Admissions to Norwegian Hospitals during the COVID-19 Pandemic.

BACKGROUND: In mid-March 2020, the Norwegian government implemented measures to contain the coronavirus disease 2019 (COVID-19) pandemic, and hospitals prepared to handle an unpredictable inflow of patients with COVID-19. AIM: The study was performed to describe the changes in hospital admissions during the first phase of the pandemic. METHODS: The Norwegian Institute of Public Health established a national preparedness register with daily updates on COVID-19 cases and the use of health services. We used individual-level information on inpatients from the electronic journal systems for all hospitals in Norway to estimate daily hospital admissions. RESULTS: Before the onset of the pandemic in March, there was an average of 2400 inpatient admissions per day in Norway, which decreased to approximately 1500 in the first few days after lockdown measures were implemented. The relative magnitudes of the decreases were similar in men and women and across all age groups. The decreases were substantial for both elective (54%) and emergency (29%) inpatient care. The admission rate gradually increased and reached pre-pandemic levels in June. However, the reductions in admissions for pneumonia and chronic obstructive pulmonary disease seemed to persist. CONCLUSIONS: The elective and emergency inpatient admission rates were substantially reduced a few days after the pandemic response measures were implemented. The ways in which the lack or postponement of care may have affected the health and well-being of patients is an important issue to be addressed in future research.

Ethnic differences in risk factors and total risk of cardiovascular disease based on the Norwegian CONOR study.

BACKGROUND: Risk of cardiovascular disease varies between ethnic groups and the aim of this study was to investigate differences in cardiovascular risk factors, and total cardiovascular risk between ethnic groups in Norway. DESIGN: Cross-sectional study using data from the Cohort of Norway (CONOR). METHODS: A sample of 62,145 participants, 40-65 years of age, originating from 11 geographical regions, were included in our study. Self-reported variables, blood samples and physical measurements were used to estimate age- and time-adjusted mean values of cardiovascular risk factors for different ethnic groups. The 10-year risks of cardiovascular mortality and cardiovascular events were calculated using the Framingham and NORRISK risk models. RESULTS: We observed differences between ethnic groups for cardiovascular risk factors and both Framingham and NORRISK risk scores. NORRISK showed significant differences by ethnicity in women only. Immigrants from the Indian subcontinent had the lowest high-density lipoprotein (HDL) levels, the highest levels of blood glucose, triglycerides, total cholesterol/HDL ratio, waist hip ratio and diabetes prevalence. Immigrants from the former Yugoslavia had the highest Framingham scores, high blood pressure, high total cholesterol/HDL ratio, overweight measures and smoking. Low cardiovascular risk was observed among East Asian immigrants. CONCLUSION: The previously reported excess cardiovascular risk among immigrants from the Indian subcontinent was supported in this study. We also showed that immigrants from the former Yugoslavian countries had a higher total 10-year risk of cardiovascular events than other ethnic groups. This study adds information about ethnic groups in Norway which needs to be addressed in further research and targeted prevention strategies.

A prospective study of intake of trans-fatty acids from ruminant fat, partially hydrogenated vegetable oils, and marine oils and mortality from CVD.

Trans-fatty acids (TFA) have adverse effects on blood lipids, but whether TFA from different sources are associated with risk of CVD remains unresolved. The objective of the present study was to evaluate the association between TFA intake from partially hydrogenated vegetable oils (PHVO), partially hydrogenated fish oils (PHFO) and ruminant fat (rTFA) and risks of death of CVD, CHD, cerebrovascular diseases and sudden death in the Norwegian Counties Study, a population-based cohort study. Between 1974 and 1988, participants were examined for up to three times. Fat intake was assessed with a semi-quantitative FFQ. A total of 71,464 men and women were followed up through 2007. Hazard ratios (HR) and 95 % CI were estimated with Cox regression. Energy from TFA was compared to energy from all other sources, carbohydrates or unsaturated cis-fatty acids with different multivariable models. During follow-up, 3870 subjects died of CVD, 2383 of CHD, 732 of cerebrovascular diseases and 243 of sudden death. Significant risks, comparing highest to lowest intake category, were found for: TFA from PHVO and CHD (HR 1.23 (95 % CI 1.00, 1.50)) and cerebrovascular diseases (HR 0.65 (95 % CI 0.45, 0.94)); TFA from PHFO and CVD (HR 1.14 (95 % CI 1.03, 1.26)) and cerebrovascular diseases (HR 1.32 (95 % CI 1.04, 1.69)); and rTFA intake and CVD (HR 1.30 (95 % CI 1.05, 1.61)), CHD (HR 1.50 (95 % CI 1.11, 2.03)) and sudden death (HR 2.73 (95 % CI 1.19, 6.25)) in women. These associations with rTFA intake were not significant in men (P interaction ≥ 0.01). The present study supports that TFA intake, irrespective of source, increases CVD risk. Whether TFA from PHVO decreases risk of cerebrovascular diseases warrants further investigation.

Nonfasting triglycerides and risk of cardiovascular death in men and women from the Norwegian Counties Study.

The association between nonfasting triglycerides and cardiovascular disease (CVD) has recently been actualized. The aim of the present study was to investigate nonfasting triglycerides as a predictor of CVD mortality in men and women. A total of 86,261 participants in the Norwegian Counties Study 1974-2007, initially aged 20-50 years and free of CVD were included. We estimated hazard ratios (HRs) for deaths from CVD, ischemic heart disease (IHD), stroke and all causes by level of nonfasting triglycerides. Mean follow-up was 27.0 years. A total of 9,528 men died (3,620 from CVD, 2,408 IHD, 543 stroke), and totally 5,267 women died (1,296 CVD, 626 IHD, 360 stroke). After adjustment for CVD risk factors other than HDL-cholesterol, the HRs (95% CI) per 1 mmol/l increase in nonfasting triglycerides were 1.16 (1.13-1.20), 1.20 (1.14-1.27), 1.26 (1.19-1.34) and 1.09 (0.96-1.23) for all cause mortality, CVD, IHD, and stroke mortality in women. Corresponding figures in men were 1.03 (1.01-1.04), 1.03 (1.00-1.05), 1.03 (1.00-1.06) and 0.99 (0.92-1.07). In a subsample where HDL-cholesterol was measured (n = 40,144), the association between CVD mortality and triglycerides observed in women disappeared after adjustment for HDL-cholesterol. In a model including the Framingham CHD risk score the effect of triglycerides disappeared in both men and women. In conclusion, nonfasting triglycerides were associated with increased risk of CVD death for both women and men. Adjustment for major cardiovascular risk factors, however, attenuated the effect. Nonfasting triglycerides added no predictive information on CVD mortality beyond the Framingham CHD risk score in men and women.

Ethnic differences in SCORE cardiovascular risk in Oslo, Norway.

AIM: To compare the estimated 10-year risk of cardiovascular death between ethnic Norwegians and five immigrant groups in Norway, according to the European Systematic Coronary Risk Evaluation (SCORE) system. METHODS: Data were obtained from the Oslo Health Study and the Oslo Immigrant Health Study (2000-2002). Fourteen thousand eight hundred and fifty-six individuals born between 1940 and 1971 in Norway, Turkey, Iran, Pakistan, Sri Lanka and Vietnam were included in the study. The European SCORE high-risk models, one including total cholesterol and the other including total cholesterol/HDL cholesterol ratio, were used to estimate 10-year cardiovascular mortality risk. A model assuming no smoking was also applied. Age was projected to 60 years and estimates were adjusted for age at screening. RESULTS: Norwegians had higher total cholesterol and systolic blood pressure, but lower triglycerides and higher HDL cholesterol compared with immigrants. The mean SCORE (total cholesterol model) varied between 6.6% (Turkey) and 5.4% (Sri Lanka) in men, and 2.1% (Norway) and 1.5% (Pakistan, Sri Lanka and Vietnam) in women. Application of the ratio model gave higher estimated risk in all immigrant groups except for Vietnamese, with 10-year risk varying between 7.7% (Turkey/Pakistan) and 5.7% (Vietnam) in men, and 2.0% (Norway) and 1.5% (Vietnam) in women. When the ratio model was applied assuming no smoking in all ethnic groups, the mean SCORE risk was reduced by 30% in Turkish men and 25% in Norwegian women, with less significant reductions observed in the other groups. CONCLUSION: Norwegians ranked high with the SCORE total cholesterol model and Norwegian men low with the SCORE ratio model. Although the predictive accuracy of the SCORE models for immigrants in Norway remains to be evaluated, our findings suggest that the ratio model could be more applicable to the entire population in Norway.

The ability of the SCORE high-risk model to predict 10-year cardiovascular disease mortality in Norway.

AIMS: To evaluate the predictive accuracy of the Systematic Coronary Risk Evaluation (SCORE) project high-risk function in Norway. METHODS AND RESULTS: We included 57 229 individuals screened in 1985-1992 from two population-based surveys in Norway (age groups 40-49, 50-59, and 60-69 years). The data have been linked to the Norwegian Cause of Death Registry. The SCORE high-risk algorithm for the prediction of 10-year cardiovascular disease (CVD) mortality was applied, and the risk factors entered into the model were age, sex, total cholesterol, systolic blood pressure, and smoking (yes/no). The number of expected events estimated by the SCORE model (E) was compared with the observed numbers (O). The SCORE low-risk algorithm was studied for comparison. In men, the observed number of CVD deaths was 718, compared with 1464 estimated by the SCORE high-risk function (O/E ratios 0.53, 0.53 and 0.45, for age groups 40-49, 50-59 and 60-69, respectively). In women, the observed and expected numbers were 226 and 547. The O/E ratios decreased with age (ratios 0.60, 0.45 and 0.37, respectively), i.e. the overestimation increased with age. The low-risk function predicted reasonably well for men (ratios 0.85, 0.92 and 0.79, respectively), whereas an overestimation was found for women aged 50-59 and 60-69 years (ratios 0.69 and 0.56, respectively). CONCLUSION: The SCORE high-risk model overestimated the number of CVD deaths in Norway. Before implementation in clinical practice, proper adjustments to national levels are required.

The SCORE risk model applied to recent population surveys in Norway compared to observed mortality in the general population.

AIMS: To compare the predictions of the Systematic Coronary Risk Evaluation (SCORE) high- and low-risk functions applied to a recent population study with observed cardiovascular disease (CVD) mortality estimated from annual official mortality statistics in Norway. METHODS: Data were obtained from large epidemiological surveys conducted in five Norwegian counties in 2000-2003. RESULTS: A total of 32 251 men and women were investigated (aged 30-31, 40-41, 45-46, and 59-61). For men aged >or=59, more than 75% qualified for preventive treatment by having a 10-year risk >or=5%. Few women and practically no men younger than 46 years can be considered at high risk according to the SCORE risk prediction models. For men, the high-risk function overestimated and the low-risk model underestimated the CVD mortality as compared to the 10-year risks calculated from official mortality statistics (1999-2003). For women, however, both functions underestimated mortality in young individuals, whereas in the elderly an overestimation was observed. CONCLUSIONS: The risk predictions depended strongly on age and gender. The SCORE high-risk function overestimates the risk of fatal CVD for men in Norway, and before implementation in clinical practice, proper adjustments to national levels are required.

The effects of long-term diet and omega-3 fatty acid supplementation on coagulation factor VII and serum phospholipids with special emphasis on the R353Q polymorphism of the FVII gene.

The aim of the present study was to investigate the effect of long-term diet and very long chain n-3 fatty acids (VLC n-3) intervention on plasma coagulation factor VII (FVII), choline-containing phospholipids (PC) and triglycerides (TG), especially related to the R353Q polymorphism of the FVII gene. The present investigation included 219 subjects from the Diet and Omega-3 Intervention Trial on atherosclerosis (DOIT), a 2x2 factorial designed study in elderly men with long-standing hypercholesterolemia. The subjects were randomly allocated to receive placebo capsules (corn oil) (control), placebo capsules and dietary advice ("Mediterranean type" diet), VLC n-3 capsules, or VLC n-3 capsules and dietary advice combined. The R353Q genotype and the levels of FVIIc, FVIIag, FVIIa, PC, and TG at baseline and after 6 months were determined. Diet intervention was followed by a significant reduction of 5.1% in the levels of FVIIag and 2.4 mU/ml in FVIIa (95% CI -7.4, -2.9, and -3.8, -1.1, respectively) (both p<0.001) compared to the no diet group, independent of genotype. No effects of diet intervention on FVIIc, PC or TG were observed. After VLC n-3 supplementation the TG levels were significantly reduced compared to placebo (p=0.01), whereas all FVII levels and PC remained unchanged. Dietary advice towards a "Mediterranean type" diet, but not VLC n-3 supplementation, was shown to reduce the levels of FVIIag and FVIIa after 6 months, independent of genotype. The results indicate the dietary advice to be more favourable in reducing this risk factor for CVD as compared to specific VLC n-3 supplementation.

Coagulation factor VII, R353Q polymorphism, and serum choline-containing phospholipids in males at high risk for coronary heart disease.

INTRODUCTION: Elevated levels of coagulation factor VII (FVII) have been associated with increased risk for myocardial infarction (MI). The R353Q polymorphism of the FVII gene has been shown to modify plasma levels of FVII, and has in some studies also been associated with reduced risk for MI. OBJECTIVES: To examine the R353Q polymorphism of the FVII gene and the relation to myocardial infarction (MI), cardiovascular disease (CVD), and diabetes, and furthermore, to elucidate the association between the polymorphism and plasma levels of FVII coagulant activity (FVIIc), FVII antigen (FVIIag), activated FVII (FVIIa), and serum choline-containing phospholipids (PC). METHODS: In 560 elderly men characterised as hypercholesterolemic in 1972, we examined the R353Q polymorphism by melting curve analysis after real-time PCR. In a subgroup of 205 individuals, FVIIc, FVIIag, FVIIa, and PC were analysed. RESULTS: There were no significant associations between genotype and the disease states, although we observed a lower number of MI cases among subjects with the Q allele, compared to the RR individuals (14% vs. 19%). FVIIag and FVIIc levels were lower in RQ compared to RR subjects, whereas for FVIIa the opposite was observed (p<0.001 for all). PC correlated positively with FVIIag (r=0.24, p<0.001), but negatively with FVIIa (r=-0.25, p<0.001). No genotype specific interactions were found for the association between FVII and PC. CONCLUSION: No significant associations between the R353Q polymorphism and MI, CVD, or diabetes were observed, although the polymorphism strongly influenced plasma levels of FVII. Serum PC correlated significantly with FVIIag and inversely with FVIIa, independently of genotype.

A diet rich in coconut oil reduces diurnal postprandial variations in circulating tissue plasminogen activator antigen and fasting lipoprotein (a) compared with a diet rich in unsaturated fat in women.

The effects of high and low fat diets with identical polyunsaturated/saturated fatty acid (P/S) ratios on plasma postprandial levels of some hemostatic variables and on fasting lipoprotein (a) [Lp(a)] are not known. This controlled crossover study compared the effects of a high fat diet [38.4% of energy (E%) from fat; HSAFA-diet, P/S ratio 0.14], a low fat diet (19.7 E% from fat; LSAFA-diet, P/S ratio 0.17), both based on coconut oil, and a diet with a high content of monounsaturated fatty acids (MUFA) and PUFA (38.2 E% from fat; HUFA-diet, P/S ratio 1.9) on diurnal postprandial levels of some hemostatic variables (n = 11) and fasting levels of Lp(a) (n = 25). The postprandial plasma concentration of tissue plasminogen activator antigen (t-PA antigen) was decreased when the women consumed the HSAFA-diet compared with the HUFA-diet (P = 0.02). Plasma t-PA antigen was correlated with plasminogen activator inhibitor type 1 (PAI-1) activity when the participants consumed all three diets (Rs = 0.78, P < 0.01; Rs = 0.76, P < 0.01; Rs = 0.66, P = 0.03; on the HSAFA-, the LSAFA- and the HUFA-diet, respectively), although the diets did not affect the PAI-1 levels. There were no significant differences in postprandial variations in t-PA activity, factor VII coagulant activity or fibrinogen levels due to the diets. Serum fasting Lp(a) levels were lower when women consumed the HSAFA-diet (13%, P < 0.001) and tended to be lower when they consumed the LSAFA-diet (5.3%, P = 0.052) than when they consumed the HUFA-diet. Serum Lp(a) concentrations did not differ when the women consumed the HSAFA- and LSAFA-diets. In conclusion, our results indicate that a coconut oil-based diet (HSAFA-diet) lowers postprandial t-PA antigen concentration, and this may favorably affect the fibrinolytic system and the Lp(a) concentration compared with the HUFA-diet. The proportions of dietary saturated fatty acids more than the percentage of saturated fat energy seem to have a beneficial influence on Lp(a) levels.

The serum LDL/HDL cholesterol ratio is influenced more favorably by exchanging saturated with unsaturated fat than by reducing saturated fat in the diet of women.

We compared the effects of a high fat diet [38.4% of energy (E%) from fat; HSAFA diet, polyunsaturated/saturated fatty acid (P/S) ratio = 0.14], a low fat diet (19.7 E% from fat; LSAFA diet, P/S = 0.17), both based on coconut oil, and a diet with a high content of mono- and polyunsaturated fatty acids (PUFA; 38.2 E% from fat; HUFA diet, P/S = 1.9) on serum lipoproteins. The 25 women studied consumed each diet for 3-wk periods in a crossover design. The two high fat diets were identical except for the quality of the test fat. The LSAFA diet was identical to the HSAFA diet except that half the fat was replaced by carbohydrates. Serum total cholesterol, LDL cholesterol and apoB concentrations did not differ between the HSAFA and the LSAFA diet periods. Total cholesterol, LDL cholesterol and apoB were lower when women consumed the HUFA diet than when they consumed the other two diets. HDL cholesterol and apoA-I were 15 and 11%, respectively, higher when women consumed the HSAFA diet than when they consumed the LSAFA diet; HDL cholesterol and apoA-I were lower when women consumed the HUFA diet than when they consumed the HSAFA diet, but not the LSAFA diet. The LDL cholesterol/HDL cholesterol and apoB/apoA-I ratios were higher when women consumed the LSAFA diet than when they consumed the HSAFA diet. The LDL/HDL cholesterol ratio was higher when women consumed either the LSAFA or the HSAFA diet than when they consumed the HUFA diet, whereas apoB/apoA-I was higher when women consumed the LSAFA diet than when they consumed the HUFA diet. Triacylglycerol and VLDL cholesterol were higher when women consumed the LSAFA diet than when they consumed either the HSAFA or the HUFA diet. We conclude that, to influence the LDL/HDL cholesterol ratio, changing the proportions of dietary fatty acids may be more important than restricting the percentage of total or saturated fat energy, at least when derived mainly from lauric and myristic acids, both of which increase HDL cholesterol.