AIMS: Influenza infection leads to increased morbidity and mortality in those with heart failure, and individuals with heart failure exhibit reduced antibody responses to influenza vaccine. We hypothesized that patients with heart failure randomized todouble dose (DD) influenza vaccine will mount more vigorous humoral immune responses compared with those given standard dose (SD) vaccine. METHODS AND RESULTS: We randomized 28 heart failure patients to DD (30 μg/strain) or SD (15 μg/strain) influenza vaccine. We assessed antibody production by haemagglutination inhibition assay (reported as log haemagglutination units) prior to, at 2-4 weeks and at 4-6 months following vaccination. Baseline antibody titres between DD (n = 12, mean age 64 ± 10 years) and SD (n = 16, mean age 63 ± 9 years) did not differ significantly. At 2-4 weeks, DD haemagglutination unit changes were significantly higher than those of SD (3.3 vs. 1.6 for A/H3N2, P < 0.001; 1.9 and 1.1 for A/H1N1, P = 0.009; and 1.7 and 1 for B-type, P = 0.02). At 4-6 weeks, there were no differences in titres in any of the virus types between treatment groups and, although titres decreased, levels remained above the seroprotective threshold. CONCLUSIONS: Higher influenza vaccine doses may elicit increased antibody-mediated responses in patients with heart failure; further studies should assess whether clinical outcomes are improved with this strategy.
RCT Entities:
AIMS: Influenza infection leads to increased morbidity and mortality in those with heart failure, and individuals with heart failure exhibit reduced antibody responses to influenza vaccine. We hypothesized that patients with heart failure randomized to double dose (DD) influenza vaccine will mount more vigorous humoral immune responses compared with those given standard dose (SD) vaccine. METHODS AND RESULTS: We randomized 28 heart failurepatients to DD (30 μg/strain) or SD (15 μg/strain) influenza vaccine. We assessed antibody production by haemagglutination inhibition assay (reported as log haemagglutination units) prior to, at 2-4 weeks and at 4-6 months following vaccination. Baseline antibody titres between DD (n = 12, mean age 64 ± 10 years) and SD (n = 16, mean age 63 ± 9 years) did not differ significantly. At 2-4 weeks, DD haemagglutination unit changes were significantly higher than those of SD (3.3 vs. 1.6 for A/H3N2, P < 0.001; 1.9 and 1.1 for A/H1N1, P = 0.009; and 1.7 and 1 for B-type, P = 0.02). At 4-6 weeks, there were no differences in titres in any of the virus types between treatment groups and, although titres decreased, levels remained above the seroprotective threshold. CONCLUSIONS: Higher influenza vaccine doses may elicit increased antibody-mediated responses in patients with heart failure; further studies should assess whether clinical outcomes are improved with this strategy.
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