High C-reactive protein levels have been linked to a higher risk for heart disease, and levels vary according to people’s ancestry, researchers have revealed in a study published in the American Heart Association journal Circulation: Cardiovascular Genetics. The authors explain that how doctors determine statin treatment may be impacted by patients’ C-reactive protein values.
C-reactive protein is found in blood; its levels rise in response to inflammation. It is synthesized by the liver in response to factors released by adipocytes (fat cells). Experts say that even though high C-reactive protein (CRP) blood levels have been associated with a greater chance of developing heart disease, the link is uncertain if the association is casual. Researchers are not sure whether the CRP-lowering effects of statins have any health benefits. Statins are medications which are known to lower cholesterol and CRP levels.
A consensus statement from the American Heart Association and Centers for Disease Control, says:
CRP may be used at the discretion of the physician as part of a global coronary risk assessment in adults without known cardiovascular disease.
Anything above a CRP value cut-point of 3mg/L indicates high risk.
Researchers evaluated statin efficacy using a risk cut-point for CRP at values over 2mg/L in a recent study called JUPITER (Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin). Based on those findings the FDA (Food and Drug Administration) recently approved rosuvastatin for males over 50 and females over 60 who have one other heart disease risk factor as well as CRP values over 2mg/L (to prevent cardiovascular disease).
Tina Shah, Ph.D., co- author of the study and a post-doctoral research fellow at University College London, England, said:
The difference in average population CRP values in populations of different ancestry are sufficiently large as to have bearing on clinical management and statin eligibility based on single CRP cut-point values.
In this study, the investigators examined data on 221,287 individuals from 89 published studies. They found that CRP blood levels vary according to ethnicity, even after such factors as age and BMI (body mass index) have been taken into account.
They found the following CRP levels according to ancestry:
- African-Americans – 2.6mg/L
- Hispanics – 2.51mg/L
- South Asians – 2.34mg/L
- Caucasians – 2.03mg/L
- East Asians – 1.01 mg/L
The order remained unchanged when the investigators calculated the probability that individuals in each ethnic group would exceed the 2mg/L CRP threshold at any age. Over 50% of Hispanics and African-Americans were over the 2 mg/L CRP threshold at the age of 50, compared to under half of East Asians. At the age of 60 under 40% of East Asians and nearly two-thirds of African-Americans and Hispanics would likely have a CRP greater than 2mg/L.
A gene linked to CRP levels varied in frequency according to ethnicity, a genetic analysis in the multi-ethnic Wandsworth Heart and Stroke Study revealed. This study surveyed a population in South London to estimate major heart and stroke risk factors among individuals of different ethnic backgrounds. Even though such lifestyle factors as BMI, blood pressure and tobacco consumption were factors that impacted in CRP values between groups, the majority of the CRP differences could not be explained, the authors wrote.
Aroon D. Hingorani, Ph.D., co-author of the study and professor of genetic epidemiology and British Heart Foundation Senior Research Fellow at University College London, said:
There is ongoing debate over the ability of CRP to predict the risk of heart disease over established cardiovascular risk factors, even in individuals of European origin where there is the most evidence pertaining to the CRP-coronary disease association “If clinicians still want to use CRP as part of heart risk prediction, the results of the current study suggest they should bear ethnicity in mind in interpreting a CRP value.
Hingorani added that the absolute heart disease risk for varying ethnic groups and individuals should be based on established risk factors using the Framinghan risk equation.
Tina Shah; Paul Newcombe; Liam Smeeth; Juliet Addo; Juan P. Casas; John Whittaker; Michelle A. Miller; Lorna Tinworth; Steve Jeffery; Pasquale Strazzullo; Francesco P. Cappuccio and Aroon D. Hingorani
Circulation: Cardiovascular Genetics. 2010
Published online before print September 28, 2010, doi: 10.1161/CIRCGENETICS.110.957431
Written by Christian Nordqvist