TROKE IS A MAJOR CAUSE OF death and disability in the United States and is a growing public health concern. The latest projections estimate that more than 1 million strokes will occur every year by the year 2010. Moreover, stroke has a disproportionate impact on elderly, black, and Hispanic persons, who are among the fastest growing segments of the US population. Many studies have provided strong evidence for lipids as a risk factor for coronary artery disease (CAD). These studies demonstrate a direct relationship between total cholesterol, low-density lipoprotein cholesterol (LDL-C), and CAD and an inverse relationship between highdensity lipoprotein cholesterol (HDL-C) and CAD. 1-4 These relationships have not been as clearly established for ischemic stroke with some studies even questioning whether cholesterol is a risk factor for stroke. The advent of statin agents, which significantly lower lipid levels by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, has focused more research on lipids in all vascular outcomes, in particular stroke. Compelling data from statin trials show impressive reductions in stroke risk among persons with CAD. 5 Some researchers have suggested that the

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 Columbia University Informatics for Diabetes Education and Telemedicine (IDEATel) Project is a four-year demonstration project funded by the Centers for Medicare and Medicaid Services with the overall goals of evaluating the feasibility, acceptability, effectiveness, and cost-effectiveness of telemedicine in the management of older patients with diabetes. The study is designed as a randomized controlled trial and is being conducted by a state-wide consortium in New York. Eligibility requires that participants have diabetes, are Medicare beneficiaries, and reside in federally designated medically underserved areas. A total of 1,500 participants will be randomized, half in New York City and half in other areas of the state. Intervention participants receive a home telemedicine unit that provides synchronous videoconferencing with a project-based nurse, electronic transmission of home fingerstick glucose and blood pressure data, and Web access to a project Web site. End points include glycosylated hemoglobin, blood pressure, and lipid levels; patient satisfaction; health care service utilization; and costs. The project is intended to provide data to help inform regulatory and reimbursement policies for electronically delivered health care services.

Asymmetric dimethylarginine (ADMA), a compound detectable in human plasma, is an endogenous inhibitor of NO synthase. Endothelial dysfunction is an early event in atherogenesis, and large-vessel atherosclerosis is a major cause of morbidity and mortality in patients with type 2 diabetes mellitus. Fifty patients with type 2 diabetes mellitus were studied at baseline and 5 hours after ingestion of a high-fat meal. Plasma ADMA measured by using high-performance liquid chromatography increased from 1.04+/-0.99 to 2.51+/-2.27 micromol/L (P:<0.0005). Brachial arterial vasodilation after reactive hyperemia, a NO-dependent function, measured by high-resolution ultrasound, decreased from 6.9+/-3.9% at baseline to 1.3+/-4.5% (P:<0.0001). These changes occurred in association with increased plasma levels of triglycerides and very low density lipoprotein triglycerides, with reduced low density lipoprotein cholesterol and high density lipoprotein cholesterol, and with no changes in total cholesterol. The increase in plasma ADMA in response to a high-fat meal was significantly and inversely related to the decrease in percent vasodilation. In 10 of the subjects studied with a similar protocol on another day, no significant changes in the brachial artery flow responses or in plasma ADMA were observed 5 hours after ingestion of a nonfat isocaloric meal. The data suggest that ADMA may contribute to abnormal blood flow responses and to atherogenesis in type 2 diabetics.