Hypercoagulable state under low-intensity warfarin anticoagulation assessed with hemostatic markers in cardiac disorders

Takano, Kentaro; Iino, Kozo; Ibayashi, Setsuro; Tagawa, Koichi; Sadoshima, Seizo; Fujishima, Masatoshi

doi:10.1016/0002-9149(94)90590-8

Cited by 16 publications

(9 citation statements)

References 29 publications

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“…Many previous studies have indicated that hemostatic markers are not affected by aspirin. 3,5,27 Third, we could not determine the mechanism by which coexistence of severe atheroma and nonrheumatic AF could promote activation of coagulation and fibrinolysis, nor the effect of cholesterol-lowering statin therapy for stroke risk reduction. The site of activation of coagulation and fibrinolysis would be in the localized region with severe atheroma of the thoracic aorta, as well as in the fibrillating atria.…”

Section: Study Limitationsmentioning

confidence: 99%

Thoracic Aortic Plaque Enhances Hypercoagulability in Patients With Nonrheumatic Atrial Fibrillation

Nakagawa

Hirai

Sakurai

et al. 2007

Circ J

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trial fibrillation (AF) is associated with higher thromboembolic risk, possibly because of the hypercoagulable state. 1,2 Elevated levels of hemostatic markers have been shown in patients with nonrheumatic AF. [2][3][4][5][6] During AF, stagnation of blood flow in the left atrial appendage (LAA) could contribute to the hypercoagulable state and clot formation in the fibrillating atria. Hemostatic markers could be therefore used for stratification of patients at high risk vs low risk for thromboembolism as demonstrated in previous studies. [1][2][3][4][5][6] Aortic atheroma is recognized as an important marker of stroke and peripheral embolism in patients with AF. 7-9 The SPAF-III investigators reported that complex aortic plaque emerged as a risk factor of thromboembolism in patients with nonrheumatic AF, and warfarin was effective in reducing stroke in patients with AF and complex aortic plaque. 10 Complex aortic plaques with ulcerated or mobile plaques and superimposed thrombi would activate hemostatic markers. The Framingham Offspring Study raised the possibility that the increases in hemostatic factors in patients with AF were mainly caused by the confounding effect of traditional risk factors and coexistent cardiovascular diseases rather than by AF itself. 2 We recently reported that patients with nonrheumatic AF had elevated levels of D-dimer when complicated with spontaneous echocardiographic contrast (SEC) in the descending thoracic aorta. 11Because AF and aortic atherosclerosis might contribute synergistically to increased levels of hemostatic markers, and could be associated with increased risk of thromboembolism, we determined the relationship between plasma levels of hemostatic markers and atherosclerosis in the descending thoracic aorta assessed by transesophageal echocardiography (TEE) in patients with nonrheumatic AF and in those in sinus rhythm (SR). Methods Study PatientsEchocardiographic and hematologic studies were performed in 106 consecutive patients (79 men, 27 women; mean age of 67±11 years) referred to a university hospital for cardiovascular assessment for stroke risk or identification of the cardiogenic source of recent embolism. Patients who received anticoagulant therapy were not included in the present study. Of these 106 patients, AF was documented electrocardiographically in 60 patients (AF group) but not in the remaining 46 patients (SR group). The study protocol was approved by the institutional ethics committee and written informed consent was given by all patients. Underlying heart diseases included the following: ischemic heart disease (n=8), hypertrophic cardiomyopathy (n=4), dilated cardiomyopathy (n=5), sick sinus syndrome (n=3), atrial septal defect (n=5), post pericarditis (n=6), and miscellaneous diseases (n=20). No apparent underlying diseases were identified in 55 patients. Baseline clinical characteristics, including body mass index, diabetes mellitus, hyperlipidemia, smoking, previous cerebral or peripheral embolic event and the use of oral antiplatelet medication at...

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Section: Study Limitationsmentioning

confidence: 99%

Thoracic Aortic Plaque Enhances Hypercoagulability in Patients With Nonrheumatic Atrial Fibrillation

Nakagawa

Hirai

Sakurai

et al. 2007

Circ J

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“…[12][13][14] The critical issue that remains unresolved at this time is the minimal degree of suppression of coagulation that is required to provide antithrombotic protection in various clinical settings. Using specific and sensitive immunologic assays of activation of the coagulation system, several groups have shown that lower-dose warfarin regimens are able to suppress coagulation in vivo in various populations of patients.…”

Section: However Kearon Et Al Have Reported In Preliminary Formmentioning

confidence: 99%

Warfarin for Venous Thromboembolism — Walking the Dosing Tightrope

Schafer¹

2003

N Engl J Med

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“…20 Insufficient VKA treatment was independently associated with higher severity of stroke and higher prevalence of proximal artery occlusion in the present study, and this seems pharmacokinetically plausible: the functional activity of protein C -the protein that has the anticoagulant effect -is decreased even in the subtherapeutic PT-INR range. 22 Insufficient VKA therapy may lead to larger thrombus formation than in those without anticoagulant medication through insufficient suppression of coagulation factors plus suppression of functional activity of protein C, and it may be associated with more severe stroke via proximal artery occlusion. This association was found only in patients with anterior-circulation stroke, probably because the relationship between vessel occlusion and NIHSS score in posteriorcirculation stroke patients was relatively weaker than in anterior-circulation stroke.…”

Section: Resultsmentioning

confidence: 99%

Insufficient Warfarin Therapy Is Associated With Higher Severity of Stroke Than No Anticoagulation in Patients With Atrial Fibrillation and Acute Anterior-Circulation Stroke

Sakamoto

Okubo

Nito

et al. 2018

Circ J

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Hypercoagulable state under low-intensity warfarin anticoagulation assessed with hemostatic markers in cardiac disorders

Cited by 16 publications

References 29 publications

Thoracic Aortic Plaque Enhances Hypercoagulability in Patients With Nonrheumatic Atrial Fibrillation

Thoracic Aortic Plaque Enhances Hypercoagulability in Patients With Nonrheumatic Atrial Fibrillation

Warfarin for Venous Thromboembolism — Walking the Dosing Tightrope

Insufficient Warfarin Therapy Is Associated With Higher Severity of Stroke Than No Anticoagulation in Patients With Atrial Fibrillation and Acute Anterior-Circulation Stroke

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