Lancet: C-reactive protein levels not causal for heart disease
There has been intense interest among researchers during the past decade about whether blood concentrations of C-reactive protein (CRP)—a sensitive indicator of tissue injury inflammation produced by the liver—is a causal factor in heart disease. Study findings published online Dec. 21 in the Lancet negated this supposition.
Earlier studies had suggested that this protein might be as important in the causation of heart attack as are blood cholesterol levels, according to the authors.
In this study of associations of blood levels of CRP with major diseases, John Danesh, FRCP, from the University of Cambridge, England, and 269 other scientists in the Emerging Risk Factors Collaboration (ERFC) combined information from 54 long-term medical surveys comprised of more than 160,000 people in 18 countries.
The researchers demonstrated that CRP concentration is associated with future risk of a wide range of common diseases, including: heart attack, stroke, deaths from various cancers, chronic lung disease, injuries and other conditions.
According to the authors, most of the associations between CRP levels and heart disease were explained, however, by risk factors already known to cause heart disease (e.g., smoking, blood pressure, obesity, cholesterol levels). This finding reduces the likelihood that CRP is a cause of heart disease, they wrote.
"Although our results support the idea that some process related to persistent inflammation is associated with vascular disease and other chronic disorders, most of the association with ischemic vascular disease depends on conventional risk factors and fibrinogen concentration," Danesh and colleagues wrote.
The authors concluded that further large studies are needed to assess other markers of inflammation, as well as their genetic and lifestyle determinants.
"Further work is also needed to assess whether evidence of low-grade inflammation mainly indicates external triggers (e.g., socioeconomic position or infection), insulin resistance, hereditary predisposition, or some combination of such factors," they wrote.
In an accompanying commentary, S. Matthijs Boekholdt, MD, PhD, from the department of cardiology, and John J.P. Kastelein, MD, PhD, chair of vascular medicine at the Academic Medical Center in Amsterdam, said: "One of the prominent topics in this debate is CRP's role in guiding decision-making for the primary prevention of cardiovascular disease.”
“Current guidelines advise the use of established risk factors to quantify an individual's cardiovascular risk,” Boekholdt and Kastelein wrote. “These guidelines recommend that people at high risk should be treated, whereas for people at intermediate risk, additional information should be obtained to guide decision-making. CRP measurement might be valuable in the fine-tuning of the choice of treatment in this specific subgroup... The wealth of data collected by ERFC will be an excellent source for future analyses to more accurately define the role of CRP in clinical decision-making.”
Earlier studies had suggested that this protein might be as important in the causation of heart attack as are blood cholesterol levels, according to the authors.
In this study of associations of blood levels of CRP with major diseases, John Danesh, FRCP, from the University of Cambridge, England, and 269 other scientists in the Emerging Risk Factors Collaboration (ERFC) combined information from 54 long-term medical surveys comprised of more than 160,000 people in 18 countries.
The researchers demonstrated that CRP concentration is associated with future risk of a wide range of common diseases, including: heart attack, stroke, deaths from various cancers, chronic lung disease, injuries and other conditions.
According to the authors, most of the associations between CRP levels and heart disease were explained, however, by risk factors already known to cause heart disease (e.g., smoking, blood pressure, obesity, cholesterol levels). This finding reduces the likelihood that CRP is a cause of heart disease, they wrote.
"Although our results support the idea that some process related to persistent inflammation is associated with vascular disease and other chronic disorders, most of the association with ischemic vascular disease depends on conventional risk factors and fibrinogen concentration," Danesh and colleagues wrote.
The authors concluded that further large studies are needed to assess other markers of inflammation, as well as their genetic and lifestyle determinants.
"Further work is also needed to assess whether evidence of low-grade inflammation mainly indicates external triggers (e.g., socioeconomic position or infection), insulin resistance, hereditary predisposition, or some combination of such factors," they wrote.
In an accompanying commentary, S. Matthijs Boekholdt, MD, PhD, from the department of cardiology, and John J.P. Kastelein, MD, PhD, chair of vascular medicine at the Academic Medical Center in Amsterdam, said: "One of the prominent topics in this debate is CRP's role in guiding decision-making for the primary prevention of cardiovascular disease.”
“Current guidelines advise the use of established risk factors to quantify an individual's cardiovascular risk,” Boekholdt and Kastelein wrote. “These guidelines recommend that people at high risk should be treated, whereas for people at intermediate risk, additional information should be obtained to guide decision-making. CRP measurement might be valuable in the fine-tuning of the choice of treatment in this specific subgroup... The wealth of data collected by ERFC will be an excellent source for future analyses to more accurately define the role of CRP in clinical decision-making.”