Hostname: page-component-78c5997874-dh8gc Total loading time: 0 Render date: 2024-11-17T20:16:12.188Z Has data issue: false hasContentIssue false

Endothelial function state following repair of cyanotic congenital heart diseases

Published online by Cambridge University Press:  29 October 2013

Mohammad Reza Sabri
Affiliation:
Child Growth and Development Research Center, Department of Pediatrics, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
Hooman Daryoushi*
Affiliation:
Department of Pediatrics, School of Medicine, Felowship in Pediatric Cardiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
Mojgan Gharipour
Affiliation:
Isfahan Cardiovascular Research Center, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
*
Correspondence to: Dr H. Daryoushi, MD, Department of Pediatrics, School of Medicine, Felowship in Pediatric Cardiology, Isfahan University of Medical Sciences, Isfahan, Iran. E-mail: mojgangharipour@gmail.com

Abstract

Background

Repairing cyanotic congenital heart disease may be associated with preserving endothelial function. The present study aimed to evaluate vascular endothelial function in patients with repaired cyanotic congenital heart disease.

Methods

In a case–control study conducted in 2012 in Isfahan, Iran, 42 consecutive patients aged <35 years who had suffered from different types of cyanotic congenital heart disease and had undergone complete repair of their congenital heart defect were assessed in regard to their endothelial function state by measuring flow-mediated dilatation and other cardiac function indices. They were paired with 42 sex- and age-matched healthy controls.

Results

The mean flow-mediated dilatation was lower in patients with repaired cyanotic congenital heart disease than in the controls [6.14±2.78 versus 8.16±1.49 respectively (p<0.001)]. Significant adverse correlations were found between flow-mediated dilatation, age, and body mass indexes, in those who underwent repair surgery. In addition, flow-mediated dilatation had a positive association with the shortening fraction, ejection fraction, and tricuspid annular plane systolic excursion value, and it was also inversely associated with carotid intima-media thickness and the myocardial performance index. The mean of the flow-mediated dilatation was significantly higher in the group with tetralogy of Fallot along with complete repair before the age of 2.5 years and also in those patients with total anomalous pulmonary venous connection or transposition of the great arteries repaired with an arterial switch operation before 6 months of age, compared with the other two subgroups. This includes patients with a tetralogy of Fallot defect repaired after 4 years of age and those with complex cyanotic congenital heart disease that was repaired after 2.5 years of age (mean age at repair 9±6.1 years).

Conclusion

Early repair of a cyanotic defect can result in the protection of vascular endothelial function and prevent the occurrence of vascular accidents at an older age.

Type
Original Articles
Copyright
Copyright #x00A9; Cambridge University Press 2013 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Herbst, U, Toborek, M, Kaiser, S, Mattson, MP, Hennig, B. 4-Hydroxynonenal induces dysfunction and apoptosis of cultured endothelial cells. J Cell Physiol 1999; 181: 295303.3.0.CO;2-I>CrossRefGoogle ScholarPubMed
2. Gimbrone, MA Jr. Vascular endothelium: an integrator of pathophysiologic stimuli in atherosclerosis. Am J Cardiol 1995; 75: 67B70B.Google Scholar
3. Schachinger, V, Britten, MB, Zeiher, AM. Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease. Circulation 2000; 101: 18991906.Google Scholar
4. Ridker, PM, Stampfer, MJ, Rifai, N. Novel risk factors for systemic atherosclerosis: a comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein(a), and standard cholesterol screening as predictors of peripheral arterial disease. JAMA 2001; 285: 24812485.Google Scholar
5. Anderson, TJ, Uehata, A, Gerhard, MD, et al. Close relation of endothelial function in the human coronary and peripheral circulations. J Am Coll Cardiol 1995; 26: 12351241.Google Scholar
6. Farouque, HM, Meredith, IT. The assessment of endothelial function in humans. Coron Artery Dis 2001; 12: 445454.CrossRefGoogle ScholarPubMed
7. Cordina, RL, Celermajer, DS. Chronic cyanosis and vascular function: implications for patients with cyanotic congenital heart disease. Cardiol Young 2010; 20: 242253.Google Scholar
8. Fichtlscherer, S, Breuer, S, Zeiher, AM. Prognostic value of systemic endothelial dysfunction in patients with acute coronary syndromes: further evidence for the existence of the “vulnerable” patient. Circulation 2004; 110: 19261932.Google Scholar
9. Schachinger, V, Britten, MB, Zeiher, AM. Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease. Circulation 2000; 101: 18991906.Google Scholar
10. Zeineh, NS, Champion, HC. Utility of tricuspid annular plane systolic excursion in the assessment of right ventricular function. PVRI Review 2010; 2: 1721.Google Scholar
11. Kelm, M. Flow-mediated dilatation in human circulation: diagnostic and therapeutic aspects. Am J Physiol Heart Circ Physiol 2002; 282: 15.Google Scholar
12. Anderson, TJ, Meredith, IT, Yeung, AC, et al. The effect of cholesterollowering and antioxidant therapy on endothelium-dependent coronary vasomotion. N Engl J Med 1995; 332: 488493.Google Scholar
13. Anderson, TJ. Assessment and treatment of endothelial dysfunction in humans. J Am Coll Cardiol 1999; 34: 631638.Google Scholar
14. de Groot, PC, Thijssen, D, Binkhorst, M, Green, DJ, Schokking, M, Hopman, MT. Vascular function in children with repaired tetralogy of Fallot. Am J Cardiol 2010; 106: 851855.CrossRefGoogle ScholarPubMed
15. Reriani, MK, Lerman, LO, Lerman, A. Endothelial function as a functional expression of cardiovascular risk factors. Biomark Med 2010; 4: 351360.Google Scholar
16. Walther, C, Gielen, S, Hambrecht, R. The effect of exercise training on endothelial function in cardiovascular disease in humans. Exerc Sport Sci Rev 2004; 32: 129134.Google Scholar
17. Wilcox, JN, Subramanian, RR, Sundell, CL, et al. Expression of multiple isoforms of nitric oxide synthase in normal and atherosclerotic vessels. Arterioscler Thromb Vasc Biol 1997; 17: 24792488.Google Scholar
18. Pou, S, Pou, WS, Bredt, DS, Snyder, SH, Rosen, GM. Generation of superoxide by purified brain nitric oxide synthase. J Biol Chem 1992; 267: 2417324176.Google Scholar
19. Shimokawa, H, Flavahan, NA, Vanhoutte, PM. Loss of endothelial pertussis toxin-sensitive G protein function in atherosclerotic porcine coronary arteries. Circulation 1991; 83: 652660.Google Scholar
20. Wei, Y, Liu, G, Yang, J, Zheng, R, Jiang, L, Bao, P. The association between metabolic syndrome and vascular endothelial dysfunction in adolescents. Exp Ther Med 2013; 5: 16631666.Google Scholar
21. Brili, S, Tousoulis, D, Antonopoulos, AS, et al. Effects of atorvastatin on endothelial function and the expression of proinflammatory cytokines and adhesion molecules in young subjects with successfully repaired coarctation of aorta. Heart 2012; 98: 325329.Google Scholar
22. Pedersen, CM, Schmidt, MR, Mortensen, B, et al. Preserved flow-mediated dilation in adults with cyanotic congenital heart disease. Pediatr Cardiol 2009; 30: 965970.Google Scholar