Aim: Inflammation is highlighted in the pathogenesis and destabilization of atherosclerotic lesions. Noninvasive identification of inflammation of atherosclerotic lesions has been challenging. 18-Fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) is a useful technique for detecting inflamed atherosclerotic plaques in vivo. However, it is time consuming, expensive, and accompanied by radiation. Therefore, we investigated the relationship between levels of circulating inflammatory markers and the degree of inflammation of atherosclerotic plaques shown by 18F-FDG uptake. We aimed to identify high-risk patients with inflamed, unstable atherosclerotic plaques on the basis of the determination of inflammatory markers.Methods: The study included 37 patients, 21 with high-grade stenosis of internal carotid artery (ICA group) and 16 with occlusion of common femoral artery (CFA group), who underwent endarterectomy. Mean age of the study population was 69.43 ± 6.2 years. Eight out of 21 patients with ICA stenosis and all patients with CFA occlusion were symptomatic. In all patients before endarterectomy, 18F-FDG-PET imaging was performed and blood samples were obtained for determination of circulating inflammatory markers: high-sensitivity C-reactive protein (hsCRP), tumor necrosis factor alpha (TNF-α), interleukins, and selectins. Both groups were compared with a sex- and age-matched control group composed of 27 healthy volunteers.Results: 18F-FDG uptake, calculated by target-to-background ratio (TBR) was not significantly different between the groups. Levels of inflammatory markers were elevated, and there were no significant differences between ICA and CFA groups, with an exception of interleukin 6 (IL-6) levels, which was higher in the ICA group (3.2 ± 2.5 ng/L vs. 1.8 ± 1.3 ng/L, p < 0.05). There was a positive interrelationship between 18F-FDG-PET and most of the systemic inflammatory markers: hsCRP (r = 0.417, p = 0.010), IL-6 (r = 0.603, p < 0.001), and TNF-α (r = 0.374, p = 0.023). However, correlation between 18F-FDG-PET and P-selectin, E-selectin, and t-PA was not found.Conclusion: Our study showed that an interrelationship exists between the intensity of inflammatory process of atherosclerotic lesions shown by FDG uptake and circulating inflammatory markers. Therefore, the determination of circulating inflammatory markers can have a potential to identify individuals with unstable, inflamed atherosclerotic plaques.

Some inflammatory markers and indicators of endothelial dysfunction are increased in varicose vein blood. This is most probably the consequence of deteriorated blood flow in dilated and tortuous superficial veins, and increased venous pressure. Damage to the venous wall, which causes a chronic inflammatory response, together with the procoagulant properties of local blood may promote further progression of the disease and thrombotic complications.

The aim of this study was to follow the thrombus progression and regression in superficial veins of lower limbs in patients with superficial vein thrombosis (SVT) treated with low-molecular-weight heparin. Patients (n = 68) with a first symptomatic SVT of the lower limbs received 2 different dosages of dalteparin. The primary outcome was a change in the diameter and length of thrombus in the affected veins. The regression of thrombus was not significantly different between the groups (P = .19). The reduction in the length of thrombus as well as thrombus diameter was significantly greater in females. At the end of the observation period, the length of thrombus in the distal part was more reduced than in the proximal segments. It seems that the dosage of anticoagulant drug does not have a significant impact on thrombus resolution.

IntroductionLittle is known about pathogenetic mechanisms of superficial venous thrombosis (SVT). We aimed to investigate the systemic inflammatory response in the acute phase of SVT, the time course of inflammatory markers and involvement of inflammation in resolution of thrombus in SVT.Material and methodsThe circulatory inflammatory parameters high-sensitivity C-reactive protein (hsCRP), tumor necrosis factor α (TNF-α), interleukins 6, 8 and 10 (IL-6, IL-8, IL-10), and markers of fibrinolytic activity tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and fibrinogen were determined in 68 patients with acute SVT of lower limbs, who were allocated to two groups, dalteparin 5000 IU once daily or 10 000 IU once daily. Recanalization of occluded veins was monitored by ultrasonography at regular intervals. Blood was drawn in the acute phase and after 12 weeks.ResultsIn the acute phase a majority of the measured inflammatory markers were increased, while after 12 weeks most of them significantly dropped: hsCRP: 13.6 ±11.9 vs. 7.4 ±4.4, p < 0.001; IL-6: 3.8 ±3.1 vs. 2.6 ±1.9, p = 0.007. Significant changes in endogenic fibrinolytic parameters were also observed: t-PA activity decreased (0.81 ±0.35 vs. 0.68 ±0.34, p = 0.003), while PAI-1 levels increased (5.6 ±5.1 vs. 8.8 ±8.5, p < 0.001). Levels of inflammatory markers at inclusion and after 12 weeks were related to less effective thrombus resolution: CRP: r = 0.386, p = 0.001; IL-6: r = 0.384; TNF-α: r = 0.255, p = 0.037.ConclusionsIn the acute phase of SVT, most of the circulating inflammatory markers were increased and most of their levels decreased after 12 weeks. Levels of inflammatory markers were negatively correlated with the recanalization rate.

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