C-Reactive Protein and the Prediction of Cardiovascular Events Among Those at Intermediate RiskMoving an Inflammatory Hypothesis Toward Consensus
Paul M. Ridker, MD, MPH, FACC*
Center for Cardiovascular Disease Prevention, the Divisions of Preventive Medicine and Cardiovascular Diseases, Brigham and Women’s Hospital, the Harvard Medical School, and the Harvard School of Public Health, Boston, Massachusetts.
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Figure 1 Independent Impact of hsCRP on Cardiovascular Risk
Multivariate adjusted relative risks of future cardiovascular events according to baseline levels of high-sensitivity C-reactive protein (hsCRP) <1 mg/l, 1 to 3 mg/l, and >3 mg/l in 14 major prospective cohort studies. Data adapted from references 1,11–13,16–20,22,23,51–54. ARIC = Atherosclerosis Risk in Communities study; CHS = Cardiovascular Health Study; EPIC = Evaluation for Prevention of Ischemic Complications-Norfolk study; FHS = Framingham Heart Study; HPFUS = Health Professionals Follow-Up Study; Iceland = Reykjavik Heart Study data; Kuopio = Kuopio Heart Study; MONICA = Monitoring Trends and Development in Cardiovascular Disease study; NHS = Nurses Health Study; PHS = Physicians Health Study; PIMA = Pima Indian study; Strong = Strong Heart Study; UK = British general practice cohort; WHS = Women’s Health Study.
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Figure 2 Risk Reclassification Using hsCRP and Parental History
Impact of high-sensitivity C-reactive protein (hsCRP) (representing inflammation) and family history (representing genetics) on estimates of global cardiovascular risk for a representative population of 100,000 U.S. women at 5% to 10% and 10% to 20% 10-year risk according to the Adult Treatment Panel III (ATP-III). Data adapted from references 34 and 35. BP = blood pressure; CVD = cardiovascular disease; HDLC = high-density lipoprotein cholesterol; TC = total cholesterol.
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Figure 3 LDL Cholesterol, hsCRP, and Clinical Outcomes on Statin Therapy
Cumulative rates of recurrent myocardial infarction or cardiovascular death among statin-treated patients according to achieved levels of LDL cholesterol in mg/dl and achieved levels of hsCRP in mg/l in the PROVE-IT–TIMI-22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction-22) trial (left) and in the A to Z (Aggrastat to Zocor) trial (right). Data adapted from references 77 and 80. hsCRP = high-sensitivity C-reactive protein; LDL = low-density lipoprotein.
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