Cardiovascular events (CVEs), in particular acute coronary syndrome (ACS), complicate the course of a significant number of patients hospitalised for community-acquired pneumonia (CAP) or influenza. Emerging evidence suggests that this increased risk of CVEs could be mitigated by the use of acetylsalicylic acid (aspirin). The ASCAP study investigates whether the addition of aspirin to standard therapy in hospitalised patients with moderate-to-severe CAP or influenza can reduce the incidence of CVEs.

The ASCAP study is a multicentre, double-blind, placebo-controlled randomised trial in 16 university and general hospitals in the Netherlands, in which patients are randomised to acetylsalicylic acid or matching placebo for 90 days. Eligible patients are adults hospitalised for moderate-to-severe CAP or influenza. Patients with antithrombotic or anticoagulant drugs, or those with contraindications for aspirin, are excluded. The primary outcome is the incidence of ACS up to day 180. Secondary outcomes include the incidence of 4-point major adverse cardiovascular events up to day 180, as well as the incidence of major bleeding and clinically relevant non-major bleeding events up to day 90, all-cause mortality up to day 180 and quality of life and societal costs up to day 180. Survival time will be analysed by the log-rank test, stratified for CAP and influenza, with a two-sided alpha of 0.05. Assuming an average baseline ACS risk of 7.5% over 180 days with up to 30% variation across strata, and a 60% hazard reduction due to aspirin, the required sample size to achieve 80% power is 760 patients. Currently, 114 patients are enrolled in the study.

This study is approved by the Medical Ethics Committee Amsterdam UMC (Amsterdam, The Netherlands) under reference number 2023.0741 and registered under EU trial number 2023-504553-12-01 in the EU portal CTIS (Clinical Trials Information System). Results of the study will be published in a peer-reviewed journal.

EU CTIS: 2023-504553-12-01.

Frontotemporal lobar degeneration (FTLD) is the second most common early-onset dementia. Several studies demonstrated that neuroinflammation and iron accumulation occur in FTLD. However, the timing and relevance of these processes and whether these two are merely cause or consequence remains unclear. Elucidating the role is crucial to assess the rationale for using anti-inflammatory therapies in FTLD. Additionally, the process of glymphatic brain clearance has gained attention as a potential contributor in the disease pathophysiology.

In this multimodal biomarker study, we use a combination of ultra-high field (7T) MR, blood and cerebrospinal fluid (CSF) biomarkers to investigate the role of neuroinflammation, iron accumulation and brain clearance in FTLD, and to identify biomarkers to differentiate FTLD-TDP from FTLD-tau. We aim to include 25 patients with probable FTLD-tau, 25 with probable FTLD-TDP and 50 healthy individuals with 50% risk to develop FTLD. We will use several MRI techniques, including magnetic resonance spectroscopy, diffusion weighted spectroscopy and quantitative susceptibility mapping. In addition, we will assess the prevalence of perivascular spaces (PVS) and the mobility of CSF to address glymphatic brain clearance. We will compare quantitative MR markers between patients with FTLD-tau and FTLD-TDP, presymptomatic mutation carriers and healthy controls, and correlate these measures with clinical data and biomarkers in blood and CSF.

We obtained ethical approval from the Medical Ethics Committee Leiden Den Haag Delft (NL78272.058.21). The results will be disseminated through presentations at national and international conferences, open-access peer-reviewed publications, ClinicalTrials.gov and to the public through social media posts and annual newsletters.

NCT06870838; Pre-results.