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Biomedical subjects

A G Turpie

Publications and source records attributed to A G Turpie.

At least 145 records · Page 8Linked to original sources
PubMed1983

Platelet tests and antiplatelet drugs in coronary artery disease.

This study was designed to clarify discrepancies in the literature concerning platelet survival time and beta-thromboglobulin (beta TG) levels in patients with coronary artery disease (CAD) and the effect of platelet-suppressant drugs on these tests. Platelet survival time and plasma beta TG levels were determined in 48 patients with angiographically documented CAD. The effect of sulfinpyrazone or aspirin/dipyridamole on these measurements was investigated in a double-blind, crossover trial that included a placebo phase. In patients with CAD, the mean plasma beta TG concentration was significantly elevated, but the mean platelet survival time was not significantly different from that in controls. Treatment with sulfinpyrazone or aspirin/dipyridamole did not produce changes in platelet survival time or plasma beta TG concentration that were significantly different from the values during the placebo phase. This study demonstrates that compared with the spontaneous variation in platelet survival time or beta TG concentration, there was no measureable effect of sulfinpyrazone or aspirin/dipyridamole on the results of the tests.

Adult↗
PubMed1983

The diagnosis of acute, recurrent, deep-vein thrombosis: a diagnostic challenge.

Recurrent venous thrombosis presents a diagnostic challenge. Venography, impedance plethysmography and fibrinogen leg scanning all have potential limitations, and their role in this context has not been evaluated. We performed a prospective cohort study evaluating impedance plethysmography and leg scanning, plus venography, using outcome on long-term follow-up as the end point in 270 patients with clinically suspected recurrent deep-vein thrombosis. Anticoagulant treatment was withheld in the 181 patients negative by noninvasive testing and was given in patients positive by impedance plethysmography if leg scanning was positive or if intraluminal filling defects were detected by venography. The validity of this approach was tested by long-term follow-up. Three of 181 patients (1.7%) negative by noninvasive testing had a recurrence, compared with 18 of 89 (20%) with positive findings (p less than 0.001). Our objective diagnostic approach has high clinical utility; an objective rationale for withholding or giving treatment was established in 95% of patients.

Acute Disease↗
PubMed1983

Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan.

Inherent contradictions in current diagnostic recommendations for pulmonary embolism have created considerable confusion and controversy. To resolve these contradictions, we did a prospective study of ventilation-perfusion scanning, pulmonary angiography, and venography in consecutive patients with clinically suspected pulmonary embolism and abnormal perfusion scans. Ventilation scanning increased the probability of pulmonary embolism in patients with large perfusion defects and ventilation mismatch, but a ventilation-perfusion match was not helpful in ruling out pulmonary embolism. Small perfusion defects with mismatch had neither sufficiently high nor low probability to be of diagnostic value. The observed frequency of proximal vein thrombosis (19% to 51%) and its association with the range of ventilation-perfusion defects have important implications for management of pulmonary embolism. Pulmonary angiography is required in combination with venography in most patients with perfusion abnormalities because the probability of pulmonary embolism is neither sufficiently high nor low to confirm or exclude pulmonary embolism.

Adolescent↗
PubMed1982

Different intensities of oral anticoagulant therapy in the treatment of proximal-vein thrombosis.

We have previously reported that long-term therapy with warfarin is effective for preventing recurrent venous thromboembolism in patients with proximal-vein thrombosis but that there is an appreciable risk of hemorrhage. To determine whether that risk could be reduced without a loss of effectiveness, we randomly allocated 96 patients with proximal-vein thrombosis to a group receiving less intense anticoagulant therapy, with a mean prothrombin time of 26.9 seconds using the Manchester comparative reagent (corresponding Simplastin time, 15 seconds), or a group given more intense therapy, with a mean Simplastin time of 19.4 seconds (corresponding prothrombin time 41 seconds with the Manchester comparative reagent) (P less than 0.001). Two of 47 patients (4 per cent) in the less intensely treated group had hemorrhagic complications, as compared with 11 of 49 patients (22 per cent) in the more intensely anticoagulated group (P = 0.015 by the two-tailed test). This difference was due to minor bleeding episodes. The frequency of recurrent venous thromboembolism was low in both groups (2 per cent). Our findings indicate that less intense anticoagulant therapy is associated with a low frequency of recurrent venous thromboembolism (2 per cent) and a reduced risk of hemorrhage.

Administration, Oral↗
PubMed1982

Platelet consumption in cardiovascular disease.

Many tests have been devised to investigate the role of platelets in arterial or venous thromboembolism. The mechanisms of platelet reactivity that the tests have measured have been variable and the early studies have been of little value in determining the contribution of platelet consumption in thromboembolic diseases. More recently, tests of in vivo platelet release and of platelet survival and turnover have been introduced and thought to be of great potential in the investigation of thromboembolic disorders. However, the data published thus far using more tests are far from conclusive that platelet activation and consumption occurs in thromboembolic disorders associated with arteriosclerosis. It may be that they are neither sensitive nor specific enough to detect minor changes in platelet activation. There is, however, some consistency that in conditions involving the larger vessels, prosthetic surfaces, or in association with active and recurrent venous thromboembolism, platelet release and platelet consumption measured by platelet survival time may occur. In particular, the abnormal results are consistently found in acute and recurrent venous thromboembolism, cardiac valve replacement with the older prosthetic devices, and arteriosclerosis of the larger arteries with clinical episodes of thromboembolism. However, in coronary artery disease, cerebrovascular disease, and peripheral vascular disease, the data are inconclusive, probably because the tests lack sensitivity. In addition, the value of the tests in the management of patients with thromboembolic disorders appears to be limited.

Angina Pectoris↗
PubMed1982

Plasma betathromboglobulin and serum fragment E in acute partial stroke.

Plasma betathromboglobulin (BTG) and serum fragment E (FgE) were measured serially by radioimmunoassay for 7 d in 67 patients admitted with acute partial stroke. Twelve patients progressed within 7 d of admission. Plasma BTG was not different from normal in patients with acute partial stroke and did not increase significantly with stroke progression. Serum FgE was elevated in patients with acute partial stroke compared with normal values, and was significantly higher in patients who progressed compared with those who remained stable. The results indicate that fibrin formation may be more important in the process of stroke progression than activation of platelets.

Acute Disease↗
PubMed1982

Platelet release and thromboxane synthesis in symptomatic coronary artery disease.

The incidence and significance of platelet activation in myocardial ischemia was evaluated by serial measurement of plasma thromboxane B2 (TXB2) and beta thromboglobulin (beta TG) in plasma and urine in 98 patients admitted to a coronary care unit with chest pain. All measurements were normal in the 26 patients with noncardiac chest pain. Mean plasma TXB2 and beta TG concentration, but not urine beta TG, were elevated in the 25 patients with myocardial infarction and the 47 patients with angina. The beta TG levels remained normal in 61% of the patients with angina or infarction. The TXB2 levels were significantly higher in patients with recurrent episodes of angina at rest than in those without ischemic episodes after admission. There was a weak correlation between plasma TXB2 and plasma beta TG (r = 0.20, p less than 0.01) and between plasma and urine beta TG (r = 0.31, p less than 0.01). Results indicate that platelets are frequently activated with myocardial ischemia or infarction. However, the measurement of beta TG and TXB2 is of limited value in detecting or differentiating myocardial ischemia from infarction and therefore lacks clinical value in the management of patients with ischemic heart disease.

Aged↗
PubMed1982

Antithrombotic effects of drugs which suppress platelet function: their potential in prevention growth of tumour cells.

Four drugs that inhibit platelet function have been evaluated for their antithrombotic effects in humans. These are aspirin, dipyridamole, hydroxychloroquine and sulphinpyrazone. Aspirin has been shown to reduce the number of transient ischemic attacks (TIA), stroke and death in patients with multiple TIA. The reduction in TIA was greatest in males who were normotensive and when there was an angiographically demonstrated lesion in the carotid artery that accounted for the symptoms. Aspirin reduced venous thrombosis and non-fatal and fatal pulmonary embolism in patients after surgery for fractured hip and after elective hip replacement. There is evidence that the prophylactic effect of aspirin may be greater in male patients. Aspirin reduced the frequency of arteriovenous shunt thrombosis. Aspirin abolished symptoms in patients with peripheral ischemia associated with thrombocytosis and spontaneous platelet aggregation. There is no conclusive evidence at the present time that aspirin is effective in patients with coronary artery artery disease. Dipyridamole in combination with oral anticoagulants is effective in reducing the frequency of systemic embolism in patients with prosthetic heart valve replacement but is ineffective in patients with transient cerebral ischemic attacks or for the prevention of venous thromboembolism. Hydroxychloroquine was effective in reducing postoperative venous thrombosis in patients undergoing general abdominothoracic surgery but the evidence that it was effective in patients undergoing orthopaedic surgery is inconclusive. Sulphinpyrazone may be effective in reducing the frequency of sudden cardiac deaths in patients in the first year after myocardial infarction when it is started within 25 to 35 days after the infarction. Sulphinpyrazone reduced the incidence of arteriovenous shunt thrombosis in patients undergoing chronic hemodialysis and in combination with anticoagulants, it reduced the frequency of recurrent venous thrombosis. There have been no large scale trials of platelet suppressant drugs in clinical cancer and successful treatment of thromboembolic disorders cannot be used to predict success in the treatment of malignant disease.

Aspirin↗
PubMed1982

The diagnostic value of the fibrinogen/fibrin fragment E antigen assay in clinically suspected deep vein thrombosis.

We have evaluated the fibrinogen/fibrin fragment E antigen assay as a diagnostic test in patients with clinically suspected venous thrombosis by comparing the results of this assay with venography in 272 patients. The result of the fragment E antigen assay was elevated in 79 of 80 patients with positive venograms for recent venous thrombosis (sensitivity 99%) and within the normal range in 161 of 192 patients with normal venograms (specificity 84%). The fragment E assay was also evaluated in 130 medical and surgical controls without evidence of venous thrombosis by leg scanning and the test was found to be relatively nonspecific. However, in the patient group under study, a correct clinical diagnosis of no thrombosis, based on a normal fragment E result, was made in 161 of 162 cases (negative predictive value of 99%). Therefore, a normal test result effectively excludes a diagnosis of venous thrombosis in clinically symptomatic patients. The assay, as currently performed, is technically demanding and takes 24 hr to complete. Therefore, it will have to be simplified before it can be applied to clinical practice.

Adolescent↗
PubMed1981

Clinical validity of a negative venogram in patients with clinically suspected venous thrombosis.

Although it is generally accepted that negative venography excludes deep vein thrombosis (DVT) in patients in whom it is clinically suspected, there is no evidence to support this conclusion. To test the correctness of withholding anticoagulant therapy in these patients, we followed 160 consecutive patients who had clinically suspected DVT and negative venograms to determine the frequency of postvenographic DVT. Anticoagulant therapy was withheld in all patients. No patient died or developed pulmonary embolism during 3 months of follow-up. Two of the 160 patients (1.3%) attended the clinic on an emergency basis during follow-up with new symptoms of DVT and in both patients, DVT was confirmed by objective testing. These events developed within 5 days of venography, which suggests that they were induced by venography. Nevertheless, the findings indicate it is safe to withhold treatment in patients with clinically suspected DVT and negative venograms.

Adolescent↗
PubMed1981

Replacement of venography in suspected venous thrombosis by impedance plethysmography and 125I-fibrinogen leg scanning: a less invasive approach.

Noninvasive diagnostic testing is gaining acceptance in the evaluation of patients with clinically suspected venous thrombosis. Although clinically useful, all these tests have limitations, and the safety of basing therapeutic decisions on their outcome has not been assessed. We have done a prospective study of 322 symptomatic patients to ascertain the safety of replacing venography with impedance plethysmography and leg scanning. To provide a diagnostic reference, we did venography in all patients but withheld anticoagulants if the noninvasive tests were negative irrespective of the results of venography. None of the 163 patients with negative noninvasive tests died or developed clinical pulmonary embolism during 3 months' follow-up, confirming the safety of this approach. In two, clinically evident postvenographic venous thrombosis developed, confirmed by repetition of these objective tests. Also, the positive predictive values indicate that therapeutic decisions can be based on a positive noninvasive outcome in patients without clinical disorders known to produce false-positive results.

Adolescent↗
PubMed1981

Plasma and urine beta-thromboglobulin concentration in patients with deep vein thrombosis.

Plasma and urine beta-thromboglobulin (BTG) were measured in 52 patients with established deep vein thrombosis (DVT) and in 100 patients with clinically suspected DVT but with a negative venogram. Both plasma BTG (geometric mean 54: 95% range 12--239 ng/ml) and urine BTG (0.25; 0.03--3.1 ng/ml) were significantly elevated (p less than 0.005) in patients with DVT compared to symptomatic patients with a negative venogram (plasma BTG 32, 9--112 ng/ml; urine BTG 0.12, 0.02--0.58 ng/ml). Sensitivity (35%) and specificity (80%) of the plasma BTG assay for the diagnosis of DVT were low. The urine BTG assay had a sensitivity of 37% but a specificity of 100%. There was a significant correlation between plasma and urine BTG (r = 0.68, p less than 0.005). Serial BTG measurements were made in urine (40 patients) and plasma (20 patients) from high-risk neurosurgical cases who were screened with 125I-fibrinogen leg scanning and impedance plethysmography. BTG was elevated postoperatively and returned to normal within 2 or 3 days, but rose again in 10 patients in association with the development of DVT. The rise of BTG preceded the uptake of 125I-fibrinogen and lasted for only a few days. The return to normal of BTG was not related to treatment with anticoagulants. While measurement of BTG in plasma and urine is of limited value in the clinical diagnosis of venous thrombosis, the data indicate platelet activation occurs in venous thrombosis, but is maximal or perhaps limited to the initial phase of thrombus development.

Adolescent↗
PubMed1980

Beta-thromboglobulin radioimmunoassay. A laboratory characterization and evaluation.

Platelets release beta-thromboglobulin from alpha-granules when they are activated by various stimuli. An evaluation and optimization of a radioimmunoassay for beta-thromboglobulin is described. The optimum conditions for the reaction have been characterized, and the use of second antibody and polyethylene glycol allows completion of the assay within 24 hours. Similar BTG concentrations were obtained using a 1-hour non-equilibration assay but the 1-hour assay was inefficient for processing large volumes of specimens and has the potential for cross reactivity. BTG standards were unstable but the shelf-life was prolonged with aprotinin or by storage at -70 degrees C. Plasma BTG concentration in 80 normal individuals was 28 +/- 18 ng/ml. (mean +/- 2 S.D.).

Adult↗