Sayed, Ahmed

BACKGROUND: Mortality due to ischemic heart disease (IHD) has declined in countries with high socioeconomic development. Whether these declines extend to other settings, and whether socioeconomic development influences IHD mortality among men and women differently, is unknown. METHODS: We obtained annual data on sex-specific IHD mortality rates for countries/territories in the GBD study (Global Burden of Disease) from 1980 to 2021. The sociodemographic index (SI), a measure of socioeconomic development, was retrieved for each country/territory. Age-adjusted IHD mortality rates were modeled as a smooth function of sex, year, and SI. RESULTS: From 1980 to 2021, IHD mortality rates did not decrease in low SI settings for men or women. In contrast, mortality rates relative to 1980 declined by >25% in average SI settings (age-adjusted mortality per 100 000, 153–107 for women and 218–161 for men) and >50% in high SI settings (age-adjusted mortality per 100 000, 162–69 for women and 258–114 for men). Comparing the 20th versus 80th percentile of SI in 2021 (corresponding to lower versus higher socioeconomic development), mortality rates were 81% higher for men and 111% higher for women living in socioeconomically deprived settings ( P for difference by sex: 0.01), although absolute differences were larger in men. The association of low SI with higher IHD mortality was especially pronounced for mortality attributable to environmental/occupational risk factors (eg, particulate matter air pollution, lead exposure, and extremes of temperature), with mortality rates being 174% higher among women and 199% higher among men. CONCLUSIONS: Across the past 4 decades, low socioeconomic development was associated with no improvement in IHD mortality rates for men or women, in contrast to the large reductions observed in settings with high socioeconomic development. In contemporary settings, socioeconomic deprivation is associated with larger relative excess mortality in women and larger absolute excess mortality in men.

This research analyzes immunological response patterns to SARS-CoV-2 infection in blood and urine in individuals with serum cotinine-confirmed exposure to nicotine. Samples of blood and urine were obtained from a total of 80 patients admitted to hospital within 24 h of admission (tadm), 48 h later (t48h), and 7 days later (t7d) if patients remained hospitalized or at discharge. Serum cotinine above 3.75 ng/mL was deemed as biologically significant exposure to nicotine. Viral load was measured with serum SARS-CoV-2 S-spike protein. Titer of IgG, IgA, and IgM against S- and N-protein assessed specific antiviral responses. Cellular destruction was measured by high mobility group box protein-1 (HMGB-1) serum levels and heat shock protein 60 (Hsp-60). Serum interleukin 6 (IL-6), and ferritin gauged non-specific inflammation. The immunological profile was assessed with O-link. Serum titers of IgA were lower at tadm in smokers vs. nonsmokers (p = 0.0397). IgM at t48h was lower in cotinine-positive individuals (p = 0.0188). IgG did not differ between cotinine-positive and negative individuals. HMGB-1 at admission was elevated in cotinine positive individuals. Patients with positive cotinine did not exhibit increased markers of non-specific inflammation and tissue destruction. The blood immunological profile had distinctive differences at admission (MIC A/B↓), 48 h (CCL19↓, MCP-3↓, CD28↑, CD8↓, IFNγ↓, IL-12↓, GZNB↓, MIC A/B↓) or 7 days (CD28↓) in the cotinine-positive group. The urine immunological profile showed a profile with minimal overlap with blood as the following markers being affected at tadm (CCL20↑, CXCL5↑, CD8↑, IL-12↑, MIC A/B↑, GZNH↑, TNFRS14↑), t48h (CCL20↓, TRAIL↓) and t7d (EGF↑, ADA↑) in patients with a cotinine-positive test. Here, we showed a distinctive immunological profile in hospitalized COVID-19 patients with confirmed exposure to nicotine.