Hypercoagulopathy in Stroke Patients with Nonvalvular Atrial Fibrillation: Hematologic and Cardiologic Investigations

Turgut, Nilda; Akdemir, Osman; Turgut, Burhan; Demir, Muzaffer; Ekuklu, Galip; Vural, Özden; Özbay, Gültaç; Utku, Ufuk

doi:10.1177/107602960601200104

Cited by 34 publications

(19 citation statements)

References 29 publications

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“…Increases in prothrombin fragment and thrombin-antithrombin complexes have been observed in patients with AF-related strokes 191 and in those with transesophageal spontaneous echo contrast. 192 Other hemostatic factors have been implicated in contributing to the hypercoagulable state including fibrinogen, D-dimer, factor VIII, and von Willebrand factor.…”

Section: Clinical Outcomesmentioning

confidence: 99%

“…192 Other hemostatic factors have been implicated in contributing to the hypercoagulable state including fibrinogen, D-dimer, factor VIII, and von Willebrand factor. 191, 193–196 However, in an adjusted model, the FHS showed that such abnormalities are ascribed to AF RFs and presence of cardiovascular disease rather than AF alone. 197 Finally, inflammation may mediate endothelial dysfunction and hypercoagulability.…”

Section: Clinical Outcomesmentioning

confidence: 99%

“…Several studies have shown that AF is associated with a hypercoagulable state attributed to elevated hemostatic factors including fibrinogen, D-dimer, prothombin fragment, factor VIII, and von Willebrand factor; 191, 193–196 however, many of these studies were not adjusted for co-existing cardiovascular RF. In an adjusted model, the FHS showed no significant difference in levels of fibrinogen, von Willebrand factor, or tissue plasminogen activator suggesting that co-existing RFs rather than AF may explain elevated thrombotic risk.…”

Section: Clinical Outcomesmentioning

confidence: 99%

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Atrial Fibrillation

Stærk

Sherer

et al. 2017

Circulation Research

900

380

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The last three decades have been characterized by an exponential growth in knowledge and advances in the clinical treatment of atrial fibrillation (AF). It is now known that AF genesis requires a vulnerable atrial substrate and that the formation and composition of this substrate may vary depending on comorbid conditions, genetics, sex, and other factors. Population-based studies have identified numerous factors that modify the atrial substrate and increase AF susceptibility. To date, genetic studies have reported seventeen independent signals for AF at fourteen genomic regions. Studies have established that advanced age, male sex, and European ancestry are prominent AF risk factors. Other modifiable risk factors, including sedentary lifestyle, smoking, obesity, diabetes mellitus, obstructive sleep apnea, and elevated blood pressure predispose to AF and each factor has been shown to induce structural and electrical remodeling of the atria. Both heart failure and myocardial infarction increase risk of AF and vice versa creating a feed forward loop that increases mortality. Other cardiovascular outcomes attributed to AF, including stroke and thromboembolism, are well established and epidemiology studies have championed therapeutics that mitigate these adverse outcomes. However, the role of anticoagulation for preventing dementia attributed to AF is less established. Our review is a comprehensive examination of the epidemiological data associating unmodifiable and modifiable risk factors for AF and of the pathophysiological evidence supporting the mechanistic link between each risk factor and AF genesis. Our review also critically examines the epidemiological data on clinical outcomes attributed to AF and summarizes current evidence linking each outcome with AF.

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Section: Clinical Outcomesmentioning

confidence: 99%

Section: Clinical Outcomesmentioning

confidence: 99%

Section: Clinical Outcomesmentioning

confidence: 99%

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Atrial Fibrillation

Stærk

Sherer

et al. 2017

Circulation Research

900

380

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“…16 This conclusion is disputed by others. 17 In our patients with elevated D-dimer levels, none of them had atrial fibrillation. However, high-grade carotid stenosis (≥75%) or carotid occlusion was found in five of our patients with elevated D-dimer levels.…”

Section: Discussionmentioning

confidence: 54%

The follow-up of patients of sixty-five years of age and younger with acute ischemic stroke and transient ischemic attacks, and elevated D-dimer levels in plasma

Vrethem¹,

Lindahl²

2009

Neurol Int

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D-dimer levels in plasma, a degradation product of fibrin, have been shown to correlate with the severity of ischemic stroke. In order to investigate the outcome of patients with elevated D-dimer we have carried out a follow-up study of patients of 65 years of age and younger with acute ischemic stroke or transient ischemic attacks (TIA) admitted to our stroke unit from 1991 to 1992. Twenty-two of the 57 patients had elevated D-dimer levels in the plasma. High levels were associated with cardioembolic stroke. On follow-up after a mean of 12 years, 15 patients had died and six patients had suffered another stroke or TIA (three of whom were dead). Ten patients had suffered other cardiovascular events and seven of them were dead. We concluded that high levels of D-dimer in acute ischemic stroke patients on admission were associated with cardioembolic stroke and might have prognostic value for the development of further cardioor cerebrovascular events. Advanced age was found to be an independent risk factor.

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“…In fact, AF is often characterized by endocardial damage, from dilatation of the atria, 7 blood slowdown and stasis, 8 related to the anatomy of the atria, and abnormal changes in blood constituents, including platelet activation, 9 as well as inflammation 10 and changes in growth factor. 11 For these reasons, AF can favor a prothrombotic and hypercoagulable state.…”

mentioning

confidence: 99%

Clinical Significance of Non-Vitamin K Antagonist Oral Anticoagulants in the Management of Atrial Fibrillation

Santarpia

Curcio

Sibilio

et al. 2015

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp mation, described 150 years ago by Rudolph Virchow, 6 are present in AF. In fact, AF is often characterized by endocardial damage, from dilatation of the atria, 7 blood slowdown and stasis, 8 related to the anatomy of the atria, and abnormal changes in blood constituents, including platelet activation, 9 as well as inflammation 10 and changes in growth factor. 11 For these reasons, AF can favor a prothrombotic and hypercoagulable state. Warfarin, a VKA, is the most commonly used agent among the OACs used for thromboembolic prophylaxis in AF patients. Its effectiveness is proven by 64% relative risk reduction of stroke compared with placebo, 12 and it also shows superior results to aspirin 13 and to aspirin plus clopidogrel. 14 However, VKAs have some faults: (a) it takes time (days) to achieve a satisfactory therapeutic effect; (b) intricate superimposition with parenteral anticoagulants; (c) narrow therapeutic window; (d) significant interaction with several drugs and food, making regular monitoring of the therapeutic effect obligatory. For these reasons, a review found that up to 65% of patients at risk were not taking OACs, and the international normalized ratio (INR) was out of range in a further 19% of patients. 15 Thus, the impetus for the development of the nonvitamin K antagonist oral anticoagulants (NOACs), such as espite recent improvements in pharmacologic and electrical therapies, atrial fibrillation (AF) still remains the most common supraventricular tachyarrhythmia encountered in daily clinical practice. It affects 1-2% of the general population and its incidence increases in older patients. 1 The disease is frequently asymptomatic, but associated with a 2-fold increase in mortality, a 3-fold increase in congestive heart failure and a 5-fold increase in the risk of thromboembolic events, leading to frequent hospitalizations and worsened quality of life. 2 Although the use of antiarrhythmic medications leads to a significant improvement in symptoms, 3 assessment of thromboembolic risk and the use of adequate anticoagulation is mandatory in the proper therapeutic management of AF. 4,5 Physiopathology of Thromboembolism and Anticoagulants in AFThe association between AF and thromboembolic risk is widely recognized and the genesis of thrombus formation in AF is multifactorial. All the anatomical and physiopathological features of the triad of events necessary for thrombus for- Atrial fibrillation (AF) is the most commonly observed rhythm disorder in clinical practice. It is associated with a high risk of thromboembolic stroke and increased cardiovascular mortality. Vitamin K antagonists (VKAs), the only oral anticoagulants used for thromboembolic prophylaxis in AF patients over the past 60 years, have been effective in reducing thromboembolic stroke, compared with placebo and aspirin, in this group of patients. However, VKAs have a very narrow therapeutic window, so regular monitoring of the therapeutic ef...

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Hypercoagulopathy in Stroke Patients with Nonvalvular Atrial Fibrillation: Hematologic and Cardiologic Investigations

Cited by 34 publications

References 29 publications

Atrial Fibrillation

Atrial Fibrillation

The follow-up of patients of sixty-five years of age and younger with acute ischemic stroke and transient ischemic attacks, and elevated D-dimer levels in plasma

Clinical Significance of Non-Vitamin K Antagonist Oral Anticoagulants in the Management of Atrial Fibrillation

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