Lovenox-bridge Therapy

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Carla Sloan Says:


How does Lovenox bridge therapy work? I need an explanation in full detail.
Thanks



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Verwon Says:

Lovenox contains the active ingredient Enoxaparin, it is used for its ability to thin the blood, to prevent clotting.

Bridge therapy refers to using it, for its immediate effects, during a time period when the patient is started on a new medication, such as Warfarin, or when they are at higher risks of blood clots.

The dosage of a medication like Warfarin must be carefully adjusted to get the desired results and like many medications, it takes some time to reach its full effect in the body.

And since it does, the Lovenox is often used during that time period, to help prevent clotting in the patient, until the Warfarin or another medication can reach its full effectiveness, then the Lovenox is usually stopped.

https:/­/­www.medschat.com/­wiki/­Enoxaparin/­

https:/­/­www.medschat.com/­wiki/­Warfarin/­

Are there any other questions?

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Critch Says:

I'm afraid I'll have to disagree with Verwon, in that Lovenox (heparin) is NOT a blood thinner. It does nothing to change the viscosity of the blood. What it is is an injectable, quickly effective drug for reducing the blood's ability to coagulate. In other words it's an anticoagulant, not a blood thinner. For an explanation in "full detail" the following is from the Wikipedia article on heparin:

Mechanism of action
Heparin and its low molecular weight derivatives (e.g. enoxaparin, dalteparin, tinzaparin) are effective at preventing deep vein thromboses and pulmonary emboli in patients at risk,[12][13] but there is no evidence that any one is more effective than the other in preventing mortality.[14] Heparin binds to the enzyme inhibitor antithrombin III (AT) causing a conformational change that results in its activation through an increase in the flexibility of its reactive site loop.[15] The activated AT then inactivates thrombin and other proteases involved in blood clotting, most notably factor Xa. The rate of inactivation of these proteases by AT can increase by up to 1000-fold due to the binding of heparin.[16]
AT binds to a specific pentasaccharide sulfation sequence contained within the heparin polymer:
GlcNAc/NS(6S)-GlcA-GlcNS(3S,6S)-IdoA(2S)-GlcNS(6S)
The conformational change in AT on heparin-binding mediates its inhibition of factor Xa. For thrombin inhibition, however, thrombin must also bind to the heparin polymer at a site proximal to the pentasaccharide. The highly negative charge density of heparin contributes to its very strong electrostatic interaction with thrombin.[2] The formation of a ternary complex between AT, thrombin, and heparin results in the inactivation of thrombin. For this reason, heparin's activity against thrombin is size-dependent, the ternary complex requiring at least 18 saccharide units for efficient formation.[17] In contrast, anti-factor Xa activity requires only the pentasaccharide binding site.
This size difference has led to the development of low-molecular-weight heparins (LMWHs) and, more recently, to fondaparinux as pharmaceutical anticoagulants. Low-molecular-weight heparins and fondaparinux target anti-factor Xa activity rather than anti-thrombin activity, with the aim of facilitating a more subtle regulation of coagulation and an improved therapeutic index. The chemical structure of fondaparinux is shown above. It is a synthetic pentasaccharide, whose chemical structure is almost identical to the AT binding pentasaccharide sequence that can be found within polymeric heparin and heparan sulfate.
With LMWH and fondaparinux, there is a reduced risk of osteoporosis and heparin-induced thrombocytopenia (HIT). Monitoring of the activated partial thromboplastin time is also not required and does not reflect the anticoagulant effect, as APTT is insensitive to alterations in factor Xa.
Danaparoid, a mixture of heparan sulfate, dermatan sulfate, and chondroitin sulfate, can be used as an anticoagulant in patients that have developed HIT. Because danaparoid does not contain heparin or heparin fragments, cross-reactivity of danaparoid with heparin-induced antibodies is reported as less than 10%.[18]
The effects of heparin are measured in the lab by the partial thromboplastin time (aPTT), one of the measures of the time it takes the blood plasma to clot. Partial thromboplastin time should not be confused with Prothrombin time, or PT, which measures blood clotting time through a different pathway of the coagulation cascade.

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