Paul Ridker, MD, discusses inflammation and cardiometabolic risk by highlighting the Jupiter study.
For his presentation, “Inflammation and Cardiometabloic Risk: Integrating the Science into Clinical Practice” Paul Ridker, MD, highlighted research that goes on to measure inflammation markers and how they relate to predicting the risk of myocardial infarction, stroke, and cardiovascular events.
Ridker is the director of the Center for Cardiovascular Disease Prevention, at the Brigham and Women’s Hospital.
Lowering ldl cholesterol remains the fundamental issue in treating atherosclerosis risk, Ridker said. While it is essential to focus in this aspect, Ridker said growing evidence points to the inflammation factor. Ridker said atherosclerosis can be compared to common autoimmune diseases, such as psoriasis, he said.
Ridker provided data from a research study, the Jupiter Trial. The study included 7,000 women and those who participated had CRP levels that were in the range marked as high risk for cardiovascular events, but would normally not be treated with statin therapy due to their normal LDL levels. The tests available to assess cardiovascular risks are the Framingham test and the Reynolds Risk score. Currently, the Reynolds test includes a CRP component while the Framingham does not.
In this group of participants, CRP and IL-6 measures, which are associated with inflammation levels, were used. Patients with a reading of .05-1.0 are at low risk, those with 1.0 to 3.0 are at moderate risk, and those with 3.0 or greater are at high risk. The magnitude of impending risk with high CRP scores is at least as large or larger than with high blood pressure measures. Most of the women in the study had Framingham scores of less than 10% and would not normally be considered at risk.
The trial treated this group of women with statins and found that their risk had been reduced so effectively and quickly that it had to be stopped early, he said.
Weight had not played much of a factor in the results, he said. What was a key indicator of risk was high CRP scores, so that if a patient were thin with a high score she would be at more risk than an overweight patient with a low CRP score and the same Framingham score.
Among the key findings were that inflammation and thrombosis were linked, and the risk of unprovoked venous thrombosis was reduced, without the side effect of hemorrhaging.
The Jupiter trial delivered a 45-50% reduction in risk. Ridker made the case that targeted anti-inflammatory therapy may directly influence cardiovascular risks. Additionally, he cited an Aspirin study in 1997 that used the well-known anti-inflammatory agent as a treatment in prevention.
Due to the evidence, Ridker suggested that changing current guidelines to include CRP and Il-6 testing may be beneficial in improving the estimation of cardiovascular event risks. He highlighted current guidelines in Canada, which incorporate the Reynolds score, and also suggested that the moderate risk level score in the Framingham score test be modified from 5-10% to 5-20%.