We examined the prognostic significance of left ventricular hypertrophy determined by echocardiography in a cohort beginning renal replacement therapy. No patient had hemodynamically significant valvular disease or echocardiographic signs of obstructive cardiomyopathy. Using the Cox proportional hazards model, left ventricular hypertrophy was significantly associated with survival. The relative risk, based on comparison of upper and lower quintiles of left ventricular mass index, was 3.7 (95% confidence intervals, 1.6 to 8.3) for all-cause mortality and 3.7 (95% confidence intervals, 1.2 to 11.1) for cardiac mortality. The independent risk, adjusted for age, known coronary artery disease, diabetes, level of systolic blood pressure, and treatment (dialysis or transplantation), was 2.9 (95% confidence intervals, 1.3 to 6.9) for all-cause mortality and 2.7 (95% confidence intervals, 0.9 to 8.2) for cardiac mortality. Therefore, left ventricular hypertrophy appears to be an important, independent, determinant of survival in patients receiving therapy for end-stage renal failure.

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The authors carried out a population-based case-control study to estimate the risk of an acute coronary disease event associated with various definitions of a family history of coronary heart disease (CHD). A detailed family history questionnaire was completed by 403 cases and 236 controls in Newcastle, New South Wales, Australia from 1992 to 1994. Odds ratios of an acute coronary disease event adjusted for proband age and sex ranged from 2.7 (95% confidence interval (CI) 1.8-4.1) for the simplest definition (one or more first-degree relatives with CHD at any age) to 5.4 (95% CI 1.7-16.8) for the most stringent definition (two or more first-degree relatives with CHD before age 55 years). In a series of nested models, the authors examined the improvement in model fit as each component of the detailed family history was added. Additional information was provided by accounting for "don't know" responses, the number of affected relatives, the age of the affected relative, and whether the first-degree relative was a sibling rather than a parent. The results were similar when the data were analyzed as a cohort design with proband disease status as the exposure variable. The authors suggest that, to facilitate preventive efforts in a population, more detailed family history definitions should be used to better target high risk subjects.

The reproducibility of FMD measured by brachial artery ultrasound was poor and likely to render the measurements inaccurate for clinical research in our hands. Between-study variation contributed the largest proportion of total study variability. We suggest that investigators using this technique conduct their own careful reproducibility studies in order to avoid the misinterpretation of 'negative' studies.

In this paper, the authors report on the design of a population-based case-control study of family history as a risk factor for coronary heart disease (CHD). They studied the characteristics of subjects who completed a detailed family history questionnaire in 1992-1994 as well as the accuracy of recall of family history in order to quantify both selection and recall biases. Coronary disease cases were enrolled through the Newcastle MONICA Project (Monitoring Trends and Determinants in Cardiovascular Disease), which registered all suspected heart attacks and sudden cardiac deaths in the Lower Hunter region of New South Wales, Australia, between August 1984 and March 1994. Controls were selected at random from the New South Wales electoral roll. The response rate was 76% in cases and 62% in controls; the major factor associated with participation in the study was perceived family history of CHD, more so in the control series than in the case series. Accuracy was determined by comparing information obtained from the proband with that recorded on death certificates. In first-degree relatives, sensitivity of CHD recall was 85% (95% confidence interval (CI) 74-92%) in cases and 95% (95% CI 84-99%) in controls, while specificity was 59% (95% CI 49-69%) and 74% (95% CI 65-82%), respectively. The net bias in both selection and recall is toward the null and hence the comparisons provide a conservative estimate of risk of CHD associated with a positive family history.

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