Numerous observational studies have identified a decline in cerebro-/cardiovascular (CV) admissions during  the initial phase of the COVID-19 pandemic. Recent studies and meta-analyses indicated that the overall decrease was smaller than that found in initial studies during the first months of 2020. Two years later we still do not have clear evidence about the potential causes and impacts of the reduction of CV hospitalizations during the COVID-19 pandemic. It has becoming increasingly evident that collateral damage (i.e., incidental damage to the public and patients) from the COVID-19 outbreak is the main underlying cause that at least somewhat reflects the effects of imposed measures such as social distancing and self-isolation. However, a smaller true decline in CV events in the community due to a lack of triggers associated with such acute syndromes cannot be excluded. There is currently indirect epidemiological evidence about the immediate impact that the collateral damage had on excess mortality, but possible late consequences including a rebound increase in CV events are yet to be observed. In the present narrative review, we present the reporting milestones in the literature of the rates of CV admissions and collateral damage during the last 2 years, and discuss all possible factors contributing to the decline in CV hospitalizations during the COVID-19 pandemic. Healthcare systems need to be prepared so that they can cope with the increased hospitalization rates for CV events in the near future.

Purpose: Metabolic and cardiovascular disease prevention starting in childhood is critical for reducing morbidity later in life. In the present study, the association of novel biomarkers with metabolic syndrome (MS) and vascular function/structure indices of early atherosclerosis in children was investigated. Methods: This was a prospective study of 78 children (8–16 years of age) grouped based on the presence or absence of MS. The serum biomarkers investigated included fibroblast growth factor 21 (FGF21), leptin, adiponectin, and insulinlike growth factor binding protein-1 (IGFBP1). Endothelial function and carotid atherosclerosis were assessed based on brachial artery flow-mediated dilation (FMD) and carotid intima-media thickness, respectively. Results: Children with MS (n=12) had higher levels of FGF21 (median [interquartile range]: 128 [76–189] pg/mL vs. 60 [20–98] pg/mL, P=0.003) and leptin (18.1 [11–34.8] pg/mL vs. 7.5 [1.9–16.5] ng/mL, P=0.003), and lower levels of IGFBP1 (1.5 [1.2–2.1] ng/mL vs. 2.3 [1.5–6] ng/mL, P=0.028) compared with children without MS. FMD inversely correlated with FGF21 (Spearman rho= -0.24, P=0.035) and leptin (rho= -0.24, P=0.002) in all children. The best cutoff value of FGF21 levels for MS diagnosis was above 121.3 pg/mL (sensitivity/specificity, 58/86%). Only FGF21 was significantly associated with the presence of MS after adjustment for body mass index, age, and sex (odds ratio per 10 pg/mL increase: 1.10 [95% confidence interval, 1.01–1.22]; P=0.043). Conclusion Increased FGF21 levels were associated with the presence of MS and worse endothelial function in children. Larger studies are needed to evaluate the potential value of FGF21 as a biomarker that could predict future metabolic/cardiovascular disease at an early stage.