Biomedical subjects

I Hjermann

Publications and source records attributed to I Hjermann.

At least 37 records · Page 2Linked to original sources

PubMed1998

Effects of doxazosin and atenolol on atherothrombogenic risk profile in hypertensive middle-aged men.

The alpha-blockers prazosin and doxazosin reduce hypertriglyceridemia (HTG) and increase serum levels of high-density lipoprotein (HDL)-cholesterol, whereas beta-blockers such as atenolol have the opposite effect. As HTG is associated with reduced fibrinolysis and hypercoagulability, we investigated the effects of doxazosin and atenolol on serum lipids and hemostatic factors in hypertensive men with an atherothrombogenic risk profile. The study was randomized and open, but blinded to investigator of biochemical results. Forty-five men (mean age, 44.5 years) with central obesity [median body-mass index (BMI), 28 kg/m2] and moderate hypertension [median diastolic blood pressure (DBP), 104.5 mm Hg] were treated with atenolol (n = 22) or doxazosin (n = 23) for 22 weeks, after which changes in between-group differences from baseline were estimated. After intervention, significant between-group differences in favor of doxazosin were found: lower triglycerides (p = 0.008) and higher HDL cholesterol (p = 0.036); furthermore, improvement of fibrinolysis: lower plasminogen activator inhibitor-1 (PAI-1) activity (p = 0.012), higher tissue plasminogen activator (tPA) activity after venous occlusion (VO); and higher levels of serum D-dimer, both unstimulated (p = 0.0016) and after VO (p = 0.0032). In addition, lower levels of serum testosterone were found in the atenolol group (p = 0.0016). A profile with reduced HTG, increased HDL cholesterol, and improved fibrinolysis was obtained with doxazosin when compared with atenolol. Furthermore, the observed decrease in serum testosterone on atenolol treatment would rather favor long-term treatment with doxazosin in this study population.

Adult↗

PubMed1998

Associations between central obesity and indexes of hemostatic, carbohydrate and lipid metabolism. Results of a 1-year intervention from the Oslo Diet and Exercise Study.

The relationships of central obesity and physical fitness to indexes of hemostatic, lipid and glucose metabolism both at baseline and after 1 year of diet and exercise intervention were examined in 209 sedentary middle-aged men and women with increased coronary risk factor levels. Central obesity was measured as either waist circumference or waist/hip ratio. Maximal oxygen uptake was used as a measure of physical fitness. The cross-sectional results show that there were significant correlations between waist circumference and euglobuline clot lysis time (r = 0.23), factor VII (r = 0.16), glucose and insulin before and after 1 h glucose load (r ranging from 0.32 to 0.50). The 1-year intervention gave the following associations between changes in waist circumference and changes in: euglobuline clot lysis time (r = 0.27), factor VII (r = 0.19), carbohydrate variables and lipids (magnitude of r ranging from 0.19 to 0.43). Also the other indexes of obesity and physical fitness showed significant correlations to indexes of hemostatic, lipid and glucose variables, both cross-sectionally and for changes after the 1-year intervention. The associations between changes in central obesity and changes in indexes of hemostatic, carbohydrate and lipids were generally stronger during 1 year of diet and exercise intervention than those found at baseline. Multiple regression analyses with waist circumference, waist/hip ratio, percent body fat and Vo2 max as independent variables and indexes of hemostatic, carbohydrate and lipid metabolism as dependent variables showed that waist circumference was a significant predictor for indexes of the hemostatic, carbohydrate and lipid metabolism, mostly independent of physical fitness. The cross-sectional and 1-year change results support each other and therefore underscore the importance of abdominal obesity as an important risk factor for cardiovascular disease.

Adult↗

PubMed1997

[Cholesterol lowering therapy after myocardial infarction. Consequences of the CARE study].

In the recently published CARE-study, 4,159 patients aged 21-75 years were included and randomised to treatment with pravastatin 40 mg once daily or placebo 3-20 months following a myocardial infarction. Inclusion criteria were a total cholesterol < 6.2 mmol/l and LDL-cholesterol 3.0-4.5 mmol/l. Mean follow-up time was five years. Average reduction of total cholesterol was 20% and of LDL-cholesterol 28% in the treatment group. The incidence of coronary death or non-fatal myocardial infarction was reduced by 24% (p = 0.003). The cholesterol levels in the CARE-study were similar to those in most western populations and lower than in the 4S study. This must be considered when evaluating the different results of the treatment in the two studies. It seems fair not only to offer statin treatment to patients complying with the 4S inclusion criteria, but also to patients with values as in the CARE population.

Adult↗

PubMed1997

Peroxidation of LDL from combined-hyperlipidemic male smokers supplied with omega-3 fatty acids and antioxidants.

The effects of marine omega-3 polyunsaturated fatty acids (FAs) and antioxidants on the oxidative modification of LDL were studied in a randomized, double-blind, placebo-controlled trial. Male smokers (n = 41) with combined hyperlipidemia were allocated to one of four groups receiving supplementation with omega-3 FAs (5 g eicosapentaenoic acid and docosahexaenoic acid per day), antioxidants (75 mg vitamin E, 150 mg vitamin C, 15 mg beta-carotene, and 30 mg coenzyme Q10 per day), both omega-3 FAs and antioxidants, or control oils. LDL and human mononuclear cells were isolated from the patients at baseline and after 6 weeks of supplementation. LDL was subjected to cell-mediated oxidation by the patients' own mononuclear cells, as well as to Cu(2+)-catalyzed and 2,2'-azobis-(2-amidinopropane hydrochloride) (AAPH)-initiated oxidation. Extent of LDL modification was measured as lag time, the formation rate of conjugated dienes (CDs), the maximum amount of CDs formed, formation of lipid peroxides, and the relative electrophoretic mobility of LDL on agarose gels. Dietary supplementation with omega-3 FAs increased the concentration of total omega-3 FAs in LDL and reduced the concentration of vitamin E in serum. The omega-3 FA-enriched LDL particles were not more susceptible to Cu(2+)-catalyzed, AAPH-initiated, or autologous cell-mediated oxidation than control LDL. In fact, enrichment with omega-3 FAs significantly reduced the formation rate of CDs when LDL was subjected to AAPH-induced oxidation. Supplementation with moderate amounts of antioxidants significantly increased the concentration of vitamin E in serum and increased the resistance of LDL to undergo Cu(2+)-catalyzed oxidation, measured as increased lag time, reduced formation of lipid peroxides, and reduced relative electrophoretic mobility compared with control LDL. Supplementation with omega-3 FAs/antioxidants showed oxidizability of LDL similar to that of control LDL and omega-3 FA-enriched LDL. In conclusion, omega-3 FAs neither rendered the LDL particles more susceptible to undergo in vitro oxidation nor influenced mononuclear cells' ability to oxidize autologous LDL, whereas moderate amounts of antioxidants protected LDL against oxidative modification.

Administration, Oral↗

PubMed1997

Lifestyle changes may reverse development of the insulin resistance syndrome. The Oslo Diet and Exercise Study: a randomized trial.

OBJECTIVE: To compare and assess the single and joint effect of diet and exercise intervention for 1 year on insulin resistance and the development leading toward the insulin resistance syndrome. RESEARCH DESIGN AND METHODS: An unmasked, randomized 2 x 2 factorial intervention trial was applied with a duration of 1 year for each participant. The trial comprised 219 men and women with diastolic blood pressure of 86-99 mmHg, HDL cholesterol < 1.20 mmol/l, triglycerides > 1.4 mmol/l, total cholesterol of 5.20-7.74 mmol/l, and BMI > 24 kg/m2. Participants were randomly allocated to diet group (n = 35), diet and exercise group (n = 67), exercise group (n = 54), and control group (n = 43). The diet included increased intake of fish and reduced total fat intake. The exercise program entailed supervised endurance exercise three times a week. Baseline cross-sectional changes and 1-year changes in insulin resistance, fasting serum levels of insulin, C-peptide, proinsulin, glucose, and lipids as well as weight, mean blood pressure, and plasminogen activator inhibitor 1 (PAI-1) values were recorded. RESULTS: The cross-sectional results at baseline showed significant correlations between the calculated insulin resistance and BMI (r = 0.54) and correlations between the mean blood pressure (mBP) (r = 0.26) and PAI-1 (r = 0.40). The 1-year diet intervention gave a significant decrease in the calculated insulin resistance from 4.6 to 4.2 and a positive correlation between the changes in insulin resistance and changes in BMI (r = 0.40). The diet and exercise intervention also led to significantly decreased insulin resistance (from 5.0 to 4.0). The exercise intervention did not significantly change insulin resistance. CONCLUSIONS: The cross-sectional and 1-year intervention results supported each other and underscored the important connection between increased BMI and the development leading toward the insulin resistance syndrome.

Blood Glucose↗

PubMed1996

Exercise-induced increase in lipoprotein (a).

In the Oslo Diet and Exercise Study (ODES) 219 healthy middle-aged physically inactive persons with moderately deranged risk factor levels (increased bodyweight, diastolic blood pressure, serum cholesterol, triglycerides, decreased HDL-cholesterol) were randomized to 4 intervention groups: dietary intervention, exercise, diet + exercise and control. The purpose of the study was to test if these interventions maintained for a year, isolated or in combination, would change coronary risk factor levels as compared to control. One of the risk factors included was lipoprotein (a) (Lp(a)). The hypothesis to be tested was if physical exercise would be associated with increased levels of Lp(a) as a result of intervention. Those who exercised increased their Lp(a) levels with 15.4 (S.E. = 8.0) mg/l as compared to no exercise (P < 0.05). Also, dietary intervention tended to increase Lp(a), but the increase did not reach statistical significance. There was no detectable interaction on the effect on Lp(a) of the two intervention modalities. A dose-response relationship was found between change in the exercise-specific variables heart rate and peak oxygen uptake, and Lp(a)-change and this dose-response was most pronounced in the exercise group. Change in Lp(a) was associated to change in several lifestyle related variables such as alcohol intake and waist circumference, pointing to the possibility that Lp(a), at least in some subpopulations, is more amenable to change through lifestyle alterations than reported so far.

Adult↗

PubMed1996

LPS induced release of IL-1 beta, IL-6, IL-8 and TNF-alpha in EDTA or heparin anticoagulated whole blood from persons with high or low levels of serum HDL.

We have examined the lipopolysaccharide (LPS) induced release of interleukin 1 beta (IL-1 beta), IL-6, IL-8 and tumour necrosis factor alpha (TNF-alpha), in EDTA or heparin anticoagulated whole blood, from persons with high or low levels of high density lipoprotein (HDL), incubated at 37 degrees C for up to 20 h. In general, 100 ng LPS/ml gave two to twenty times higher responses than 1 ng LPS/ml, and heparin ten to hundred times higher than EDTA. The release of IL-8 was significantly higher in persons with high HDL, and was correlated with HDL, and inversely correlated with triglycerides and sCD14. The release of IL-1 beta, IL-6 and TNF-alpha was correlated with total cholesterol at medium doses of LPS (100 ng/ml), and inversely correlated with lipopolysaccharide-binding protein (LBP) at low doses of LPS (1 ng/ml). Serum levels of LBP were higher in persons with HDL, although not significantly. These results show LPS responsiveness of pro-inflammatory cytokines in whole blood from persons with high and low levels of HDL to be different, presumably of importance in inflammation and atherogenesis.

Anticoagulants↗

PubMed1996

Improved carbohydrate metabolism after physical training and dietary intervention in individuals with the "atherothrombogenic syndrome'. Oslo Diet and Exercise Study (ODES). A randomized trial.

OBJECTIVES: To compare the single and joint effect of 1-year diet and exercise intervention on carbohydrate metabolism and associated coronary risk variables. DESIGN: Unmasked, randomized, 2 x 2 factorial intervention trial with 1-year duration for each participant. SETTING: The participants were recruited from a screening examination of 40-year-old persons in Oslo, Norway. SUBJECTS: Two hundred and nineteen sedentary men and women, with diastolic blood pressure 86-99 mmHg, HDL cholesterol < 1.20 mmol L-1, triglycerides > 1.4 mmol L-1, total cholesterol 5.20-7.74 mmol L-1 and BMI > 24. Participants were randomly allocated to control (n = 43), diet (n = 55), exercise (n = 54) and diet+exercise (n = 67). INTERVENTIONS: Exercise: supervised endurance exercise three times a week. Diet: reduce weight, increase the intake of fish and reduce total fat intake. MAIN OUTCOME MEASURES: One-year changes in insulin and glucose before and after a standardized glucose load. RESULTS: As compared with controls fasting insulin in pmol L-1 decreased significantly in the combined diet and exercise group (3.9 +/- 6.2 versus -22.6 +/- 4.7 respectively, P = 0.003). Insulin in pmol L-1 after glucose load decreased significantly in all intervention groups compared to controls (diet: -82.2 +/- 49.9 P = 0.02; exercise: -92.4 +/- 60.1 P = 0.03; diet + exercise: -179.6 +/- 46.1 P = 0.0004). Fasting glucose in mmol L-1 decreased significantly in the diet alone group (0.21 +/- 0.07 P = 0.006) and in the diet+exercise group (-0.26 +/- 0.08 P = 0.005). In a subgroup analysis of the good responders, the observed changes with respect to total cholesterol (-0.76 mmol L-1), HDL cholesterol (0.16 mmol L-1), triglycerides (-0.72 mmol L-1), systolic and diastolic blood pressure (-8.5/ -6.8 mmHg) were all statistically significant compared to the control with P < 0.001). CONCLUSIONS: Exercise and diet intervention and in particular the combination of the two, were effective in improving carbohydrate metabolism. Associated risk factors were also affected in a beneficial direction.

Adult↗

PubMed1996

Smoking habits and risk of fatal stroke: 18 years follow up of the Oslo Study.

STUDY OBJECTIVE: To examine the risk of fatal stroke in relation to smoking habits in men screened for the Oslo study. DESIGN: The Oslo study is a prospective, cohort study of the epidemiology and preventive aspects of cardiovascular diseases in middle aged men. Screening started in May 1972 and results after 18 years of follow up are reported. PARTICIPANTS: There were 16209 men aged 40-49 years, of whom 16173 had no stroke history. Eighty five men died from stroke, of whom 48 were daily cigarettes smokers, 7 were pipe and cigar smokers, 15 smoked cigarettes and pipe or cigars daily, 11 were previous cigarette smokers, and 4 had never smoked cigarettes. MAIN RESULTS: Results of proportional hazards regression analysis adjusted for age, diastolic blood pressure, and glucose concentration showed the following rate ratios (RR) (95% confidence interval) of smoking groups compared with those who had never smoked or had previously smoked: combined cigarette and cigar or pipe smokers, RR = 6.1 (3.0, 12.5); cigarettes only, RR = 4.1 (2.3,7.4); and pipe and/or cigars only RR = 2.2 (0.9,5.5). The overall, age adjusted risk of smoking cigarettes daily was 3.5 and was found to increase with increasing cigarette consumption. Regardless of their smoking group, stroke cases had increased diastolic (DBP) and systolic blood pressure (SBP) when compared with men who had not had a stroke. The absolute differences in DBP and SBP between stroke cases and others for never and previous cigarette smokers versus daily smokers were twice as large: DBP, 12.1 mmHg versus 6.5 mmHg respectively and SBP, 16.0 mmHg versus 7.1 mmHg respectively. A high BMI increased the risk of fatal stroke of never and previous cigarette smokers. Men being treated for hypertension at the time of screening had three times the crude risk of fatal stroke of men who were not taking hypertensive treatment. CONCLUSIONS: Daily cigarette smoking increased the risk of fatal stroke three and a half times. Combined cigarette and pipe or cigar smoking had a higher risk than smoking cigarettes only. An increased risk was found in relation to increased daily cigarette consumption.

Adult↗

PubMed1996

Lipid composition of mononuclear cell membranes and serum from persons with high or low levels of serum HDL cholesterol.

High density lipoprotein (HDL) levels have been shown to be inversely correlated with the incidence of coronary artery disease (CAD). Since we have previously found that peripheral blood mononuclear cells (PBMC) from persons with high (n = 10) or low HDL (n = 10) have different functional properties, we wanted to examine the PBMC membrane lipid composition and fluidity, as well as to characterize the serum lipoproteins in greater detail. In persons with high HDL, PBMC membrane phospholipids were higher, and the cholesterol/phospholipid (CH/PL) ratio lower than in persons with low HDL. Membrane cholesterol and phospholipids were positively correlated with serum HDL2. The fatty acid composition of membrane phospholipids, and membrane fluidity was similar. The median saturated/unsaturated fatty acid (SFA/UFA) ratio tended to be lower in PBMC membranes and in serum from persons with high HDL; however this was not statistically significant. In serum, total phospholipids and HDL2 components (cholesterol, phospholipids and protein) were higher in persons with high HDL, whereas non-esterified fatty acids (NEFA) and very low density lipoprotein (VLDL) components (triglycerides, cholesterol, phospholipids and protein) were lower. Furthermore, serum cholesterol esters and the cholesterol esters/free cholesterol (CE/FC) ratio was higher, and the atherogenic index, i.e. (apoB X (total cholesterol-HDLc)/apoA-I X HDLc, lower in persons with high HDL. These results demonstrate that PBMC from persons with high or low serum HDL have a different lipid composition presumably of importance for cell function, lipid transport and atherogenesis.

Cell Membrane↗

PubMed1996

Different binding of 125I-LPS to plasma proteins from persons with high or low HDL.

In severe trauma, sepsis or during surgery, bacterial lipopolysaccharide (LPS) frequently enters the circulation. Persons with high levels of high-density lipoprotein (HDL) have previously demonstrated higher monocyte procoagulant activity (PCA) when whole blood is challenged with LPS. The aim of the study was to investigate the distribution of radiolabelled LPS (125I-LPS) in plasma from six persons with high (2.14-2.82 mmol l-1) and six persons with low (0.54-1.04 nmol l-1) HDL, subjecting plasma to fast protein liquid chromatography (FPLC), or agarose electrophoresis followed by quantitative autoradiography. In heparin plasma 125I-LPS was located mainly in parts of plasma containing low-density lipoprotein (LDL) or very low-density lipoprotein (VLDL) and the immunoglobulins, and located to a lesser extent in HDL. However, persons with high HDL showed significantly higher binding of 125I-LPS to HDL and the immunoglobulins, probably to IgG, and significantly lower binding to LDL/VLDL. In calcium-depleted plasma (EDTA) 125I-LPS demonstrated a sharp increase in the binding to HDL, combined with a persistently high binding to LDL/VLDL and binding to the immunoglobulins was almost eliminated in all subjects investigated. Likewise, the binding of 125I-LPS to HDL in EDTA plasma was also significantly higher and to LDL/VLDL significantly lower in persons with high HDL. This study demonstrates that the distribution of 125I-LPS in heparin and EDTA plasma from persons with high or low HDL is different, which is presumed to be of importance concerning the various bioactivities of LPS.

Autoradiography↗

PubMed1995

LPS induced procoagulant activity and plasminogen activator activity in mononuclear cells from persons with high or low levels of HDL lipoprotein.

UNLABELLED: We have examined spontaneous and lipopolysaccharide (LPS) induced procoagulant activity (PCA) and plasminogen activator activity (PA) in peripheral blood mononuclear cells (PBMC) from ten persons with high, and ten persons with low levels of serum high-density lipoprotein (HDL). PBMC were incubated +/- 100 ng LPS/ml up to 160 h. Additionally, we have measured the release of urokinase (uPA), tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI-1) and plasminogen activator inhibitor 2 (PAI-2) into the cell culture media. Spontaneous PA was significantly higher in PBMC from persons with low HDL, combined with lower release of uPA to the media and higher uPA-receptor (uPA-R) bound uPA on PBMC. Upon stimulation with LPS, PCA and released PAI-2 increased sharply, while PA and released uPA declined. These changes were not significantly different between the two groups. tPA and PAI-1 were not detected in cell lysates or in cell culture media. CONCLUSIONS: 1) LPS sharply stimulated PBMC PCA (similar in both groups). 2) PBMC from persons with low HDL showed higher spontaneous PA, due to higher uPA-R bound uPA, probably of importance in cell migration during the early events of atherosclerosis.

Blood Cell Count↗

PubMed1995

LPS-induced release of EGF, GM-CSF, GRO alpha, LIF, MIP-1 alpha and PDGF-AB in PBMC from persons with high or low levels of HDL lipoprotein.

We have examined basal and lipopolysaccharide (LPS)-induced release of epidermal growth factor (EGF), granulocyte-macrophage colony-stimulating factor (GM-CSF), growth-regulated peptide alpha (GRO alpha), leukaemia inhibitory factor (LIF), macrophage inflammatory protein-1a (MIP-1 alpha) and platelet-derived growth factor-AB (PDGF-AB) in peripheral blood mononuclear cells (PBMC) from 20 persons with either high (n = 10) or low (n = 10) levels of high-density lipoprotein (HDL). PBMC were incubated with 100 ng LPS/ml for up to 160 h, and showed a significantly higher release of the chemokines GRO alpha (P = 0.04) and MIP-1 alpha (P < 0.01) in persons with high HDL, whereas levels of GM-CSF were similar. Levels of EGF, LIF and PDGF-AB were always low, and remained unaltered during 160 h of incubation. These findings indicate that PBMC from persons with high or low levels of HDL have different functional properties, of importance in cell recruitment and activation.

Chemokine CCL4↗

PubMed1995

Effect of dietary counselling on blood pressure and arterial plasma catecholamines in primary hypertension.

There is still a need of support for nonpharmacologic treatment of uncomplicated, mild-to-moderate essential hypertension. We investigated whether a low sodium-based diet implemented by a nutritionist could lower blood pressure and affect sympathetic activity. Middle-aged, otherwise healthy men with never-treated essential hypertension (n = 95) were randomized to an intervention group, a blood pressure control group, and a time control group. The intervention group was advised to use less sodium chloride in their diet, and if necessary, less saturated fat and decrease body weight. They attended regular clinic visits as did the blood pressure control group. After 1 year, the intervention group had achieved on average 72 mmol/24 h lower urinary sodium excretion (P < .001) and a decrease in body weight of 2.7 +/- 0.5 kg (P < .001). Both supine and standing mean blood pressure were on average 8 to 10 mm Hg lower after intervention compared with the two control groups (P < .001). Arterial plasma epinephrine, measured in all 40-year-old subjects (n = 30), decreased in parallel in all three groups (P < .05), indicating some habituation to the invasive procedure and clinic visits. However, the decrease in norepinephrine was significant (P < .001) only in the intervention group; it correlated with the weight loss (r = 0.76, P < .05) and was significantly higher (P < .05) than in both control groups. These results suggest that broad dietary advice (ie, low intake of sodium chloride, saturated fat and energy), implemented by a nutritionist, may have a significant blood pressure lowering effect and a favorable sympathicolytic effect in uncomplicated, mild-to-moderate essential hypertension.

Adult↗

PubMed1995

Risk of fatal stroke according to blood pressure level: an 18-year follow-up of the Oslo Study.

OBJECTIVE: To determine how blood pressure level predicts the incidence of fatal stroke. DESIGN: The Oslo Study is a prospective cohort study of preventive and epidemiological aspects of cardiovascular disorders in middle-aged men. Of 25,915 men invited, 16,209 aged 40-49 years attended the screening. A 7% random sample of men aged 20-39 years were also invited to attend. METHODS: The screening started in May 1972 and the analysis presented is an 18-year follow-up for fatal strokes. Men with a history of stroke were excluded from the analyses. RESULTS: Of 16,173 men with no history of stroke 85 died from stroke. Results from Cox proportional hazards regression analysis confirm diastolic (DBP) and systolic blood pressure (SBP) as strong independent risk factors of fatal stroke, with DBP being the stronger predictor. Analyses of risk of fatal stroke by quintile values show SBP to give significantly increased risk from the third quintile (136 mmHg), and DBP from the fifth quintile (95 mmHg) relative to the first quintile. No levelling off at highest levels can be seen when analysing decile values. No J-shape of the curve was evident. Men on drug treatment for hypertension with no stroke history (n = 440) had 4.7-fold (crude) and 2.8-fold (adjusted for age and DBP) the rate of stroke mortality of men not on drug treatment for hypertension. CONCLUSION: DBP was a stronger predictor than SBP, with increasing risk from the fifth quintile of DBP and the third quintile of SBP. Men on drug treatment for hypertension at screening were at increased risk during the follow-up period, indicating that their treatment did not sufficiently reduce their risk of stroke.

Adult↗

PubMed1995

Is responsiveness to lovastatin in familial hypercholesterolaemia heterozygotes influenced by the specific mutation in the low-density lipoprotein receptor gene?

Lovastatin is one of the most commonly used lipid-lowering drugs in familial hypercholesterolaemia (FH) heterozygotes. In order to study whether the response to lovastatin is influenced by the underlying mutation in the low-density lipoprotein (LDL) receptor gene, the authors compared the response in 24 heterozygotes in whom the mutation has been classified and in 34 heterozygotes in whom the mutation has not been classified. Those possessing a classified mutation had significantly higher pre-trial values of LDL-cholesterol than those possessing an unclassified mutation. However, no difference was found in the response to lovastatin. Nor were there any differences in the response between subjects possessing one of the three different classified mutations. Furthermore, irrespective of whether or not the mutation had been classified, no difference in the response was found between subjects in the upper and lower quartile with respect to pre-trial values of LDL-cholesterol. The authors conclude that the response to lovastatin is independent of both the specific mutation in the LDL receptor gene and the actual cholesterol level in FH heterozygotes.

Adult↗

PubMed1995

Hypertension therapy and risk of coronary heart disease: how do antihypertensives affect metabolic factors?

A recent meta-analysis of hypertension treatment trials demonstrated a marked reduction in the incidence of cerebrovascular disease, but a less pronounced reduction in coronary heart disease. Treatment consisted mainly of diuretics and beta-blockers, and this paper discusses the possible influences of their metabolic side effects on coronary risk factors compared with newer agents: angiotensin-converting enzyme (ACE) inhibitors, selective alpha 1-adrenoceptor inhibitors and calcium channel blockers. Several studies are underway to compare the effect of these compounds with diuretics and beta-blockers with respect to long-term cardiovascular morbidity and mortality. Until the results of these studies are available, young patients (i.e. < 60-65 years) at high risk of coronary heart disease, especially patients with the insulin resistance syndrome or diabetes mellitus, should in our opinion be treated with ACE-inhibitors, selective alpha 1-adrenoceptor inhibitors or calcium channel blockers.

Antihypertensive Agents↗

PubMed1995

Nonfasting serum glucose and the risk of fatal stroke in diabetic and nondiabetic subjects. 18-year follow-up of the Oslo Study.

BACKGROUND AND PURPOSE: The association between nonfasting serum glucose and stroke mortality for diabetic and nondiabetic subjects is presented for participants of the Oslo Study. METHODS: The study started in 1972; of 16,209 men aged 40 to 49 years, 16,172 had no previous history of stroke and 151 were known to be diabetic. Five diabetic and 80 nondiabetic subjects died of stroke during the 18 years of follow-up, giving a rate ratio of 7.87 (95% confidence interval [CI], 2.48 to 19.14). The rate of mortality for all causes in diabetic subjects was more than five times that of those who were nondiabetic. RESULTS: Nonfasting serum glucose was a predictor of fatal stroke in all participants (diabetic subjects included) without a history of stroke in age-adjusted univariate analysis. The relative risk was 1.13 (CI, 1.03 to 1.25) by increase of 1 mmol/L of serum glucose according to results of proportional hazards regression analysis. Accordingly, relative risk for nondiabetic subjects was 1.02 (CI, 0.83 to 1.26) with no linear trend. The rate ratio of the fifth quintile to the rest was 1.57 (CI, 0.94 to 2.56) for all participants and 1.28 (CI, 0.72 to 2.18) for nondiabetics. CONCLUSIONS: There was an interaction between glucose level and body mass index versus stroke for all participants but not for nondiabetic subjects, with an increased risk for men with above-median values of glucose and body mass index. Analysis of nondiabetic subjects failed to show glucose as a definite predictor of fatal stroke.

Adult↗