Article

Pathogenesis of venous thromboembolism.

Sezione di Medicina Interna e Cardiovascolare, Dipartimento di Medicina Interna, Università di Perugia, Perugia, Italy.
Current opinion in pulmonary medicine (Impact Factor: 2.96). 10/2002; 8(5):360-4. DOI: 10.1097/00063198-200209000-00003
Source: PubMed

ABSTRACT Three factors are related with the pathogenesis of venous thrombosis: (1) blood stasis, (2) hypercoagulability, and (3) vessel damage. Local and systemic factors are implicated in blood stasis. Remarkable advances have been recently achieved regarding the understanding of the concept of hypercoagulability, with special emphasis to thrombophilic molecular abnormalities. Increased thromboembolic risk has been described in patients with antithrombin III, protein C, or protein S deficiencies as well as factor V Leiden, prothrombin mutation G20210A, or hyperhomocystinemia. Vessel wall has a remarkable role in protecting against and in promoting thrombosis. The role of inflammation on venous thrombosis is under investigation.

0 Followers
 · 
135 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: To determine the incidence of arterial and venous thromboembolic (VTE) events, to determine the effect of raloxifene on the incidence of combined vascular (arterial and VTE) events, and to identify patient characteristics associated with these vascular events, in women participating in the MORE trial. In a post hoc analysis using MORE data, arterial, VTE, and combined vascular event rates were compared between participants receiving placebo (n = 2,576) and those receiving 60 mg/d of raloxifene (n = 2,557). Baseline characteristics were compared between those who did and did not experience an arterial event. The same analysis was performed for VTE events. Overall, during a mean follow-up time of 41 months, 178 women experienced an arterial event and 40 experienced a VTE event. In the placebo group, the incidence of arterial events exceeded VTE events by at least sevenfold. Raloxifene had no significant effect on the incidence of combined vascular events in the overall cohort (hazard ratio 0.95, 95% CI, 0.73-1.24). In a subset of women retrospectively determined to be at increased cardiovascular risk, raloxifene was associated with a lower incidence of combined vascular events (hazard ratio 0.63, 95% CI, 0.40-0.97). Baseline characteristics differed between those who did and those who did not experience an arterial event, but this was generally not the case for VTE events. Arterial events were more common than VTE events. The characteristics of women experiencing an arterial event differed from those experiencing a VTE event. Raloxifene had a neutral effect on the risk of combined vascular events in the overall population, and was associated with a reduced combined vascular event rate in women at increased cardiovascular risk. Additional studies are needed to confirm the effect of raloxifene on overall vascular outcomes.
    Menopause 01/2005; 12(4):444-52. DOI:10.1097/01.GME.0000151653.02620.89 · 2.81 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The intent of the study was to determine whether ultrasonic tissue characterization (UTC) could indicate acuteness and stability of deep venous thrombosis (DVT) of the lower extremities. Thrombi presenting as filling defects on color Doppler imaging in the common or superficial femoral or popliteal veins in 50 extremities in 45 patients with DVT were studied. Acute DVT was less than 4 days duration, and chronic DVT was greater than 21 days duration. UTC analysis of parameters from the normalized power spectrum of backscattered ultrasound signals from venous filling defects was performed. This spectrum approaches a straight line, and its basic parameters, slope, and Y-intercept are related to scatterer size, concentration, and the square of the scatterer-to-medium acoustic impedances. Ten of the DVT extremities were reexamined at 1 week to assess UTC changes that would indicate thrombus instability. Acute DVT (19 of the 50 extremities) could be distinguished from chronic DVT, mainly on the basis of significantly higher intercept values for the acute group, which were 11.6 relative decibels (dBr) higher than those of the chronic DVT group. Discriminant linear analysis of the two parameters indicated a sensitivity of 94.7% and specificity of 90.3% in correctly diagnosing acute DVT. In a small sample of 10 extremities reexamined at 1 week, acute DVT extremities showed a mean 9.4 dBr decrease in intercept values with no significant change in slope. UTC distinguished clinically defined acute from chronic DVT. In a small series of extremities, UTC revealed significant instability of acute thrombi in a selected patient population.
    Journal of Vascular Surgery 07/1995; 21(6):976-84. DOI:10.1016/S0741-5214(95)70226-1 · 2.98 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Recent report, particularly the Women's Health Initiative, demonstrated that hormone therapy with combined estrogen plus progestin increased the incidence of heart attacks, stroke, blood clots, breast cancer and dementia in women over 65 years old. We investigated the role of synthetic progestins in initiating the adverse events associated with estrogen therapy. We used a fluorescence imaging technique, which allows video microscopic recordings of blood flow, blood vessel morphology and activities of various blood cells in a live animal. The acute peripheral and cerebrovascular responses were measured following intraperitoneal (5 or 10 mg) or intravenous (10 or 100 microg) administration of progesterone, synthetic progestins (medroxyprogesterone acetate and norethindrone) or estrogens (conjugated equine estrogens and 17 beta-estradiol). In both peripheral and cerebral vasculature, synthetic progestins caused endothelial disruption, accumulation of monocytes in the vessel wall, platelet activation and clot formation, which are early events in atherosclerosis, inflammation and thrombosis. Natural progesterone or estrogens did not show such toxicity. The risk associate with combined estrogen plus progestin therapy may be a consequence of vascular actions of progestins. Using progestins with minimal vascular toxicity may lead to safer estrogen preparations for menopausal women.
    Climacteric 01/2004; 6(4):293-301. DOI:10.1080/cmt.6.4.293.301 · 2.24 Impact Factor
Show more