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Biomedical subjects

G D Lowe

Publications and source records attributed to G D Lowe.

At least 163 records · Page 9Linked to original sources
PubMed1993

The relationship between blood viscosity and blood pressure in a random sample of the population aged 55 to 74 years.

Blood viscosity is elevated in hypertensive subjects, but the association of viscosity with arterial blood pressure in the general population, and the influence of social, lifestyle and disease characteristics on this association, are not established. In the Edinburgh Artery Study, 1592 men and women aged 55-74 years selected randomly from the general population attended a university clinic. A fasting blood sample was taken for the measurement of blood viscosity and its major determinants (haematocrit, plasma viscosity and fibrinogen). Systolic pressure was related univariately to blood viscosity (P < 0.001), plasma viscosity (P < 0.001) and plasma fibrinogen (P < 0.01), but the association with fibrinogen did not persist after adjusting for body mass index. Diastolic pressure was related univariately to blood viscosity (P < 0.001) and plasma viscosity (P < 0.001) and haematocrit (P < 0.001) but not to fibrinogen. The only difference between the sexes was that the association between blood viscosity and systolic pressure was confined to males. Blood viscosity was associated equally with systolic and diastolic pressures in males, and remained independently related on multivariate analysis adjusting for age, sex, body mass index, social class, smoking, alcohol intake, exercise, angina, HDL and non-HDL cholesterol, diabetes mellitus, plasma viscosity, fibrinogen, and haematocrit.

Aged↗
PubMed1993

The incidence and mechanism of hypotension following thrombolytic therapy for acute myocardial infarction with streptokinase-containing agents--lack of relationship to pretreatment streptokinase resistance.

The incidence, amplitude, mechanism and relationship to prior exposure to streptococcal antigen of blood pressure changes to streptokinase-containing thrombolytic agents were investigated in 125 patients treated with either 1.5 x 10(6) IU streptokinase over 60 min or 30 U anistreplase over 5 min, within 6 h of onset of acute myocardial infarction. Twenty-one of 52 patients with anterior and 34 of 73 with inferior myocardial infarction had a hypotensive response. There were no significant differences in the incidence, duration or amplitude of hypotension between the two treatment groups. The maximum mean fall in systolic blood pressure was 16.9 mmHg (95% confidence limits, CL 12.2 to 24.5 mmHg), and the maximum mean fall in diastolic blood pressure was 13.7 mmHg (CL 10.3 to 17.1 mmHg), starting 4 min after start of therapy and resolving within 34 min. Blood pressure changes were well tolerated. Hypotension was not related to pretreatment streptokinase resistance titre, or anti-SK IgG concentration, to changes in plasma fibrinogen, B-beta 15-42 peptide, D-dimer--as indices of thrombin activation and fibrin (-ogen) breakdown--to plasma viscosity. The blood pressure changes following treatment with streptokinase-containing thrombolytic agents in acute myocardial infarction are frequent but well tolerated. The mechanism of hypotension remains unclear, but is not related to prior exposure to streptococcal antigen.

Anistreplase↗
PubMed1993

Reduced coagulation activation following infusion of a highly purified factor IX concentrate compared to a prothrombin complex concentrate.

We have looked for evidence of coagulation activation in six subjects with haemophilia B by performing a single-blind active control cross-over study comparing a recently developed factor IX concentrate with a conventional prothrombin complex concentrate (PCC). Samples were obtained before infusion and at 0.25, 0.5, 1, 2, 4, 6, 12, 24, 36 and 48 h for assay of factor IX, prothrombin time, fibrinopeptide A (FPA), prothrombin fragment F1 + 2, D-dimer, thrombin-antithrombin complexes (TAT) and antithrombin III (ATIII). Following administration of the PCC there was evidence of coagulation activation in five of the six recipients for up to 6 h after the infusion. The factor IX concentrate induced a moderate degree of coagulation activation in one subject. There was no significant difference between the two products in respect of either recovery or half-life. This study provides further evidence that the new high purity preparations of factor IX concentrates produce significantly less coagulation activation than currently available PCCs. It remains to be established whether this will result in a corresponding reduction in thromboembolic complications in clinical use.

Adolescent↗
PubMed1993

Plasma fibrinogen in women: relationships with oral contraception, the menopause and hormone replacement therapy.

Plasma fibrinogen was measured in 4837 women aged 25-64 years as part of the Scottish Heart Health Study and Scottish MONICA population surveys. The relationships of oral contraceptive use, the menopause and hormone replacement therapy were examined. Univariate analyses found that women with a history of oral contraceptive use, premenopausal women and those on hormone replacement therapy all had significantly lower fibrinogen levels than women who had never used oral contraceptives, postmenopausal women and non-hormone replacement users respectively. These differences persisted after age standardization. On multivariate analysis, menopausal status and hormone replacement therapy had independent effects on fibrinogen levels. Together with the common risk factors, 9.9% of the total variation in plasma fibrinogen levels was explained. However, less than 1% of this was from the combined menopausal and hormonal factors. These results confirm a postmenopausal rise in fibrinogen level which may be relevant to an increased risk of coronary heart disease. In addition, a protective effect with hormone replacement therapy is noted, although this was probably due to selection bias.

Adult↗
PubMed1993

Fibrinogen in relation to personal history of prevalent hypertension, diabetes, stroke, intermittent claudication, coronary heart disease, and family history: the Scottish Heart Health Study.

OBJECTIVE: To determine the relations of plasma fibrinogen to family history of premature heart disease, personal history of hypertension, diabetes, stroke, coronary heart disease, and to presence of intermittent claudication. DESIGN: Random population survey across 22 local government districts in Scotland. PARTICIPANTS: 10,359 men and women aged 40 to 59 years. Plasma fibrinogen was measured in 8824. MAIN OUTCOME MEASURE: Plasma fibrinogen concentration. RESULTS: Persons with a family history of heart disease or a personal history of high blood pressure, diabetes, stroke, or presence of intermittent claudication all had higher plasma fibrinogen concentrations than those without. When compared with participants without cardiovascular or related disease (men: 2.27 (SE = 0.01) g/l, n = 3367; women 2.34 (0.01) g/l, n = 3096), predefined cases of either myocardial infarction (men: 2.51 (0.02) g/l, n = 248; women: 2.63 (0.04) g/l, n = 72) or angina (men: 2.45 (0.02) g/l, n = 394; women: 2.50 (0.02) g/l, n = 398) had significantly higher plasma fibrinogen concentrations (p < 0.001). After adjustment for 10 other coronary risk factors, there was a noticeable linear trend in the odds ratios for myocardial infarction across all quartiles (quarters) of plasma fibrinogen concentrations in both sexes. Similarly, the risk of angina increased linearly with increasing fibrinogen concentrations, although the test for a linear trend was NS among women. CONCLUSIONS: This large population study confirms that plasma fibrinogen is not only a risk factor for coronary heart disease and stroke, but it is also raised with family history of premature heart disease and with personal history of hypertension, diabetes, and presence of intermittent claudication.

Adult↗
PubMed1993

Blood viscosity, fibrinogen, and activation of coagulation and leukocytes in peripheral arterial disease and the normal population in the Edinburgh Artery Study.

BACKGROUND: Increased blood and plasma viscosity, hematocrit, fibrinogen, and activation of coagulation and leukocytes have been reported in patients with claudication; however, their associations with symptomatic and asymptomatic peripheral arterial disease have not been reported in an epidemiological study. METHODS AND RESULTS: Blood and plasma viscosity, hematocrit, fibrinogen, urinary fibrinopeptide A, plasma leukocyte elastase, and uric acid were measured in a random sample of 1,581 men and women aged 55-74 years in Edinburgh, Scotland, and related to peripheral arterial stenosis (ankle-brachial systolic pressure index, ABPI) and to lower limb ischemia (intermittent claudication and reactive hyperemia test). Each variable (except fibrinopeptide A) was significantly related to prevalent symptomatic and asymptomatic peripheral arterial disease. On multivariate analysis, blood viscosity (p < 0.05) and fibrinogen (p < 0.01) were independently associated with peripheral arterial narrowing (ABPI); a positive interaction was found between fibrinogen and smoking in the association with ABPI. Plasma viscosity was associated with claudication in the presence of a given degree of arterial narrowing (odds ratio of claudication in top quintile compared with bottom quintile of plasma viscosity, 3.35; 95% CI, 1.32, 8.51). Leukocyte elastase and uric acid were each associated with reactive hyperemia independently of arterial narrowing (p < 0.01). CONCLUSIONS: Blood rheological factors and leukocyte activation as well as arterial narrowing are associated with lower limb ischemia in the general population and may be implicated in its pathogenesis.

Aged↗
PubMed1993

Dental disease, fibrinogen and white cell count; links with myocardial infarction?

Plasma fibrinogen and white blood cell count were compared in fifty patients aged 25-50 years with periodontal disease and in fifty age-matched controls with relatively healthy periodontal tissues. Patients had significantly higher levels of fibrinogen and white cell count, and dental indices correlated significantly with these two cardiovascular risk factors on multivariate analyses. We suggest that inflammatory dental disease may be a determinant of fibrinogen level and white cell count in the general population, and that fibrinogen and white cell count may be two mediators of the link between dental disease and myocardial infarction.

Adult↗
PubMed1993

Anabolic steroids and fibrinolysis.

Anabolic steroids increase the activity of the fibrinolytic system by reducing plasma levels of inhibitors (plasminogen activator inhibitor type I, histidine-rich glycoprotein, alpha-2-macroglobulin) and increasing plasma levels of tissue-type plasminogen activator activity, plasminogen, and plasmin activity (B beta 15-42 fragment of fibrinogen). Plasminogen activator inhibitor levels are elevated, and tissue-type plasminogen activator activity is depressed, in a variety of disease states, including premature venous or arterial thrombosis, connective tissue disorders, and cancer. Such abnormalities can be reversed by anabolic steroids. However the clinical benefits and adverse effects of such treatment remain to be established by large, randomized controlled trials.

Anabolic Agents↗
PubMed1992

Fibrinogen genotype and risk of peripheral atherosclerosis.

There is conflicting evidence about the influence of fibrinogen genotype on plasma fibrinogen concentrations, and the relation between genotype and atherosclerotic disease has not been studied. In a population-based case-control study we aimed to find out whether certain fibrinogen genotypes are associated with an increased risk of peripheral atherosclerosis. 121 subjects with peripheral arterial disease and 126 healthy controls matched for age and sex were selected from a random population sample aged 55-74 years in the Edinburgh Artery Study. Mean fibrinogen concentrations were higher in cases than in controls (3.12 [95% confidence interval 2.99-3.26] vs 2.75 [2.64-2.85], p less than 0.001). A greater proportion of cases than controls were homozygous or heterozygous for an allele at the beta fibrinogen locus (4.2 kb allele, Bcl I digestion); the allele frequency was 0.197 in cases and 0.097 in controls (p less than 0.005). Extended haplotypes for 4.2 kb heterozygotes were also associated with an increased risk of peripheral arterial disease. However, haplotype had only a small effect on the association of plasma fibrinogen concentration with disease, and the relation of haplotype with disease was independent of age, sex, social class, smoking status, plasma fibrinogen, alcohol consumption, body mass index, and diabetes mellitus. We conclude that variation at the beta fibrinogen locus is associated with an increased risk of peripheral atherosclerosis. The influence is not mediated simply by way of increased fibrinogen concentrations but could be due to a structurally variant fibrinogen or linkage disequilibrium with a neighbouring gene.

Aged↗
PubMed1992

Prevention of venous thromboembolism after surgery: a review of enoxaparin.

This review discusses the problem of deep vein thrombosis (DVT) after operation and identifies three levels of risk of DVT: low (less than 10 per cent), moderate (10-40 per cent) and high (40-80 per cent). Special emphasis is placed on the most recent prophylactic treatment, low molecular weight heparins (LMWHs), particularly enoxaparin. Several LMWHs are now available, but they differ slightly and each must be evaluated on its own merits. In general, however, LMWHs are both effective and safe in those patients at moderate or high risk of DVT. Thromboprophylaxis is cost effective when analysed using health-economic methodology.

Adult↗
PubMed1992

Rheological determinants of blood pressure in a Scottish adult population.

OBJECTIVES: To examine the relationship of blood pressure with haematocrit, plasma viscosity, whole blood viscosity and plasma fibrinogen. DESIGN: A random population sample of 1264 men and women aged 25-64 years from the west of Scotland, UK. RESULTS: Strong correlations between age, body mass index and blood pressure were noted: these were higher for women than men. Blood viscosity, haematocrit and plasma viscosity correlated with blood pressure independently of age, body mass index and smoking status. No evidence was found for an effect of erythrocyte rigidity upon blood pressure; plasma fibrinogen showed an inverse correlation with blood pressure and the rheological variables on multivariate analysis. CONCLUSIONS: Our findings support the role of blood viscosity in determining blood pressure as suggested by other, smaller studies. The magnitude of the effect upon blood pressure levels across the normal range of blood viscosity was of clinical importance. Further studies of factors that influence blood and plasma viscosity may help in the understanding of the aetiology of essential hypertension and its management.

Adult↗
PubMed1992

Increased interleukin 6 concentrations in the absence and presence of HIV-1 infection in haemophilia.

AIMS: To measure IL-6 concentrations in asymptomatic HIV-1 antibody positive and negative haemophilic patients and to correlate these with IgG concentrations and CD4 positive cell numbers. METHODS: IL-6 concentrations were measured by bioassay in stored serum from a prospective cohort of haemophilic patients in whom immunoglobulins and T cell subsets had been determined. Values of IL-6 and immunoglobulins were also correlated with severity of liver disease. RESULTS: IL-6 concentrations were raised in haemophilic patients independent of HIV-1 antibody status. In HIV-1 antibody positive patients there was no correlation between IL-6 concentrations and CD4 positive cell numbers, but there was a correlation with IgG (r = 0.4; p = 0.05). In HIV-1 antibody negative patients there were no significant correlations. CONCLUSIONS: Haemophilic patients have increased IL-6 concentrations; in HIV-1 positive patients this is independent of the decline in CD4 cell count. The raised concentrations do not correlate with the clinical severity of liver disease.

Adult↗
PubMed1992

Changes in neutrophil deformability following in vitro smoke exposure: mechanism and protection.

We have previously demonstrated a reduction in the deformability of neutrophils, exposed to whole particulate cigarette smoke in vitro, by measuring their ability to filter through a micropore membrane with pore dimensions similar to those of the average pulmonary capillary segment. In this study, we exposed neutrophils to the vapor phase of cigarette smoke and investigated the mechanism of the reduction in neutrophil filterability. Although both stimulated neutrophils and smoke-exposed neutrophils demonstrated an increase in filtration pressures, and thus a reduction in cell deformability, compared with control untreated cells, the spontaneous release of the reactive oxygen intermediates hydrogen peroxide and the superoxide anion was depressed following in vitro smoke exposure and there was no shape change to suggest that smoke-exposed cells were activated. The presence of erythrocytes, plasma, or the antioxidants albumin and glutathione prevented the reduction in cell filterability following smoke exposure, suggesting that in vitro smoke exposure, in our system, was mediated by oxidants. Indeed, the increase in filtration pressures, produced by smoke, could be mimicked by the addition of the oxidant hypochlorous acid. The cytoskeletal inhibitors cytochalasin B and D improved the filterability of smoke-exposed cells, suggesting that smoke may change neutrophil deformability through an effect on the actin component of the cytoskeleton. By contrast, colchicine, a specific inhibitor of the microtubules, had no effect. Preincubation with a monoclonal antibody to the CD18 antigen, to block this major neutrophil adhesive glycoprotein, did not alter the filtration pressure developed by stimulated or smoke-exposed neutrophils, suggesting that increased adhesivity was not the mechanism of the increase in filtration pressures observed following smoke exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Antioxidants↗