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C Kluft

Publications and source records attributed to C Kluft.

At least 73 records · Page 4Linked to original sources
PubMed1998

Factor VIIa response to a fat-rich meal does not depend on fatty acid composition: a randomized controlled trial.

A fat-rich meal increases activated factor VII (FVIIa), but it is not clear whether this increase depends on the fatty acid composition of the meal. Therefore, we studied the FVIIa response to fat-rich meals with different fatty acid composition in a randomized controlled crossover trial and investigated whether this response is mediated by an increase in serum triglycerides. Elderly women (> 60 years, n=91) received on separate days four different fat-rich breakfasts (50 energy percent [en%] of fat) and a control breakfast (1.5 en% fat; crossover). The fat-rich breakfasts differed in fatty acid composition: one rich in palmitic acid (21.7 g), one in stearic acid (18.6 g), and the other two in linoleic and linolenic acid-one with a ratio 3:1 (12.5/3.9 g) and the other with a ratio of 15:1 (18.8/1.2 g). At 8 AM before the breakfast (fasting) and at 1 and 3 PM, blood samples were taken, in which FVIIa and serum triglycerides were measured. FVIIa response to the fat-rich meals ranged from 11.6 mU/mL (95% confidence interval: 8.3,14.9) on the stearic meal to 15.9 mU/mL (12.0,19.8) on the linoleic/linolenic 15:1 meal at 1 PM and from 14.9 mU/mL (10.6,19.2) to 21.1 mU/mL (16.6,25.6) for the same meals at 3 PM. The responses did not differ between the fat-rich meals. After the control breakfast, FVIIa decreased, with 6.3 mU/mL (3.9,8.7) at 1 PM and 8.7 mU/mL (6.3,11.1) at 3 PM. The triglyceride response was lower after both linoleic/linolenic rich breakfasts compared with the palmitic and stearic breakfast (P<.05) and was not associated with the FVIIa response at any of the blood sampling occasions. The results of this study show that the response of FVIIa to a fat-rich meal is independent of its fatty acid composition and is not mediated by serum triglycerides.

Aged↗
PubMed1998

Elevated plasma fibrinogen: cause or consequence of cardiovascular disease?

An association between increased plasma fibrinogen and an increased risk for myocardial infarction (MI) is well established, but the nature of this association is subject to debate. Our aim was to shed light on the potentially causal nature of this association. We examined whether increased plasma fibrinogen, due to a condition that is independent of cardiovascular events, also increases the risk for MI. A case-control study was performed in 139 subjects with a history of MI and 287 control subjects selected from the Rotterdam Study, a population-based cohort of 7983 subjects aged 55 years and older. The genotype of the -455G/A polymorphism in the fibrinogen beta-gene was determined by polymerase chain reaction. Functional plasma fibrinogen levels were determined according to von Clauss. The plasma level of fibrinogen was significantly higher in subjects with one or two A alleles compared with subjects with the GG genotype: 3.8 (95% confidence interval [CI], 3.6 to 3.9) g/L and 3.6 (3.5 to 3.7) g/L, respectively. With increasing plasma fibrinogen level, the risk for MI increased gradually; a rise in fibrinogen of 1 g/L was associated with a 45% increased risk (odds ratio adjusted for age, sex, and smoking, 1.45; 95% CI, 1.12 to 1.88). There was no association between the genotype of the -455G/A polymorphism and the risk for MI. The -455G/A polymorphism is therefore associated with increased plasma fibrinogen levels but not with an increased risk for MI. These findings indicate that an increased plasma fibrinogen level due to this genetic factor does not increase the risk for MI.

Aged↗
PubMed1998

The CAMCOG: a useful screening instrument for dementia in stroke patients.

BACKGROUND AND PURPOSE: Most mental screening tests focus on the detection of cognitive deficits compatible with Alzheimer's disease. Stroke patients who develop a dementia syndrome, however, constitute a more heterogeneous group with both cortical and subcortical disturbances. We assessed the diagnostic accuracy of the CAMCOG (the cognitive and self-contained part of the Cambridge Examination for Mental Disorders of the Elderly) and the Mini-Mental State Examination (MMSE) for dementia in patients with a recent stroke. METHODS: In patients aged 55 and older who were admitted in the Rotterdam Stroke Databank, cognitive functioning was assessed between 3 and 9 months after the most recent stroke. The "gold standard" diagnosis of dementia was compatible with the criteria of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised. The CAMCOG and MMSE scores were obtained independent of the diagnostic procedure. RESULTS: Of 300 consecutive patients, 71 (23.7%) were demented. Sixteen severely demented patients could not be tested and were excluded. The CAMCOG and MMSE scores were significantly related to dementia (both P<0.0001) in a logistic regression model. Receiver operating characteristic analysis showed that the CAMCOG was a more accurate screening instrument (area under the curve for CAMCOG, 0.95; for MMSE, 0.90). Two other clinical variables independently improved the diagnostic accuracy of the MMSE and CAMCOG: patients with a left hemispheric lesion had a lower (odds ratio, 0.3; 95% confidence interval, 0.1 to 0.7), and patients with hemorrhagic stroke had a greater chance of being demented (odds ratio, 3; 95% confidence interval, 1 to 10). The effect of left hemispheric lesion as an independent diagnostic factor could not be explained by selection or its association with aphasia alone. CONCLUSIONS: The CAMCOG is a feasible instrument for use in patients with a recent transient ischemic attack or stroke. It is a more accurate screening tool for dementia than the MMSE, especially when type and site of stroke are taken into account.

Aged↗
PubMed1998

Clot accumulation characteristics of plasminogen-bearing liposomes in a flow-system. Groningen Utrecht Institute for Drug Exploration.

In this study, the clot accumulation properties of liposome-coupled plasminogen were compared to those of free (non-liposomal) plasminogen in an in vitro, closed-loop, flow-system. After introduction of a clot into the closed system, double-radiolabelled plasminogen-liposomes were administered and the accumulation of radiolabel on the entire clot was measured. Liposomal plasminogen showed improved accumulation over free plasminogen, on both a fibrin clot and a whole blood clot. Moreover, once liposomal plasminogen was fibrin associated, it could not be washed away with buffer, in contrast to free plasminogen. Liposomal plasminogen was able to compete successfully with an excess of free plasminogen. The plateau levels for the accumulated amount of plasminogen depended on the incubated amount of plasminogen and were influenced by partial degradation of the clot. Furthermore, it was shown that a threshold liposomal plasminogen surface-density was needed for optimum clot accumulation.

Buffers↗
PubMed1998

[Clinical presentation of unstable angina may influence the formation of thrombin during spontaneous episodes of ischemia].

In order to evaluate whether different clinical presentations of unstable angina are associated with a different degree or pattern of activation of the hemostatic, fibrinolytic and inflammatory systems, we measured plasma levels of thrombin-antithrombin III, plasmin-alpha2- antiplasmin complexes and C-reactive protein, as markers of activation of coagulation, fibrinolysis and inflammation respectively, in two groups of patients: 7 patients with de novo unstable angina (Group 1) and 7 patients with destabilizing unstable angina (Group 2). Blood samples were taken on admission for measuring levels of C-reactive protein and during ischemic episodes at the onset of ECG changes and pain (0 min) and after 5, 15 and 60 min in order to assess the peak values of thrombin-antithrombin III and plasmin-alpha2-antiplasmin during the episode. Thrombin-antithrombin III levels in Group 1 were 1.8 microgram/l (0.3-4.15) at 0 min and increased to 17 micrograms/l (2.8-60) after 5 to 15 min (p = 0.013); conversely thrombin-antithrombin III levels in Group 2 were 2.15 microgram/l (1.4-3.8) at 0 min and raised to 4 micrograms/l (2-43) after 5 to 15 min (NS). No significant differences in both groups were observed in plasmin-alpha2-antiplasmin levels (Group 1:650 micrograms/l, ranged 492-956, at 0 min vs 670 microgram/l, range 415-977, at peak; Group 2: 480 micrograms/l, range 274-955, at 0 min vs 502 micrograms/l, range 304-1027, at peak; NS). Inversely, C-reactive protein levels on admission were 4 mg/dl (range 2-27) in Group 1, and 1 mg/dl (range 0.6-4) in Group 2 (p = 0.006). In conclusion, patients with de novo unstable angina have significantly enhanced thrombin (but not plasmin) production during spontaneous ischemic episodes than patients with destabilizing unstable angina. Furthermore, patients with de novo unstable angina have enhanced acute phase responses than patients with destabilizing unstable angina. Our data suggest that different pathogenetic mechanisms may be responsible for acute ischemic episodes in unstable angina and may explain different response to antithrombotic therapy in unstable angina patients.

Aged↗
PubMed1998

EUROPA substudies, confirmation of pathophysiological concepts. European trial on reduction of cardiac events with perindopril in stable coronary artery disease.

In patients with coronary disease, ACE inhibitors may improve endothelial function in the coronary arteries as well as peripheral arteries, and may have anti-proliferative effects which might result in retardation of progression of coronary artery disease. In order to verify these pathophysiological concepts, a series of substudies will be conducted as part of the EUROPA programme. Angiographic and intravascular ultrasound examination of coronary arteries will be performed in approximately 400 patients before and after 3 years' treatment with either perindopril or placebo, in order to assess progression and possible regression of coronary lesions. B-mode ultrasonography of the brachial artery will be used as a model for changes in the coronary arteries, to assess endothelial function in response to ischaemia (reactive hyperaemia) and to vasoconstriction (cold pressor test). Three hundred patients will be investigated before and at different intervals after initiation of study treatment. In addition genetic characterization will be performed of patients participating in EUROPA in order to assess whether specific genotypes do respond more or less favourably to perindopril. In addition, the effect of perindopril will be investigated in patients with diabetes type II, since ACE inhibition in such patients may improve microvascular function and renal function. Integration of these substudies, as well as detailed analysis of other specific subgroups in EUROPA, will help us understand the effects of treatment with perindopril in patients with stable coronary artery disease.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Genetic modulation of coagulation factor VII plasma levels: contribution of different polymorphisms and gender-related effects.

We studied the relationships among different polymorphisms of FVII gene in determining FVII levels, in a sample of 335 male and female Italian volunteers. The hypervariable region 4 (HVR4), the promoter decanucleotide insertion (-323 0/10 bp) and the R353Q polymorphisms of FVII gene were evaluated. The association of HVR4 or -323 0/10 bp polymorphism with plasma FVII levels differed between gender (Interaction term: p = 0.02 and p = 0.03, respectively), showing stronger effect in males than in females. In males, the R353Q and the HVR4 polymorphisms showed an incremental influence on FVII variance (F = 8.9, p <0.001 and F = 4.4, p = 0.01, respectively). Moreover, the effects of Q and 10 bp alleles on the reduction of FVII activity levels were significantly potentiated by the presence of H7 allele of HVR4 (Interaction term p = 0.03 for R353Q*HVR4 and p = 0.03 for -323 0/10 bp*HVR4). In conclusion, the effect of FVII polymorphisms on FVII levels was gender dependent and derived from a complex interaction among them. The HVR4 polymorphism seems to add an independent, albeit small, contribution to the regulation of FVII plasma levels.

Adult↗
PubMed1998

The risk of mortality and the factor V Leiden mutation in a population-based cohort.

The factor V Leiden mutation (conferring resistance to activated protein C) has been implicated in the risk of arterial thrombosis and is a well-established risk factor for venous thrombosis especially in the elderly. We studied whether the disease association of the factor V mutation is reflected in an increased all-cause and cause-specific mortality. First, the prevalence of the factor V Leiden mutation was determined in a population-based study among subjects aged 85 years and over (4.7%, n = 660) and was found to correspond to the prevalence in young subjects aged 18 to 40 years (5.0%, n = 321). Secondly, we studied the association of factor V Leiden with the risk of all-cause mortality and specific causes of death in the elderly cohort during a 10-year follow-up period. Neither the all-cause mortality risk (RR 1.0; 95% CI, 0.7-1.5), nor the risk of death due to cardiovascular disease (RR 0.9; 95% CI, 0.5-1.7) were increased in elderly subjects heterozygous for factor V Leiden. Our study thus indicates that heterozygosity for factor V Leiden does not affect population mortality.

Adolescent↗
PubMed1997

Tissue plasminogen activator and risk of myocardial infarction. The Rotterdam Study.

BACKGROUND: Impaired fibrinolytic capacity, as assessed by euglobulin clot lysis time or plasma concentration of fibrinolytic parameters, has been associated with an increased risk of myocardial infarction (MI). We studied the association of a polymorphism in the gene for TPA and of plasma concentrations of TPA (antigen and activity) with the prevalence of MI. METHODS AND RESULTS: A case-control study was performed. Subjects with a history of MI (n = 121) and controls (n = 250) were drawn from the Rotterdam Study, a population-based cohort study of 7983 subjects > or = 55 years old. We determined TPA antigen and activity in plasma and genotyped all subjects for the Alu repeat insertion/deletion polymorphism in intron h in the TPA gene. Homozygosity for the insertion was associated with twice as many cases of MI as was homozygosity for the deletion (odds ratio, 2.24; 95% CI, 1.11-4.50). TPA antigen was positively associated with the risk of MI; compared with that in the lowest quartile, the relative risks (odds ratio) in the second, third, and upper quartiles were 1.7 (CI, 0.9-3.3), 2.3 (1.2-4.4), and 2.0 (1.0-3.8), respectively. When adjusted for body mass index, HDL and total cholesterol, systolic and diastolic blood pressures, and current smoking, the risk associated with TPA antigen concentration was attenuated. Increased concentrations of TPA activity tended to be associated with an increased risk of MI. CONCLUSIONS: This study provides evidence for an independent association of the insertion allele of the insertion/deletion polymorphism in the TPA gene with nonfatal MI. Increased TPA antigen is associated with an increased risk of MI; however, this association was not independent of cardiovascular disease risk factors.

Aged↗
PubMed1997

The effect of chemical anti-inhibitors on fibrinolytic enzymes and inhibitors.

Fibrinolytic enzyme inhibitors hamper the determination of the specific fibrinolytic serine protease activity. Reportedly, chemical anti-inhibitors eliminate the influence of fibrinolytic inhibitors, but it remains unclear to what extent they change the specific activity of fibrinolytic serine proteases. We studied the influence of chemical anti-inhibitors (chloramine T, flufenamate, sodium lauryl sulfate, and methylamine) on fibrinolytic serine proteases and fibrinolytic enzyme inhibitors using the physiological substrate fibrin as plasmin substrate. Low concentrations of chloramine T (0.01 mmol/l) prevent the inhibition of plasminogen activators. Higher concentrations (1 mmol/l) reduce the inhibition of plasmin, but simultaneously quench the plasminogen activator activity. Flufenamate eliminates most fibrinolytic enzyme inhibitors, but increases the activity of plasmin (apparent recovery 140%) and plasminogen activators (apparent recovery > 200%). Sodium lauryl sulfate eliminates the major fibrinolytic enzyme inhibitors, but increases the activity of plasmin (apparent recovery > 200%) and plasminogen activator, urokinase type (apparent recovery 130%). Methylamine affects only plasmin inhibition. We conclude that chemical anti-inhibitors may invalidate the analytical specificity of methods for the determination of fibrinolytic serine protease activity.

Chloramines↗
PubMed1997

Short-term oestrogen replacement therapy improves insulin resistance, lipids and fibrinolysis in postmenopausal women with NIDDM.

Oestrogen replacement therapy is associated with a decreased risk of cardiovascular disease in postmenopausal women. Patients with non-insulin-dependent diabetes mellitus (NIDDM) have an increased cardiovascular risk. However, oestrogen replacement therapy is only reluctantly prescribed for patients with NIDDM. In a double blind randomized placebo controlled trial we assessed the effect of oral 17 beta-estradiol during 6 weeks in 40 postmenopausal women with NIDDM. Glycated haemoglobin (HbA1c), insulin sensitivity, suppressibility of hepatic glucose production, lipoprotein profile and parameters of fibrinolysis were determined. The oestrogen treated group demonstrated a significant decrease of HbA1c and in the normotriglyceridaemic group a significantly increased suppression of hepatic glucose production by insulin. Whole body glucose uptake and concentrations of non-esterified fatty acids did not change. LDL-cholesterol- and apolipoprotein B levels decreased, and HDL-cholesterol, its subfraction HDL2-cholesterol and apolipotrotein A1 increased. The plasma triglyceride level remained similar in both groups. Both the concentration of plasminogen activator inhibitor-1 antigen and its active subfraction decreased. Tissue type plasminogen activator activity increased significantly only in the normotriglyceridaemic group. Oestrogen replacement therapy improves insulin sensitivity in liver, glycaemic control, lipoprotein profile and fibrinolysis in postmenopausal women with NIDDM. For a definite answer as to whether oestrogens can be more liberally used in NIDDM patients, long term studies including the effect of progestogens are necessary.

C-Peptide↗
PubMed1997

Factor VII polymorphisms in populations with different risks of cardiovascular disease.

Increased plasma factor VII coagulant activity (FVII:C) has been associated with the risk of ischemic heart disease (IHD). Differences in plasma FVII:C among individuals are associated with three common polymorphisms in the FVII gene. Therefore, we investigated FVII polymorphisms in four populations that differ in their risk of developing cardiovascular disease, namely, Europeans, Greenland Inuit, Gujarati Indians, and Afrocaribbeans. We studied (1) the promoter polymorphism, which is the result of a decanucleotide insertion in the FVII promoter at position -323 from the start of translation; (2) the hypervariable region 4 polymorphism (HVR4), which is the result of a variable number of tandem repeats in intron 7; and (3) the RQ353 polymorphism, a guanine-to-adenine substitution in the position of the codon for amino acid 353 resulting in an amino acid replacement of arginine (R) by glutamine (Q) in the FVII protein. The frequencies of these three polymorphisms and their linkage disequilibrium were different in the four populations studied. The frequencies of the alleles associated with higher plasma FVII:C were lower in the Europeans than in the Inuit, a population with a lower incidence of IHD. There was an association between both the promoter polymorphism and the RQ353 polymorphism and the plasma FVII:C in the Europeans, the Inuit, and the Gujarati Indians, and an association only between the RQ353 polymorphism and plasma FVII:C in the Afrocaribbeans. Only in the Inuit was the HVR4 polymorphism associated with plasma FVII:C. In multiple regression analysis, the additional information provided by the promoter polymorphism when the other polymorphisms were already included in the model was the most pronounced, suggesting that the promoter polymorphism may be the functional mutation having the greatest effect on determining plasma FVII:C.

Adult↗
PubMed1997

Effect of 17 beta-estradiol on plasma lipids and LDL oxidation in postmenopausal women with type II diabetes mellitus.

In type II diabetes mellitus the altered hormonal state after menopause may represent an additional cardiovascular risk factor. Estrogen replacement therapy (ERT) is associated with a decreased cardiovascular risk, at least in nondiabetic postmenopausal women. We studied the effect of ERT on plasma lipids and lipoproteins and on LDL oxidation in 40 postmenopausal women with type II diabetes but with minimal vascular complications in a randomized placebo-controlled trial. Twenty patients were treated orally with 2 mg/d micronized 17 beta-estradiol and 20 patients with placebo for 6 weeks. Plasma total cholesterol (-6%, P = .04), LDL cholesterol (-16%, P = .0001), and apoB (-11%, P = .001) levels decreased and HDL cholesterol (20%, P = .0001) and apoA-I (14%, P = .0001) levels increased after ERT compared with placebo. Glycated hemoglobin (HbA1c) decreased significantly after ERT (-3%, P = .03), the cholesterol content of the LDL particles decreased (-5%, P = .006), triglyceride content increased (16%, P = .01), and LDL particle size did not change significantly. ERT had no effect on parameters of LDL oxidation. We conclude that plasma levels of HDL cholesterol, apoA-I, LDL cholesterol, apoB, and glycated hemoglobin are improved in postmenopausal women with type II diabetes mellitus after treatment with 17 beta-estradiol, indicative of a better metabolic control, and that ERT has no effect on LDL oxidizability.

Aged↗
PubMed1997

No effect of unfractioned or low molecular weight heparin treatment on markers of vascular wall and hemostatic function in incipient diabetic nephropathy.

OBJECTIVE: The high risk for cardiovascular disease in IDDM patients with nephropathy may be mediated by abnormal function of the vascular wall. We investigated whether heparin was able to modulate markers of vascular wall and hemostatic function in patients with incipient nephropathy. RESEARCH DESIGN AND METHODS: Thirty-five IDDM patients with incipient nephropathy were randomized to treatment with placebo, unfractioned heparin, or low molecular weight heparin in a double-blind trial. The treatment was given as 1 h of conventional intravenous high-dose treatment and in a conventional subcutaneous low-dose regime for 3 months. Transcapillary escape rate of albumin and plasma levels of von Willebrand factor, fibrinogen, prothrombin fragment 1 + 2, thrombin-antithrombin III complexes, tissue type plasminogen activator, tissue plasminogen activator inhibitor type 1, total cholesterol, HDL cholesterol, and triglycerides were measured before and after treatment. Of the patients, 31 completed the study. RESULTS: We found no significant effect of heparin on markers of vascular wall and hemostatic function by any of the treatments. CONCLUSIONS: Treatment with high- or low-dose heparin induced no modulation of markers of vascular wall or hemostatic function in IDDM patients with incipient diabetic nephropathy.

Adult↗
PubMed1997

Modulation of plasma fibrinogen levels by ciprofibrate and gemfibrozil in primary hyperlipidaemia.

An elevated plasma fibrinogen level is increasingly accepted as an independent risk indicator of cardiovascular disease. This has enhanced the interest in identifying agents that can normalize elevated plasma fibrinogen levels. One group of agents with this capacity are the fibric acid derivatives, e.g. ciprofibrate and gemfibrozil. We studied fibrinogen levels after 12 weeks of treatment with ciprofibrate (n = 48) and gemfibrozil (n = 51) in hypercholesterolenic patients. The correlation of the decrease in fibrinogen with lipid lowering and the contribution of the acute phase and genetic polymorphisms to this decrease were also evaluated. After 12 weeks of treatment, the fibrinogen levels were significantly decreased (p < 0.0005) with both drugs, although the decrease in the ciprofibrate group (mean 3.4 g/l pre-treatment to 2.4 g/l after 12 weeks) was larger than in the gemfibrozil group (mean 3.4 g/l to 3.0 g/l). The lipid lowering effect was comparable for the two drugs but there was no correlation for either ciprofibrate or gemfibrozil between the lipid lowering and the magnitude or the velocity of the fibrinogen lowering effect. An attenuation of the major regulatory mechanism of plasma fibrinogen levels, the acute phase reaction, was invoked as the underlying mechanism. However, pre-treatment C-reactive protein levels were not increased and did not change after treatment. Moreover, no effects of the polymorphisms of the fibrinogen beta-gene on the decrease of the plasma fibrinogen levels were observed. This suggests that a new, as yet unknown, mechanism is involved in fibrinogen lowering by fibrates.

Adult↗
PubMed1997

Effect of oral contraceptives on haemostasis variables.

Combined oral contraceptives (COCs) have effects on a large number of haemostasis variables. We have summarised literature data on effects of COCs containing 30-35 micrograms ethinyl estradiol for the third generation of progestogens (PGs): desogestrel, gestodene and norgestimate. It is concluded that about 15 variables show a shift in distribution of the order of magnitude of their interindividual variation coefficient. When comparing the third generation of PGs with the second one (norgestrel, levonorgestrel) stronger increases are noted for the former for some haemostatic variables. Also differences between desogestrel and gestodene for factor VII were apparent. It indicates that the role of PGs in the effects of COCs is significant and their design may in addition to reduction of oestrogen dosage be important in reducing haemostatic complications. The survey on molecular and cellular mechanisms by which the sex steroids might operate showed a great lack of knowledge. Only for factor XII has a functional oestrogen response element in the DNA definitely been identified. The study of molecular markers of coagulation and fibrinolysis have shown a distinct increased activation of coagulation (F 1 + 2, FPA) and fibrinolysis (PAP), and an increased fibrin turn-over (increased FDPs); platelet products are not found increased (beta TG, PF-4). The increase in fibrinolysis represent a counterforce, but individual changes in variables in coagulation and fibrinolysis do not correlate indicating independent effects and no evidence for a individually regulated balance. A first step in further research might be in understanding the increase in coagulation activation (F 1 + 2) which has so far not been satisfactorily related to changes in blood concentrations of haemostatic factors and possibly local factors.

Biomarkers↗
PubMed1997

Effect of strenuous exercise on fibrinogen and fibrinolysis in healthy elderly men and women.

The elevated incidence of thrombotic disease in elderly people may be associated with an increase in PAI-1 and fibrinogen with ageing. Cross-sectional studies report an inverse relation of PAI-1 and fibrinogen with physical activity, but training studies show inconsistent results. In a controlled intervention study among elderly subjects (aged 60-80 years) we observed a moderate decrease in PAI-1 antigen (4%, -2.1 +/- 2.4 ng/ml), a significant increase in t-PA activity (11%, 0.07 +/- 0.04 IU/ml) and an unexpected significant increase in fibrinogen (6%, 0.18 +/- 0.07 g/l) in subjects following a 6-month intensive training program as compared to controls. Reduction in PAI-1 antigen was significantly associated with a decrease in triglycerides (beta = 10.3 ng/ml per 1 mM, p <0.01) and insulin (beta = 2.37 ng/ml per 1 mU/l, p = 0.07). Increase in fibrinogen coincided with a rise in C-reactive protein (p <0.001). These data suggest that regular intensive activity may increase fibrinolytic activity in a moderate way, but also may cause chronically elevated plasma levels of acute phase proteins in elderly persons.

Aged↗