Summary. Background: Whether atherosclerotic disease predisposes to venous thrombosis is uncertain. Objective: To determine whether subclinical atherosclerosis, manifested as increased carotid intima-media thickness (IMT) or presence of carotid plaque, is associated with increased incidence of venous thromboembolism (VTE). Patients and methods: The Atherosclerosis Risk in Communities study is a prospective cohort of adults aged 45-64 years, examined at baseline (1987-89) and followed for cardiovascular events. Bilateral carotid ultrasound for IMT measurements was done at baseline for portions of the common and internal carotid arteries, and carotid bifurcation and also to detect the presence of carotid plaque. Exclusion criteria included baseline anticoagulant use, history of coronary heart disease, stroke, or VTE, and incomplete data. First VTE during follow-up was validated using abstracted medical records. Results: Among 13 081 individuals followed for a mean of 12.5 years, 225 first VTE events were identified. Unadjusted hazard ratios (HR) (95% CI) of VTE across quartiles of baseline IMT were 1.0, 1.16 (0.77-1.75), 1.64 (1.12-2.40), and 1.52 (1.03-2.25). However, this association disappeared after adjustment for age, sex, and ethnicity (HRs: 1.0, 1.06, 1.40, and 1.18). Further adjustment for body mass index and diabetes weakened the relative risks even further. Presence of carotid plaque at baseline also was not associated with VTE occurrence; adjusted HR ¼ 0.97, 95% CI ¼ 0.72-1.29. Conclusion: Increased carotid IMT or presence of carotid plaque was not associated with an increased incidence of VTE in this middle-aged cohort, suggesting subclinical atherosclerosis itself is not a VTE risk factor.
Summary. Background: Recent reports have suggested an association of atherosclerosis with risk of venous thrombosis. Objective: To confirm whether subclinical atherosclerosis is a risk factor for venous thrombosis (VT) among men and women age 65 and older. Methods: Participants of the Cardiovascular Health Study (n ¼ 4108) without baseline clinical cardiovascular disease, anticoagulant use or previous VT were followed for a median of 11.7 years after non-invasive assessment of subclinical atherosclerosis using carotid ultrasound (intimamedia thickness and presence of plaques), ankle-brachial blood pressure index and electrocardiogram. Each event was classified as idiopathic or secondary. We used Cox proportional hazards regression to estimate the relative risk of overall and idiopathic VT for individuals with and without baseline subclinical atherosclerosis. Results: There were 133 first time VT events. No subclinical atherosclerosis measures were associated with increased risk of overall or idiopathic VT. The adjusted relative risks of overall and idiopathic VT for presence of any type of subclinical disease were 0.60 (95% confidence interval 0.39-0.91) and 0.32 (0.18-0.59), respectively. Most of this association was explained by an inverse association of high-risk carotid plaques (prevalent in 54% of those at risk) with VT. Conclusion: Non-invasively measured subclinical atherosclerosis was not associated with increased risk of overall or idiopathic VT in this observational study. Carotid plaques and arterial events during follow up were inversely associated, a finding that requires further study.
To determine whether elevated levels of hemostatic and inflammatory markers [von Willebrand factor (vWF), fibrinogen, D-dimer, factor VII, factor VIII, PAI-1, tPA, beta-thromboglobulin (beta-TG), CRP, and WBC count] are associated with increased peripheral arterial disease (PAD) prevalence, measured by low ABI, we studied 13,778 participants from the ARIC study in a cross-sectional analysis after adjustment for major cardiovascular risk factors. PAD was positively associated with fibrinogen, vWF, factor VIII, WBC count, D-dimer, beta-TG, and CRP (p for trend <0.05) but not with the other markers. Adjusted odds ratios for the highest versus the lowest quartile of fibrinogen in men and women, respectively, were 3.49 (95% CI 1.68-7.26) and 2.44 (95% CI 1.58-3.77); for vWF 2.36 (95% CI 1.36-4.07) and 1.45 (95% CI 1.00-2.10); for factor VIII 2.31 (95% CI 1.36-3.94) and 1.68 (95% CI 1.14-2.48). In a smaller subset, the sex and risk factor adjusted odds ratio for the highest versus the lowest quartile of D-dimer was 2.70 (95% CI 1.56-4.65), for beta-TG was 1.80 (95% CI 1.12-2.88), and for CRP was 1.57 (95% CI 0.84-2.95). Plasma levels of hemostatic and inflammatory markers are elevated in PAD, suggesting these processes are involved in the pathophysiology of PAD.
Intermittent claudication is the most common symptom in patients with peripheral arterial disease (PAD). As such, it is mandatory for clinicians to treat both the PAD-specific symptoms (to decrease functional impairment and thereby improve quality- of-life, as well as to decrease rates of amputation) and the underlying systemic atherosclerosis (and thereby reduce cardiovascular ischemic events, especially myocardial infarction and stroke). Most patients with claudication can successfully decrease their exertional limb symptoms via a combination of exercise (preferably supervised) and pharmacotherapeutic interventions (eg, cilostazol). Endovascular revascularization currently serves as an effective therapy for patients with high-grade stenoses of the proximal limb arterial segments, (eg, the distal aorta, common iliac artery, or external iliac artery, and occasionally the proximal common femoral artery). Surgical revascularization usually is reserved for patients who present with severe aortoiliac disease in whom long-term patency is likely to be achieved (eg, aortobifemoral or femoral-femoral bypass) and who have a low cardiovascular perioperative ischemic risk. Patients who undergo successful revascularization also are likely to benefit from exercise rehabilitation programs. All patients with PAD, of any severity, must successfully normalize atherosclerosis risk factors and use antiplatelet therapies. Such interventions include complete smoking cessation, glycemic control, normalization of blood pressure (less than 130/90 mm Hg), and lowering of low-density lipoprotein (LDL) cholesterol to less than 100 mg/dL. Antiplatelet agents (eg, clopidogrel, aspirin) should be prescribed to decrease rates of cardiovascular ischemic events in all patients with PAD, unless otherwise contraindicated.
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