Presence Of Thrombus Formation Research Articles

Тромбоутворення в порожнині лівого шлуночка. Частина 2. Можливості лікування

Попри давню проблему внутрішньопорожнинного тромбоутворення питання його лікування і сьогодні досить складне для будь-якого клініциста. На початку лікування перед лікарем постає вибір, якому з антикоагулянтів надати перевагу. Помилки щодо вибору препарату та його дозування збільшують ризик у хворого, з одного боку, виникнення кровотечі, а, з другого боку, ризик розвитку ускладнень за наявності тромбоутворення в порожнині лівого шлуночка. Стаття присвячена проблемі тромбоутворення в порожнині лівого шлуночка з огляду на аналіз даних реєстрів, метааналізів, пілотних та рандомізованих багатоцентрових клінічних досліджень.

Abstract 919: Suppression of Abdominal Aortic Aneurysms in the Angiotensin II-infused ApoE Deficient Mice by Treatment with Chymase Inhibitor

Chymase promotes not only angiotensin II production but also matrix metalloproteinase (MMP)-9 activation, which have a critical role on development of abdominal aortic aneurysms (AAAs). The purpose of this study is to examine the effects of chymase inhibitor, NK3201, on the MMP-9 activity and development of AAA in the angiotensin II-induced apolipoprotein E (apoE)-deficient mice. Method: Angiotensin II (1000ng/kg/min) (vehicle group) or saline (control group) were infused into 16-week-old male apoE-deficient mice for 4 weeks. To examine the effect of chymase inhibition for AAA, we administered NK3201 (30mg/kg/day) to angiotensin II-infused group (NK3201-treated group) for the same period. At the end of angiotensin II infusion, we measured the diameters of suprarenal and infrarenal aorta. AAA severities were scored using the suprarenal aortic diameter/infrarenal aortic diameter ratio and presence of thrombus formation, i.e. under 2.0 was 0, from 2.0 to 2.5 was 1, from 2.5 to 3.0 was 2, over 3.0 was 3, and presence of thrombus was 4. We also determined the chymase and MMP-9 activities using total aorta. Results: The scores that reflected the progression and severity of AAA were increased in vehicle group compared with control group ( 2.35±0.30 vs. 0.27±0.12, p<0.01). This progression was inhibited in NK3201-treated group compared with vehicle group (1.13±0.35, p<0.05 vs. vehicle group). Chymase activity was significantly increased in vehicle group compared with control group. MMP-9 activity was also increased in vehicle group, however it was decreased significantly in NK3201-treated group.Discussion: We demonstrated that chymase inhibition could reduce AAA progression through inhibition of MMP-9 in angiotensin II-induced apoE-deficient mice. Chymase inhibitor might be a novel strategy for preventing AAAs.

Incidence of thrombus formation on the CardioSEAL and the Amplatzer interatrial closure devices

Transcatheter closure for atrial septal defect (ASD) and patent foramen ovale (PFO) is a promising alternative to surgical closure or anticoagulant therapy. A potential complication is thrombus formation on the device after implantation. From February 2001 to June 2003, 66 patients with atrial communication were treated successfully with the Amplatzer device (16 septal and 20 PFO occluders) or the CardioSEAL device (30). Patients were discharged on antiplatelet medication (aspirin and clopidogrel) and/or anticoagulation. Fifty patients (76%) had transesophageal echocardiography (TEE) 1 month after device implantation (28 ± 10 days). No patient experienced a thromboembolic episode during follow-up. TEE revealed that thrombus formation occurred more frequently on the CardioSEAL device (5 of 23 patients; 22%) than on the Amplatzer device (0 of 27 patients; 0%) (p = 0.02). Although thrombus disappeared or markedly diminished after additional anticoagulation therapy in 3 patients, 1 patient had surgical explantation of the device due to progressive increase in the size of thrombus with hypermobility despite intensive anticoagulation therapy. There was no variable associated with the presence of thrombus formation on the occluder other than the use of the CardioSEAL device. One month after insertion, the CardioSEAL device is more likely to have thrombus present than the Amplatzer device.

Coronary angiographic findings do not predict clinical outcome in patients with unstable angina

Objectives. The presence of thrombus formation and type of coronary artery lesion were determined in patients with unstable angina and correlated with the angiographic findings and clinical outcome.Background. Some previous studies have suggested that thrombus formation and lesions are predictive of the angiographic and clinical findings. This was evaluated in a retrospective analysis of 159 patients participating in the placebo-controlled Unstable Angina Study Using Eminase (UNASEM) trial on the effect of thrombolysis in unstable angina.Methods. Patients without a previous myocardial infarction who presented with a typical history of unstable angina in the presence or abnormal findings on the electrocardiogram indicative of ischemia were included in the study. After baseline angiography, study medication (anistreplasc or placebo) was given to 126 of 159 patients. Thirty-three patients did not receive medication because of significant main stem disease or normal coronary arteries or for other reasons. Angiography was repeated after 12 to 28 h.Results. Quantitative angiography showed a significant decrease in diameter stenosis in the anistreplase-treated group compared with the placebo-treated group (decrease 11% vs. 3%, p = 0.008). No differences in clinical outcome were found when thrombolytic treatment was compared with placebo (p = 0.98). Neither the presence nor absence of thrombus formation (p = 0.98) nor the type of lesion (p = 0.96) was related to the changes in diameter stenosis or to clinical outcome (p = 0.90 and p = 0.77, respectively). The power of these analyses to detect a 20% difference varied between 56% and 74%.Conclusions. In this selected group of patterns with unstable angina, type of coronary artery lesion and the presence or absence of thrombus formation does not predict clinical outcome.

Effect of Low Molecular Weight Heparin, Dextran and Their Combinations on Experimental Venous Thrombosis in Rabbits

An experimental model based on the combination of endothelial damage and flow reduction was used to induce jugular vein thrombosis in rabbits. The effect on thrombosis of a low molecular weight heparin (LMWH [Fragmin]), dextran 70, placebo and their combination was studied in a double-blind fashion with actual doses used in clinical thromboprophylaxis. Saline and polygeline were used as placebo in the control group. Four groups with 120 isolated vein segments in 60 animals were studied for presence of thrombus formation, occlusive thrombi and thrombus weights. Dextran reduced the thrombus weights (p = 0.048) and the formation of occlusive thrombi (p = 0.01), but not the formation of thrombi when compared with the placebo control group. Similarly, LMWH reduced the thrombus weights (p = 0.046), the formation of thrombi (p = 0.007) and occlusive thrombi (p = 0.0001). Compared with the LMWH group the group treated with the combination of LMWH and dextran was found to reduce the frequency of occlusive thrombi (p = 0.03) and numerically, but not significantly, further reduce the overall frequency of thrombosis (p = 0.18) and thrombus weights (p = 0.11). The results are consistent with an augmentation of the antithrombotic effect of LMWH by dextran 70. The need for further evaluation of the combined efficacy of LMWH and dextran is apparent from this study.