Valeria Pergola

Congenital heart disease (CHD) affects approximately one in every one hundred infants worldwide, making it one of the most prevalent birth abnormalities globally. Despite advances in medical technology and treatment choices, CHD remains a significant health issue and necessitates specialized care throughout an individual′s life. Childhood obesity has emerged as a novel global epidemic, becoming a major public health issue, particularly in individuals with lifelong conditions such as CHD. Obesity has profound effects on cardiac hemodynamics and morphology, emphasizing the importance of addressing obesity as a significant risk factor for cardiovascular health. Obesity-induced alterations in cardiac function can have significant implications for cardiovascular health and may contribute to the increased risk of heart-related complications in obese individuals. Moreover, while diastolic dysfunction may be less apparent in obese children compared to adults, certain parameters do indicate changes in early left ventricular relaxation, suggesting that obesity can cause cardiac dysfunction even in pediatric populations. As most children with CHD now survive into adulthood, there is also concern about environmental and behavioral health risk factors in this particular patient group. Addressing obesity in individuals with CHD is essential to optimize their cardiovascular health and overall quality of life. This review aims to succinctly present the data on the impact of obesity on CHD and to enhance awareness of this perilous association among patients, families, and healthcare providers.

Aims Spontaneous coronary artery dissection (SCAD) is an uncommon cause of acute myocardial infarction in women and has an unclear pathophysiology. Autoantibodies (AAs) targeting angiotensin-II receptor type 1 (AT1R) and endothelin-1 receptor type A (ETAR) have known detrimental effects on endothelial function. We investigated the prevalence of these AAs in SCAD-affected female patients. Methods and results Female patients diagnosed at coronary angiography with myocardial infarction and SCAD were consecutively enrolled. Autoantibodies targeting angiotensin-II receptor type 1 and ETAR-AA titres and seropositivity prevalence were compared between SCAD patients, ST-elevation myocardial infarction (STEMI) patients, and healthy women. Ten women with SCAD and 20 age-matched controls (10 women with STEMI and 10 healthy women) were included. Six out of 10 (60%) women with myocardial infarction and SCAD were seropositive for AT1R-AAs and ETAR-AAs. In contrast, only one (10%) healthy woman and one (10%) STEMI patient were seropositive for AT1R-AAs (P = 0.03 and P = 0.03, respectively). One STEMI patient was seropositive for ETAR-AAs, while none of the healthy women was found to be seropositive (P = 0.03 and P = 0.01, respectively). The median AA titre was significantly higher in SCAD patients than in healthy women (P = 0.01 for AT1R-AAs; P = 0.02 for ETAR-AAs) and STEMI patients (P < 0.001 for AT1R-AAs; P = 0.002 for ETAR-AAs). Conclusion Autoantibodies targeting angiotensin-II receptor type 1 and ETAR-AA seropositivity is significantly higher in SCAD women with myocardial infarction than in healthy women or female patients with STEMI. Our findings, corroborated by previous data in the literature and biological plausibility, suggest a possible role for AT1R-AAs and ETAR-AAs in the pathophysiology of SCAD in women with acute myocardial infarction and should warrant further studies with larger sample sizes.