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The antithrombic drugs in clinical practice
The rational use of antithrombic drugs centres on the fundamental differences in the pathogenesis of arterial or venous thrombosis. The major role of platelets in the development of occlusion in arteries contrasts with prominent fibrin deposition in the slower moving venous blood. Logically, antiplatelet agents are used to treat patients at high risk from arterial disease and anticoagulants for those with venous thrombo-embolism. These sound theoretical principles have been linked to steady improvement in diagnostic techniques, and there now exists an extensive literature on available drugs and their clinical evaluation. It is therefore surprising how little agreement exists on the practical use of the antithrombic drugs. In patients with coronary artery disease, secondary prevention of myocardial infarction is favourably influenced by administration of aspirin, dipyridamole or sulphinpyrazone. However, differences are not statistically significant so that confident recommendations for their use cannot yet be made. In mitral valve disease, anticoagulants are effective in reducing systemic thrombo-embolism; in patients with cardiac prostheses, dipyridamole should be added. In the cerebral circulation, vertebrobasilar and carotid ischaemia need to be distinguished and suitable lesions surgically corrected. Patients not undergoing endarterectomy are divided into two groups. In those with symptoms stable for more than 3 months, aspirin alone is sufficient; patients with recent deterioration or a shorter history are best treated with conventional anticoagulants followed by the addition of aspirin. In venous thrombo-embolic disease, heparin prophylaxis should be combined with reversal of identifiable risk factors. In treating the acute event, anticoagulation, with or without preceding thrombolytic therapy, is preferred. In addition, the clinician must select an antithrombic regimen o take into account the possibility of drug interaction, the need for and feasibility of laboratory monitoring, and the total number of medicines prescribed for the patient. Failure to restrict tablets to manageable numbers will lead to poor compliance and unpredictable therapeutic response.
The rational use of antithrombic drugs centres on the fundamental differences in the pathogenesis of arterial or venous thrombosis. The major role of platelets in the development of occlusion in arteries contrasts with prominent fibrin deposition in the slower moving venous blood. Logically, antiplatelet agents are used to treat patients at high risk from arterial disease and anticoagulants for those with venous thrombo-embolism. These sound theoretical principles have been linked to steady improvement in diagnostic techniques, and there now exists an extensive literature on available drugs and their clinical evaluation. It is therefore surprising how little agreement exists on the practical use of the antithrombic drugs. In patients with coronary artery disease, secondary prevention of myocardial infarction is favourably influenced by administration of aspirin, dipyridamole or sulphinpyrazone. However, differences are not statistically significant so that confident recommendations for their use cannot yet be made. In mitral valve disease, anticoagulants are effective in reducing systemic thrombo-embolism; in patients with cardiac prostheses, dipyridamole should be added. In the cerebral circulation, vertebrobasilar and carotid ischaemia need to be distinguished and suitable lesions surgically corrected. Patients not undergoing endarterectomy are divided into two groups. In those with symptoms stable for more than 3 months, aspirin alone is sufficient; patients with recent deterioration or a shorter history are best treated with conventional anticoagulants followed by the addition of aspirin. In venous thrombo-embolic disease, heparin prophylaxis should be combined with reversal of identifiable risk factors. In treating the acute event, anticoagulation, with or without preceding thrombolytic therapy, is preferred. In addition, the clinician must select an antithrombic regimen o take into account the possibility of drug interaction, the need for and feasibility of laboratory monitoring, and the total number of medicines prescribed for the patient. Failure to restrict tablets to manageable numbers will lead to poor compliance and unpredictable therapeutic response.