Appropriate preoperative assessment of the dental patient should always include an analysis of the patient's medications. Cardiovascular diseases are the most common group of medical disorders that dentists encounter, and the number of drugs prescribed for managing these conditions is staggering. This justifiably raises concern and probable confusion regarding side effects and possible drug interactions with medications the dentist may deem necessary for dental care. This continuing education article is the second in a series that will address essential pharmacology of medications commonly prescribed for chronic medical care. A reasonable understanding of these agents will allow the dentist to better appreciate the medical status of their patients, to appreciate the actual risks associated with antithrombotic medications, and to avoid adverse interactions with drugs the dentist might administer or prescribe.Abstract
Summary of thrombogenesis and thrombolysis. A thrombus consists of 2 principal components: an aggregate of platelets and a fibrin mesh. Platelet activity consists of adherence to vessel walls (adhesion) and to one another (aggregation). The fibrin mesh is synthesized during a complex cascade of enzymatic reactions leading to the formation of fibrin strands (coagulation). The body also has a natural thrombolytic system, essentially comprised of plasmin, an enzyme that cleaves fibrin strands. Antithrombotic drugs are classified according to action on each of these processes: antiplatelet drugs, anticoagulants, and thrombolytics (fibrinolytics).
Resting platelets are activated by a variety of chemical mediators, each of which can be targeted by antiplatelet drugs summarized in Table 2. Activated platelets aggregate by binding to strands of fibrinogen, which can be prevented by drugs that block the activated receptors.
The coagulation pathway and target sites for anticoagulant drugs.1,4 The coagulation pathway is a cascade of enzymatic conversions, each activating the next enzyme (Factor) in the sequence. The final enzyme in this pathway is thrombin, also called Factor IIa, which catalyzes the conversion of fibrinogen to fibrin strands. Warfarin (W) acts by inhibiting synthesis of factors in the liver. In contrast, heparin (H) acts to inhibit factors that have become activated within the bloodstream. Thrombin can be activated by either of 2 pathways. The intrinsic pathway is initiated within the bloodstream by platelet thromboplastin. H influences this pathway by inhibiting Factor IXa. However, it also inhibits Factors Xa and IIa within the common pathway, and its activity must be monitored using the activated partial thromboplastin time (aPTT). The extrinsic pathway functions outside the bloodstream, initiated by tissue thromboplastin. This pathway is influenced most by W because it inhibits hepatic synthesis of Factor VII, the most essential factor in this pathway. The anticoagulant activity of W is monitored using the prothrombin time (PT), which is now standardized as the international normalized ratio (INR). Newer agents, commencing with the low–molecular-weight Hs (L) have greater specificity for inhibiting Factor Xa and thrombin within the common pathway and generally do not require therapeutic monitoring.
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