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Infarct venous

Hemorrhagic transformation of cerebral infarction, venous more often than arterial Intracranial venous thrombosis (Ch. 29)... [Pg.92]

Plasmin is a proteolytic enzyme with specific affinity for fibrin of clots. The indications for Streptokinase are acute cardiac infarction, venous and arterial thrombosis, lung and arterial emboli. [Pg.66]

In general, arterial thrombi are platelet-rich ( white clots ) and form at ruptured atherosclerotic plaques, leading to intraluminal occlusion of arteries that can result in end-organ injury (e.g., myocardial infarction, stroke). In contrast, venous thrombi consist mainly of fibrin and red blood cells ( red clots ), and usually form in low-flow veins of the limbs, producing deep vein thrombosis (DVT) the major threat to life results when lower extremity (and, occasionally, upper extremity) venous thrombi embolize via the right heart chambers into the pulmonary arteries, i.e., pulmonary embolism (PE). [Pg.108]

Fondaparinux, the factor Xa-binding pentasaccharide (Arixtra, MW 1,728 Da), is prepared synthetically, unlike UFH, LMWH and danaparoid, which are obtained from animal sources. Despite only inactivating free factor Xa, clinical trials indicate that fondaparinux is an effective antithrombotic agent, both for venous thromboembolism prophylaxis and treatment, as well as for acute coronary syndrome and ST elevation myocardial infarction [4]. [Pg.110]

Although more data are required, particularly in the setting of hemorrhagic venous infarction, based on the current evidence it seems reasonable to conclude that anticoagulation with UFH and LMWH is safe and probably effective in CVST. The optimal duration of therapy has not been well studied. [Pg.154]

Age >40 yr, previous venous thromboembolism, chronic heart failure, acute respiratory failure, recent major surgery (within 2 wk), confined air/ground travel (>6 h duration within 1 wk of admission), inflammatory bowel disease, myocardial infarction, nephrotic syndrome, and ischemic stroke... [Pg.48]

Venous stasis is slowed blood flow in the deep veins of the legs resulting from damage to venous valves, vessel obstruction, prolonged periods of immobility, or increased blood viscosity. Conditions associated with venous stasis include major medical illness (e.g., heart failure, myocardial infarction), major surgery, paralysis (e.g., stroke, spinal cord injury), polycythemia vera, obesity, or varicose veins. [Pg.176]

Morphine produces venous and arteriolar dilation, which may result in orthostatic hypotension. Hypovolemic patients are more susceptible to morphine-induced hypotension. Morphine is often considered the opioid of choice to treat pain associated with myocardial infarction, as it decreases myocardial oxygen demand. [Pg.639]

Thrombin, a serine protease, cleaves fibrinogen into fibrin to create a fibrous plug and also amplifies its own production through the activation of factor XI and cofactors V and Vlll. Thrombin also plays a crucial role in the activation of platelets through the cleavage of the protease-activated receptors on the platelet surface. Antagonists of G-protein-coupled protease-activated receptor PARi have been synthesised to study the role of thrombin PARi receptor in thrombosis and vascular injury. Thrombosis is the most common cause of death in the industrialised world and, whether through venous thromboembolism, myocardial infarction or stroke, ultimately involves the inappropriate activity of... [Pg.50]

In September 2001, however, a news item in the British Medical Journal reported that further analyses confirmed the increase in rates of myocardial infarction and questioned whether this was an adverse reaction affecting the whole class of COX 2 drugs. The debate continued for the next 3 years with the main emphasis remaining on GI toxicity. A PEM study that included more than 15 000 patients made no mention of cardiovascular adverse events. However, a second paper compared rofecoxib and meloxicam with respect to thromboembolic events which showed that both, to a variable extent were associated with cardiovascular, cerebrovascular and peripheral venous pathology. A meta-analysis published recently in The Lancet suggests that Merck, the licence holder... [Pg.437]

Siminiak T, Fiszer D, Jerzykowska O, Grygielska B, Rozwadowska N, Kalmucki P, Kurpisz M. Percutaneous trans-coronary-venous transplantation of autologous skeletal myoblasts in the treatment of post-infarction myocardial contractility impairment the POZNAN trial. Eur i/eart / 2005 26 1188-1195. [Pg.126]

A 75 year old man was examined on a routine visit 1 month after discharge from hospital for a myocardial infarction. No communication had been received from the hospital on the patients stay and management. The patient seemed well but had a few purpuric 1 cm round lesions on his hands. The doctor assessed these as senile purpura. He then noticed that there were several more on both legs. He felt that these were both more extensive than with senile purpura and in an unusual site. He questioned the patient about injury, which the patient denied. On ringing the hospital it was learned that the patient had had a deep venous thrombosis and was treated with warfarin. They apologised for not informing the doctor earlier ... [Pg.232]

It is used for myocardial infarction, for venous thrombosis and pulmonary embolism. [Pg.246]

The other serious side effects include high blood pressure, increased risk of myocardial infarction, thromboembolic diseases like thrombophlebitis, venous thrombosis, cerebral thrombosis. [Pg.298]

In present times, because of early mobilization and shorter stays in hospital, venous thrombosis in the legs and resulting pulmonary embolism has declined to a large degree. In persons with acute myocardial infarction, prophylactic low-dose heparin has reduced the incidence of venous thrombosis in the legs. It is considered as a reasonable alternative to warfarin in selected patients. Preventive anlicoagulalion may be indicated in some cases to prevent strokes due to left ventricular mitral thrombi embolizing in tire brain. [Pg.133]

Much of the work on both sides of the argument was less than watertight. Some studies failed to consider the confounding effects of other risk factors (notably smoking) or the likelihood of detection bias (particularly for venous thromboembolism, which is much more common in young women than myocardial infarction or stroke). The results of some studies were also confounded by uncertainties in the history of drug exposure. A landmark paper to... [Pg.215]

There is also fairly strong evidence that immunological mechanisms play a role in thrombotic episodes associated with oral contraceptives, especially when they occur in the absence of risk factors for vascular disease (71), although this has been contested (72). In one series of reports on cerebral infarction, circulating immune complexes and/or specific antihormone antibodies were found in 15 of 20 patients (37). In a large series of women with venous or arterial thrombosis, anti-ethinylestradiol antibodies were absent in non-users but present in 72% of users they were also present in 33% of healthy oral contraceptive users without thrombosis (SEDA-16, 465). In half of the cases there were both anti-ethinylestradiol antibodies and a history of smoking were found jointly in half of the cases. [Pg.219]

Vandenbroucke JP, Bloemenkamp KW, Helmerhorst FM, Rosendaal FR. Mortality from venous thromboembolism and myocardial infarction in young women in the Netherlands. Lancet 1996 348(9024) 401-2. [Pg.245]


See other pages where Infarct venous is mentioned: [Pg.252]    [Pg.448]    [Pg.262]    [Pg.1211]    [Pg.252]    [Pg.448]    [Pg.262]    [Pg.1211]    [Pg.111]    [Pg.170]    [Pg.392]    [Pg.418]    [Pg.550]    [Pg.7]    [Pg.9]    [Pg.153]    [Pg.154]    [Pg.147]    [Pg.189]    [Pg.401]    [Pg.394]    [Pg.256]    [Pg.744]    [Pg.754]    [Pg.763]    [Pg.1331]    [Pg.765]    [Pg.214]    [Pg.215]    [Pg.216]    [Pg.217]    [Pg.217]    [Pg.219]    [Pg.224]   
See also in sourсe #XX -- [ Pg.167 ]




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