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Biomedical subjects

A G Turpie

Publications and source records attributed to A G Turpie.

At least 127 records · Page 7Linked to original sources
PubMed1989

Detection of previous proximal venous thrombosis with Doppler ultrasonography and photoplethysmography.

To evaluate the reliability of two noninvasive tests, the photoplethysmograph (PPG) and venous Doppler ultrasound, in determining the presence or absence of previous proximal deep vein thrombosis (DVT), we performed a blinded retrospective cohort study of patients with objectively confirmed (DVT+) or refuted (DVT-) previous episodes of suspected DVT. Twenty-nine of 33 DVT+ patients had abnormal PPG and/or reflux by venous Doppler ultrasound, whereas 39 of 49 DVT- patients had normal PPG and no Doppler reflux (sensitivity, 88%; specificity, 80%). Of 33 DVT+ patients, 20 had abnormal Doppler results (sensitivity, 61%), in contrast to 46 of 49 DVT- patients with normal results (specificity, 94%). Moreover, 23 of 33 DVT+ patients showed abnormal PPG results (sensitivity, 70%), whereas 40 of 49 DVT- patients had normal PPG (specificity, 82%). Based on our findings, the presence of Doppler reflux is specific for previous proximal DVT, whereas a combination of normal PPG and Doppler ultrasound is reliable for excluding previous proximal DVT. Abnormal PPG with normal Doppler ultrasound does not reliably predict the presence or absence of previous DVT. However, this occurred in only 16 of 82 patients. Therefore, the combination of PPG and venous Doppler ultrasound can reliably predict the presence or absence of previous proximal DVT in most patients.

Female↗
PubMed1989

Therapy of deep vein thrombosis.

Adequate anticoagulation treatment in patients with deep vein thrombosis reduces the risk of thrombus extension or embolization to less than 5%. Thrombolytic treatment may possibly prevent subsequent postthrombotic syndrome. Heparin is the initial treatment of choice for most patients with deep vein thrombosis. The dose is adjusted according to the results of tests such as the whole blood clotting time, thrombin clotting time, activated partial thromboplastin time or plasma heparin concentration. The most commonly used test is the activated partial thromboplastin time which should be maintained at 1 1/2 to two times the control level. Initially the test should be performed two to three times daily and when optimal adjustment has been established, clotting studies are required only at 24-hour intervals. In general, treatment with intravenous heparin should be continued for seven to ten days. Thereafter, for secondary prophylaxis, treatment with oral anticoagulants is carried out for six to eight weeks for symptomatic lower leg thrombosis, for twelve weeks in the case of proximal venous thrombosis and pulmonary embolism. Oral anticoagulant therapy with warfarin should be given overlapping the last few days of heparin with the dose adjusted to prolong the prothrombin time to 1.3 to 1.5 times control. Initially, the prothrombin time should be monitored weekly, thereafter at intervals of two to three weeks. If oral anticoagulant therapy is contraindicated, secondary prophylaxis with subcutaneous heparin given twice daily in doses sufficient to prolong the activated partial thromboplastin time to 1 1/2 times control is an effective and safe alternative. The major side effect of oral anticoagulant therapy, as well as that of heparin, is bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Anticoagulants↗
PubMed1988

Randomised comparison of two intensities of oral anticoagulant therapy after tissue heart valve replacement.

After tissue heart valve replacement 108 patients were randomised to standard anticoagulant control with rabbit brain thromboplastin (Dade C reagent, therapeutic range 18-24 s; international normalised ratio 2.5-40) and 102 to a less intensive regimen controlled with human brain thromboplastin (Manchester Comparative Reagent, therapeutic range 26-30 s; INR 2.0-2.25). Treatment was continued for three months, outcome measures being major or minor embolism or haemorrhage. 2 patients in each group had major embolic events and 11 in each group had minor embolic events. The 95% confidence intervals on the differences are -3.4% to 3.2% for major embolism and -9.3% to 8.2% for minor embolism. Haemorrhagic complications were significantly more frequent with standard treatment (15 patients) than with the less intensive regimen (6 patients); and of the 5 patients with major haemorrhagic complications, all were in the standard treatment group, again a significant difference. The less intensive regimen is thus no less effective and safer than standard anticoagulant therapy in patients with tissue heart valve replacement.

Administration, Oral↗
PubMed1988

Clinical studies: evidence for intervention with specific antiplatelet drugs in arterial thromboembolism.

There is conclusive evidence that aspirin is beneficial in patients with unstable angina and that a combination of preoperative dipyridamole with post-operative aspirin is beneficial after coronary artery bypass. The evidence for a beneficial effect of aspirin after myocardial infarction is consistent but inconclusive. The evidence for the use of aspirin alone following coronary bypass is inconclusive. There is convincing evidence that aspirin will reduce the rate of recurrent TIA, stroke, and death in patients with TIA.

Cardiovascular Diseases↗
PubMed1988

The Canadian American Ticlopidine Study (CATS) in thromboembolic stroke. Design, organization, and baseline results.

The Canadian American Ticlopidine Study is a randomized, placebo-controlled, double-blind, multicenter study to assess the efficacy and safety of ticlopidine hydrochloride in patients who have suffered a thromboembolic stroke no less than 1 week and no more than 4 months before entry into the study. The primary assessment of efficacy will be based on the cluster of outcome events recurrent stroke, myocardial infarction, or vascular death. Twenty-five clinical centers, 12 in Canada and 13 in the United States, entered a total of 1,072 patients during a 3-year recruitment period; these patients were randomly allocated to receive either 250 mg ticlopidine or identical-appearing placebo tablets twice daily for up to 3 years. Patient recruitment was completed in December 1986. Patients were followed for a maximum of 3 years or until the close of the study in December 1987; at that time an average follow-up of 25 months had been achieved. We summarize the protocol and organization of the study and document the methods of execution and analysis, with corresponding criteria, before disclosure of the treatment code to any of the study investigators. We also provide a clinical description of the patients at entry into the study.

Aged↗
PubMed1987

Double-blind randomised trial of Org 10172 low-molecular-weight heparinoid in prevention of deep-vein thrombosis in thrombotic stroke.

In a double-blind, randomised trial Org 10172 low-molecular-weight (LMW) heparinoid was compared with placebo in the prevention of deep-vein thrombosis in patients with acute thrombotic stroke. Prophylaxis was started within 7 days of the onset of stroke with a loading dose of 1000 anti-factor-Xa units intravenously followed by a fixed dose of 750 anti-factor-Xa units twice a day subcutaneously; it was continued for 14 days or until hospital discharge, if earlier. 50 patients were randomised to receive Org 10172 and 25 to receive placebo. All patients underwent surveillance with I125-fibrinogen leg scanning and impedance plethysmography. Venography was carried out if either test became positive. Venous thrombosis occurred in 2 of 50 patients (4.0%) given Org 10172 and 7 of 25 patients (28.0%) given placebo (p = 0.005); the corresponding rates of proximal-vein thrombosis were 0% and 16%, respectively (p = 0.01). There was one major haemorrhage in the Org 10172 group and one minor bleed in the placebo group.

Acute Disease↗
PubMed1987

Effect of nafazatrom on platelet function and release: relationship to symptomatic episodes in patients with peripheral vascular disease.

We studied the effect of nafazatrom on plasma prostacyclin (PGI2) levels, platelet function, and thromboxane B2 (TxB2), and 12-hydroxy-eicosatetraenoic acid (12-HETE) production and clinical improvement in 12 patients with peripheral vascular disease (PVD) by means of a double-blind crossover trial of placebo, 800 or 1600 mg of nafazatrom four times daily for 1 week, with intervening 2-week washout periods. Plasma PGI2 levels were measured as 6-keto-PGF1 alpha by radioimmunoassay. Platelet function ex vivo was measured as collagen and adenosine diphosphate (ADP)-induced platelet aggregation, release of 12-HETE and thromboxane A2 (measured as TxB2), and was determined by high-pressure liquid chromatography (HPLC) and radioimmunoassay, respectively. The plasma 6-keto-PGF1 alpha levels were unaffected by nafazatrom treatment (p greater than 0.25). Nafazatrom treatment had no effect on TxB2 production, but significantly altered the production of the platelet 12-HETE (p less than 0.05). There was a significant association between the changes in 12-HETE production and clinical improvement. These results suggest that the mechanism of action of nafazatrom is in part related to the inhibition of platelet function via the lipoxygenase pathway, independent of PGI2 stimulation.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1987

Adjusted subcutaneous heparin or continuous intravenous heparin in patients with acute deep vein thrombosis. A randomized trial.

STUDY OBJECTIVE: To determine the efficacy and safety of adjusted subcutaneous calcium heparin compared with continuous intravenous calcium heparin as the initial treatment for acute deep vein thrombosis. DESIGN: Randomized control trial. SETTING: University-affiliated general hospital. PATIENTS: Of 111 consecutive patients considered, 103 had acute proximal or calf vein thrombosis confirmed by ascending venography and met all other eligibility criteria. INTERVENTIONS: PATIENTS were randomly assigned to receive subcutaneous or intravenous heparin. The subcutaneous regimen consisted of an initial dose of 15,000 U, adjusted thereafter to prolong the activated partial thromboplastin time to 50 to 70 seconds. The continuous intravenous regimen was begun as a bolus injection of 5000 U, followed by an infusion of 1250 U/h, adjusted to maintain the activated partial thromboplastin time at 50 to 70 seconds. MEASUREMENTS AND MAIN RESULTS: There was no significant difference in the rate of new pulmonary embolism between the two groups, as defined by new high-probability defect on repeat ventilation-perfusion scintigrams of the lung in 96 (93%) of the patients after 7 to 10 days of treatment. Five of forty-seven patients in the subcutaneous group and 5 of 49 in the intravenous group developed pulmonary embolism (95% confidence interval [CI] for the difference, -13.1% to 12.2%). Similarly, there was no significant difference in the frequency of hemorrhagic complications. Five of fifty-one patients in the subcutaneous group and 5 of 52 in the intravenous group had hemorrhagic complications (95% CI for the difference, -11.2% to 11.6%). CONCLUSION: Adjusted subcutaneous calcium heparin may be an effective and safe alternative to continuous intravenous calcium heparin in the initial treatment of acute proximal deep vein thrombosis.

Acute Disease↗
PubMed1986

A randomized controlled trial of a low-molecular-weight heparin (enoxaparin) to prevent deep-vein thrombosis in patients undergoing elective hip surgery.

There is experimental evidence that low-molecular-weight fractions of heparin are as effective as the standard form but cause less bleeding. We therefore performed a double-blind, randomized trial comparing PK10169 low-molecular-weight heparin with placebo for the prevention of venous thrombosis in patients undergoing elective hip surgery. Prophylactic treatment with a fixed dose was begun postoperatively and continued for 14 days. Fifty patients in each treatment group underwent surveillance with [125I]fibrinogen leg scanning and impedance plethysmography. In the first 24 patients, venography was performed only if either surveillance test was positive. Because the rate of venous thrombosis detected in those patients was unexpectedly low, venography was requested in the remaining 76 patients, even if the screening tests were negative. In this latter group, venous thrombosis occurred in 4 patients (10.8 percent) given PK10169 heparin and 20 patients (51.3 percent) given placebo (P = 0.0002); the corresponding rates for proximal-vein thrombosis were 5.4 percent and 23.1 percent, respectively (P = 0.029). In the entire group of 100 patients, venous thrombosis occurred in 12 percent of those given PK10169 heparin and 42 percent of those given placebo (P = 0.0007), and the corresponding rates for proximalvein thrombi were 4 percent and 20 percent, respectively (P = 0.014). The observed hemorrhagic rate was 4 percent in each treatment group. We conclude that prophylaxis with fixed-dose PK10169 heparin is effective and safe for patients undergoing elective hip replacement.

Aged↗
PubMed1986

Intravenous heparin for the prevention of stroke progression in acute partial stable stroke.

In a double-blind, placebo-controlled trial, 225 patients with acute partial stable thrombotic stroke were randomly assigned to receive continuous intravenous heparin therapy or placebo for 7 days for the prevention of stroke progression or death. No statistically significant difference between the two groups was found in degree of neurologic change; incidence of stroke progression after 7 days; or functional activity level of survivors at 7 days, 3 months and at 1 year after treatment. Compared with controls, a statistically significant greater number of patients in the group receiving heparin died in the year after the stroke. These deaths occurred 3 to 12 months after the initial stroke and probably were not related to treatment. Results of this study do not support the use of intravenous heparin to treat patients who have had acute partial stroke.

Aged↗
PubMed1985

An evaluation of suloctidil in the prevention of deep vein thrombosis in neurosurgical patients.

Suloctidil (200 mg t.i.d.) was compared with placebo in a randomized, double-blind trial to assess its value in preventing deep venous thrombosis (DVT) in high-risk neurosurgical patients, comprising 136 patients with brain or spinal tumour, head or spinal injury, or subarachnoid or intracranial hemorrhage. 125I fibrinogen leg scanning and impedance plethysmography were performed for up to 14 days to detect DVT. The two groups were also evenly balanced for DVT risk factors. Seventeen of 68 patients (25%) (95% confidence interval, 15-35%) treated with suloctidil and 12 of 68 patients (21%) (95% confidence interval, 11-32%) treated with placebo developed deep venous thrombosis. This observed difference in outcomes is not statistically significant (X2 = 1.096; p = 0.30). The estimated 95% confidence interval for the true difference in the incidence of DVT between suloctidil-treated and placebo-treated patients ranges from an 11% benefit in favour of suloctidil to an 18% benefit in favour of placebo. Major deep vein thrombosis occurred in two patients on suloctidil and three patients in the placebo group; there were no fatal pulmonary emboli during the 14-day study period, during which time four patients in each group died of non-thromboembolic complications. There was no observed difference in hemorrhagic complications. Long-term outcomes at three-months follow-up were similar between the two treatment groups. It is concluded that there is no real evidence that suloctidil (200 mg t.i.d.) is an effective regimen for the prevention of DVT in high-risk neurosurgical patients.

Brain Neoplasms↗
PubMed1985

Diagnostic efficacy of impedance plethysmography for clinically suspected deep-vein thrombosis. A randomized trial.

Impedance plethysmography is an accurate noninvasive method to test for proximal vein thrombosis, but it is insensitive to calf-vein thrombi. We randomly assigned patients on referral with clinically suspected deep-vein thrombosis and normal impedance plethysmographic findings to either serial impedance plethysmography alone or combined impedance plethysmography and leg scanning (which has been shown to be essentially as sensitive as venography) and compared the long-term outcomes. During the initial surveillance, deep-vein thrombosis was detected in 6 of 311 patients (1.9%) tested by serial impedance plethysmography alone and in 30 of 323 patients (9.3%) (most with calf-vein thrombi) tested by the combined approach (p less than 0.001). During long-term follow-up, no patient died from pulmonary embolism; but 6 patients (1.9%; 95% confidence limits, 0.7% to 4.2%) tested by serial impedance plethysmography developed deep-vein thrombosis compared with 7 patients (2.2%; 95% confidence limits, 0.9% to 4.4%) tested by the combined approach. Serial impedance plethysmography used alone is an effective strategy to evaluate such symptomatic patients.

Adult↗
PubMed1984

Effect of suloctidil on platelet function in patients with shortened platelet survival time.

The effect of suloctidil (600 mg/day) on platelet survival time (PST) and plasma and urine betathromboglobulin (BTG) was studied in a double-blind, placebo-controlled six-week crossover trial in 13 patients with shortened PST (less than 110 hrs, exponential model). Mean PST after suloctidil (110.6 hrs) was significantly higher than in the placebo phase (94.5 hrs) (p = 0.04). Mean plasma BTG was significantly lower during the suloctidil phase (42.8 ng/ml) compared with the placebo phase (65.8 ng/ml) (p = 0.02), but there was no significant difference in urine BTG. These results suggest that suloctidil provides a platelet protective effect and therefore may be of benefit in reducing the frequency of platelet mediated thromboembolic events.

Blood Platelets↗
PubMed1984

Evaluation of a commercial kit for the radioimmunoassay of fibrinopeptide A.

Measurement of fibrinopeptide A (FpA) provides a sensitive and specific marker of thrombin generation and is important in the investigation of the mechanisms involved in thrombosis and hemostasis. However, current methods available for determination of FpA by radioimmunoassay (RIA) require rigorous method development. Recently, a commercial kit (Mallinckrodt Corp: M-Kit) for the RIA of FpA has become available which contains all the necessary reagents for the assay. We evaluated this kit and compared it to an assay prepared from a commercial kit (IMCO Corp: I-Kit) which contains only the raw materials. Both assays had similar characteristics and duplicate plasma samples assayed using both methods were not significantly different. Separation of FpA from fibrinogen using bentonite slurry (M-Kit) proved superior to the ethanol precipitation method (I-Kit). The complete kit (M-Kit) will provide the routine hemostasis laboratory with an RIA for FpA which is immediately available.

Evaluation Studies as Topic↗
PubMed1984

Clinical usefulness of testing for a heparin-dependent platelet-aggregating factor in patients with suspected heparin-associated thrombocytopenia.

It is important to confirm the diagnosis of heparin-associated thrombocytopenia, because discontinuation of heparin requires the institution of other antithrombotic therapy. Reports describing a heparin-dependent platelet-aggregating factor in the serum of patients with heparin-associated thrombocytopenia suggest the potential for a specific diagnostic test. No study has evaluated the diagnostic usefulness of testing for this factor, and we tested for a heparin-dependent platelet-aggregating factor in sera from (1) 14 patients with heparin-associated thrombocytopenia, (2) 14 nonthrombocytopenic controls given heparin, (3) 16 patients with consumptive thrombocytopenic disorders not associated with heparin, and (4) 13 healthy laboratory personnel. Coded serum samples plus varying concentrations of heparin (final concentration 0.01, 0.1, 1.0, and 5 U/ml) plus platelets from healthy individuals were incubated together, and aggregation was measured. Positive results (greater than 20% aggregation) occurred in (1) five of 14 patients with heparin-associated thrombocytopenia, (2) 0 of 16 consumptive thrombocytopenic controls not given heparin therapy, (3) one of 14 nonthrombocytopenic controls given heparin, and (4) one of 13 healthy controls, giving a sensitivity of 36% and specificities of 100%, 93%, and 92%, respectively. No unique clinical or laboratory feature distinguished those patients with heparin-associated thrombocytopenia with positive aggregation results from those patients with heparin-associated thrombocytopenia with negative results. Fourteen of the 16 patients (86%) with heparin-associated thrombocytopenia had elevated levels of platelet-associated IgG; however, the test was also positive in 67% of the 16 patients with other consumptive (and probably immune) thrombocytopenic disorders not associated with heparin administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

The sex-related differences in aspirin pharmacokinetics in rabbits and man and its relationship to antiplatelet effects.

There are a number of reports which suggest that the antithrombotic effect of aspirin is limited to males. It is unclear whether this effect is due to sex-related differences in the effect of aspirin on platelets, the vessel wall, or the pharmacokinetics of aspirin. To test these possibilities we examined the sex-related differences in (1) vessel wall PGI2 release and its inhibition by and recovery from aspirin in rabbits; (2) the effects of aspirin on platelet aggregation, thromboxane B2 and beta-thromboglobulin (BTG) release in man, and (3) the pharmacokinetic characteristics of aspirin, in both rabbits and man. Vascular wall PGI2 measured as 6-keto-PGF1 alpha, was not different in male and females rabbits, and was inhibited to a similar extent by identical concentrations of aspirin. The duration of this inhibitory effect was also the same in males and females. The pattern of inhibition of collagen-induced platelet aggregation, and collagen-induced thromboxane B2 and BTG release by aspirin were not different in either sex. There was, however, a sex-related difference in a number of pharmacokinetic characteristics of aspirin both in rabbits and man. Thus, aspirin was absorbed more rapidly, distributed in larger apparent volume and was hydrolysed more rapidly in females. These observations suggest that the sex-related differences in the antithrombotic effects of aspirin seen in clinical studies are not due to differences in the effects of aspirin on the inhibition of platelet function mediated by the inhibition of cyclo-oxygenase in either the platelet or the vessel wall. An effect of aspirin on platelet function independent of the inhibition of cyclo-oxygenase has been described and it is possible that this effect may be influenced by sex-related differences in the pharmacokinetics of aspirin.

6-Ketoprostaglandin F1 alpha↗