When DOACs first appeared, they were meant to completely replace VK antagonists. And the first clinical trials that were done evaluated the use of DOACs versus vitamin K antagonists in patients that didn’t have atrial fibrillation. They were very successful. They showed that their efficacy was similar and with less bleeding risk. But when they translated those clinical trials to patients with valvular heart disease, they found that DOACs had less efficacy...
When DOACs first appeared, they were meant to completely replace VK antagonists. And the first clinical trials that were done evaluated the use of DOACs versus vitamin K antagonists in patients that didn’t have atrial fibrillation. They were very successful. They showed that their efficacy was similar and with less bleeding risk. But when they translated those clinical trials to patients with valvular heart disease, they found that DOACs had less efficacy. So they started to think that probably they shouldn’t be used at all in patients with valvular heart disease. So there was also another clinical trial that avoided use of DOACs in patients with severe mitral stenosis that also showed that there were less efficacy than vitamin K antagonists. So for a while, cardiologists and people in general would be too reluctant to use DOACs in patients with valvular heart disease. But we know now from some observational studies that they are safe and they have some efficacy in patients that don’t have mechanical heart valves or severe to moderate mitral stenosis. So if you have a patient with mechanical valves or with moderate to severe mitral stenosis you should not use DOACs, otherwise it seems to be safe.
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