Myocardial scar and remodelling predict long-term mortality in severe aortic stenosis beyond 10 years

Aortic stenosis (AS) is characterized by the narrowing of the aortic valve and compensatory myocardial remodelling.1 However, ultimately the left ventricle decompensates, leading to heart failure and death, and intervention is advised for severe AS accompanied by either symptoms or left ventricular (LV) dysfunction.2 Yet, over half of patients receiving aortic valve replacement (AVR) have irreversible myocardial scarring.3 Our multi-centre UK consortium linked pre-operative myocardial scarring, detected by late gadolinium enhancement (LGE) on cardiovascular magnetic resonance (CMR) with increased all-cause and cardiovascular (CV) mortality, regardless of intervention type, after a median of 3.5 years.4 With the integration of machine learning for CMR analysis, we achieve 40% greater precision than human assessment, potentially uncovering patterns obscured by human variability.5 We now examine whether the association of myocardial scar with mortality persists over longer-term follow-up

Myocardial scar and remodelling predict long-term mortality in severe aortic stenosis beyond 10 years

Aortic stenosis (AS) is characterized by the narrowing of the aortic valve and compensatory myocardial remodelling.1 However, ultimately the left ventricle decompensates, leading to heart failure and death, and intervention is advised for severe AS accompanied by either symptoms or left ventricular (LV) dysfunction.2 Yet, over half of patients receiving aortic valve replacement (AVR) have irreversible myocardial scarring.3 Our multi-centre UK consortium linked pre-operative myocardial scarring, detected by late gadolinium enhancement (LGE) on cardiovascular magnetic resonance (CMR) with increased all-cause and cardiovascular (CV) mortality, regardless of intervention type, after a median of 3.5 years.4 With the integration of machine learning for CMR analysis, we achieve 40% greater precision than human assessment, potentially uncovering patterns obscured by human variability.5 We now examine whether the association of myocardial scar with mortality persists over longer-term follow-up.</p

The immune response to infection in the bladder

International audienceThe bladder is continuously protected by passive defences such as a mucus layer, antimicrobial peptides and secretory immunoglobulins; however, these defences are occasionally overcome by invading bacteria that can induce a strong host inflammatory response in the bladder. The urothelium and resident immune cells produce additional defence molecules, cytokines and chemokines, which recruit inflammatory cells to the infected tissue. Resident and recruited immune cells act together to eradicate bacteria from the bladder and to develop lasting immune memory against infection. However, urinary tract infection (UTI) is commonly recurrent, suggesting that the induction of a memory response in the bladder is inadequate to prevent reinfection. Additionally, infection seems to induce long-lasting changes in the urothelium, which can render the tissue more susceptible to future infection. The innate immune response is well-studied in the field of UTI, but considerably less is known about how adaptive immunity develops and how repair mechanisms restore bladder homeostasis following infection. Furthermore, data demonstrate that sex-based differences in immunity affect resolution and infection can lead to tissue remodelling in the bladder following resolution of UTI. To combat the rise in antimicrobial resistance, innovative therapeutic approaches to bladder infection are currently in development. Improving our understanding of how the bladder responds to infection will support the development of improved treatments for UTI, particularly for those at risk of recurrent infection