Lipids are indispensable in the SARS-CoV-2 infection process. The clinical significance of plasma lipid profile during COVID-19 has not been rigorously evaluated. We aim to ascertain the association of the plasma lipid profile with SARS-CoV-2 infection clinical evolution. Observational cross-sectional study including 1411 hospitalized patients with COVID-19 and an available standard lipid profile prior (n: 1305) or during hospitalization (n: 297). The usefulness of serum total, LDL, non-HDL and HDL cholesterol to predict the COVID-19 prognosis (severe vs mild) was analysed. Patients with severe COVID-19 evolution had lower HDL cholesterol and higher triglyceride levels before the infection. The lipid profile measured during hospitalization also showed that a severe outcome was associated with lower HDL cholesterol levels and higher triglycerides. HDL cholesterol and triglyceride concentrations were correlated with ferritin and D-dimer levels but not with CRP levels. The presence of atherogenic dyslipidaemia during the infection was strongly and independently associated with a worse COVID-19 infection prognosis. The low HDL cholesterol and high triglyceride concentrations measured before or during hospitalization are strong predictors of a severe course of the disease. The lipid profile should be considered as a sensitive marker of inflammation and should be measured in patients with COVID-19.

Education and cardiovascular disease (CVD) are inversely associated but the mediating factors have not been totally elucidated. Our aim was to analyze the mediating role of modifiable risk factors. Cohort study using the REGICOR population cohorts. Participants without previous CVD were included (n = 9226). Marginal structural models were used to analyze the association between education and CVD incidence at 6 years of follow-up. Mediation by modifiable risk factors (diabetes, dyslipidemia, hypertension, smoking, body mass index, and physical activity) was assessed using the counterfactual framework. Participants with a university degree had a CVD incidence hazard ratio (HR) of 0.51 (95% confidence interval (CI) = 0.30, 0.85), compared to those with primary or lower education. Only hypertension, BMI, and diabetes mediated the association between education and CVD incidence, accounting for 26% of the association (13.9, 6.9, and 5.2%, respectively). Sensitivity analyses showed that hypertension was the strongest mediator (average causal mediation effect [95% CI] = increase of 2170 days free of CVD events [711, 4520]). The association between education and CVD incidence is partially mediated by hypertension, BMI, and diabetes. Interventions to decrease the prevalence of these risk factors could contribute to diminish the CVD inequalities associated with educational level.

Familial hypercholesterolemia (FH), the most frequent hereditary cause of premature coronary heart disease (CHD), is underdiagnosed and insufficiently treated. The objectives of the study were to estimate the prevalence of the FH phenotype (FH-P) and to describe its clinical characteristics in a Mediterranean population. Data were obtained from the Catalan primary care system's clinical records database (Catalan acronym: SIDIAP). Patients aged >7 years with at least 1 low-density lipoprotein cholesterol measurement recorded between 2006 and 2014 (n = 2,554,644) were included. Heterozygous FH-P and homozygous FH-P were defined by untreated low-density lipoprotein cholesterol plasma concentrations. The presence of cardiovascular diseases and risk factors was defined by coded medical records from primary care and hospital discharge databases. The age- and sex-standardized prevalence of heterozygous FH-P and homozygous FH-P were 1/192 individuals and 1/425,774 individuals, respectively. In the group aged 8 to 18 years, 0.46% (95% confidence interval: 0.41-0.52) had FH-P; overall prevalence was 0.58% (95% confidence interval: 0.58-0.60). Among patients with FH-P aged >18 years, cardiovascular disease prevalence was 3.5 times higher than in general population, and CHD prevalence in those aged 35 to 59 years was 4.5 times higher than in those without FH-P. Lipid-lowering therapy was lacking in 13.5% of patients with FH-P, and only 31.6% of men and 22.7 of women were receiving high or very high-intensity lipid-lowering therapy. Prevalence of FH-P was higher than expected, but underdiagnosed and suboptimally treated, especially in women. Moreover, treatment started late considering the high CHD incidence associated with this condition.

Aim: Assessing the effect of statin therapy (ST) at hospital admission for COVID-19 on in-hospital mortality. Methods and results : Retrospective observational study. Patients taking statins were 11 years older and had significantly more comorbidities than patients who were not taking statins. A genetic matching (GM) procedure was performed prior to analysis of the mortality risk. A Cox proportional hazards model was used for the cause-specific hazard (CSH) function, and a competing-risks Fine and Gray (FG) model was also used to study the direct effects of statins on risk. Data from reverse transcription-polymerase chain reaction-confirmed 2157 SARS-CoV-2-infected patients [1234 men, 923 women; age: 67 y/o (IQR 54–78)] admitted to the hospital were retrieved from the clinical records in anonymized manner. Three hundred and fifty-three deaths occurred. Five hundred and eighty-one patients were taking statins. Univariate test after GM showed a significantly lower mortality rate in patients on ST than the matched non-statin group (19.8% vs. 25.4%, χ2 with Yates continuity correction: P = 0.027). The mortality rate was even lower in patients (n = 336) who maintained their statin treatments during hospitalization compared with the GM non-statin group (17.4%; P = 0.045). The Cox model applied to the CSH function [HR = 0.58(CI: 0.39–0.89); P = 0.01] and the competing-risks FG model [HR = 0.60 (CI: 0.39–0.92); P = 0.02] suggest that statins are associated with reduced COVID-19-related mortality. Conclusions : A lower SARS-CoV-2 infection-related mortality was observed in patients treated with ST prior to hospitalization. Statin therapy should not be discontinued due to the global concern of the pandemic or in patients hospitalized for COVID-19.