BOSTON — Patients with heart failure do not maintain protective levels of antibody titres following influenza vaccination, leaving this already at-risk population even more vulnerable to influenza-related complications, according to a study presented at the annual scientific meeting of the Heart Failure Society of America.
To determine whether heart failure patients sustain postvaccination influenza seroprotection throughout the flu season, Orly Vardeny, Pharm.D., of the University of Wisconsin at Madison, and colleagues evaluated 62 heart failure patients (median age 57) and 40 healthy controls (median age 49) during the 2006-2007 and 2007-2008 influenza seasons. The investigators measured serum antibody production via hemagglutination inhibition assay before influenza vaccination and 2-4 weeks and 6 months after vaccination, and compared antibody titers to individual vaccine viral strains after flu season to measure the persistence of antibody response.
All participants showed early antibody seroprotection, defined as postvaccination hemagglutination inhibition (HAI) antibody titer greater of at least 40, with similar rates of seroconversion between the heart failure patients and the healthy controls. Antibody titers decreased over time in both groups throughout the influenza season, said Dr. Vardeny. But the decreases observed among the healthy controls did not drop below the threshold of protective levels, whereas those observed in the heart failure patients did, “which made the heart failure patients more susceptible to influenza,” she said.
Specifically, titer levels to the A(H3N2) viral strain fell from a peak of 320 to 60 post season in the healthy controls and from 160 to 30 in the heart failure patients, and titer levels to the A(H1N1) strain fell from 160 to 80 in the healthy controls and from 60 to 30 in the heart failure patients, Dr. Vardeny reported. Titers to the less virulent B-type strain fell similarly in both groups, she noted.
In a study published earlier this year, Dr. Vardeny and her colleagues identified differences in immune responses to influenza vaccination in heart failure patients compared to healthy controls. The investigators determined that patients with heart failure had higher vaccine-induced interleukin-10 concentrations, suggesting a different cytotoxic T-lymphocyte phenotype for vaccine responses, and that heart failure patients mounted a less vigorous antibody immune response to the newest vaccine viral strain than did the healthy controls (J. Card. Fail. 2009;15:368-73).
The findings may help explain the reduced efficacy in heart failure patients of the vaccine targeting the more powerful influenza A strain and they highlight the need for a solution, said Dr. Vardeny. “It's clear that people with heart failure, who are already at risk for influenza-related complications, need better protection against influenza,” she said. Possible solutions that should be considered include higher doses of the vaccine, which might offer season-long seroprotection, or mid-season booster shots, she suggested.
Dr. Vardeny reported having no financial relationships to disclose.