A Long‐term Coronary Prevention Evaluation Program*

Abstract

Since the mid-l950's, major prospective epidemiological studies in large living population groups have shown unequivocal relationships between several traits and habits (singly and in combination) and the risk of premature clinical atherosclerotic coronary heart disease ( CHD) .1-20 The findings of our group in a sizeable cohort of men originally aged 40 to 59, employed by the Peoples Gas, Light and Coke Company in Chicago, are representative.' Of the 1,594 male employees in this age group on January 1, 1958, 1,465 were examined for the first time for the purposes of this study in 1958. Of these 1,465 men, 1,329 were free of evidence of definite clinical coronary heart disease, were followed without loss over the subsequent years, and underwent no systeinatic intervention by the research group. Data on the relationship between the major coronary risk factors and mortality from new coronary heart disease and from all causes (for the eight-year period 1958-66) are presented in TABLES 1 through 6. The men with frankly elevated serum cholesterol levels in 1958 had subsequent death rates from coronary heart disease and from all causes significantly higher than the men with levels less than 250 mg/100 ml had (TABLE 1). Similarly, men with elevated blood pressures had markedly elevated mortality rates, as 'did cigarette smokers (TABLES 2 and 3). These findings are typical of those reported by others. Correspondingly, overweight was found to be associated with increased risk of dying, at least among nonsmokers (TABLE 4), and the cumulative impact of combined risk factors is well illustrated by TABLES 5 and 6. Diabetes (symptomatic or asymptomatic) is another major coronary risk factor, as is an habitual diet high in calories, total fat, saturated fat, cholesterol, total carbohydrate, refined carbohydrate, sugar, and salt. Physical inactivity, tension-generating personality-behavior patterns, and a family history of premature vascular disease are also important, as are "silent" abnormalities in the resting, exercise, and postexercise electrocardiogram.As indicated, significant evidence on the role of several risk factors was already available by the mid-1950's. In 1957, therefore, our research group

Primary Prevention of Ischemic Heart Disease: Evaluation of Community Interventions

“…less than 130 mm Hg systolic and 90 mm Hg diastolic (36). The maximum reduction in serum cholesterol (10.8%) was achieved in the fi rst year for these 33 men, and the overall average reduction for ten years was 8.9% (37). Smokers comprised 36.8% of the project population in 1953.…”

“…However, two efforts that can be considered prototypes for such interventions have been undertaken. In one, the Chicago Coronary Prevention Evaluation Program (CPEP), the follow up data for more than ten years are available (36)(37)(38). In the other, the Multiple Risk Factor Intervention Trial (MRFIT), the project is only par tially completed, and the results have not been extensively reported (39-43).…”

Experience with Simplified Scheme of Treatment of Hyperlipidaemia

“…Though the significance of this association has been reinforced by prospective studies showing that raised cholesterol and triglyceride levels are predictive of ischaemic heart disease (Stanler, 1967;Carlson and Bottiger, 1972) rigorous proof is lacking that the association is causal. Nevertheless, it is now common clinical practice to attempt to correct hyperlipidaemia, and this practice obtains further justification from the encouraging results of the "first generation" trials of serum lipid reduction in the primary (Christakis et al, 1966;Stamler et al, 1968;Dayton et al, 1969;Miettinen et al, 1972) and of some (Leren, 1970;Dewar, 1971;Oliver, 1971) but not all (Morris, 1968) trials of secondary prevention-that is of relapse. Animal experimental evidence that diet-induced hyperlipidaemia leads to atherosclerosis-like lesions has existed for twothirds of a century, and recent suggestions have been made that such lesions are partly reversible by lipidlowering regimens (Armstrong and Megan, 1972).…”

Συναισθηματική Νοημοσύνη Και Διατροφική Συμπεριφορά Ασθενών Με Στεφανιαία Νόσο

“…Οι πρώτες του µελέτες που έλαβαν χώρα γύρω στα 1940, έδειξαν ότι η προσθήκη χοληστερίνης και λίπους στη τροφή των πουλερικών είναι πιθανό να προκαλέσει το σχηµατισµό αθηρωµατικών πλακών (Stamler, 1950), ενώ η αύξηση της αρτηριακής πίεσης µπορεί να οδηγήσει σε αθηροσκλήρωση (Stamler & Katz, 1950). Ο Stamler έδειξε ότι οι πολυπαραγοντικές παρεµβάσεις στον τρόπο ζωής, ειδικά όταν αυτές περιλαµβάνουν αλλαγές στη Διδακτορική διατριβή ΜΕΡΟΣ Α' -1 ο Κεφάλαιο διατροφή, µπορούν να µειώσουν τον κίνδυνο για εµφάνιση στεφανιαίας νόσου (Stamler & Katz, 1951, Stamler et al, 1968.…”