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Yaz Lawsuit News 1/23/2012: Until recently, it had appeared self-evident that (nonembolic) arterial thrombosis was the culmination of slow enlargement of the mature atherosclerotic lesion with progressive encroachment into the arterial lumen. This pathobiological construct supported the view that the risk of acute thrombosis was dominated by the severity of arterial stenosis. However, over the past decade, angiographic and pathological data obtained in the coronary arterial bed have challenged this construct. Angiography performed prior to or at the time of acute myocardial infarction has demonstrated that the infarct-related coronary atherosclerotic lesion is frequently not ‘‘critical’’ by standard angiographic criteria. Similarly, pathological examination of culprit lesions has demonstrated that the majority of acute coronary events occur with the formation of thrombus at the site of plaques obstructing <50% of the arterial lumen. Taken together with evidence for the importance of plaque disruption in the development of superimposed thrombus (56,6569), such data have shifted focus from the degree of luminal stenosis to the morphological and histological characteristics of the atheromatous plaque that determine its propensity to rupture.
Lending further support to the contribution of inflammatory mechanisms to plaque destabilization, onset of acute thrombosis with or without myocardial necrosis is marked by the production of a number of inflammatory cytokines. In addition, a series of studies have suggested a link between the elaboration of inflammatory cytokines and impairment of the ability of smooth muscle cells to maintain the integrity of the fibrous cap (52). Interferon-gamma (IFN-y), a cytokine produced by T-lymphocytes within the atheroma core, decreases the production of collagen by vascular smooth muscle cells (80-82). Smooth muscle cells at the site of plaque rupture or erosion have been found to express high levels of the transplant antigen HLA-DRa, a protein induced only by IFN-y among a wide spectrum of cytokines evaluated
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Vascular inflammation may also influence arterial vasomotor function through several possible mechanisms. Increased concentrations of thromboxane A2 and its metabolites produced in acute coronary syndromes (99,100) mediate further platelet aggregation as well as arterial vasoconstriction (101). Leukocytes also produce en- dothelin-1, a potent modulator of vasoconstriction. In addition, certain inflammatory cytokines may increase vascular smooth muscle cell reactivity, as demonstrated in an animal model with IL-1 (102). Finally, inflammatory infiltrates have been documented in the arterial adventitia with vascular nerve involvement and thus have been hypothesized to directly stimulate coronary vasospasm.
In spite of continued advancements in the management of acute ischemic heart disease, morbidity and mortality due to atherosclerotic vascular disease continue to rise globally. Thus, the impetus for improving our strategies for the prevention and management of atherosclerosis has remained strong. In this regard, laboratory and experimental research describing key processes in the initiation, progression, and destabilization of the atheroma have pointed to novel directions for cardiovascular evaluation and management. In particular, recognition of the role of inflammation in atherothrombosis has directed attention to inflammatory mediators and indicators as potential targets for risk assessment and for treatment.
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Epidemiological data have established a well-characterized set of vascular risk factors, including advanced age, tobacco use, obesity, diabetes, hypertension, and dyslipidemia. However, up to one-third of first coronary events occur among individuals without these traditional risk factors. Researchers have thus sought to identify inflammatory indicators that might add to these clinical factors for predicting myocardial infarction and stroke. Candidate markers have included several of the cytokines (77,108,109) that promote the recruitment of monocytes in response to endothelial cell dysfunction; intercellular adhesion molecules that mediate the migration of activated monocytes into the subendothelial space; enzymes that might compromise the integrity of the protective fibrous cap, as well as the acute-phase proteins that are produced and released into the systemic circulation in response to inflammatory cytokines.
With systemic levels that are dependent on the rate of de novo hepatic production, CRP levels remain stable over long periods of time in the absence of new stimuli. However, in response to acute tissue injury, infection, or other inflammatory stimuli, CRP levels rise several hundred-fold. As such, CRP and its acute-phase counterpart, serum amyloid A, have been useful in following disease activity in chronic inflammatory conditions such as systemic lupus, inflammatory bowel disease, and rheumatoid arthritis. Traditional semiquantitative latex agglutination or standard turbidometric methods have been adequate to evaluate such marked elevation of CRP in these disease processes. In contrast, the development of high-sensitivity assays for CRP (hs-CRP) has now enabled detection of CRP within the normal range for healthy individuals. Further, the introduction of high through-put methods with high analytical sensitivity and reproducibility has provided a simple clinical tool to carefully evaluate the extent of underlying systemic inflammation.
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Antiphospholipid antibodies (APLA) are a heterogeneous group of autoantibodies associated with both arterial and venous thrombosis, recurrent pregnancy loss, and thrombocytopenia. They can occur either in association with other autoimmune conditions, most frequently systemic lupus erythematosus (SLE), or in isolation, a condition known as the primary antiphospholipid antibody syndrome. In the research laboratory, many antiphospholipid antibodies (with varying epitope specificity) can be identified. However, in clinical practice, the antiphospholipid antibodies are divided into two large groups, the lupus anticoagulants and the anticardiolipin antibodies.
Lupus anticoagulants or nonspecific inhibitors interfere with the assembly of procoagulant complexes. In vitro, these antibodies are associated with the prolongation of phospholipid-dependent blood-clotting times. Characteristically, clotting times return to normal with the addition of exogenous phospholipid. Lupus anticoagulants may demonstrate specificity for blood-clotting proteins, in particular prothrombin. However, the mechanism by which they promote thrombosis is unknown. Lupus anticoagulants are likely associated with a high risk of first and recurrent thrombosis as well as recurrent pregnancy loss.
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APLA are found in about 20% of patients presenting with venous thromboembolism (1,2), in about 10% of patients presenting with first ischemic stroke (3), and in approximately 5 to 10% of young people presenting with first myocardial infarction (4). Their prevalence in the unselected population is unknown; reported rates vary widely with the test system used and the population being studied. About 30% of individuals with systemic lupus erythematosus have an APLA (5). Low-titer anticardiolipin antibodies are frequently detected in otherwise well individuals; repeat testing reveals a high rate of spontaneous resolution.
All patients with unexplained venous thrombosis, in particular those with thrombosis in unusual sites (such as the cerebral veins or mesenteric veins), should be screened for an antiphospholipid antibody. Both a lupus and an anticar- diolipin antibody should be sought. Testing should be carried out in accordance with the recommendations of the International Society of Thrombosis and He- mostasis, with appropriate confirmatory assays for suspected lupus anticoagulants.
Many questions remain unanswered in patients with antiphospholipid antibodies. First, many patients, particularly those with systemic lupus erythematosus, are screened for the presence of an antiphospholipid antibody despite their never having had an episode of thrombosis. When detected, the clinical importance of the antibody is unknown. As a result, some such patients (who are suspected to have a high risk of first thrombosis) are treated with warfarin with varying INR target ranges, while others are treated with aspirin or other antiplatelet agents, and many receive no antithrombotic prophylaxis. To address the need for routine antithrombotic prophylaxis in this problematic patient population, a large, randomized clinical trial is currently being carried out. Within this study, adults and children, with both an antiphospholipid antibody and systemic lupus erythematosus, are allocated to long-term warfarin with a target INR of 2.0, or no therapy. The primary outcome measure of the study is the rate of objectively confirmed arterial and venous thrombosis.
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