Journals / Dokuz Eylül Üniversitesi Tıp Fakültesi Dergisi / 2018 / Cilt: 32 - Sayı: 2

THE RELATIONSHIP BETWEEN LEFT TO RIGHT SHUNTING CONGENITAL HEART DISEASE AND CARDIOTROPHIN-1 IN CHILDREN

Soldan sağa şantlı doğumsal kalp hastalıklı çocuklarda şant miktarı ile kardiyotrofin–1 ilişkisi

Pages
123–130
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Furthermore, it was indicated that the increase in CT-1 was related to the number of shunts in the group having more intracardiac shunts and a higher risk of failure.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: In our study, it was aimed to investigate the interaction of serum cardiotrophin-1 (CT-1) levels in left to right shunting congenital heart disease in children and to evaluate the change of this biomarker with intracardiac defect features.Material and Method: We investigated 45 patients and 23 healthy children between 1 months and 13 years of age in our study.
📊
Key Findings & Data:In the patient group, we identified an atrial septal defect (ASD) in 19 cases, a ventricular septal defect (VSD) in 17 cases, an ASD and VSD (ASD+VSD) in 6 cases and a patent ductus arteriosus (PDA) in 3 cases.
💡
Conclusion & Impact:Furthermore, it was indicated that the increase in CT-1 was related to the number of shunts in the group having more intracardiac shunts and a higher risk of failure.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: In our study, it was aimed to investigate the interaction of serum cardiotrophin-1 (CT-1) levels in left to right shunting congenital heart disease in children and to evaluate the change of this biomarker with intracardiac defect features.Material and Method: We investigated 45 patients and 23 healthy children between 1 months and 13 years of age in our study. In the patient group, we identified an atrial septal defect (ASD) in 19 cases, a ventricular septal defect (VSD) in 17 cases, an ASD and VSD (ASD+VSD) in 6 cases and a patent ductus arteriosus (PDA) in 3 cases. All children underwent a classical echocardiography (twodimensional, M-Mode, two-dimensional Doppler and colour Doppler echocardiography). In all patients, plasma BNP levels were measured by chemiluminescence and CT-1 levels were estimated by enzyme-linked immunosorbent assay (ELISA) method, synchronously with echocardiographic studies. Results: A positive correlation was detected between CT-1 and the number of shunts (p 2) (p<0.001, r=0.71). Conclusion: CT-1 has been found to increase in the group with left to right shunting heart disease. Furthermore, it was indicated that the increase in CT-1 was related to the number of shunts in the group having more intracardiac shunts and a higher risk of failure.

Özet

Amaç: Çalışmamızda çocuklarda soldan sağa şantlı doğumsal kalp hastalıklarında serum kardiyotrofin-1 (CT-1) düzeyleri ile şant miktarının karşılıklı etkileşimlerini araştırmak, bu belirtecin intrakardiyak defekt tipine göre değişimlerini incelemek amaçlanmıştır. Gereç ve Yöntem: Çalışmamızda, 1 ay–13 yaşları arasında, 45 hasta ve 23 sağlıklı çocuk incelendi. Hasta grubu içinde 19 olguda atriyal septal defekt (ASD), 17 olguda ventriküler septal defekt (VSD), 6 olguda ASD ve VSD (ASD+VSD) ve 3 olguda patent duktus arteriyozus (PDA) mevcuttu. Tüm çocuklara konvansiyonel ekokardiyografi incelemesi (iki boyutlu, M-Mode, iki boyutlu Doppler ve renkli Doppler ekokardiyografileri) yapıldı. Tüm olgulardan ekokardiyografi çalışmaları ile eş zamanlı olarak plazma BNP düzeyleri kemilüminisans ve CT-1 düzeyleri de “enzyme-linked immunosorbent assay” (ELISA) yöntemleriyle ölçüldü. Bulgular: Hasta grubunda CT-1 ile şant miktarı arasında (p 2) CT-1 ile EF ve FS arasında negatif korelasyon bulundu (p<0,001, r=0,71). Sonuç: CT-1’in soldan sağa şantlı kalp hastalıkları grubunda yükselmiş olduğu bulundu. Bunun yanı sıra intrakardiyak şantı fazla, kalp yetersizliği riski yüksek olan grupta da CT-1’in şant miktarıyla korele olarak arttığı saptandı. Sonuç olarak CT-1, erişkinlerde olduğu gibi çocuklardaki kalp yetmezliğinin değerlendirilmesinde de kullanılmaya aday bir belirteçtir. Ancak, çocukluk çağında CT-1 ile kalp fonksiyonları arasındaki ilişkiyi ortaya koymak için daha fazla sayıda hastanın incelendiği prospektif çalışmalara ihtiyaç vardır.

🔖

Cite This Article

ÇETİN, B. Ş., KIR, M., ÜNAL, N., KÜME, T., YILMAZ, N. (2018). THE RELATIONSHIP BETWEEN LEFT TO RIGHT SHUNTING CONGENITAL HEART DISEASE AND CARDIOTROPHIN-1 IN CHILDREN. Dokuz Eylül Üniversitesi Tıp Fakültesi Dergisi, Cilt: 32 - Sayı: 2, 123–130. https://ajindex.com/articles/153438

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (9)

  1. Hsu DT, Pearson GD. Heart failure in children: part I: history, etiology, and pathophysiology. Circulation 2009;2(1):63-70.
  2. Kuwahara K, Saito Y, Harada M ve ark. Involvement of cardiotrophin-1 in cardiac myocyte-nonmyocyte interactions during hypertrophy of rat cardiac myocytes in vitro. Circulation. 1999;100(10):1116-24.
  3. Freed DH, Moon MC, Borowiec AM ve ark. Cardiotrophin-1: expression in experimental myocardial infarction and potential role in post-MI wound healing. Mol Cell Biochem. 2003;254:247-56.
  4. Freed DH, Borowiec AM, Angelovska T ve ark. Induction of protein synthesis in cardiac fibroblasts by cardiotrophin-1: integration of multiple signaling pathways. Cardiovasc Res. 2003;60:365- 75. Latchman DS. Cardiotrophin-1 (CT-1): a novel hypertrophic and cardioprotective agent. Int J Exp Pathol. 1999;80:189-196.
  5. Jougasaki M, Tachibana I, Luchner A ve ark. Augmented cardiac cardiotrophin-1 in experimental congestive heart failure. Circulation. 2000;101:14-7. Berezin AE.Prognostication in different heart failure phenotypes: The Role of Circulating Biomarkers. J Circ Biomark. 2016; 16:6. Pennica D, King KL, Shaw KJ ve ark. Expression cloning of cardiotrophin 1, a cytokine that induces cardiac myocyte hypertrophy. Proc Natl Acad Sci USA. 1995;92:1142-46.
  6. Stephanou A, Brar B, Heads R ve ark. Cardiotrophin-1 Induces Heat Shock Protein Accumulation in Cultured Cardiac Cells and Protects them from Stressful Stimuli. J Mol Cell Cardiol. 1998;30:849-55.
  7. Wollert K, Taga T, Saito M ve ark. Cardiotrophin-1 activates a distinct form of cardiac muscle cell hypertrophy. Assembly of sarcomeric units in series VIA gp130/leukemia inhibitory factor receptor-dependent pathways. J Biol Chem. 1996;271:9535-45.
  8. Talwar S, Downie P, Squire I ve ark. An immunoluminometric assay for cardiotrophin-1: a newly identified cytokine is present in normal human plasma and is increased in heart failure. Biochem Biophys Res Commun. 1999;261:567-71 Lorenzo-Almorós A, Tuñón J, Orejas M, Cortés M, Egido J, Lorenzo Ó. Diagnostic approaches for diabetic cardiomyopathy. Cardiovasc Diabetol. 2017;16:28. Tsutamoto T, Asai S, Tanaka T ve ark. Plasma level of cardiotrophin-1 as a prognostic predictor in patients with chronic heart failure. Eur J Heart Fail. 2007;9:1032-7.
  9. Cantinotti M, Giovannini S, Murzi B ve ark. Diagnostic, prognostic and therapeutic relevance of B-type natriuretic hormone and related peptides in children with congenital heart diseases. Clin Chem Lab Med. 2011;49:567-80. Jougasaki M