Title: Carotid Intima-Media Thickness and Presence or Absence of Plaque Improves Prediction of Coronary Heart Disease: The ARIC (Atherosclerosis Risk In Communities) Study
Topic: Noninvasive Cardiology
Date Posted: 4/29/2010
Author(s): Nambi V, Chambless L, Folsom AR, et al.
Citation: J Am Coll Cardiol 2010;55:1600-1607.
Clinical Trial: No
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JACC Article: Carotid Intima-Media Thickness and Presence or Absence of Plaque Improves Prediction of Coronary Heart Disease: The ARIC (Atherosclerosis Risk In Communities) Study
Trial: Atherosclerosis Risk in Communities (ARIC)
Study Question: Does carotid intima-media thickness (CIMT) and the presence of plaque improve coronary heart disease (CHD) risk prediction when used with traditional risk factors?
Methods: Data from the Atherosclerosis Risk in Communities (ARIC) study, of 15,792 subjects (between 45 and 64 years old) from four US communities were used for the present analysis. Risk factor prediction models were considered for the total cohort of men and women. Models included traditional risk factors only, or risk factors with CIMT. Additional models included traditional risk factors and the presence of carotid plaque, and the traditional risk factors with CIMT together with plaque. Models were compared using the receiver-operating characteristic curve (AUC). Cox proportional hazard models were used to estimate 10-year risk for CHD. Number of subjects reclassified was also determined for each of the models.
Results: Of the 13,145 subjects included (5,682 men and 7,463 women), there were 1,812 CHD events over a 15.1-year follow-up. Plaque was observed in 13.6% of those with a CIMT in the <25th percentile, in 26.6% of those with a CIMT in the 25th-75th percentile, and 65.3% of those with a CIMT in the >75th percentile. An estimated 23% of the subjects were reclassified when CIMT and plaque were added to the models. CIMT and plaque resulted in the greatest improvement in the AUC; increasing from 0.742 for traditional risk factors only to 0.755 when both CIMT and plaque were added to the model. These models (containing both CIMT and plaque) also had the best net reclassification index in the overall population. For women, adding plaque to the traditional risk factors model had a more pronounced effect on the AUC than did the addition of CIMT. In contrast, adding CIMT to the traditional risk factors model had a more pronounced effect on the AUC than did the addition of plaque for men.
Conclusions: The authors concluded that the addition of CIMT and plaque to traditional risk factors improved risk prediction for CHD events.
Perspective: Addition of characteristics to present risk prediction models is in part dependent on added accuracy in prediction. However, examining the cost-benefit is needed prior to wide-scale adoption of measures such as CIMT. Elizabeth A. Jackson, M.D., F.A.C.C.
Title: Lipoprotein-Associated Phospholipase A2 and Risk of Coronary Disease, Stroke, and Mortality: Collaborative Analysis of 32 Prospective Studies
Topic: Prevention/Vascular
Date Posted: 4/29/2010 8:00:00 PM
Author(s): The Lp-PLA2 Studies Collaboration.
Citation: Lancet 2010;375:1536-1544.
Clinical Trial: No
Study Question: What is the association between circulating lipoprotein-associated phospholipase A2 (Lp-PLA2) mass and activity with risk of coronary heart disease (CHD), stroke, and mortality under different circumstances?
Methods: A meta-analysis was performed using individual records from 79,036 participants in 32 prospective studies (yielding 17,722 incident fatal or nonfatal outcomes during 475,000 person-years at risk). Within study regressions were used to calculate risk ratios (RRs) per 1 standard deviation (SD) higher value of Lp-PLA2 or other risk factor. The primary outcome was CHD.
Results: Mean age at entry of the 79,036 participants was 64 years (SD 10). Lp-PLA2 activity and mass were associated with each other (r = 0.51; 95% confidence interval, 0.47-0.56) and pro-atherogenic lipids. There were rough log-linear associations of Lp-PLA2 activity and mass with risk of CHD and vascular death. RRs, adjusted for conventional risk factors, were 1.10 with Lp-PLA2 activity and 1.11 with Lp-PLA2 mass for CHD; 1.08 and 1.14 for ischemic stroke; 1.16 and 1.13 for vascular mortality; and 1.10 and 1.0 for nonvascular mortality, respectively. RRs with Lp-PLA2 were similar in people with and without initial stable vascular disease, apart from vascular death with Lp-PLA2 mass. Adjusted RRs for CHD were 1.10 with non–high-density lipoprotein (HDL) cholesterol and 1.10 (1.00-1.21) with systolic blood pressure.
Conclusions: Lp-PLA2 activity and mass each show continuous associations with risk of CHD, similar in magnitude to that with non-HDL cholesterol or systolic blood pressure in this population. Associations of Lp-PLA2 mass and activity are not exclusive to vascular outcomes, and the vascular associations depend at least partly on lipids.
Perspective: The additive relative risk of cardiovascular events associated with Lp-PLA2, an inflammatory enzyme expressed in atherosclerotic plaques, is modest. It is presently being evaluated as a therapeutic target for vascular disease prevention. Melvyn Rubenfire, M.D., F.A.C.C.
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