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ARTERIAL THROMBOSIS
Arterial thrombosis may result from a variety of factors. As with venous thrombosis, the priniciples expressed as Virchow’s triad (vascular injury, stasis, hypercoagulability) predict the risk for thrombosis. Atherosclerosis is a primary disorder of arteries, which begins with an inciting process illiciting an inflammatory response in the vessel wall. The result is endothelial dysfunction, subendothelial proliferation of smooth muscle cells and the deposition of minimally oxidized low-density lipoprotein molecules, which coalesce within monocytes to form lipid pools. An important aspect of the process is the development of a number of abnormalities of the coagulation system. Atherosclerotic placques sustain injury due to spontaneous fissuring or interventional procedures, which acutely activates the clotting system. The result is acute arterial thrombosis in as many as 90% of patients who sustain myocardial infarction. At least 70% of the thrombosed arteries are less than 50% occluded from the athersoclerotic placque. To one degree or another, a similar process is responsible for peripheral arterial thrombosis and cerebrovascular thrombosis. Recognized risk factors for arterial thrombosis are listed below. At CALIFORNIA CLINICAL THROMBOSIS CENTER every effort is made to identify these underlying risk factors and present a comprehensive recommendation for appropriate treatment.
Risk Factors for Arterial Thrombosis
- Atherosclerosis
- Cigarette smoking
- Hypertension
- Diabetes mellitus
- LDL elevation
- Hypertriglyceridemia
- Family history
- Oral contraception
- Left ventricular failure
- Lipoprotein (a)
- Polycythemia
- Hyperviscosity
- Leukostasis
- Heparin induced thrombocytopenia
Many patients with myocardial infarction, peripheral arterial thrombosis and stroke, have underlying Thrombophilic disorders predisposing them to acute thrombosis. Identifying these disorders allows specific treatment for specific disorders. Disorders associated with arterial thrombosis include: Activated protein C resistance (including factor V Leiden mutation and factor V Cambridge mutation); Prothrombin G20210A mutation, Protein S and C deficiency, Antithrombin deficiency; Antiphospholipid antibodies (anticardiolipin antibodies, lupus anticoagulant and others), Hyperhomocysteinemia (methylene tetrahydrofolate reductase mutation C677T), Myeloproliferative disorders, Trousseau’s Syndrome, Sticky Platelet Syndrome, Wein Penzing platelet defect, Dysfibrinogenemia, Factor XII deficiency (Hageman factor), Heparin co-factor II defect, Plasminogen deficiency, Tissue –plasminogen activator deficiency, Plasminogen activator inhibitor Type-1 elevation, and von Willebrand’s factor elevation.
The treatment with aspirin (usually prescribed for patients with coronary artery disease, transient ischemic attacks and stroke) is not adequate in many of these patients. More potent anticoagulation therapy may be required to prevent recurrence. The underlying etiology determines the appropriate therapy.
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