Right ventricular pressure overload: hemodynamic and proteomic changes

The incidence of congenital heart disease (CHD) is estimated to vary between 4 to 50 per 1000 live births [1, 2] . This wide range of incidence is due to different phenotypes of CHD, as well as the inclusion criteria used. All together, CHD can be seen as the most common birth defect worldwide with approximately 1 million children born with a CHD each year [3]. Epidemiological studies in the Netherlands report an incidence of 6 per 1000 children born with a CHD each year [4]. When looking at causes of infant death, congenital anomalies are the leading cause. One third of these deaths are due to CHD [5]. However, the introduction of modern surgery as well as improved treatment strategies for CHD resulted in a decline in mortality from CHD [6]. In addition, death resulting form CHD shifted from newborns to young adults [7]. Thus, this prolonged survival results in an increase in patients with CHD that need treatment not only at birth, but also during adolescence and even during their adult live. In a selected group of these patients, the structural abnormalities that define a particular CHD phenotype results in prolonged RV pressure overload, such as Tetralogy of Fallot, left hypoplastic heart syndrome or congenitally corrected transposition of the great vessels. In addition, other diseases such as pulmonary hypertension or even ischemic heart disease can result in increased RV loading conditions. The effects of prolonged RV pressure overload on the heart’s function, as well as the effects on molecular and cellular level is not yet fully understood. However, patient data suggest that the RV is unable to cope with prolonged periods of (systemic) overload resulting in RV failure [8-12]. Therefore, it is of utmost importance to understand the effects of prolonged pressure overload on the RV in terms of ventricular function, as well as at the molecular level.

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