Infective endocarditis in adult patients with congenital heart disease

Congenital heart disease plus infective endocarditis: complexity squared, but what is the outcome?

“…In their ACHD population, that resembles the complexity of patient load in a tertiary centre, the first notable finding is that the 1-year mortality rate reported by Verzelloni Sef et al is considerably lower than the mortality reported in a previous international substudy from the EURO-ENDO registry [2] (7.3% vs 12.9%, respectively). Several reasons for this discrepancy come to mind.…”

“…The satisfactory results for conservative treatment found by Verzelloni Sef et al in patients with PVE and/or moderate and complex ACHD IE highlights the importance for further research on indications for surgery in this specific subgroup. However, we want to emphasize that renouncement of indicated surgical treatment in CHD patients with IE is an independent risk factor for all-cause mortality [2]. Lastly, the relatively low prevalence of cardiac abscesses (11.9%), which is regarded to be an independent risk factor for mortality, may suggest limited extensiveness of IE in their cohort and may have resulted in lower mortality rates.…”

Discovery and functional investigation of BMP4 as a new causative gene for human congenital heart disease

“…As an array of cardiovascular developmental deformations, CHD is clinically categorized into > 30 distinct isoforms, encompassing double-outlet right ventricle (DORV) and ventricular septal defect (VSD) [2,[7][8][9][10][11][12][13][14]. Though certain mild/minor forms of CHD may resolve spontaneously [2], severe/complex forms of CHD usually lead to worse quality of life [15][16][17], reduced exercise performance [18][19][20][21], neurodevelopmental delay and structural brain anomaly [22][23][24][25][26], ischemic/thromboembolic stroke [27,28], acute renal injury/chronic kidney disease [29][30][31][32], hepatic fibrosis [33,34], pulmonary dysplasia/ pulmonary arterial hypertension [35][36][37], bacte-Am J Transl Res 2024;16 (5):2034-2048 rial endocarditis [38][39][40][41][42], chronic heart failure [43][44][45], supraventricular/ventricular arrhythmias [46][47]…”

Discovery of BMP10 as a new gene underpinning congenital heart defects

“…As a vast collection of cardiovascular developmental anomalies, CHD is clinically assorted to >26 diverse isoforms, including patent ductus arteriosus (PDA), aortic/pulmonary atresia, aortic/pulmonary stenosis, aortic coarctation, aortopulmonary window, atrial/ ventricular septal defect, tetralogy of Fallot (the Am J Transl Res 2024;16(1):109-125 commonest cyanotic CHD), atrioventricular septal defect, single ventricle, endocardial cushion defect, transposition of the major arteries, double outlet right ventricle, aortic arch interruption, abnormal coronary artery connection, cor triatriatum, and left heart hypoplasia/left ventricular noncompaction/spongy myocardium [2,[6][7][8][9][10][11]. Though some minor types of CHD do resolve spontaneously [2], severe types of CHD may give rise to degraded health-correlated quality of life [12][13][14][15], impaired exercise capacity [16][17][18], pulmonary arterial hypertension [19][20][21], acute brain injury and delayed neurodevelopment [22][23][24][25], thromboembolic/ischemic cerebral stroke [26][27][28], acute renal injury and chronic kidney disease [29][30][31], liver fibrosis and dysfunction [32], infective endocarditis [33][34][35][36][37], chronic/congestive heart failure [38][39][40], miscellaneous supraventricular and life-threatening ventricular dysrhythmias [41]…”