A cohort of 4 475 Finnish men was followed up during 1964-80 in order to study regional differences in mortality from cardiovascular diseases, especially ischaemic heart disease (IHD). The west/east gradient in cardiovascular mortality recorded in several previous studies was greatly age-dependent. The excess eastern risk was a feature of younger age groups; with increasing age the risk pattern was reversed. The risk factors in IHD in eastern Finland have an element which somehow accelerates the process of this disease.
The combined effects of age, leisure-time physical activity, smoking, alcohol consumption, and different forms of shift work on the prevalence of sleep complaints and daytime sleepiness were studied among workers in industry, transport, and traffic.
Altogether 3020 subjects were studied using a psychosocial questionnaire. The participants were currently employed men, aged 45-60 years, from a postal and telecommunication agency, the railway company, and 5 industrial companies. On the basis of a factor analysis of an 11-item sleep questionnaire, the sleep complaints were grouped into the categories of insomnia, sleep deprivation, daytime sleepiness, and snoring. The importance of the shift schedule, age, and life-style factors as simultaneous predictors of the complaints was studied in a logistic regression analysis and an analysis of covariance.
The prevalence of insomnia, sleep deprivation, and daytime sleepiness depended significantly on the shift system. All sleep complaints were more common in 2- and 3-shift work and in irregular shift work than in day work. The prevalence of daytime sleepiness was 20-37%, depending on the shift system. Leisure-time physical activity and alcohol consumption were the most important life-style factors predicting all sleep complaints, except snoring. The effects of physical activity and alcohol consumption differed for different shift schedules.
Different shift systems, also 2-shift work and permanent night work, seem to increase the frequency of sleep complaints. Especially 3-shift work seems to interact with life-style factors by increasing the adverse effects and decreasing the beneficial effects on sleep and sleepiness.
The aim of the Helsinki Heart Study, a 5-year primary prevention placebo-controlled study involving 4081 dyslipidaemic men (aged 40 to 55 years), was to investigate if increasing high density lipoprotein (HDL)-cholesterol plasma levels and decreasing low density lipoprotein (LDL)-cholesterol levels would reduce the incidence of coronary heart disease. Gemfibrozil 600mg twice daily was administered to induce these changes in lipoprotein levels. Baseline HDL-cholesterol levels in the study group were similar to those in the general population. Data from patients treated with placebo were analysed to investigate the influence of HDL-cholesterol levels on the incidence of coronary heart disease. Using the number of cardiac end-points per 1000 person-years to indicate the risk of coronary heart disease, it was clear that elevated HDL-cholesterol levels reduced the risk of coronary heart disease while the incidence increased at low HDL-cholesterol levels. This relationship was not altered when the effect of HDL-cholesterol levels was analysed jointly with other coronary risk factors (age, smoking or blood pressure). A weaker association was seen between LDL-cholesterol and risk of coronary heart disease, and triglycerides appeared to have no significant effect on the incidence of the disease. The data clearly suggest that HDL-cholesterol is a strong predictor of the incidence of coronary heart disease in the placebo group of the Helsinki Heart Study.
To confirm that coronary heart disease (CHD) can be prevented by gemfibrozil treatment and to estimate the long-term effect of the treatment.
All participants of the Helsinki Heart Study, a controlled 5-year CHD primary prevention trial with gemfibrozil and placebo, were offered gemfibrozil treatment and biannual follow-up for 3.5 more years.
By the end of the multi-clinic double-blind trial, a 34% difference in definite cardiac events (56 vs. 84; P
Information on coronary heart disease (CHD) obtained from the Finnish Hospital Discharge and Cause-of-Death Registers was compared with that collected in the Helsinki Heart Study (HHS) during an 8.5-year follow-up. The purpose of the comparison was two-fold, firstly, to study the accuracy of registration of CHD and secondly, to find out what diagnostic codes to use for CHD in register-based follow-up studies. The HHS cases were used as the 'golden standard' and the CHD deaths and definite nonfatal acute myocardial infarctions (AMIs) (all diagnoses) were taken from the registers to establish the sensitivity of the Hospital Discharge and Cause-of-Death Registers combined. The sensitivity was 0.84 during the period 1980-86 and 0.87 during 1987-90, with the positive predictive values 0.94 and 0.92 respectively. The treatment effects seen in the HHS were compared with the effects that would have emerged, if register-based information only had been used with different definitions of CHD. Of the register-based calculations, the one with the definition 'all CHD deaths and hospitalizations with the ICD-8 code 410' came closest to the HHS result, with a 32% reduction (P=0.028 one-sided) of CHD incidence, while the original HHS result was a 34% reduction (P=0.008 one sided). However, when comparing Kaplan-Meier plots of cumulative hazards of CHD, the plot with a wider definition of CHD (ICD-8 and ICD-9 codes 410-414) came closest to the HHS experience, especially if revascularizations were included in the latter. Definite AMI as a single definition of CHD might thus not be sufficient when studying CHD risk, instead, at least two parallel definitions of CHD should be used.
In the 1960s, lung cancer among Finnish men was about 3.5 times as common as among Norwegian men. A study by Pedersen et al. in 1962 indicated that the difference in contemporary smoking habits could account for only part of the difference in lung cancer incidence in men between the countries. In that study, smoking habits in Finland and Norway were investigated via interviews of 8,700 people from six areas of each country. For the present study the Finnish and Norwegian cancer registries have followed lung cancer morbidity in those areas. When the interval between the recording of smoking habits and lung cancer incidence was 15 years, after adjustment for age and smoking habits, the Finnish males had a relative risk between 1.1 and 1.6 compared with Norwegian men. The results suggest that, given a sufficiently long latency period, almost the entire difference between Finnish and Norwegian men could be attributed to smoking habits.
The joint effect of shift work and certain adverse life-style factors on coronary heart disease (CHD) was studied.
Base-line measurements were obtained for a 6-year follow-up of an industrially employed cohort (N= 1806), whose shiftwork status was recorded from a questionnaire filled out by a sample of the cohort. The CHD end points (codes 410-414 of the 9th revision of the International Classification of Diseases) were obtained from official Finnish registers. In order that the joint effects of shift work and life-style factors on the risk of CHD could be studied, dichotomized variables and their combinations as a dummy variable system in Cox's proportional hazards models were used.
The relative risks were 1, 1.6[95% confidence interval (95% CI) 1.1-2.5], 1.3(95% CI 0.9-2.1), and 2.7(95% CI 1.8-4.1) for the following combinations of shift work (SW) and smoking (SM): SW-&SM-, SW-&SM+, SW+&SM-, and SW+&SM+, respectively; and the corresponding figures for shift work and obesity (BMI > or =28 kg/m2) were 1, 1.2(95% CI0.8-1.9), 1.3(95% CI0.9-1.9), and 2.3(95% CI1.5-3.6), respectively. In both cases the effect was at least multiplicative. For the shift workers the relative risk for CHD rose gradually with increasing numbers of adverse life-style factors, but for the day workers there was no clear dose-response pattern.
Shift work seems to trigger the effect of other, lifestyle-related risk factors of CHD and therefore calls for active prevention among shift workers.
The -344C allele of a 2-allele (C or T) polymorphism in the promoter of the gene encoding aldosterone synthase (CYP11B2) is associated with increased left ventricular size and mass and with decreased baroreflex sensitivity, known risk factors for morbidity and mortality associated with myocardial infarction (MI). We hypothesized that this polymorphism was a risk factor for MI.
We used a nested case-control design to investigate the relationships between this polymorphism and the risk of nonfatal MI in 141 cases and 270 matched controls from the Helsinki Heart Study, a coronary primary prevention trial in dyslipidemic, middle-aged men. There was a nonsignificant trend of increasing risk of MI with number of copies of the -344C allele. However, this allele was associated in a gene dosage-dependent manner with markedly increased MI risk conferred by classic risk factors. Whereas smoking conferred a relative risk of MI of 2.50 (P=0.0001) compared with nonsmokers in the entire study population, the relative risk increased to 4.67 in -344CC homozygous smokers (relative to nonsmokers with the same genotype, P=0.003) and decreased to 1.09 in -344TT homozygotes relative to nonsmokers with this genotype. Similar joint effects were noted with genotype and decreased HDL cholesterol level as combined risk factors.
Smoking and dyslipidemia are more potent risk factors for nonfatal MI in males who have the -344C allele of CYP11B2.
Notes
Comment In: Circulation. 2000 Dec 12;102(24):E18311113060
An association between human herpesvirus 8 (HHV8) and multiple myeloma (MM) has been reported, though most studies have not confirmed such association. To follow-up on a previous prospective seroepidemiological study, where HHV8 tended to associate with MM risk, we linked five large serum banks in the Nordic countries with the Nordic cancer registries and 329 prospectively occurring cases of MM were identified, together with 1631 control subjects matched by age and gender. The HHV8 seroprevalences among cases and controls were similar (12 and 15%, respectively) and HHV8 seropositivity did not associate with the risk of MM, neither when considering positivity for lytic antibodies (relative risk (RR) = 0.8, 95% confidence interval (CI) = 0.5-1.1) nor for latent antibodies (RR = 0.6, 95% CI = 0.1-2.7). Similar risks were seen when analysis was restricted to case-control sets with at least 2 years lag before diagnosis (RR = 0.8, 95% CI = 0.5-1.2 and RR = 0.9, 95% CI = 0.1-4.2). In conclusion, the data indicate that HHV8 infection is not associated with MM.
The role of an elevated serum leukocyte count (WBC) as a coronary risk factor was investigated using a nested case-control design in dyslipidemic middle-aged men (n = 420) participating in the Helsinki Heart Study, a coronary primary prevention trial. Baseline WBC was significantly higher, 6.93 (2.11) x 10(9)/L in subjects with cardiac events, than in controls, 6.26 (1.88) x 10(9)/L; p less than 0.002. This association was time-dependent, however, since the difference was not significant for events occurring during the second half of the 5-year study. Using nonsmokers in the lowest WBC tertile as the reference sample, the relative risks in the highest WBC tertile were 1.86 (95% confidence intervals [CI] 0.81 to 4.28) for nonsmokers and 3.07 (95% CI 2.23 to 8.19) for smokers. Logistic regression analysis including smoking in the model disclosed an independent contribution of elevated WBC to coronary heart disease. We conclude that elevated leukocyte count was a coronary risk factor even in this dyslipidemic population.
