ABSTRACT
BACKGROUND: Venous thoracic outlet syndrome resulting in the upper limb deep venous thrombosis is known as Paget-Schroetter syndrome or effort thrombosis. A general treatment algorithm includes catheter-directed thrombolysis followed by surgical thoracic outlet decompression. There are limited data regarding endovascular treatment of rethrombosis presenting early after the surgery. CASE PRESENTATION: Two cases of early rethrombosis successfully treated with percutaneous mechanical thrombectomy by two different techniques are described. In both cases, rethrombosis was diagnosed soon after thrombolysis and first rib resection with scalenectomy. After 12 months, both patients remain symptom-free, with patent subclavian veins confirmed by duplex ultrasonography. CONCLUSION: Percutaneous mechanical thrombectomy devices may offer a safe treatment option for patients with recurrent thrombosis after thoracic outlet surgery, even when thrombolytic therapy is contraindicated.
ABSTRACT
Platelets are required for the recruitment of bone marrow-derived mononuclear cells (BMMNC) into ischemia-induced vasculature, which underlines their key role in angiogenesis. The difference in platelet immunophenotype between healthy controls and patients with critical limb ischemia (CLI) treated with therapeutic angiogenesis (TA) using BMMNC was assessed. The impact of TA on the expression of platelet membrane markers was studied as well. CLI patients (N = 26) and blood donors as controls (N = 21) were enrolled. Bone marrow (600 ± 50 ml) was centrifuged (3200 g, 20 min, 22 °C). BMMNC (100-120 ml) were separated by Optipress I and implanted to the ischemic limb using deep intramuscular injections. Flow cytometry was employed for the peripheral blood platelets immunophenotyping. CD41FITC, CD62PE, CD36FITC, CD29FITC antibodies were used. Patients were followed up prior to the procedure and at months 1, 3 and 6. The expression of CD41 was lower in CLI patients than in the controls. P-selectin (CD62P) was higher in CLI patients than in controls at the baseline and at month 6. It was significantly down-regulated at month 3, however not at months 1 and 6 compared to baseline. Platelet GPIV (CD36) was higher at the baseline, but not during the follow-up compared to the controls. ß1-integrin (CD29) progressively decreased during the follow-up as compared to the baseline value. Platelets in CLI express P-selectin, GPIV and ß1-integrin more abundantly than platelets of healthy subjects. TA down-regulates the expression of the respective markers. Possible mechanism could be higher clearance of the activated platelets in the ischemic tissues during angiogenesis.
