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The association between physical activity at work and at leisure, coronary risk factors, social class and mortality has been studied in about 15000 Oslo men, aged 40-49, without known cardiovascular disease or diabetes at a screening examination for coronary risk factors. Four-year total and CHD mortality showed a decrease with increasing degree of leisure activity, and an increase with increasing work activity. The three conventional coronary risk factors--serum cholesterol, systolic blood pressure (SBP) and number of cigarettes--associated negatively with physical leisure activity, whereas they all associated positively with physical activity at work. Men in lower social classes were less active at leisure but more active at work than men in the higher classes. In a multivariate analysis of variance with coronary risk score (based on SBP, serum total cholesterol and number of cigarettes), social class and physical activity, the predictive power of physical leisure activity for future death was almost as good as the coronary risk score. Physical activity at work, on the other hand, was not an independent risk factor either for total or for CHD mortality.

Both arterial and venous plasma adrenaline and noradrenaline concentrations were elevated in 20 middle-aged men with long-standing, untreated essential hypertension compared to 19 normotensive control men (p less than 0.01). The mean a-v (arterial-venous) difference of adrenaline and v-a difference of noradrenaline were increased in the hypertensive (p less than 0.05) consistent with raised adrenal adrenaline release and release of noradrenaline from the peripheral vascular beds of the forearm.

A screening for coronary risk factors in 18000 Oslo men yielded 16525 “healthy” men, aged 20–49. The intercorrelation of serum cholesterol, body weight and cigarette smoking was found to be more pronounced than described in other studies. Increasing daily exposure to cigarette smoke in the order: never-smoker, ex-smoker, non-inhaling smoker, inhaling smoker and present non-filter smoker, was parallelled by increasing cholesterol levels, but not by increasing body weight. Daily cigarette-smokers had lower body weight and higher serum cholesterol values than never-cigarette-smokers, with the exception of the 20+ cigarette-smokers who had higher serum cholesterol values and body weight than the never-cigarette-smokers. As regards ex-cigarette-smokers, both body weight and serum cholesterol tended to increase with the number of cigarettes smoked before quitting. Possible explanations of these findings are discussed.

Seventeen 50-year-old hypertensive men (157 +/- 4/110 +/- 2 mmHg, mean +/- SE) were given low sodium diet for one week, which was supplemented with potassium the following week. The urinary Na+/K+ excretion ratio changed from 2:1 to 1:5 and 1:12, respectively, during dietary intervention. Arterial plasma vasopressin decreased by 3.4 +/- 1.7 ng/l (0.05 less than p less than 0.10) and urinary excretion of vasopressin was reduced by nearly 50% (p less than 0.001) during sodium depletion, while plasma noradrenaline increased by 38% (p less than 0.001) and plasma dopamine showed an increase by 58% (p less than 0.001). Plasma renin concentration increased four-fold during sodium depletion (p less than 0.001). With combined salt depletion and potassium supplementation, arterial plasma vasopressin decreased by 9.5 +/- 4.0 ng/l (p less than 0.05) compared to control. Urinary excretion of vasopressin together with plasma noradrenaline and dopamine were unchanged during the second week. The reduction of blood pressure was most marked during the first week (143 +/- 3/103 +/- 2 mmHg, p less than 0.05), but continued to fall also during the second week. Thus, during sodium restriction in middle-aged hypertensive men, blood pressure reduction occurs concomitantly with inhibited vasopressin release, despite enhanced renin and catecholamine release. Potassium supplementation during sodium restriction induces only minor changes in these variables.

Electrocardiograms of 412 male postmyocardial infarction patients recorded 1–2 years after their first infarction have been classified according to the Minnesota Code by two independent readers (physicians). A study of the inter- and intra-observer error or reliability was then performed. The degree of accuracy and reproducibility thus obtained was related to degree of experience in the use of the Minnesota Code. Reproducibility was greater towards the end of the study when the readers were more experienced. The importance of substantial and continuous experience with the use of the Minnesota Code is stressed as well as the importance of at least two observers reading the ECGs independently. A final arbitration is no problem. These criteria must be fulfilled before the use of the Minnesota Code in clinical or epidemiological studies on coronary heart disease.

Blood lipid studies with lipoprotein typing a.m. Fredrickson were performed in 1 155 persons including 207 normals, 559 coronary heart disease patients, and 101 patients with atherosclerosis obliterans of the lower limbs. The results of lipoprotein typing were as follows. Type Normal: 43.2%, 54.8%, and 66.8%. Type II: 43.9%, 32.3%, and 20.3%. Type IV: 9.2%, and 3.7% could not be classified. (The figures refer to upper cutoff points of normal cholesterol of 275, 300 and 325 mg/100 ml, respectively.) Triglyceride levels were distinctly correlated to body weight.

The association between socioeconomic status, measured by a combination of income and education, and CHD mortality has been studied in a cohort of 40–49 year old Oslo men. Socio–economic status was significantly associated with CHD mortality. However, the lowest CHD mortality was found in social status Group III (middle class) and this could not be explained by the risk factor gradients seen among those studied. Although the number of fatalities is small (68 CHD deaths during 4.5 years) socio–economic status seems to be independently associated with coronary risk after adjusting for serum cholesterol, systolic blood pressure and cigarette smoking.

A screening for coronary risk factors in 18 000 Oslo men yielded 16 525 "healthy" men, aged 20-49. The intercorrelation of serum cholesterol, body weight and cigarette smoking was found to be more pronounced than described in other studies. Increasing daily exposure to cigarette smoke in the order: never-smoker, ex-smoker, non-inhaling smoker, inhaling smoker and present non-filter smoker, was parallelled by increasing cholesterol levels, but not by increasing body weight. Daily cigarette-smokers had lower body weight and higher serum cholesterol values than never-cigarette-smokers, with the exception of the 20+ cigarette-smokers who had higher serum cholesterol values and body weight than the never-cigarette-smokers. As regards ex-cigarette-smokers, both body weight and serum cholesterol tended to increase with the number of cigarettes smoked before quitting. Possible explanations of these findings are discussed.

In a 24-week randomized, single-blind study Timolol (n = 63) and Enalapril (n = 57) proved to be potent and safe antihypertensive drugs. However, the effect on lipid metabolism was fundamentally different, despite the fact that the effect on total serum cholesterol did not significantly differ between the two groups. Enalapril had no adverse effect on any lipid fractions, while Timolol increased very low (VLDL) + low (LDL) density lipoprotein cholesterol by 7.6% (p less than 0.001) and total triglycerides by 34.5% (p less than 0.001), and decreased the favorable high density lipoprotein (HDL) cholesterol by 11.3% (p less than 0.001). Thus, the ratio HDL/VLDL + LDL cholesterol was reduced by 17.1% (p less than 0.001). Enalapril reduced uric acid by 3.4% (NS), while Timolol increased uric acid by 4.0% (p less than 0.05). The difference between the groups was statistically significant (p less than 0.01). The first steps in any attempt to solve the hypertension-coronary dilemma should be to take into consideration all pharmacologic effects of antihypertensive drugs.