RESUMEN
PURPOSE OF REVIEW: There are over a million adults living with congenital heart disease (CHD) in the USA. There have been improvements in CHD management which have led to an expansion of the adult congenital heart disease (ACHD) population. There is a high prevalence of atherosclerotic cardiovascular disease (ASCVD) encountered in the aging ACHD population. This review focuses on the most recent literature regarding the primary prevention of ASCVD in young ACHD patients. RECENT FINDINGS: There are unique considerations for ASCVD risk reduction in ACHD patients. ASCVD may be as prevalent in ACHD compared in the general population. However, there may be a perceived shorter life expectancy in ACHD patients; therefore, primary prevention of ASCVD may not be considered important. Preventative strategies for ASCVD are underutilized in ACHD patients. As these patients are followed for a lifetime by cardiologists, we can truly pursue primary prevention in this aging population.
Asunto(s)
Aterosclerosis , Enfermedades Cardiovasculares , Cardiopatías Congénitas , Adulto , Anciano , Aterosclerosis/prevención & control , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/etiología , Enfermedades Cardiovasculares/prevención & control , Cardiopatías Congénitas/complicaciones , Cardiopatías Congénitas/epidemiología , Humanos , Prevalencia , Factores de Riesgo , Adulto JovenRESUMEN
PURPOSE OF REVIEW: The right ventricle (RV) and left ventricle (LV) have different developmental origins, which likely plays a role in their chamber-specific response to physiological and pathological stress. RV dysfunction is encountered frequently in patients with congenital heart disease (CHD) and right heart abnormalities emerge from different causes than increased afterload alone as is observed in RV dysfunction due to pulmonary hypertension (PH). In this review, we describe the developmental, structural, and functional differences between ventricles while highlighting emerging therapies for RV dysfunction. RECENT FINDINGS: There are new insights into the role of fibrosis, inflammation, myocyte contraction, and mitochondrial dynamics in the pathogenesis of RV dysfunction. We discuss the current state of therapies that may potentially improve RV function in both experimental and clinical trials. A clearer understanding of the differences in molecular alterations in the RV compared to the LV may allow for the development of better therapies that treat RV dysfunction.