüksektir. Nabız, PR aralığı, QRS, QT, QTc, RV5, SV1 ve RV5+SV1 değerleri arasında anlamlı fark yoktur. Paket/yıl değeri, Tp-e aralığı, Tp-e/QT ve Tp-e/QTc değerlerinin her üçünü de etkileyen bir faktör olarak bulunmuştur. Sonuç: Sigara içenlerde Tp-e aralığı, Tp-e/QT ve Tp-e/QTc değerleri daha yüksektir. Ayrıca içilen sigara miktarı (paket/yıl) bu değerlerin artmasını sağlayan anlamlı bir faktör olduğu gösterilmiştir.

Effects of chronic smoking on ECG parameters

Objectives: We aimed to investigate the effect of chronic smoking on ventricular repolarization and ECG parameters by using Tp-e/QT, Tp-e/QTc, and Tp-e intervals. Methods: This cross-sectional descriptive study was conducted on hospital registrations. A total of 120 patients, 60 of whom were chronic smokers and 60 were never smoked, were included in the study. ECGs were taken with a recording speed of 25 mm/sec. The Tp-e is the time from the peak of the T wave to the end of the T wave. The time from the beginning of the Q wave to the end of the T wave is the QT interval. ECG measurements were made manually by two researchers using a magnifying glass to reduce measurement errors. Measurements were made using the DII lead. Results: Tp-e/QT, Tp-e/QTc, and Tp-e were found to be higher in smokers than in non-smokers. There wasn’t difference between heart rate, PR interval, QRS, QT, QTc, RV5, SV1 and RV5+SV1 values. The package/year value was found to be a factor affecting all three of the Tp-e interval, Tp-e/QT and Tp-e/QTc values. Conclusion: Tp-e/QT, Tp-e/QTc values, and Tp-e interval were found to be higher in smokers than in non-smokers. The number of cigarettes smoked (pack/year) has been shown to be a significant factor that increases these values.

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  • 1. Walton K, Wang TW, Schauer GL, et al. State-specific prevalence of quit attempts among adult cigarette smokers - United States, 2011-2017. MMWR Morb Mortal Wkly Rep 2019;68(28):621-6.
  • 2. Heart Disease and Stroke, Smoking & Tobacco Use, CDC. https://www.cdc.gov/tobacco/basic_information/health_effects/heart_disease/index.htm. Accessed on Jan 10, 2022.
  • 3. Taşolar H, Balli M, Bayramoğlu A, et al. Effect of smoking on Tp-e interval, Tp-e/QT and Tp-e/QTc ratios as indices of ventricular arrhythmogenesis. Hear Lung Circ 2014;23(9):827-32.
  • 4. Ilgenli TF, Tokatli A, Akpinar O, Kiliçaslan F. The effects of cigarette smoking on the Tp-e interval, Tp-e/QT ratio and Tp-e/QTc ratio. Adv Clin Exp Med 2015;24(6):973-8.
  • 5. D’Alessandro A, Boeckelmann I, Hammwhöner M, Goette A. Nicotine, cigarette smoking and cardiac arrhythmia: an overview. Eur J Prev Cardiol 2012;19(3):297-305.
  • 6. Gupta P, Patel C, Patel H, et al. T(p-e)/QT ratio as an index of arrhythmogenesis. J Electrocardiol 2008;41(6):567-74.
  • 7. Kors JA, RitsemavanEck HJ, vanHerpen G. The meaning of the Tp-Te interval and its diagnostic value. J Electrocardiol 2008;41(6):575-80.
  • 8. Erikssen G, Liestøl K, Gullestad L, Haugaa KH, Bendz B, Amlie JP. The terminal part of the QT interval (T peak to T end): a predictor of mortality after acute myocardial infarction. Ann Noninvasive Electrocardiol 2012;17(2):85-94.
  • 9. Smokerlyzer ® Range for use with piCO, piCO baby and Micro +, user manual. https://www.bedfont.com/documents/smokerlyzer-manual.pdf. Accessed on 17 Apr, 2021.
  • 10. Ulubay G, Dilektaşlı AG, Börekçi Ş, et al. Turkish Thoracic Society Consensus report: interpretation of spirometry. Turkish Thorac J 2019;20(1):69-89.
  • 11. Tanaka T, Yahagi K, Asami M, et al. Prognostic impact of electrocardiographic left ventricular hypertrophy following transcatheter aortic valve replacement. J Cardiol 2021;77(4):346-52.
  • 12. Ip M, Diamantakos E, Haptonstall K, et al. Tobacco and electronic cigarettes adversely impact ECG indexes of ventricular repolarization: implication for sudden death risk. Am J Physiol Heart Circ Physiol 2020;318(5):1176-84.
  • 13. Wang H, Shi H, Zhang L, et al. Nicotine is a potent blocker of the cardiac A-type K(+) channels. Effects on cloned Kv4.3 channels and native transient out ward current. Circulation 2000;102(10):1165-71.
  • 14. Yashima M, Ohara T, Cao JM, et al. Nicotine increases ventricular vulnerability to fibrillation in hearts with healed myocardial infarction. Am J Physiol Heart Circ Physiol 2000;278(6):2124-33.
  • 15. Mehta MC, Jain AC, Mehta A, Billie M. Cardiac arrhythmias following intravenous nicotine: experimental study in dogs. J Cardiovasc Pharmacol Ther 1997;2(4):291-8.
  • 16. Zareba KM, Truong VT, Mazur W, et al. T-wave and its association with myocardial fibrosis on cardiovascular magnetic resonance examination. Ann Noninvasive Electrocardiol 2021;26(2):e12819.
  • 17. Leone A. Biochemical markers of cardiovascular damage from tobacco smoke. Curr Pharm Des 2005;11(17):2199-208.
  • 18. Skipina TM, Upadhya B, Soliman EZ. Exposure to secondhand smoke is associated with increased left ventricular mass. Tob Induc Dis 2021;19:43.
Troia Tıp Dergisi-Cover
  • ISSN: 2630-6107
  • Yayın Aralığı: Yılda 3 Sayı
  • Başlangıç: 2019
  • Yayıncı: Çanakkale Onsekiz Mart Üniversitesi