can someone please explain to me in basic terms why rivaroxaban does not need to be monitored and warfarin does? I get they work on different parts of coagulation, but I guess I just don't understand it.
rivaroxaban vs warfarin
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Mechanisms are completely different.
Warfarin has vastly variable pharmacokinetics, not just from patient to patient by from week to week for the same patient. Metabolism of coumadin itself as well as vitamin K depends on genetic polymorphisms, nutritional status, other medications the patient may or may not be taking, etc, etc, etc. On top of that, it works the synthesis of at least six different proteins (C, S, II, VII, IX, X), all of which have different half-lives, so that leads to even more variation. Honestly, it's a terrible drug, except that it was the only option we had for oral anticoagulation for 50+ years.
On the other hand, rivaroxaban (and all of the other target-specific anticoagulants) work on a single target, with simple metabolism, standard pharmacokinetics, and significantly fewer drug-drug interactions. The dose needs to be adjusted for crappy renal function, but that's really it. Just dose it and leave it alone. There's some question on whether adjustments need to be made for the super morbidly obese, but that's more of a theoretic issue than anything else.
The other, easier answer to your question is that we have a standardized way of monitoring coumadin, versus most hospitals have no reasonable way to monitor rivaroxaban and all of it's cousins. The effect on INR is super inconsistent, and the more specific assays take a lot longer to run and/or aren't widely available.
In a few years, when we have easily available reversal agents and especially when at least one of the TSOACs goes off patent, I can't imagine anyone will be on coumadin anymore except for mechanical valves.
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