Levels of Lp-PLA2 and CRP may be complementary beyond traditional risk factors in identifying middle-aged individuals at increased risk for ischemic stroke.
Abstract-Elevated levels of lipoprotein(a) [Lp(a)] and the presence of small isoforms of apolipoprotein(a) [apo(a)] have been associated with coronary artery disease (CAD) in whites but not in African Americans. Because of marked race/ethnicity differences in the distribution of Lp(a) levels across apo(a) sizes, we tested the hypothesis that apo(a) isoform size determines the association between Lp(a) and CAD. We related Lp(a) levels, apo(a) isoforms, and the levels of Lp(a) associated with different apo(a) isoforms to the presence of CAD (Ն50% stenosis) in 576 white and African American men and women. Only in white men were Lp(a) levels significantly higher among patients with CAD than in those without CAD (28.4 versus 16.5 mg/dL, respectively; Pϭ0.004), and only in this group was the presence of small apo(a) isoforms (Ͻ22 kringle 4 repeats) associated with CAD (Pϭ0.043). Elevated Lp(a) levels (Ն30 mg/dL) were found in 26% of whites and 68% of African Americans, and of those, 80% of whites but only 26% of African Americans had a small apo(a) isoform. Elevated Lp(a) levels with small apo(a) isoforms were significantly associated with CAD (PϽ0.01) in African American and white men but not in women. This association remained significant after adjusting for age, diabetes mellitus, smoking, hypertension, HDL cholesterol, LDL cholesterol, and triglycerides. We conclude that elevated levels of Lp(a) with small apo(a) isoforms independently predict risk for CAD in African American and white men. Our study, by determining the predictive power of Lp(a) levels combined with apo(a) isoform size, provides an explanation for the apparent lack of association of either measure alone with CAD in African Americans. Furthermore, our results suggest that small apo(a) size confers atherogenicity to Lp(a) for cardiovascular disease. [1][2][3] In numerous, but not all, prospective studies, mainly in white populations, elevations of plasma Lp(a) levels, usually defined as Ն30 mg/dL, were significantly correlated with coronary artery disease (CAD). 4 -13 Curiously, although mean Lp(a) levels are twice as high in African Americans compared with whites, studies to date have failed to establish a significant association between elevated Lp(a) levels (Ն30 mg/dL) and CAD among African Americans. 1,14 -16 The lack of understanding of this racial difference has made it difficult to conclude with full confidence that Lp(a) is a risk factor for CAD..In addition to high Lp(a) levels, the presence of small apo(a) isoforms has been associated with CAD in whites. [17][18][19][20][21][22][23][24] In the majority of studies using high-resolution sizing techniques, small apo(a) size has been defined as Ͻ22 kringle 4 (K4) repeats. 17,18,24 The majority of whites with high Lp(a) levels possesses at least 1 small apo(a) isoform; however, the majority of African Americans with high Lp(a) levels has no small apo(a) isoform. 25 The high degree of correlation between elevated levels of Lp(a) and small apo(a) isoforms in whites makes it difficult to ascerta...
The Working Group on research in adult congenital heart disease (ACHD) was convened in September 2004 under the sponsorship of National Heart, Lung, and Blood Institute (NHLBI) and the Office of Rare Diseases, National Institutes of Health, Department of Health and Human Services, to make recommendations on research needs. The purpose of the Working Group was to advise the NHLBI on the current state of the science in ACHD and barriers to optimal clinical care, and to make specific recommendations for overcoming those barriers. The members of the Working Group were chosen to provide expert input on a broad range of research issues from both scientific and lay perspectives. The Working Group reviewed data on the epidemiology of ACHD, long-term outcomes of complex cardiovascular malformations, issues in assessing morphology and function with current imaging techniques, surgical and catheter-based interventions, management of related conditions including pregnancy and arrhythmias, quality of life, and informatics. After research and training barriers were discussed, the Working Group recommended outreach and educational programs for adults with congenital heart disease, a network of specialized adult congenital heart disease regional centers, technology development to support advances in imaging and modeling of abnormal structure and function, and a consensus on appropriate training for physicians to provide care for adults with congenital heart disease.
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