Volume 5, Number 1—February 1999
Workshop on the Potential Role of Infectious Agents in Cardiovascular Disease and Atherosclerosis
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|EID||Workshop on the Potential Role of Infectious Agents in Cardiovascular Disease and Atherosclerosis. Emerg Infect Dis. 1999;5(1):186-187. https://dx.doi.org/10.3201/eid0501.990131|
|AMA||Workshop on the Potential Role of Infectious Agents in Cardiovascular Disease and Atherosclerosis. Emerging Infectious Diseases. 1999;5(1):186-187. doi:10.3201/eid0501.990131.|
|APA||(1999). Workshop on the Potential Role of Infectious Agents in Cardiovascular Disease and Atherosclerosis. Emerging Infectious Diseases, 5(1), 186-187. https://dx.doi.org/10.3201/eid0501.990131.|
Cardiovascular and cerebrovascular disease currently exact a substantial human and economic toll in the established market economies and are expected to become increasingly more prevalent in developing countries. The noncommunicable nature of coronary artery disease, myocardial infarction, stroke, and atherosclerotic plaques has now been questioned; Chlamydia pneumoniae, human cytomegalovirus, periodontal disease, Helicobacter pylori, and herpes simplex virus-1 have all been associated, to some extent, with these conditions. The strongest evidence links C. pneumoniae, then human cytomegalovirus, to coronary artery disease, but direct causation has not been established. Nevertheless, large antibiotic trials employing broad spectrum macrolides are now in progress, intended to treat C. pneumoniae infection in symptomatic cardiac atherosclerosis. In the future, if even a portion of vascular disease can be prevented with antimicrobial drugs, vaccines, and health education, the public health impact of these findings will be imposing.
To address this global public health issue, the National Center for Infectious Diseases and the National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention (CDC), Atlanta, Georgia, USA, cosponsored a multidisciplinary workshop of invited national and international researchers, clinicians, and state public health officials August 31—September 1, 1998. The workshop had two primary goals: 1) define the basic science and clinical applied research studies required to verify or refute the associations, within the context of other cardiovascular risk factors (emphasizing C. pneumoniae and human cytomegalovirus); 2) outline a preliminary public health strategy (noting the potential involvement of CDC) that will correctly address the role of infection in cardiovascular disease prevention and treatment.
Discussions of reviewed and new data reaffirmed that evidence of causality between any organism and atherothrombotic disease is sufficient neither to establish antibiotic treatment guidelines nor to generate a public health strategy that incorporates infection into the cardiovascular disease paradigm. To change the chronic course of disease, treatment must be specifically directed at the responsible agent and applied to the appropriate stage of pathogenesis in the population at risk. Thus, the pathobiologic interaction between infection, inflammation and free radicals, lipids, genetics, and other cardiovascular risk factors must be clarified with more sensitive, specific, and standardized tools. Reagants and methods must uniformly differentiate past exposure from active infection; they must examine how acute, recurrent, and persistent infection could initiate or aggravate atherosclerosis and acute arterial thrombotic events. Expansion of animal and in vitro models will add valuable information to human treatment trials and to epidemiologic studies that address the multifactorial nature of cardiovascular disease and focus on groups at risk. Laboratory innovations are needed to maximize interpretation of results and evaluate the impact of antimicrobial and non-antimicrobial interventions. Only in this way can a public health plan based upon sound scientific evidence be developed.
The following were among the recommendations of the workshop: 1) the basic epidemiology of C. pneumoniae should be defined, including the prevalence of past and active infection, risk factors for infection and the interaction of these determinants with traditional cardiovascular and cerebrovascular disease risk factors; 2) sensitive and specific diagnostic assays (both new and revised) for laboratory, animal, and clinical studies should be standardized to assess the true long- and short-term effects of infection and intervention; 3) pathobiologically relevant animal and in vitro models should be used to investigate the pathogenesis of single and multiple agents at different stages in the disease process, enhance the standardization of tools, and evaluate interventions; 4) activities should be linked to judicious antimicrobial useexamining baseline knowledge and use of antibiotics in cardiovascular disease, monitoring changes in disease incidence and prevalence with increasing antibiotic prescription, and investigating the effects of treatment on other microbes; 5) a close alliance should be formed between CDC, the National Institutes of Health, and investigators from diverse fields to advance these objectives in a timely fashion, accumulating high quality scientific evidence that will define the true role of infections and inflammation in atherosclerotic disease and the appropriateness of antimicrobial therapy.
For more information on the conference, contact Siobhán O'Connor, Centers for Disease Control and Prevention, 1600 Clifton Rd., NE, Mailstop C12, Atlanta, GA 30333, USA; tel: 404-639-1454; fax: 404-639-3039; e-mail: firstname.lastname@example.org.Cite This Article
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.
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