The care pathway for patients with atrial fibrillation (AF) is variable and this variability is explored in a patient pathway review. This review describes events that may take place for a patient with AF considering the “ideal” and the “real-world” pathway and attempts to rationalize them by considering the patient, clinician, health service, and societal perspective. In the “ideal” pathway, AF in a patient is either identify before or after stroke. The “real-world” pathway introduces the concepts that symptoms may influence patient decision-making to seek help, AF may be identified incidentally, and healthcare professionals may fail to identify AF. The management of AF includes no treatment or treatment such as stroke prevention, rate or rhythm control, and comorbidity management. The overall outcomes for patient depend on the presence of symptoms and response to therapies. The two major priorities for patients are symptomatic relief and avoidance of stroke. While most clinicians will find that initial AF management is not challenging but there may be incidental opportunities for earlier identification. From the healthcare service perspective, noncardiologists and cardiologists care for patients with AF, which results in much heterogeneity management. From the societal perspective, the burden of AF is significant resulting in substantial cost from hospitalizations and treatments. People with AF can take on different paths, which depend on factors related to the patient’s decision-making, clinical decision-making, and patient’s response to the treatment. A streamlined approach to a holistic and integrated care pathway approach to AF management is needed.
Among individuals with new-onset AF, favourable survival was observed for patients receiving rhythm control treatment. Among different rhythm control strategies, pulmonary vein isolation showed the most pronounced survival benefit.
Lipoprotein(a) [Lp(a)] is a circulating plasma lipoprotein with structural similarities to low-density lipoprotein (LDL), distinguished by the addition of apolipoprotein(a) to the LDL structure. Lp(a) levels are approximately 80% genetically determined, and distinct components of this complex particle are thought to confer atherogenic, inflammatory, and antifibrinolytic properties contributing to cardiovascular risk. A growing body of evidence has shown a causal association between elevated Lp(a) levels and both atherosclerotic cardiovascular disease (ASCVD) and valvular aortic stenosis. However, the link with venous thromboembolism (VTE) (encompassing deep vein thrombosis [DVT] and pulmonary embolism [PE]) has been less clear. Although <i>in vitro</i> studies suggest antifibrinolytic and prothrombotic properties for Lp(a), clinical and genetic studies have yielded inconsistent results related to thrombogenicity, with some studies suggesting an association with VTE only with very high Lp(a) levels. The effect of Lp(a) levels on outcomes in patients with incident VTE has not been comprehensively investigated. Although there are currently no approved therapies specifically targeting Lp(a) reduction, at least five agents are in development, with preliminary data demonstrating reductions in Lp(a) levels of up to 98%. The impact of these therapies on VTE events remains unknown. In turn, other lipid-modifying agents, which have no effect on reducing Lp(a), such as statins, were shown to reduce incident VTE. This review summarizes the current evidence regarding the association between Lp(a) and VTE, focusing on its pathophysiology and critically analyzing the existing evidence from experimental, epidemiological, and genetic studies.
In the BOREALIS trial, the risk of adjudicated stroke/SE, major bleedings, and all-cause death was not related to mild-moderate follow-up changes in kidney function (±30 mL/min). The risk of all-cause death was significantly increased in AF patients with abruptly deteriorating kidney function.