Is Venous Thromboembolism a Chronic Inflammatory Disease?

[摘要] Venous thromboembolism (VTE)3 traditionally has been considered a time-limited acute disease. Patients with deep vein thrombosis (DVT) or pulmonary embolism (PE) following major surgery, trauma, or periods of immobility are frequently treated with anticoagulation for a limited duration of 3 to 6 months. However, a subset of patients who suffer idiopathic (unprovoked) VTE have a high risk of recurrence, exceeding 50% over 10 years, if not treated with extended-duration anticoagulation (1, 2). Even patients who suffer VTE in the setting of identifiable provoking factors have an enduring risk of recurrence that exceeds 20% over 10 years (2). An analysis of the Danish National Registry of Patients demonstrated that patients with VTE have increased mortality over 30 years of follow-up and that recurrent PE remained an important cause of death throughout this time period (3). Extended-duration low-intensity anticoagulation with warfarin for patients with idiopathic VTE dramatically reduces the risk of recurrent events compared with time-limited anticoagulation (4). These data support the hypothesis that VTE is a chronic disease with pathophysiology rooted in enduring as well as transient risk factors.Chronic inflammation plays a key role in the pathophysiology of atherothrombosis (5). Furthermore, modulation of inflammation with antiplatelet therapy (6) and statins reduces the risk of atherothrombotic events (7). Until recently, VTE was believed to be pathophysiologically distinct from atherothrombotic disorders such as acute coronary syndromes and stroke. However, recent data have challenged this “silo thinking” and suggest that VTE should be considered as part of a pan-cardiovascular syndrome that includes coronary artery disease, cerebrovascular disease, and peripheral artery disease (8).In addition to sharing cardiovascular risk factors such as obesity, hypertension, dyslipidemia, diabetes, and smoking, VTE and atherothrombosis result from common pathophysiological mechanisms including hypercoagulability, endothelial injury, and inflammation (Fig. 1) (8). The increased frequency of DVT …

[学科分类] 过敏症与临床免疫学