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Objectives: To compare nosologist coding of underlying cause of death according to the death certificate with adjudicated cause of death for subjects aged 65 and older in the Cardiovascular Health Study (CHS)., Design: Observational., Setting: Four communities: Forsyth County, North Carolina (Wake Forest University); Sacramento County, California (University of California at Davis); Washington County, Maryland (Johns Hopkins University); and Pittsburgh, Pennsylvania (University of Pittsburgh)., Participants: Men and women aged 65 and older participating in CHS, a longitudinal study of coronary heart disease and stroke, who died through June 2004., Measurements: The CHS centrally adjudicated underlying cause of death for 3,194 fatal events from June 1989 to June 2004 using medical records, death certificates, proxy interviews, and autopsies, and results were compared with underlying cause of death assigned by a trained nosologist based on death certificate only., Results: Comparison of 3,194 CHS versus nosologist underlying cause of death revealed moderate agreement except for cancer (kappa=0.91, 95% confidence interval (CI)=0.89-0.93). kappas varied according to category (coronary heart disease, kappa=0.61, 95% CI=0.58-0.64; stroke, kappa=0.59, 95% CI=0.54-0.64; chronic obstructive pulmonary disease, kappa=0.58, 95% CI=0.51-0.65; dementia, kappa=0.40, 95% CI=0.34-0.45; and pneumonia, kappa=0.35, 95% CI=0.29-0.42). Differences between CHS and nosologist coding of dementia were found especially in older ages in the sex and race categories. CHS attributed 340 (10.6%) deaths due to dementia, whereas nosologist coding attributed only 113 (3.5%) to dementia as the underlying cause., Conclusion: Studies that use only death certificates to determine cause of death may result in misclassification and potential bias. Changing trends in cause-specific mortality in older individuals may be a function of classification process rather than incidence and case fatality.

Background and Purpose: Data from randomized clinical trials in Scotland and Sweden testing the efficacy of tamoxifen therapy in patients with breast cancer have suggested that the drug may also reduce the risk of coronary heart disease. In view of these findings, we examined mortality from coronary heart disease among patients with early stage breast cancer who were enrolled in the National Surgical Adjuvant Breast and Bowel Project B-14 trial of tamoxifen therapy., Methods: Deaths occurring among women who were randomly assigned to 5 years of either tamoxifen or placebo in the first phase of the B-14 trial were reviewed to determine the cause. Three categories of heart disease-related death were defined: 1) death from a definite fatal myocardial infarction, 2) death from definite fatal coronary heart disease/possible myocardial infarction, and 3) death from possible fatal coronary heart disease. Comparisons of the findings by treatment group were made on the basis of average annual hazard (i.e., death) rates and the corresponding relative hazard of death., Results: The average annual death rate from coronary heart disease was lower for patients who received tamoxifen than for patients who received placebo, but the difference was not statistically significant. There were eight definite heart-related deaths (i.e., definite fatal myocardial infarction or definite fatal coronary heart disease/possible myocardial infarction) among the patients who received tamoxifen, yielding an average annual rate of 0.62 per 1000 patients. There were 12 definite heart-related deaths among the patients who received placebo, yielding an average annual rate of 0.94 per 1000. The corresponding relative hazard of death from definite fatal heart disease (tamoxifen versus placebo) was 0.66 (95% confidence interval = 0.27-1.61). Eleven deaths in the tamoxifen group and 10 deaths in the placebo group were classified as possible cases of fatal coronary heart disease. When these cases and the definite cases were considered together, the average annual death rate for the patients who received tamoxifen was 1.48 per 1000, and the rate for the patients who received placebo was 1.73 per 1000. The corresponding relative hazard of death was 0.85 (95% confidence interval = 0.46-1.58)., Conclusions: The findings from the B-14 trial are consistent with the findings from the Scottish and the Swedish trials, suggesting that tamoxifen treatment reduces coronary heart disease among patients with breast cancer. Continued follow-up of the patients in these trials and in ongoing prevention trials is needed to accumulate enough data so that reliable conclusions can be drawn about the benefits of tamoxifen in preventing heart disease.

Deaths among 35- to 44-year-old black and white men and women residing in Allegheny County, Pennsylvania, were investigated. All coroner-certified nontraumatic deaths and practitioner-certified deaths coded as heart, cerbrovascular, or arterial disease, diabetes mellitus, and sudden or ill-defined causes were studied. Using autopsy, coroner, hospital, physician, and/or informant information about medical history, characteristics, and circumstances of death, physicians validated the deaths as due to coronary heart disease (CHD) or another cause. In 1984 to 1989, 616 deaths were investigated, 384 of which were sudden (within 24 hours of onset). Overall CHD mortality was 35.4/100,000/y for white males, 8.4/100,000/y for white females, 61.3/100,000/y for black males, and 19.5/100,000/y for black females. Although rates varied widely, characteristics, circumstances, and disease history were similar across race-sex groups. CHD mortality was 73% higher in black than white males. Approximately 80% of CHD deaths were sudden.

Trends in coronary heart disease mortality and sudden death were studied in 35- to 44-year-old white male residents of Allegheny County, Pennsylvania. Deaths coded as any cardiac or vascular disease, diabetes, unexplained sudden death, and other rubrics were eligible for investigation, and the cause of death was validated by physicians examining multiple data sources about the deaths. During 1970-1990, 1,424 white male deaths were investigated, with 903 validated as coronary heart disease. In that time span, white male coronary heart disease mortality fell from 93.4 to 36.7 per 100,000 population per year, a 60% decline. Little proportionate change was seen in characteristics of the deaths, which were predominantly sudden and out-of-hospital. Diabetes mellitus history increased proportionately over time, largely because diabetics' mortality rates, unlike those of all other subgroups, did not fall. These observations support the contention that the decline in coronary heart disease mortality relates to risk factor modification more than to improvements in the treatment of coronary heart disease. Differences in death certification practices must be considered when interpreting and comparing vital statistics data.

While previous prospective multicenter studies have conducted cardiovascular disease surveillance, few have detailed the techniques relating to the ascertainment of and data collection for events. The Cardiovascular Health Study (CHS) is a population-based study of coronary heart disease and stroke in older adults. This article summarizes the CHS events protocol and describes the methods of surveillance and ascertainment of hospitalized and nonhospitalized events, the use of medical records and other support documents, organizational issues at the field center level, and the classification of events through an adjudication process. We present data on incidence and mortality, the classification of adjudicated events, and the agreement between classification by the Events Subcommittee and the medical records diagnostic codes. The CHS techniques are a successful model for complete ascertainment, investigation, and documentation of events in an older cohort.

Few studies have evaluated the efficacy of cholesterol-lowering interventions in a community setting and have included a control or comparison group. As part of a preventive health demonstration project in rural Pennsylvania, Medicare beneficiaries underwent cholesterol screening to identify high-risk individuals with serum cholesterol levels > or = 240 mg/dL. These high-risk individuals were randomized to a cholesterol-lowering intervention through either local hospitals or physicians' offices or to a control group. Baseline and follow-up serum cholesterol levels collected two to three years later were compared according to service location (hospital versus physician's office), intervention attendance, degree of participation, baseline heart disease history, and cholesterol-lowering medication use at follow-up. Serum cholesterol levels decreased between 5.7% and 6.6% in the hospital-based and physician-based groups, as well as in a control group not offered the intervention. Participation rates did not differ between treatment groups, nor did participation affect serum cholesterol levels. Attendance level and heart disease history were not associated with a greater decrease in serum cholesterol levels. Individuals reporting cholesterol-lowering drug use at follow-up had significantly higher baseline serum cholesterol levels and a significantly greater decrease in total serum cholesterol (P < .0001) than those not on medication. Both nonpharmacological (diet) and pharmacological (drug) interventions will reduce serum cholesterol levels and heart attack risk. The study results suggest that, at least for older individuals, the impact of nonpharmacological interventions on the community is minimal. We conclude that only very aggressive treatment will significantly loser serum cholesterol levels in older individuals at risk for heart attack.

Trends in coronary heart disease (CHD) mortality were examined among 35-44-year-old white men during 1970-1986. Death certificates were obtained for 1,216 cases. All were coroner-certified natural deaths and noncoroner-certified deaths due to vascular diseases and diabetes mellitus. Autopsy data, coroner's reports, hospital records, physician's reports, and informants were used to validate diagnoses. The reviewers rejected 73 of 805 CHD certifications, but they validated 54 cases not certified as CHD on the death certificate as CHD. The CHD mortality rate fell from 90.6/100,000/year in 1970-1972 to 40.3/100,000/year in 1985-1986. Approximately two thirds of the decline was related to a decline in sudden deaths including 41.6% due to incident sudden CHD death. The proportion of diabetics among validated CHD deaths rose dramatically from 6.5% in 1970-1972 to 23.0% in 1985-1986. The CHD mortality rate among diabetics apparently did not decline during the 17 years of the study. We conclude that primary prevention has contributed substantially to the CHD decline in the 35-44-year age group. Better diagnoses and treatment, especially of angina pectoris and of patients after a myocardial infarction, may also have been important. Control of CHD in diabetics must take high priority in further prevention strategies.