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PubMed1991

[Platelet antiaggregants in the treatment of arterial thrombosis].

The paper contains a critical review of the major clinical controlled trials which have been carried out on the use of platelet anti-aggregating agents in the prophylactic treatment of arterial thrombosis. The drugs studied to date include aspirin, sulphinpyrazone, dipyridamole and ticlopidine. These drugs have been used in primary infarction prophylaxis and secondary prophylaxis of arterial thrombosis at a cardiac (reinfarction, instable angina, valvular prosthesis, aortocoronary bypass, coronary angioplasty), cerebral (TIA, ictus) and peripheral (obliterating arteriopathy, thromboendarterectomy, arteriovenous shunt) level. The most frequently studied end-points are non-fatal reinfarction, cardiovascular mortality (fatal reinfarction, sudden death, fatal ictus), non-fatal ictus, vascular re-occlusion after arterio-lesive surgery, and some clinico-radiographical parameters at a peripheral level. The best results, which are statistically significant, have been obtained in the prophylaxis of instable angina and re-occlusion following aortocoronary by-pass; results obtained in cerebrovascular disease and peripheral obliterating arteriopathy are less statistically significant but equally successful and worthy of attention, especially in the case of ticlopidine which showed a greater number of advantages than aspirin. Positive but statistically not reliable findings were reported regarding the secondary prophylaxis of reinfarction, whereas non-significant data were reported for secondary prophylaxis of reocclusion of coronary angioplasty, thromboendarterectomy and arterio-venous shunt, and for the primary prophylaxis of reinfarction. The Author confirms that the clinical trials carried out for the long-term prophylaxis of still asymptomatic subjects are the only way of evaluating the clinical efficacy of a platelet anti-aggregating agent; the results of these trials must however be carefully and critically assessed from a clinical and statistical point of view and at all events can only act as a guideline for the doctor; the latter continues to be solely responsible for the choice of the drug and he must be aware of possible collateral effects and the risk/benefit ratio as well as the personal characteristics of the patient.

Angina Pectoris↗
PubMed1975

[Anti-platelet aggregating drugs in the prevention of thromboembolic diseases].

The treatment and prevention of arterial thrombosis have been improved in recent years by the use of drugs acting on certain platelet characteristics, such as clumping capacity, adhesivity, release of factors 3 & 4, and survival. Many substances have been proposed for clinical employment. Mechanisms of action are discussed on the basis of personal experience, particularly with dipyrimadol and beta-blocking drugs. It would seem that the best results are obtainable with drugs whose effect on platelet clumping comes from stablisation of the membrane, such as the non-steroid anti-inflammatory preparations, in association with drugs than enhance intraplatelet cyclic AMP.

Adrenergic beta-Antagonists↗
PubMed1986

Pharmacology of the interaction between platelets and vessel wall.

The evaluation of agents inhibiting platelet function is difficult because, in addition to primary aggregation by thrombin, there are three amplification loops involving respectively arachidonate, ADP and PAF-acether (platelet activating factor). Each amplification loop seems eventually to act via a common pathway: the mobilization of calcium ions from the dense tubular system into the cytoplasm. Inhibition of this mobilization would prevent platelet aggregation by any agonist. This could be an ideal step with which to intervene pharmacologically. An intracellular increase in cAMP reduces cytoplasm calcium levels and therefore counteracts the effect of whatever agonist is used (Vermylen et al, 1982, 1983; Verstraete et al, 1985). Depending on the pro-aggregatory stimulus, the relative importance of a given pathway of platelet activation may shift. There is also uncertainty about which pathway of platelet activation predominates in a given clinical condition. The second problem relates to the pharmacology of the ideal drug for the inhibition of platelet function. It is very difficult to delineate the desired profile of such a drug considering the properties of the various compounds presently being studied (see Table 1). Prolongation of a shortened platelet survival in man was considered to be one of the key markers of an anti-aggregatory agent; this characteristic was found to be present after administration of sulphinpyrazone, clofibrate, ticlopidine, suloctidil, dipyridamole (in patients with artificial heart valves) and dipyridamole (in patients with venous thrombosis). The protective antithrombotic effect is most clearly demonstrated for aspirin; it is rather surprising that this drug does not prolong the shortened platelet survival in man, not even in those clinical conditions in which it effectively prevents thromboembolism.

Animals↗
PubMedDate not supplied

Antiplatelet drugs or dicoumarol: what is the most effective prophylaxis in occlusive arterial disease?

Arterial thromboses lead to disturbances of vital function: myocardial infarction, ischemic cerebral infarction, disorders of peripheral blood flow, nephrosclerosis. Prophylaxis of thrombosis is still an unsolved problem, since diseases caused by thrombosis remain the first cause of death, at least in Western countries. After describing the pathomorphological and pathobiochemical findings, a survey of the literature on prophylaxis of occlusive arterial diseases is presented and the difference between anticoagulants and aggregation inhibitors is pointed out.

Arterial Occlusive Diseases↗
PubMed1988

Anturan for secondary prophylaxis of myocardial infarction.

273 patients suffering from ischemic heart disease were treated with Anturan for one year at a daily dosage of 800 mg. The number of cardiovascular complications was significantly reduced, compared to the control group.

Adrenergic beta-Antagonists↗
PubMed1989

Immunoglobulin E receptor cross-linking induces oscillations in intracellular free ionized calcium in individual tumor mast cells.

Fura-2 fluorescence in single rat basophilic leukemia cells was monitored to study the rise in intracellular free ionized calcium ([Ca2+]i) produced by aggregation of immunoglobulin E receptors. Repetitive transient increases in [Ca2+]i were induced by antigen stimulation and were measured using digital video imaging microscopy at high time resolution. The [Ca2+]i oscillations were not dependent upon changes in the membrane potential of the cells and were observed in cells stimulated with antigen either with or without extracellular Ca2+. Transient oscillations in [Ca2+]i were also observed when calcium influx was blocked with La3+. These results suggested that during antigen stimulation of cells under normal physiological conditions, release of Ca2+ from intracellular stores makes an important contribution to the initial increase in [Ca2+]i. Oscillations in [Ca2+]i are not induced by elevating [Ca2+]i with the calcium ionophore ionomycin. Mitochondrial calcium buffering is not required for [Ca2+]i oscillations to occur. The results show that rat basophilic leukemia cells have significant stores of calcium and that release of calcium from these stores can participate in both the initial rise and the oscillations in [Ca2+]i.

Adenosine Triphosphate↗
PubMed1985

Secondary prevention of coronary events after myocardial infarction. Beta-blockers and/or anti-platelets: to whom, when and for how long. A review.

The institution of a "Cardioprophylactic" drug regimen after myocardial infarction should take into consideration the concept of high or low risk patients for secondary coronary events and the concept of a decremential mortality rate as time elapses after myocardial infarction. Thus, the efficacy of a particular drug in preventing secondary coronary events may vary with the time elapsed from infarction and thus with the underlying patho-physiologic mechanism. Furthermore, the administration of a possible effective or proven effective "Cardioprophylactic" drug or drug regimen at a specific time from infarction must take into account the balance between expected benefit and untoward side effects.

Adrenergic beta-Antagonists↗