Sarcopenia and aortic valve disease.

Valvular heart disease, including calcific or degenerative aortic stenosis (AS), is increasingly prevalent among the older adult population. Over the last few decades, treatment of severe AS has been revolutionised following the development of transcatheter aortic valve replacement (TAVR). Despite improvements in outcomes, older adults with competing comorbidities and geriatric syndromes have suboptimal quality of life outcomes, highlighting the cumulative vulnerability that persists despite valve replacement. Sarcopenia, characterised by loss of muscle strength, mass and function, affects 21%-70% of older adults with AS. Sarcopenia is an independent predictor of short-term and long-term outcomes after TAVR and should be incorporated as a prognostic marker in preprocedural planning. Early diagnosis and treatment of sarcopenia may reduce morbidity and mortality and improve quality of life following TAVR. The adverse effects of sarcopenia can be mitigated through resistance training and optimisation of nutritional status. This is most efficacious when administered before sarcopenia has progressed to advanced stages. Management should be individualised based on the patient's wishes/preferences, care goals and physical capability. Exercise during the preoperative waiting period may be safe and effective in most patients with severe AS. However, future studies are needed to establish the benefits of prehabilitation in improving quality of life outcomes after TAVR procedures.

Calcified Aortic Valve Disease in Patients With Familial Hypercholesterolemia.

Familial hypercholesterolemia (FH) is a rare autosomal gene deficiency disease with increased low-density lipoprotein cholesterol, xanthoma, and premature coronary heart disease. Calcified aortic valve disease (CAVD) is prevalent in FH patients, resulting in adverse events and heavy health care burden. Aortic valve calcification is currently considered an active biological process, which shares several common risk factors with atherosclerosis, including aging, hypertension, dyslipidemia, and so on. Unfortunately, the pathogenesis and therapy of CAVD in FH are still controversial. There is no pharmacological intervention recommended to delay the development of CAVD in FH, and the only effective treatment for severe CAVD is aortic valve replacement. In this review, we summarize the detailed description of the pathophysiology, molecular mechanism, risk factors, and treatment of CAVD in FH patients.

Ultrastructural Pathology of Atherosclerosis, Calcific Aortic Valve Disease, and Bioprosthetic Heart Valve Degeneration: Commonalities and Differences.

Atherosclerosis, calcific aortic valve disease (CAVD), and bioprosthetic heart valve degeneration (alternatively termed structural valve deterioration, SVD) represent three diseases affecting distinct components of the circulatory system and their substitutes, yet sharing multiple risk factors and commonly leading to the extraskeletal calcification. Whereas the histopathology of the mentioned disorders is well-described, their ultrastructural pathology is largely obscure due to the lack of appropriate investigation techniques. Employing an original method for sample preparation and the electron microscopy visualisation of calcified cardiovascular tissues, here we revisited the ultrastructural features of lipid retention, macrophage infiltration, intraplaque/intraleaflet haemorrhage, and calcification which are common or unique for the indicated types of cardiovascular disease. Atherosclerotic plaques were notable for the massive accumulation of lipids in the extracellular matrix (ECM), abundant macrophage content, and pronounced neovascularisation associated with blood leakage and calcium deposition. In contrast, CAVD and SVD generally did not require vasculo- or angiogenesis to occur, instead relying on fatigue-induced ECM degradation and the concurrent migration of immune cells. Unlike native tissues, bioprosthetic heart valves contained numerous specialised macrophages and were not capable of the regeneration that underscores ECM integrity as a pivotal factor for SVD prevention. While atherosclerosis, CAVD, and SVD show similar pathogenesis patterns, these disorders demonstrate considerable ultrastructural differences.

Percutaneous device closure of a large complex aortic root pseudoaneurysm.

Pseudoaneurysm of the aorta is a rare and high-risk complication of native aortic valve endocarditis and can develop following cardiac surgery for aortic valve and root disease. If left untreated, there is a significant risk of aortic wall rupture and fatality. Given the high risk of mortality associated with traditional open surgical repair of aortic pseudoaneurysms, endovascular approach is a potentially favourable alternative. We describe a unique case of a young woman with a large and complex paraprosthetic pseudoaneurysm with multiple communicating fistulae which was successfully percutaneously treated with two occluder devices. In this technically challenging case, a minor but unique procedural complication is also illustrated.

State of the Art Management of Aortic Valve Disease in Ankylosing Spondylitis.

PURPOSE OF REVIEW: Cardiac involvement in patients with ankylosing spondylitis (AS) generally manifests itself as aortic insufficiency, aortitis, disturbance in cardiac conduction, and myocardial dysfunction. We have used a case-based approach to review the current state of the art knowledge regarding the diagnosis and management of aortic valve disease and aortitis in patients with AS. RECENT FINDINGS: The risk for aortic valve disease and aortic valve replacement or repair is significantly higher than in people without AS, and this risk increases with age. Echocardiography, cardiac MRI, and CT can serve as effective tools for screening and follow-up. Surgical repair/replacement remains the mainstay of therapy for aortic insufficiency and aortic dilation, whereas transcatheter-based techniques may be favorable in the setting of aortic stenosis. Aortic valve and atrioventricular conduction abnormalities contribute to overall cardiovascular burden in AS. Optimal timing and therapeutic technique are dependent on assessment of overall risk and serial follow-up.