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QT Dispersion Which Predicts Cardiovascular Adverse Event Risk, Increases In Non Alcoholic Fatty Liver Disease

Alkole Bağlı Olmayan Yağlı Karaciğer Hastalığında, Kardiyovasküler Riskin Öngördürücüsü Olan QT Dağılımı Artmıştır

Journal Name:

  • Abant Tıp Dergisi

Publication Year:

  • 2014

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Abstract (2. Language): 
Objective: Association of cardiovascular morbidity and mortality with (non alcoholic fatty liver disease) NAFLD is increasing rapidly. The QT dispersion (QTd ) and QT corrected dispersion (QTcd) reflects the heterogeneity of ventricular repolarisation.Predicting cardiovascular risk of an increased QTd and QTcd has been shown in various clinical cardiovascular and non cardiovasculer groups, but has not yet been studied in NAFLD patients according to our search of literature. We hypothesised that NAFLD related heart injury may cause myocardial repolarisation abnormalities. Method: Forty five patients admitted to the department of gastroenterology outpatient clinic with the diagnose of NAFLD were included in this study. QT intervals were measured manually from the onset of QRS to the end of the T wave defined as a return to the T–P baseline. Results: We found that QT dispersion (47.8±22.7 vs 22.5±7.5 ms, p<0.001) and QTc values (55.5± 28 vs 23.7±8.7 ms, p<0.001) were significantly higher in biobsy proven NAFLD patients without overt cardiac involvement than in control subjects. Conclusion: Little is known about the possible myocardial repolarisation abnormalities NAFLD which are considered to be a risk factor for developing cardiovascular adverse events. Our study is the first to assess of myocardial repolarisation processes in NAFLD patients. Our result may indicate that prolonged QT dispersion can be a useful noninvasive and simple method of early detection of subclinical cardiac involvement in NAFLD patients.
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Abstract (Original Language): 
Amaç: Alkole bağlı olmayan yağlı karaciğer hastalığı ile kardiyovasküler morbidite ve mortalite arasındaki ilişki hızla artmaktadır. QT dağılımı (QTd) ve düzeltilmiş QT dağılımı (QTdz) ventrikül repolarizasyonunun heterojenitesini göstermektedir. Çeşitli kardiyovasküler hastalığı olan ve olmayan gruplarda artmış QTd ve QTdz’nin artmış kardiyovasküler riski öngördüğü gösterilmiştir. Ancak kaynak araştırmamıza göre, alkole bağlı olmayan yağlı karaciğer hastalığında QTd ve QTdz incelenmemiştir. Alkole bağlı olmayan yağlı karaciğer hastalığında meydana gelen myokardiyal hasar ile repolarizasyonunun anormalliği arasında ilişki olabileceğini varsaydık. Yöntem: Gastroenteroloji polikliniğine başvurmuş ve alkole bağlı olmayan yağlı karaciğer hastalığı tespit edilmiş hastalar çalışmaya alındı.Yaş ve cinsiyet eşleşmesi yapılan sağlıklı kontrol bireyler ile QTd ve QTdz değerleri karşılaştırıldı. Bulgular: Alkole bağlı olmayan yağlı karaciğer hastalığı tespit edilmiş hastalarda QTd (47.8±22.7 vs 22.5±7.5 ms, p<0,001) ve QTc (55.5± 28 vs 23.7±8.7 ms, p<0,001) değerlerinin kontrollerden anlamlı olarak yüksek olduğunu bulduk. Sonuç: Alkole bağlı olmayan yağlı karaciğer hastalığı olan hastalarda oluşan repolarizasyon anormalliği hakkında bilinenler azdır. Uzamış QT dağılımı, alkole bağlı olmayan yağlı karaciğer hastalığında oluşabilecek klinik olarak tespit edilmemiş miyokard tutulumuna bağlı olabilir.
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REFERENCES

References: 

1-Ratziu V, Charlotte F, Heurtier A, Gombert S, Giral P, Bruckert E, Grimaldi A, Capron F, Poynard T. Sampling variability of liver biopsy in nonalcoholic fatty liver disease. Gastroenterology 2005; 128: 1898–906.
2-Bugianesi E. Nonalcoholic fatty liver disease (NAFLD) and cardiac lipotoxicity: Another piece of the puzzle. Hepatology 2008; 47: 2–4.
3-Vuppalanchi R, Chalasani N. Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis: Selected practical issues in their evaluation and management. Hepatology. 2009; 49: 306–17.
4-JC, Molnar J. Usefulness of QT dispersion as an electrocardiographically derived index. Am J Cardiol, 2002; 89: 291–29
5-Barr CS, Naas A, Freeman M, Lang CC, Struthers AD. QT dispersion and sudden unexpected death in chronic heart failure. Lancet 1994; 343: 327–329.
6-Bazett HC. An analysis of the time-relations of electrocardiograms. Heart 2001; 26: 321-31
7-Sevimli S, Arslan S, Gündoğdu F. Carvedilol therapy is associated with improvement in QT dispersion in patients with congestive heart failure. Arch Turk Soc Cardiol 2007; 35:284-288.
8-Glancy JM, Garratt CJ, Woods KI, Bono DP. QT dispersion and mortality after myocardial infarction. Lancet 1995; 345: 945–948.
9-Zabel M, Woosly RL, Franz MR. Is dispersion of ventricular repolarisation rate dependent? PACE 1997; 20(Part I): 2405–2411.
10-Korenblat KM, Fabbrini E, Mohammed BS, Klein S. Liver, muscle, and adipose tissue insulin action is directly related to intrahepatic triglyceride content in obese subjects. Gastroenterology 2008; 134: 1369–75.
11-Korenblat KM, Fabbrini E, Mohammed BS, Klein S. Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity. Proc Natl Acad Sci USA 2009; 106: 15430–5.
12-Salamone F, Bugianesi E. Nonalcoholic fatty liver disease: the hepatic trigger of the metabolic syndrome. J Hepatol 2011; 53: 1146–7.
13-Lautamäki R, Borra R, Iozzo P, Komu M, Lehtimäki T, Salmi M, Jalkanen S, Airaksinen KE, Knuuti J, Parkkola R, Nuutila P. Liver steatosis coexists with myocardial insulin resistance and coronary dysfunction in patients with type 2 diabetes. Am J Physiol Endocrinol Metab 2006; 291: 282–90.
14-Speliotes EK, Massaro JM, Hoffmann U, Vasan RS, Meigs JB, Sahani DV, Hirschhorn JN, O'Donnell CJ, Fox CS. Fatty liver is associated with dyslipidemia and dysglycemia independent of visceral fat: the Framingham Heart Study. Hepatology 2010; 51: 1979–87.
15-Salamone F, Galvano F, Li Volti G. Treating fatty liver for the prevention of cardiovascular diseases. Hepatology 2010; 52: 1174–5.
16-Unger RH, Orci L. Lipotoxic diseases of nonadipose tissues in obesity. IntJ Obes Relat Metab Disord 2000; 24: 28-S32.
17-Boudina S, Abel ED. Diabetic cardiomyopathy revisited. Circulation 2007; 115: 3213-3223.
18-Mantena SK, King AL, Andringa KK, Eccleston HB, Bailey SM. Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol and obesity induced fatty liver diseases. Free Radic Biol Med 2008; 44: 1259–72.
19-Marra F. Nuclear factor-kappaB inhibition and non-alcoholic steatohepatitis: inflammation as a target for therapy. Gut 2008; 57: 570–2.
20-Mellor KM, Ritchie RH, Delbridge LM. Reactive oxygen species and insulinresistant cardiomyopathy. Clin Exp Pharmacol Physiol 2010; 37: 222–8.
21-McGavock JM, Victor RG, Unger RH, Szczepaniak LS. Adiposity of the heart, revisited. Ann Intern Med 2006; 144: 517–24.
22-Neubauer S. The failing heart an engine out of fuel. N Engl J Med 2007; 356: 1140–51.
23-Perseghin G, Lattuada G, De Cobelli F, Esposito A, Belloni E, Ntali G, Ragogna F, Canu T, Scifo P, Del Maschio A, Luzi L. Increased mediastinal fat and impaired left ventricular energy metabolism in young men with newly found fatty liver. Hepatology 2008; 47: 51–8.
24-Szczeklik W, Sokolowska B, Mastalerz L, Miszalski-Jamka T, Musial J. Heart involvement detected by magnetic resonance in a patient with Churg-Strauss syndrome, mimicking severe asthma exacerbation. Allergy. 2010; 65: 1063–1064
25-Somberg JC, Molnar J. Usefulness of QT dispersion as an electrocardiographically derived index. Am J Cardiol 2002; 89: 291–294.

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