Premium
Response to D r. S trandberg et al
Author(s) -
Matheï Catharina,
Vaes Bert,
Wallemacq Pierre,
Degryse JeanMarie
Publication year - 2012
Publication title -
journal of the american geriatrics society
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.992
H-Index - 232
eISSN - 1532-5415
pISSN - 0002-8614
DOI - 10.1111/j.1532-5415.2012.04003.x
Subject(s) - medicine , cohort , disease , comorbidity , pathogenesis , cohort study , cytomegalovirus , serology , population , immunology , viral disease , virus , herpesviridae , antibody , environmental health
To the Editor: We are grateful to Dr. Strandberg and colleagues for their interest in our article that prompted them to analyze more baseline data of the associations between cytomegalovirus (CMV) serology, functional performance, comorbidity, and health-related quality of life (HRQoL) in their cohort with a mean age of 80. We agree that the apparent lack of association between functional impairment and frailty and CMV serology in our Belfrail cohort with a mean age of 84 may be the result of selection (survival), with many of the participants representing a specific phenotype that is less susceptible to the long-term deleterious effects of CMV. Consistent with our hypothesis, we would indeed expect similar findings in other equally old populations. To the contrary, in the cohort of Strandberg and colleagues, higher baseline CMV titers were associated with more functional impairment, comparable with findings in younger populations, but their cohort represents a select population of home-dwelling older persons with a history of stable cardiovascular disease. The findings of two recent meta-analyses strongly suggest that CMV infection is associated with a higher risk of cardiovascular morbidity and mortality. There are several plausible mechanisms by which CMV might play a role in the pathogenesis of cardiovascular disease. CMV is able to establish persistent infection in endothelial cells and to cause vascular damage. CMV is also associated with chronic systemic low-grade inflammation, which may also contribute to endothelial damage and the atherosclerotic process. For these reasons, CMV may play an important role in the pathogenesis of cardiovascular disease. In light of this, it seems likely that, in many of the individuals in Strandberg and colleagues’ cohort, CMV was involved in the development of their cardiovascular disease. Therefore, it is possible that, in their study, individuals susceptible to the detrimental long-term effects of CMV, but only to the extent that it did not prevent them from reaching an advanced age, are overrepresented. In our opinion, the contrasting findings between Strandberg and colleagues’ and ours are illustrative of the heterogeneity of the CMV-seropositive older adult population. Further research is required to better understand this heterogeneity.