Re: Maze and Mitral Valve Repair and Plavix

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Posted by steve giddings on March 10, 2003 at 17:26:40:

In Reply to: Maze and Mitral Valve Repair and Plavix posted by Bill Landis on March 08, 2003 at 17:00:04:

There is a fair amount of confusion about preventing clot formation in various circumstances, what drugs are most apporiate in which circumstances, etc.

All of the drugs used, heparin, low molecular weight heparin (lovenox); warfarin (coumadin), clopidigrel (Plavix), Ticlopidine (Ticlid) aspirin, are used to prevent new or additional clots from forming, or, if already formed, from extending or getting bigger. These drugs are separate from the "clot busters" like TPA, urokinase and streptokinase (with a bunch of different brand names), which actually digest the bonds that hold clots that are already formed, together.

These drugs fall into several classes and several of them work by similar mechanisms. In general, the more effective they are in blocking clot formation, the greater risk they pose for causing bleeding episodes. Some of the drugs also have separate, distinct risks.

Heparin and lovenox (low molecular weight heparin) keep clots from forming by inhibiting a clot inducing enzyme system that forms a sticky protein scaffold that platelets bind to. They are both quite potent and effective and start to work almost immediately. They both have to be injected or even infused intravenously. Heparin levels have to be monitored by frequent blood tests (more than daily). Lovenox costs $40-60 per dose and is taken twice a day, but is injected under the skin so it can be used in outpatients.

Coumadin also works to block the formation of the protein scaffold, but by a different mechanism. Heparin keeps the proteins from sticking together. Coumadin works by slowing down or stopping the manufacture of several of these proteins, also called clotting factors, by the liver. separticular proteins require vitamin k for synthesis. Coumadin interferes with vitamin k binding. Both coumadin and heparin (and LMH) are more effective than the other agents in blocking formation of clots formed in the atria of patients in A fib.

Plavix and Ticlid act directly on platelets and interfere with their ability to become "sticky" and bind to the scaffold formed by clotting factors. Both work on the same signalling pathway in the platelet, ADP-induced platelet aggregation. Ticlid may be marginally more effective than Plavix, but damages the bone marrow's ability to make white cells and other blood elements more frequently than plavix, so it isn't used as much. Plavix is marginally better than aspirin in preventing new stroke or MI in patients who have already had one (secondary prevention).

Aspirin also prevents platelet aggregation. It works at a separate point, by irreversibly inactivating cyclooxygenase (cox). The reason it is effective and other aspirin-like drugs (termed NSAIDS, or "non-steroidal anti-inflamatory drugs) are not, is because the effect of aspirin lasts for the entire lifespan of the platelet. The other NSAIDS are reversible cox inhibitors. This is also why other NSAIDS, like motrin, can block the anti-clotting effect of ASA. They keep ASA from getting to where they need to go from having an effect, then wear off after ASA is gone from the blood.

Additional confusion occurs because a lot of the clinical trials looked at somewhat different outcomes, had different patient inclusion requirements, used different doses of drug and so on.

Bottom line: If you have a fib or may go into a fib, and are over 60-65 and have any other cardiovascular abnormality, including even mild controlled hypertension or an "innocent" heart murmur, you should be on coumadin. You usually recover from a bleeding episode. Strokes are generally irreversible and typically reduce overall quality of life and level of function longterm.



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