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Biomedical subjects

E Coyne

Publications and source records attributed to E Coyne.

15 recordsLinked to original sources
PubMed2004

Studies comparing low molecular weight heparin with heparin for the treatment of thromboembolism: a literature review.

The use of heparin for the prophylaxis and treatment of venous and arterial thrombosis had been the standard of care for clinicians until 1982. At that time the introduction of depolymerized heparin for the prophylaxis of deep vein thrombosis in surgical patients was introduced. A number of such products, low molecular weight heparins (LMWH) were patented and introduced as new drugs during the ensuing of 20 years. Each LMWH had to be given a clinical trial against standard heparin for the several thromboembolic disorders for which heparin was the standard of care. By definition LMWH had to have unequal factor Xa and IIa inhibitor potency, expressed as a Xa-IIa ratio of greater than 1. They also had a molecular weight reduction to about one third that of heparin. A major advantage of LMWH over heparin was the subcutaneous route of injection for treatment of thrombotic disorders in contrast to the intravenous route for heparin. They had greater bioavailability than heparin by the subcutaneous route, a longer half-life and better predictability of dose response. It was found that routine laboratory monitoring was unnecessary. When given a trial against heparin, LMWH was equally safe and effective for most venous and arterial disorders. A new synthetic version of (pentasaccharide) both heparin and LMWH has been at least if not more effective than one LMWH (enoxaparin).

Animals↗
PubMed1992

Frequency of late potentials on signal-averaged electrocardiograms during thallium stress testing in coronary artery disease.

Late potentials detected by signal-averaged electrocardiography (SAECG) are an important noninvasive indicator identifying patients with previous myocardial infarction at risk for developing ventricular tachycardia. The role of myocardial ischemia in the development of late potentials is undefined. This study attempts to determine if late potentials on SAECG can be produced during scintigraphically proven ischemia. A signal-averaged electrocardiogram was obtained before and immediately after single-photon emission computed tomography thallium exercise testing in 51 patients. Reversible ischemia was documented in 25 cases with no significant changes in the parameters of SAECG; patients with previous myocardial infarction (n = 10) also had no significant changes from baseline. Multivariate analysis with respect to reversible ischemia and previous myocardial infarction was unrevealing. Patients with late potentials at baseline (n = 10) who developed reversible ischemia (n = 5) had a shorter QRS duration than those with late potentials at baseline and no reversible ischemia. The data indicate that exercise-induced scintigraphically proven ischemia does not alter SAECG even in the presence of previous myocardial infarction. Patients with late potentials at baseline may actually have a shortened QRS duration during reversible ischemia as opposed to the expected lengthening of the QRS.

Coronary Disease↗
PubMed1991

Interaction of heparinoids with platelets: comparison with heparin and low molecular weight heparins.

Heparin interacts with platelets to impair collagen-induced aggregation and adhesion to collagen. Low molecular weight heparin and heparinoids have little or no inhibitory activity in these platelet-collagen interactions. Thrombin-induced aggregation of platelets is inhibited by any of the glycosaminoglycans that will block the action of thrombin on fibrinogen. However, heparin is a much more potent inhibitor than low molecular weight heparins or heparinoids at equigravimetric concentrations in these reactions. The inhibition of ristocetin or asialo-von Willebrand factor aggregation of platelets is partially blocked by high dose heparin but not by low molecular weight heparin or heparinoids. The heparin-induced IgG antibody, produced to a heparin-platelet complex, aggregates platelets strongly in the presence of heparin, less strongly in the presence of low molecular weight heparins and pentosan polysulfate and not at all with dermatan sulfate or the pentasaccharide. Heparan sulfate does interact with platelets and this antibody, which is of interest because of the heparan sulfate on endothelial cells. Clinical information to date suggests a low incidence of heparin antibodies in patients receiving only low molecular weight heparin of the depolymerized type. Whether long-term clinical use of low molecular weight heparins, heparan sulfate, and dermatan sulfate will give rise to specific antibodies that would cause a similar problem as heparin remains to be seen.

Autoantibodies↗
PubMed1989

In vitro studies of the interaction of heparin, low molecular weight heparin and heparinoids with platelets.

Heparin, low molecular weight heparins, and heparinoids were studied for their ability to inhibit the aggregation of platelets by various agonists and for their ability to adhere to collagen. Heparin was a very effective inhibitor of aggregation with collagen and with ristocetin as it was with adhesion to collagen. The heparinoids showed little effect on aggregation or adhesion. Heparan sulfate and pentosan polysulfate did show slight inhibitory activity against collagen aggregation and adhesion and both interacted with the antibody induced by heparin therapy. It is of interest that dermatan sulfate and the pentasaccharide were almost inert in these experiments, and are unlikely to induce bleeding by inhibition of platelet function. It is highly probable that interference with the interaction of von Willebrand factor with platelets and collagen is a major mechanism for bleeding in the heparinized patient.

Adenosine Diphosphate↗