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Perioperative Management of Oral Antithrombotics in Dentistry and Oral Surgery: Part 2
Benjamin J. Statman DDS
Article Category: Research Article
Volume/Issue: Volume 70: Issue 1
Online Publication Date: Mar 28, 2023
DOI: 10.2344/anpr-70-01-06
Page Range: 37 – 48

clinical trials, but observational and retrospective studies have been used to establish a general stratification of thrombotic risk ( Table 1 ). Patients prescribed acetylsalicylic acid (aspirin; ASA) for primary prevention of atherosclerotic complications are at a relatively very low risk for thrombosis. For patients on oral antiplatelet (OAP) agents for secondary prevention of thrombosis, risk is stratified based on the condition (coronary artery disease, peripheral artery disease, cerebrovascular disease), intervention (coronary artery stent or stents, coronary

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Perioperative Management of Oral Antithrombotics in Dentistry and Oral Surgery: Part 1
Benjamin J. Statman DDS
Article Category: Other
Volume/Issue: Volume 69: Issue 3
Online Publication Date: Oct 06, 2022
DOI: 10.2344/anpr-69-03-05
Page Range: 40 – 47

vWF, adenosine diphosphate (ADP), factor V, and other substances that attract and activate additional platelets. 2 , 3 Platelet aggregation is also augmented by the activation of ADP-bound P2Y 12 receptors located in the platelet membrane. Once activated by ADP, these G-inhibitory protein receptors inhibit adenylyl cyclase and thus promote more platelet aggregation. In addition, P2Y 12 receptor activation antagonizes the action of the antiplatelet eicosanoid prostacyclin, promoting further aggregation. 4 Coagulation is the next stage of hemostasis

Caution: Maintain Anti-Platelet Therapy in Patients with Coronary Artery Stents
Joel M. Weaver DDS, PhD
Article Category: Research Article
Volume/Issue: Volume 54: Issue 4
Online Publication Date: Jan 01, 2007
DOI: 10.2344/0003-3006(2007)54[161:CMATIP]2.0.CO;2
Page Range: 161 – 162

A recent science advisory from the American Heart Association, American College of Cardiology, Society for Cardiovascular Angiography and Interventions, American College of Surgeons, and the American Dental Association with representation of the American College of Physicians states that coronary artery stent thrombosis is a very serious problem. * Their new advisory states that dual antiplatelet therapy consisting of aspirin and a thienopyridine drug such as clopidogrel (Plavix) or ticlopidine (Ticlid) should be given for at least a full

Figure 2. ; Platelet aggregation and actions of antiplatelet drugs.1,3 Resting platelets have specific receptors for ligands that trigger activation: epinephrine, thrombin, serotonin, collagen, adenosine diphosphate (ADP), and thromboxane A2 (TXA2). When activated, intracellular calcium levels elevate and the platelet expresses glycoprotein (GP) IIb/IIIa receptors that bind to strands of fibrinogen. This results in platelet aggregation. The various antiplatelet drugs inhibit aggregation by targeting specific aspects of this process.
Daniel E. Becker
<bold>Figure 2.</bold>
Figure 2.

Platelet aggregation and actions of antiplatelet drugs. 1,3 Resting platelets have specific receptors for ligands that trigger activation: epinephrine, thrombin, serotonin, collagen, adenosine diphosphate (ADP), and thromboxane A2 (TXA2). When activated, intracellular calcium levels elevate and the platelet expresses glycoprotein (GP) IIb/IIIa receptors that bind to strands of fibrinogen. This results in platelet aggregation. The various antiplatelet drugs inhibit aggregation by targeting specific aspects of this process.

Figure 2; 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.
Daniel E. Becker
Figure 2
Figure 2

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.

Kawasaki Disease and General Anesthesia for Dental Treatment: A Case Report
Sarah Lee DDS,
 David B. Guthrie DMD, and
 Ralph H. Epstein DDS
Article Category: Case Report
Volume/Issue: Volume 68: Issue 3
Online Publication Date: Oct 04, 2021
DOI: 10.2344/anpr-68-01-06
Page Range: 146 – 153

treated with antiplatelet (aspirin 162 mg) and anticoagulant (warfarin titrated to a prothrombin time/international normalized ratio [PT-INR] of 2.5) medications. Figure 1. Transthoracic echocardiogram image demonstrating patient's giant tubular aneurysm of the right coronary artery (RCA) measuring 10.04 mm maximal diameter; Z score 18.7 (red arrow). Figure 2. Transthoracic echocardiogram image demonstrating patient's aneurysm of the left anterior descending

Figure 1; 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).
Daniel E. Becker
Figure 1
Figure 1

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).

Figure 1. ; Thrombogenesis. 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 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).
Daniel E. Becker
<bold>Figure 1.</bold>
Figure 1.

Thrombogenesis. 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 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).

Figure 1.; Classic coagulation cascade model featuring the extrinsic, intrinsic, and common coagulation pathways.
Benjamin J. Statman
Figure 1.
Figure 1.

Classic coagulation cascade model featuring the extrinsic, intrinsic, and common coagulation pathways.

Figure 2.; Contemporary coagulation model demonstrating the 3 phases: activation (A-C), amplification (D-F), and clot propagation (G).3
Benjamin J. Statman
Figure 2.
Figure 2.

Contemporary coagulation model demonstrating the 3 phases: activation (A-C), amplification (D-F), and clot propagation (G). 3