(A) Normal tricuspid valve. (B) Functional tricuspid regurgitation: enlargement of the right ventricle results in displacement of the papillary muscles and tethering of the tricuspid leaflets. In addition there is dilatation of the tricuspid annulus.
Infective endocarditis in adults with congenital heart disease: Is it time to change our approach to prophylaxis based on new insights into risk prediction? - Figure 1
Endocarditis in congenital heart disease. Left upper panel: schematic drawing of unrepaired tetralogy of Fallot. Right upper panel: repaired tetralogy with a VSD patch and transannular RVOT patch resulting in residual severe pulmonary regurgitation. Left lower panel: after reoperation with implantation of a homograft. Right lower panel: ultrasound image of a patient with repaired tetralogy and homograft endocarditis. The arrows indicate the vegetations on the homograft valve. Ao, aorta; LV, left ventricle; PA, pulmonary artery; RV, right ventricle; RVOT, right ventricular outflow tract; VSD, ventricular septal defect.
Centre: severe calcific aortic stenosis causes pressure overload followed by left ventricular hypertrophy, collagen deposition, relative ischaemia, and diastolic dysfunction with pulmonary congestion.
Left top: transfemoral TAVI with implantation of the Edwards Sapien prosthesis.
Left bottom: transapical TAVI with implantation of the Edwards Sapien prosthesis.
Right top: transfemoral TAVI with implantation of the Medtronic CoreValve prosthesis.
Right bottom: transsubclavian TAVI with implantation of the Medtronic CoreValve prosthesis.
This conceptual framework for the natural history of calcific aortic valve disease illustrates the spectrum of disease from the 'at risk' patient to the patient with end-stage severe symptomatic aortic stenosis. Once aortic sclerosis is detectable, there is an increased risk of cardiovascular events, as shown by deviation of the survival curve (purple line) from the expected event-free survival (light blue line). At the onset of even mild symptoms, survival deviates even more from expected, with a dramatic decline in survival with severe symptomatic aortic stenosis. Aortic valve replacement (AVR) at the onset of early symptoms prevents these late adverse outcomes.
Fluid shear stress, the arterial modelling force! But how does it work?
Schematic representation of the molecular mechanisms activated in response to ischaemia and downstream of VEGFR2 involving Src, PI3-Akt and ANGPTL4, ultimately leading to disruption of VE-cadherin and claudin-5.
A schematic representation of the chameleon-like nature of HDL. In the non-inflammatory state, HDL contains little serum amyloid A (SAA) and promotes cholesterol efflux from macrophages, inhibits the production of reactive oxygen species (ROS) and increases nitric oxide (NO) production from endothelial cells. In the presence of an acute phase response or systemic inflammation the positive acute phase reactant SAA is produced by the liver and other tissues and associates with HDL. In the process of SAA associating with HDL, the HDL proteome is remodelled by reducing cardioprotective proteins associated with HDL. As a result, HDL-mediated cholesterol efflux is reduced, ROS production is stimulated and NO production is decreased, which leads to an enhancement of the inflammatory state.
The cardiovascular overweight paradigm: weight management recommendation should clearly differentiate between the primary prevention in healthy subjects and the secondary outcome prevention in patients with established cardiovascular (CV) disease or an advanced risk profile (*see Table 1 for details). Adapted from Doehner et al.5