I do know there are different anti-platelet mechanisms with each medication you are referring as well which mechanism of action is perferred for a specific malady and the interaction with other medicaion.
My experience is with dual therapy (aspirin and plavix) and the last I heard that therapy is a appropriate post DES implant. It seems plavix helps reduce the risk for clots at implant site, and after a year the risk of clots is less than the risk of excessive bleeding with plavix.
I am not physically restricted - I walk 1 mile or more day and do 10 minutes of other light exercises most days. My BP runs under 120/80 most of the time. I understand carvedilol helps prevent stiffening of the heart muscle and can help restore LV function to some degree. How specially, so it do this? What is the biochemical mechanism?
The abnormal levels of INR may suggest that there is a problem with the bleeding and clotting mechanism. You must necessarily get the dose of Warfarin adjusted. High or low INR may lead to abnormal clotting or spontaneous bleeding. The medicine should keep the blood just thin enough to prevent clots. If the blood is too thin, you may bleed too easily. Severe headache while being on Warfarin therapy needs immediate medical attention.
is it safe to use blood clotting spray for minor wounds&cuts for warfarin user?
In three months on Warfarin, I thinned over the top and front of my hair (I am a female aged 70) and also my nails went chalky, plus I couldn't sleep well and felt very off colour. The blood tests which were weekly due to an unstable INR became an ordeal when it took two or three attempts. I took Warfarin (for AFib) for about three and a half months and then refused to take it any longer, saying that I would take my chances on aspirin only.
I take Warfarin as follows: 3mg 2xda for 2 da and 4mg 2xda rest of week. Can't seem to get my levels even. Is the dosage too little or not enough?
The proposed mechanism is that continual drinking of large amounts of alcohol induces the hepatic metabolism of anticoagulants. Effects are highly variable and significant INR/PT fluctuations are possible.
MANAGEMENT: Patients taking oral anticoagulants should be counseled to avoid large amounts of ethanol, but moderate consumption (one to two drinks per day) are not likely to affect the response to the anticoagulant in patients with normal liver function.
The mechanism of action of Campral® (acamprosate calcium) Delayed-Release Tablets in maintenance of alcohol abstinence is not completely understood. Originally, several neurotransmitter systems, including GABA, were investigated for a possible role in Campral's mechanism of action. However, recent evidence suggests Campral's main interaction is with the glutamate system. Chronic alcohol exposure is hypothesized to alter the normal balance between neuronal excitation and inhibition.
http://www.nasdaq.
2 cardiologists, an electophysiologist and my GP all denied any knowledge of the vitamin K / Calcification mechanism. I wasnt given a thyroxin test ever, I.V. Magnesium or urine test on presenting with af. Am I one of those 'read it on the internet' medical know it alls, or justified in feeling feeling a slight lack of confidence in my health system consultants? Any thoughts on my prognosis - thanks.
37 for placebo (10). In a study of 11 patients on stable warfarin, INR increased after 4 days of taking APAP 4 g/day increasing the risk of bleeding (7). A 72-year-old man was on acenocoumarol, chronically self-medicating with APAP 1 to 2 g/day for low back pain. His INR was stable at 2.5, but when APAP was stopped his INR dropped to 1.62. Two weeks later, he restarted APAP and the INR climbed to 2.0 over 4 weeks (5).
I take warfarin (generic coumadin) and have for about 15 years. I discussed changing to Pradaxa with my cardiologist when that drug first came out, I decided not to use it because of cost (warfarin cost about 12 cents a day) and the fact I do well on warfarin, albeit I have to have my blood coagulation tested once a month. Recently I have seen a lot of "bad news" about Pradaxa including law firm adds looking for new participants in a class action suit, as I understand it...
had blood choking problems and kept in hospital overnight for observation.Various amounts of congealed blood came out for 48 hours before i was completley healed.Presumably i need to reduce my INR from 2.9 (as it was for the bleed) to 2.0/2.1..care with nose blowing.on warafrin..permanent AF 66 MALE.
AFig can cause the formation of clots in the artial chamber due to the incomplete pumping action characteristic of AFib. If/when these clots move into the blood stream and if they block oxygen/blood to the brain a stroke occurs. An Anticoagulant, such as warfarin/coumadin reduce the chance that such clots will form, thus reducing the possibility of a stroke.
I do not believe the taking of meds to control the heart rate, e.g.
Factor V Leiden is a variation of normal Factor V which is part of the clotting cascade, which is essentially a chain reaction of proteins acting on proteins, ending in the formation of a (fibrin) clot. Platelets are another part of the body's clotting mechanism, they start things off by sticking together to plug the initial hole in the blood vessel & the fibrin clot then adds to this, making it stronger.
I have congestive heart failure and had an infarction rate of 24. Have a valve that leaks. I have a pacemaker/defib mechanism (2nd one) and I think I do great. I am still working (sedentary job), am an active grandmother, lovely life. I am getting tired again... feel like I have to stop and catch my breath (NOT during exercise)... dizzy. After the device, cardiologist says I just need to come in once a year... I should be fine. I am going to another doctor..
Plavix has a unique mechanism of action by blocking the amplification of platelet activation by released ADP, and often used with aspirin to prevent the risk of clots for the first year after DES implant. Plavix and aspirin have different mechanism of action to prevent clots. After a year, plavix is usually discontinue as the risk for clots is decreased, and aspirin is continued long term. The risk of a clot is about 3%.
Coumadin also has what's known as a long "offset of action". That means its effects aren't turned off quickly when the drug is stopped. It can take days. I don't really know how many.
To quickly reverse the drug's effects, vitamin K can be given orally or by IV. (Coumadin works by inhibiting vitamin K, and vitamin K is necessary for coagulation.
Recommended
