Because you are asymptomatic during AF episodes, the most important thing to do is anticoagulation medicine for stroke prevention. So I am surprised that your cardiologist didn't prescribe that for you and wants you on an AAD (anti-arrhythmic drug) instead. And I agree that with your low heart rate, it may not be a good thing. The specialist to see would be an electrophysiologist because they would have more expertize in AAD and anti-coagulants.
Coumadin pre-operatively, as you state one considers the risks of hemorrhage or thromboembolism versus the benefit from the operation. When considering noncardiac surgery, these factors and the need to weigh the risk of hemorrhage against that of thromboembolism must analyzed on an individual patient basis.
Certain procedures such as a bunion that are not procedure that threatens limb or life are easy analysis.
continue through with warfarin, or to stop the warfarin and bridge in between with enoxaparin or heparin (as snconorm had done).
http://www.circ.ahajournals.org/cgi/content/full/116/22/2531
So continuing through with warfarin seems to be the newer strategy.
What would NOT be done is to stop anticoagulation altogether.
or a deficiency of this vitamin reduces the rate at which these factors and proteins are produced, thereby creating a state of anticoagulation. Prescribing the dose that both avoids strokes, etc. sufficient suppression of clots requires a thorough understanding of the drug's unique pharmacology.
"For most indications, the dose is adjusted to maintain the patient's International Normalized Ratio (INR) at 2 to 3.
At the professional workshop that I attended, we were told by the presenter that the anticoagulation properties of warfarin are most likely present down to an INR of about 1.6. The reason doctors don't like their patients to go below 2.0 (or in some cases 2.5) is to provide a cushion of safety. Also, a bleeding incident attributable to warfarin would not be expected to happen at an INR of 4.0. Some people, such as those who have two mechanical heart valves, have a prescribed range of 3.
Unknown. Warfarin metabolism normally occurs through the cytochrome P450 (CYP450) isoenzyme system, with excretion occurring in the urine as inactive metabolites. It is postulated that large doses of acetaminophen may "exhaust" the capability of the CYP450 system to metabolize warfarin. Additionally, DARVOCET-N 100 TABLETS may reduce functional factor VII.
Management: Monitor coagulation status and adjust the dosage of COUMADIN 4MG TABLETS (BLUE) accordingly.
Your friend has experienced a worrisome series of events and is lucky to have your support. The first question relates to the "shadow on the lung." What do her doctors suspect? Is this "shadow" most likely a sign of the pulmonary emboli (PE), perhaps pulmonary infarction, or is it an incidental finding that’s unrelated to the PE?
Depending on the interpretation of the shadow, a biopsy may or may not be indicated.
Responding both posts.
The only thing I have to add is I'd ask the doctor about putting your husband on an anticoagulant, e.g., Coumadin or Warfarin. The rhythm problem doesn't sound very serious to me, compared to what my heart does, but it could cause a clot to form and put him at risk of a stroke.
For instance, I know of someone who had to be on it throughout pregnancy, because she needed anticoagulation therapy, and warfarin has effects on the fetus. I know those shots aren't fun, but I wonder if you could use them from time to time, to give your hands a break.
However, they require lifelong anticoagulation with medications such as warfarin, so that blood clots don’t form on the valve. Warfarin can cause major birth defects for unborn fetuses, and thus becomes more problematic for use during childbearing. However, with adequate planning, it can be done by switching to routine heparin injection.
Unless there are underlying reasons why it would be harmful, anticoagulation (low molecular weight heparin, followed by warfarin) is often initiated and maintained in patients who do not have cirrhosis. Anticoagulation for patients with cirrhosis who experience portal vein thrombosis is usually not advised unless they have chronic PVT 1) with thrombophilia, 2) with clot burden in the mesenteric veins, or 3) inadequate blood supply to the bowels.
The basis of therapy of AF are treating the underlying heart disease, restoring the rhythm, maintaining the rhythm and anticoagulation to prevent complication. For restoring the rhythm medications like Flecanide are used. Without rhythm control, the main complication is increased ventricular rate. Also, exercise tolerance is better with rhythm control. So, based on your present clinical symptoms and AF status, therapy can be planned.
Also, the doctors decided that I should definitely go on a blood thinner. So their choice is Plavix over Coumadin or the other blood thinners. Why do you think this is a better choice than say Coumadin?
It sounds as if your only need for anticoagulation is the prosthetic valve. If that's the case, I wouldn't add the baby aspirin. As long as your INR is in the therapeutic range, the aspirin will add minimal beneift and will increase your bleeding risk. Given your very active lifestyle, you want to minimize your bleeding risk as much as possible. Unless you have severe underlying coronary artery disease or a history of stroke, I would stick with the warfarin and skip the aspirin.
A person on warfarin with an inr of 1.2 is not at risk of bleeding out. They are at risk for a clot. People not on warfarin normal range of about 1 because they don't have a bleeding or clotting disorder, thus 1 is normal.
I take 10 MG a day everyday and my inr was 2.2 just today. It all depends o. The reason behind taking it.
I have tried to research it and have found info about warfarin (another type of blood thinner) causing hairloss, and was wondering if anyone knew wether tinzaparin could be a cause for hairloss
Thanks
Three pulmonary emboli within a 2 year period is a serious problem, assuming that each has been confirmed. It is good that you are on Coumadin® (warfarin) but, a detailed attempt to discover the factors that have predisposed you to thrombosis and embolization, such a comprehensive diagnostic investigation, should be initiated without delay.
There is no direct connection between pulmonary emboli and tuberculosis (TB), including skin test conversion.
I am a 52 year old woman with history of DVT and Pulmonary embolism (since age of 17 - hereditary). I've been off my anti-coagulants for over a year and a half now due to no insurance. I'm an LMSW and work with elderly and disabled individuals. About 2 months ago, I was doing visits and was out in the middle of nowhere, driving, when I felt a pressure across my chest and then my back started hurting pretty bad (around right shoulder blade and right arm). I could not get comfortable.
Will do.
Nothing so far. In looking at the Posts in that forum, it seems like quite a few receive no expert replies whatsoever, even weeks after they were posted. Kind of discouraging. Little point in having a forum like that, if the physicians/experts aren't going to consistently provide answers/opinions.
Oh well, we'll see.
Looking back at your post, I see your reference to "long term effects to our organs" from anticoagulation.
2005 I had asuspected acute subarachoid haemorhage related to anticoagulation[ Warfari]The summary angiogramm -negative subarachnoid bleed .warfarin reversed angiogram is normal , however the cardiologist did a cardioversion to get the rhythm back to normal .
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