Levels of IL-6 in community-dwelling participants were associated with the development of HFpEF, independent of iron deficiency, anemia, and FGF23 upregulation.
This combined cohort study suggested that IL-6 and hs-CRP levels were associated with HF hospitalization and adverse outcomes in patients with AF. The risk for HF hospitalization increased with increasing inflammation scores of both inflammation markers.
ACC 2021 The phase 2 RESCUE trial showed that the IL-6 inhibitor ziltivekimab largely reduced hsCRP and other biomarkers of inflammation and thrombosis in patients with CKD and ≥2 mg/L hsCRP.
A meta-analysis of 5 trials showed that colchicine reduced MACE by 25% compared to placebo or no colchicine with a low between-trial heterogeneity in a wide range of patients with coronary disease.
From CANTOS to COLCOT to COPS to LoDoCo2: What are the lessons from these trials with anti-inflammatory treatment, in particular those with colchicine, in patients with residual inflammatory risk?
A subanalysis of COLCOT showed that initiation of colchicine within the first 3 days after MI significantly reduced the risk of an ischemic CV event compared to patients on placebo.
This position paper discusses the cause and consequences of endothelial injury and dysfunction in COVID-19.
This viewpoint article in JAMA reviews the latest findings on the risk of heart failure, particularly HFpEF, in those who developed acute COVID-19 and those who have recovered from the illness.
An analysis of the CANTOS trial showed that IL-1β inhibition with canakinumab reduced total number of serious CV events compared to placebo in patients with prior MI and subclinical inflammation.
Investigators of the LoDoCo2 trial present the design and the major findings of this trial which evaluated colchicine in patients with chronic coronary disease.
Elevated Lp(a) levels were associated with greater risk of MACE in optimally treated patients with high-risk vascular disease when hsCRP levels ≥2 mg/L, but not in those with hsCRP levels <2 mg/L.
Elevated Lp(a) contributes to pro-inflammatory gene expression of monocytes in both healthy subjects and CVD patients. Potent Lp(a)-lowering reduced the pro-inflammatory state of circulating monocytes.