Antithrombin III and arterial disease

Meade, T. W.; Cooper, Jane; Miller, George; Howarth, D. J.; Stirling, Yvonne

doi:10.1016/0140-6736(91)91503-m

Cited by 74 publications

(32 citation statements)

References 9 publications

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“…There also was no U-shaped association with AT-III, as has been previously suggested. 6 After pooling the data for both races, fibrinogen was still the only factor showing an age-, race-, and centeradjusted association with carotid wall thickness at P<.01 (Table 4, wall thickness per each SD greater fibrinogen concentration. Adjustment for other fibrinogen correlates (Table 4, bottom half) attenuated the estimates.…”

Section: Resultsmentioning

confidence: 99%

“…Plasma fibrinogen 13 and factor VII 2 have been shown in prospective epidemiological studies to be positively associated with cardiovascular disease incidence. Clinical or epidemiological evidence suggests that other factors, such as factor VIII, 2 -4 von Willebrand factor, 45 protein C, 4 and antithrombin III (AT-III), 6 may also be related to cardiovascular disease occurrence. It is uncertain, however, whether hemostatic factors are associated only with the thrombotic component of cardiovascular disease or also with the atherosclerotic process.…”

mentioning

confidence: 99%

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Association of hemostatic variables with prevalent cardiovascular disease and asymptomatic carotid artery atherosclerosis. The Atherosclerosis Risk in Communities (ARIC) Study Investigators.

Folsom

Shahar

et al. 1993

Arterioscler Thromb

156

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Association of hemostatic variables with prevalent cardiovascular disease and asymptomatic carotid artery atherosclerosis. The Atherosclerosis Risk in Communities (ARIC) Study Investigators.

Folsom

Shahar

et al. 1993

Arterioscler Thromb

156

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“…9) Meade, et al reported that an increased risk for ischemic events occurs in both the lowest and highest tertiles of AT-III values compared to the middle tertile. 10) In patients with ACS, AT-III activity decreases after treatment with heparin. 10,11) However, the degree of this decrease is usually not significant in most patients, and AT-III activity is in the normal range 24 hours after heparin therapy.…”

Section: Discussionmentioning

confidence: 99%

“…10) In patients with ACS, AT-III activity decreases after treatment with heparin. 10,11) However, the degree of this decrease is usually not significant in most patients, and AT-III activity is in the normal range 24 hours after heparin therapy.…”

Section: Discussionmentioning

confidence: 99%

A Case of Acute Myocardial Infarction With Repetitive Stent Thrombosis During Emergent Percutaneous Coronary Intervention Transient Decrease in Antithrombin III Activity and Heparin Resistance

et al. 2009

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SummaryA 59-year-old woman was admitted to our hospital for the treatment of an acute anterior myocardial infarction. She had a history of uncontrolled diabetes mellitus, hypertension, hyperlipidemia, obesity, and smoking. Coronary angiography revealed 90% stenosis with spontaneous dissection in the proximal portion of the left anterior descending artery. At this time, heparin was initiated for the first time. Although direct stenting (Be-stent, 3.0-18 mm) was performed for the culprit lesion, coronary dissection occurred at the left main trunk and additional stenting (Multi Link ZETA stent 3.5-15mm) was performed for the left main trunk. Soon after stenting, repetitive stent thrombosis occurred. Aspiration of the thrombus using an aspiration catheter was ineffective and repetitive angioplasty and intraaortic balloon pumping were required. Although we used 17,000 units of unfractionated heparin during the intervention, the activated coagulation time (ACT) was not prolonged (157 seconds). In the coronary care unit, the ACT and activated partial prothrombin time (aPTT) were not prolonged despite the use of large amounts of heparin (69,000 units in 2 days). Protein-S, protein-C, and hepaplastin testing were within normal limits and heparin-platelet factor IV complex antibody was not detected. In the acute phase, a decrease in the antithrombin III activity (65%) was noted and with administration of argatroban, prolongation of the aPTT was achieved. In the chronic phase, the decrease in antithrombin III activity and heparin resistance had improved spontaneously. It is important to recognize the existence of transient decreases in antithrombin III activity in the acute phase of myocardial infarction. (Int Heart J 2009; 50: 111-119)

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“…In 1976 Yue et al 14 reported that high plasma concentrations of antithrombin might predispose to ischaemic heart disease. More recently, Meade et al ,15 in a prospective study of approximately 900 men, made the fascinating observation that more deaths had occurred in those with antithrombin levels in both the low and high thirds of the normal antithrombin distribution than in individuals whose result fell into the middle third of the pooled results. For men at least, this suggests that both high and low levels of antithrombin may be risk factors for death from arterial disease.…”

Section: Clinical Featuresmentioning

confidence: 99%