Table 3 and Table 4 summarize the characteristics of 31 prospective studies of Lp(a), the first of which was published in 1990,19 with 14 studies reported since the publication of a meta-analysis in 2000.32- 41,43- 46 All the studies were based in continental North America or in Western Europe except 1.36 Most studies identified participants in population registers (eg, general practitioner lists or electoral rolls) or in occupational settings, involved middle-aged men of white European continental ancestry, and reported on incident myocardial infarction and coronary death outcomes. The interval between sample collection and assay performance varied from a few hours to approximately 20 years. Eighteen studies7,8,11,14,15,17,32- 35,39- 42,44,46- 48 measured Lp(a) levels in plasma and 13 studies (including the present study)5,6,10,12,13,18,19,36,37,45 in serum, with measurements generally performed in samples thawed after long-term storage at temperatures of −70°C or colder, whereas few studies conducted assays in samples stored at temperatures ranging from −70°C to −20°C12,17,18,39,41 or in freshly collected samples.6,10,35 Apart from 6 studies6,8,10,11,32,35 that used in-house Lp(a) assays, most of the studies used commercially available immunoassays. Assay results were generally reported as mass per volume, although 1 study8 used an analytical method that measured molarity, and 2 studies6,11 used semiquantitative assay methods. Detailed information on assay methods (such as the exact antibodies used and the existence of sensitivity to Lp[a] isoforms) was reported in only a subset of studies (Table 4). Reported mean or median levels of Lp(a) in controls varied substantially across studies, ranging from approximately 10 to 300 mg/L (to convert to micromoles per liter, multiply by 0.0357) (although, as in the present study, most were 50-200 mg/L). All but 3 studies10,32,45 reported adjustment of CHD ORs for at least age, sex, smoking status, BP, and lipid concentrations. Using only within-study comparisons, a combined analysis of published data from these studies (including the present study) involving a total of 9870 incident CHD cases yielded an adjusted OR of 1.45 (95% CI, 1.32-1.58) for individuals in the top third of the baseline Lp(a) distribution compared with those in the bottom third (Figure 4). There was moderate heterogeneity among these studies (χ230 = 52.6; P = .007; I2 = 43% [95% CI, 12%-63%]), some of which was explained by period of publication (P = .004) and sample type (P = .003) but only a small part by other characteristics prespecified for investigation, notably, study size, sample storage characteristics, and Lp(a) assay isoform sensitivity or standard used (P > .10 for each characteristic) (Figure 3B). A funnel plot did not show an excess of extreme findings in smaller studies (Egger test P = .23) (data available on request).