Objectives: We conducted a case-control study to investigate the effectiveness of effor ts to increase folate intake in Western Australia (WA) for the prevention of neural tube defects (NTD). Methods: Case (36) and control (578) mothers completed questionnaires, from which their intake of folate from supplements and food (including fortified foods) was estimated.Results: Almost one-third of women took folic acid supplements periconceptionally.Supplement use was associated with a non-significant 4% reduction in risk. For women not taking supplements, dietary sources of folate were protective, and most women obtained at least some folate from fortified food. Conclusions:For the two-thirds of WA women not taking supplements, for tified food is an important source of folate for the prevention of NTD. Implications: Greater promotion of foods currently allowed to be fortified with folate, or mandatory fortification, is needed to maximise prevention of NTD in Australia.

To assess whether the site of myocardial infarction is an independent prognostic indicator, the outcome of patients with anterior myocardial infarction was compared with that of patients with inferior infarction. A consecutive series of patients who had suffered their first myocardial infarction was analyzed (398 with anterior and 391 with inferior infarction). Patients with anterior myocardial infarction had a higher 1 year mortality than those with inferior infarction (18.3% vs 10.5%, p = .002). When patients were matched for infarct size determined by peak creatine kinase (CK) level expressed as a multiple of the upper limit of normal, those with anterior myocardial infarction tended to have a higher 1 year mortality than those with inferior infarction for all subgroups of peak CK. Early mortality (day 1 to 28 after myocardial infarction) was greater in the anterior than in the inferior myocardial infarction group (10% vs 6.4%, p = .03); this was most significant when peak CK was greater than four times normal (12.4% vs 7.0%, p = .04). Late mortality was also higher in the anterior (8.4% vs 4. 1%, p = .04) than the inferior infarction group and this was most significant when peak CK was less than two times normal (15.2% vs 0%, p = .02) or greater than eight times normal (10.6% vs 4.1%, p = .04). Multivariate analysis with proportional-hazards regression confirmed the prognostic significance of location of infarction independent of peak CK level. Thus, infarct location was found to be a predictor of prognosis that is independent of infarct size based on peak CK levels. Circulation 73, No. 5, 885-891, 1986.! THE PROGNOSIS of patients with anterior myocardial infarction is significantly worse than that of patients with inferior myocardial infarction.'-5 Anterior infarction is associated with more myocardial damage than inferior infarction.5' 6 It remains unclear whether this difference in survival is due to the site or the size of myocardial infarction.Goldberg et al.7 concluded that the poorer prognosis for patients with anterior myocardial infarction was probably related to the extent of myocardial damage rather than the location of the injury. Strauss et al.' demonstrated a poorer prognosis (both early and late) for patients with anterior than for those with inferior infarction of similar size. However, they found no

Patients registered by the 1971 Perth Coronary Register as having suffered a myocardial infarction were followed up for 9 years. The Register was a community-based study that used standard methods and criteria as part of a World Health Organization collaborative investigation. Of the 1078 patients studied, 77% survived the first 24 hr and 62% the first 28 days; 0.3% were lost to follow-up. For the 666 patients alive at 28 days, the crude 1, 5, and 9 year survival rates were 88%, 67%, and 52%, respectively. The relationship between 54 variables and the survival of patients alive 28 days after myocardial infarction was examined by life-table methods and the log rank test, and then by fitting a proportional hazards model to the data. The important prognostic factors were age, sex, past history of myocardial infarction, stroke, diabetes and hypertension, tachycardia at presentation, hypotension at presentation, and the occurrence of arrhythmias as short-term complications. The most appropriate mathematical description of the joint effects of the prognostic factors was a multiplicative model with no interaction. Circulation 68, No. 5, 961-969, 1983.

T his paper describes the creation of a unique maternal identifier for use in the investigation of perinatal, postneonatal and child outcomes in relation to maternal characteristics. All Midwives' records of Western Australian (WA) births were routinely linked to registrations of births and deaths for infants born from 1980 to 1992 inclusive, then linked to WA hospital discharge data and to registries of birth defects and cerebral palsy to create a longitudinal health record for each infant. However, since each birth to a woman was recorded as a separate event, there was no way to identify siblings. Probabilistic record linkage, based on information about the mother, was used for this task. Logical inconsistencies within the data were used to test the validity of the linkages between birth records attributed to each mother. Information about the mother from other epidemiological studies and data abstracted from hospital case notes was also used to validate sibships. Linkage of the records of 310,255 births in WA during that period resulted in the formation of 181,133 sibships of one or more children. Pooling the results of all of the validation methods gave an error of 0.9%. Linkage identified 3678 sibships containing multiple births, and 305 sets of maternal twins. Ascertainment of twins and their siblings for an ongoing twin register, the WA Twin Child Health (WATCH) study, was a natural consequence of this process.