Impaired SARS-CoV-2 vaccine responsiveness is not associated with subclinical atherosclerosis or cardiovascular disease

TL;DR

This study found that subclinical atherosclerosis or cardiovascular disease does not impair SARS-CoV-2 vaccine responses in older adults.

Contribution

The study provides novel evidence that atherosclerosis or CVD is not linked to reduced vaccine immunity in older individuals.

Findings

No significant association found between atherosclerosis and SARS-CoV-2 vaccine-specific IgG or T cells.

Vaccine immunity was inversely correlated with several plasma cytokines, not lipid levels.

Results suggest subclinical atherosclerosis does not impair vaccine responsiveness in older adults.

Abstract

Although age-related immune deterioration has been implicated as a mechanistic contributor to cardiovascular disease (CVD), evidence for an impairment of adaptive immune function in individuals with clinically verified presence of atherosclerosis is lacking.

To test the association between atherosclerosis and immune function, we evaluated SARS-CoV-2 vaccine responsiveness in 65- to 71-year-old individuals (n = 644) derived from a population-based cohort, characterized for subclinical atherosclerosis by coronary computed tomography angiography and carotid ultrasound. Vaccine-specific T cells were quantified by activation-induced marker assays and antibody responses by ELISA. We did not find any significant associations between the degree of subclinical atherosclerosis or history of cardiovascular disease and vaccine-specific IgG or T cells. Vaccine immunity was not associated with lipid levels but was inversely correlated with several plasma cytokines.

Our study demonstrates that subclinical atherosclerosis or prevalent CVD is not associated with impaired responsiveness to vaccination.

Graphical Abstract

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