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Review
. 2014 Jan;10(1):219-27.
doi: 10.1016/j.hfc.2013.09.017.

Heart failure in congenital heart disease: a confluence of acquired and congenital

Affiliations
Review

Heart failure in congenital heart disease: a confluence of acquired and congenital

Akl C Fahed et al. Heart Fail Clin. 2014 Jan.

Abstract

Heart failure (HF) is a common cause of morbidity and mortality in congenital heart disease (CHD), with increasing prevalence because of improved treatment options and outcomes. Genetic factors and acquired postnatal factors in CHD might play a major role in the progression to HF. This article proposes 3 routes that lead to HF in CHD: rare monogenic entities that cause both CHD and HF; severe CHD lesions in which acquired hemodynamic effects of CHD or surgery result in HF; and, most commonly, a combined effect of complex genetics in overlapping pathways and acquired stressors caused by the primary lesion.

Keywords: Adult; Congenital heart disease; Genomics; Heart failure.

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Conflict of interest statement

The authors have no conflicts of interest to disclose

Figures

Figure 1
Figure 1
Schematic of the hypothesized mechanisms linking congenital heart disease with heart failure. We propose three putative routes which lead to HF in ACHD: rare monogenic entities that cause both CHD and HF (middle arrow), severe CHD lesions in which acquired hemodynamic effects of CHD or surgery result in HF (top arrow), and most commonly a combined effect of complex genetics in overlapping pathways and acquired stressors caused by the lesion (bottom arrow).
Figure 2
Figure 2
Current genomic technologies and proposed mechanisms of contribution to the understanding of HF in ADCHD.

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References

    1. Montana E, Khoury MJ, Cragan JD, Sharma S, Dhar P, Fyfe D. Trends and outcomes after prenatal diagnosis of congenital cardiac malformations by fetal echocardiography in a well defined birth population, Atlanta, Georgia, 1990–1994. Journal of the American College of Cardiology. 1996 Dec;28(7):1805–1809. - PubMed
    1. Webb CL, Jenkins KJ, Karpawich PP, et al. Collaborative care for adults with congenital heart disease. Circulation. 2002 May 14;105(19):2318–2323. - PubMed
    1. Greutmann M, Tobler D. Changing epidemiology and mortality in adult congenital heart disease: looking into the future. Future cardiology. 2012 Mar;8(2):171–177. - PubMed
    1. Khairy P, Ionescu-Ittu R, Mackie AS, Abrahamowicz M, Pilote L, Marelli AJ. Changing mortality in congenital heart disease. Journal of the American College of Cardiology. 2010 Sep 28;56(14):1149–1157. - PubMed
    1. Norozi K, Wessel A, Alpers V, et al. Incidence and risk distribution of heart failure in adolescents and adults with congenital heart disease after cardiac surgery. The American journal of cardiology. 2006 Apr 15;97(8):1238–1243. - PubMed