Active smoking is a well-established risk factor for myocardial infarction, but less is known about the impact of passive smoking, and possible sex differences in risk related to passive smoking. We investigated active and passive smoking as risk factors for myocardial infarction in an 11-year follow-up of 11,762 men and 13,206 women included in the Tromsø Study. There were a total of 769 and 453 incident cases of myocardial infarction in men and women, respectively. We found linear age-adjusted relationships between both active and passive smoking and myocardial infarction incidence in both sexes. The relationships seem to be stronger for women than for men. Age-adjusted analyses indicated a stronger relationship with passive smoking in ever-smokers than in never-smokers. After adjustment for important confounders (body mass index, blood pressure, total cholesterol, HDL cholesterol and physical activity) the associations with active and passive smoking were still statistically significant. Adjusting for active smoking when assessing the effect of passive smoking and vice versa, indicated that the effect of passive smoking in men may be explained by their own active smoking. In women, living with a smoker =30 years after the age of 20 increased the myocardial infarction risk by 40 %, even after adjusting for active smoking. Passive smoking is a risk factor for myocardial infarction on its own, but whereas the effect for men seems to be explained by their own active smoking, the effect in females remains statistically significant.
The acyl pattern of adipose tissue triglycerides and of plasma free fatty acids were determined after 7 yr of diet intervention on elevated plasma cholesterol in 42 men taking part in the smoking-lipid trial of the Oslo Study. Twenty-two of the men were advised to change dietary habits (mainly reduce saturated fat) whereas the remaining 20 were controls. The adipose tissue from men in the intervention group contained relatively more linoleic and linolenic acids and relatively less saturated and monounsaturated fatty acids compared to men in the control group. There were strong correlations between the relative content of several fatty acids in adipose tissue triglycerides and plasma free fatty acid. Furthermore, there was a close correlation between the intake of polyunsaturated fatty acids found in a dietary survey done 2 to 3 yr before this study and the relative content of polyunsaturated fatty acids in adipose tissue.
The Swedish Society of Anaesthetists conducted a nationwide retrospective survey of clinical experience with extradural and intrathecal opiates. Special interest was focused on the frequency and type of ventilatory depression. The questionnaire was answered by 84 of 93 departments (90%). Up to May 1981 extradural morphine had been given to approximately 6000-9150 patients, extradural pethidine to 220-450 and intrathecal morphine to 90-150 patients. Ventilatory depression requiring treatment with naloxone was reported in 23 patients treated with extradural morphine (0.25-0.40%) and in six given intrathecal morphine (4-7%). In 22 patients the administration of extradural morphine was considered as a major contributory factor for the occurrence of ventilatory depression. Only two of these 22 patients experienced ventilatory depression later than 6 h after the last dose of opiates (S.C., i.m., i.v. or extradural). Patients aged 70 yr or more, those receiving thoracic extradural puncture and those with reduced ventilatory capacity seemed to be overrepresented.
Atherosclerosis begins early in life and is the major underlying cause of cardiovascular morbidity and death. Yet, population-based information on age and sex differences in the extent and morphology of atherosclerosis throughout life is scarce. Carotid atherosclerosis can be visualized with B-mode ultrasound and is a marker of atherosclerosis elsewhere in the circulation. We assessed both the prevalence and the morphology of carotid atherosclerosis by B-mode ultrasound in 3016 men and 3404 women, 25 to 84 years old, who participated in a population health survey. The participation rate was 88%. Plaque morphology was graded according to whether a plaque was predominantly soft (echolucent) or hard (echogenic). Atherosclerotic plaques were found in 55.4% of the men and 45.8% of the women. In men, there was a linear increase with age in the prevalence of carotid atherosclerosis, whereas in women, there was a curvilinear age trend, with an inflection in the prevalence rate of women at approximately 50 years of age. The male predominance in atherosclerosis declined after the age of 50 years, the plaque prevalence being similar in elderly men and women. Men had softer plaques than women; this sex difference in plaque morphology increased significantly (P=0.005) with age. The sex difference in the prevalence of atherosclerosis and the female age trend in atherosclerosis show significant changes at the age of approximately 50 years, suggesting an adverse effect of menopause on atherosclerosis. The higher proportion of soft plaques in men compared with women increases with age and may partly account for the prevailing male excess risk of coronary heart disease in the elderly despite a similar prevalence of atherosclerosis in elderly men and women.
In a cohort of 19,731 Norwegian postmenopausal women, the authors analyzed relations between the age at natural menopause and all-cause mortality. A total of 18,533 women died during the 37 years of follow-up from 1961 to 1997. An inverse relation was found between the age at menopause and the all-cause mortality rate (p = 0.003). The strength of the association was moderate, however, with 1.6% (95% confidence interval: 0.6, 2.7) reduced mortality per 3 years' increase in age at menopause. The impact appeared to be stronger in women with an attained age of less than 70 years (3.7% reduction in risk) than in women aged 80 years or more (1.0%). The inverse relation could not be explained by extreme mortality rates in women with very early (55 years) menopause or by possible confounding variables like birth cohort, place of residence, occupational category (own or husband's occupation), body mass index, age at menarche, and first and last delivery or parity. The smoking prevalence was low in the underlying population, and the use of hormone replacement therapy was very rare. The authors conclude that age at natural menopause is inversely related to all-cause mortality.
BACKGROUND AND PURPOSE: Young age at natural menopause has been related to increased cardiovascular mortality, but few studies have examined the relationship with stroke risk specifically. METHODS: In a cohort of 19,731 Norwegian women, we analyzed the relationship between age at natural menopause and stroke mortality. A total of 3561 women died of stroke during the 37-year follow-up from 1961 through 1997. Smoking prevalence was low in the underlying population, and use of hormone replacement therapy was very rare. RESULTS: No significant linear relationship was found between age at menopause and stroke mortality. A 3-year increase in age at menopause was associated with a 1.0% estimated increase in stroke mortality (95% CI, -1.5, 3.6). No relationships were found for ischemic strokes (271 deaths) or hemorrhagic strokes (389 deaths) when considering the stroke deaths with sufficient information on death certificates. The estimate of the association between age at natural menopause and stroke mortality was hardly influenced by mortality in women with very early (aged 55 years) menopause, or by a number of possible confounding variables. CONCLUSIONS: Age at natural menopause is essentially unrelated to stroke mortality.
High levels of microalbuminuria have been associated with severe atherosclerosis. In this prospective, population-based study, we examined whether urinary albumin-to-creatinine-ratios (ACR) in the lower range were associated with the initiation and progression of atherosclerosis.
Carotid ultrasonography and measurements of ACR, fibrinogen, monocytes, white cell count, and well-established cardiovascular risk factors were performed in 4037 non-diabetic subjects, 2203 without, and 1834 with pre-existing plaques at baseline. After 7 years new ultrasound measurements were performed. In subjects without pre-existing plaques, 884 had developed at least one plaque during follow-up. Baseline ACR was significantly related to the area of the novel plaques (P for linear trend = 0.009 over the baseline ACR quartiles, after multiple adjustments). The relationship with ACR was clearly modified by fibrinogen (P = 0.001, for the interaction ACR x fibrinogen). Subjects with high levels of both ACR and fibrinogen developed plaques with the largest area. In subjects with pre-existing plaques, ACR was related to plaque-progression (P for linear trend = 0.026, after multiple adjustments). In these individuals, the interaction between fibrinogen and ACR on plaque-growth appeared only in those with minimal atherosclerosis at baseline.
ACR is positively related to plaque-initiation and plaque-growth. This relationship is substantially modified by fibrinogen in previously plaque-free subjects.
Comment In: Eur Heart J. 2007 Feb;28(3):271-317251260
Attention deficit hyperactivity disorder (ADHD) is a common behavioral disorder affecting children and adults. It has been suggested that gene variants related to serotonin neurotransmission are associated with ADHD. We tested the functional promoter polymorphism 5-HTTLPR and seven single nucleotide polymorphisms in SLC6A4 for association with ADHD in 448 adult ADHD patients and 580 controls from Norway. Replication attempts were performed in a sample of 1454 Caucasian adult ADHD patients and 1302 controls from Germany, Spain, the Netherlands and USA, and a meta-analysis was performed also including a previously published adult ADHD study. We found an association between ADHD and rs140700 [odds ratio (OR ) = 0.67; P = 0.01] and the short (S) allele of the 5-HTTLPR (OR = 1.19; P = 0.06) in the Norwegian sample. Analysis of a possible gender effect suggested that the association might be restricted to females (rs140700: OR = 0.45; P = 0.00084). However, the meta-analysis of 1894 cases and 1878 controls could not confirm the association for rs140700 [OR = 0.85, 95% confidence interval (CI) = 0.67-1.09; P = 0.20]. For 5-HTTLPR, five of six samples showed a slight overrepresentation of the S allele in patients, but meta-analysis refuted a strong effect (OR = 1.10, 95% CI = 1.00-1.21; P = 0.06). Neither marker showed any evidence of differential effects for ADHD subtype, gender or symptoms of depression/anxiety. In conclusion, our results do not support a major role for SLC6A4 common variants in persistent ADHD, although a modest effect of the 5-HTTLPR and a role for rare variants cannot be excluded.
BACKGROUND: Low levels of physical activity is associated with major health problems. However, no overview of the level of physical activity outside work or school in Norway has been made, which is important in order to implement targeted interventions. MATERIAL AND METHODS: Based on published as well as unpublished data, we present data on physical activity in Norway--among children and adolescents, adults and elderly people. RESULTS: Results from different studies differ markedly. However, the main findings are these: The level of physical activity increases in childhood up until about 13 years of age. Approximately 70% of adolescents are active two hours or more a week beyond school-hours. The proportion of physical active youngsters then decreases towards young adulthood. Adults and elderly people get more inactive with increasing age. Data on physical activity from the past 10-15 years suggest a slight increase in the proportion of moderately active Norwegians. INTERPRETATION: Research on physical activity is impeded by the fact that different studies have operationalized physical activity differently and used different age grouping. There is a need for surveys in representative samples with standardised and validated questions, with uniform age classification, covering the full spectre of physical activity. In addition, we need smaller studies with more comprehensive measures of physical activity in Norway.
To investigate the association between echocardiographic measurements with emphasis on diastolic dysfunction and risk of atrial fibrillation (AF) in a population-based cohort study.
We followed 2406 participants from the Tromsø Study from 1994 to 2010. Left atrial (LA) size and mitral Doppler indices as measured by echocardiography were used for evaluating diastolic dysfunction. Information concerning age, systolic blood pressure, height, heart rate, body mass index, total and high-density lipoprotein cholesterol, self-reported use of alcohol, smoking, coffee, physical activity, antihypertensive treatment, prevalent coronary heart disease, valvular heart disease, heart failure, hypertrophy, diabetes and palpitations were obtained at baseline. The outcome measure was clinical AF, documented by an ECG.
AF was detected in 462 subjects (193 women). Mean age at baseline was 62.6 years. Incidence rate of clinical AF was 12.6 per 1000 person-years. In multivariable Cox proportional hazards regression analysis, moderately enlarged LA was associated with 60% (95% CI 1.2 to 2.0) increased risk of AF. Severely enlarged LA had HR for AF of 4.2 (95% CI 2.7 to 6.5) with p value for linear trend