The potential problem is that if the metabolising enzyme for clopidogrel is not functioning (CYP2C19) it will not be apparent, and the NHS do not screen for it. I recently pointed out, that trial participants were not being screened for CYP2C19 loss of function or rapid function, where the administered drug is metabolised by CYP2C19. I was told that the NHS don’t screen for it (aagh!)
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I think everybody (NICE standard) gets put on aspirin (possibly with clopidogrel) immediately after a stroke. Around 80% of stokes are ischaemic (clot) and 20% are haemorrhagic (bleed). That gets a bit complicated if you have a haemorrhagic transformation (HT) after the stroke, where there is bleeding into the stroke-damaged area of the brain. Although I had an ischaemic stroke, I subsequently had an HT. The two attending GPs didn’t recognise the classic symptoms of a subarachnoid event. I was that and the one-hour delay by the ambulance paramedics who didn’t know that an absence of FAST indicators is not an absence of a stroke, that encouraged me to join Stroke Voices in Research and Stroke Association Research.
Generally, if you have an ischaemic stroke that may be related to atrial fibrillation, the long-term management will be an anticoagulant such as dabigatran (Pradaxa). If it’s haemorrhagic, the long-term management will be an antiplatelet such as clopidogrel, although there is an alternative to clopidogrel.
Although I had asymptomatic AF, that may not have directly caused my stroke. Two days beforehand, I had my usual one hour hard workout in the gym, followed by a 15 minute warm down that included yoga stretches. Those ended with a series of inverted poses - shoulder stand, candle, plough, knees to ears. It’s possible that the gym session plus my neck at right angles to my trunk, had loosened plaque in the carotid artery that made its way to my brain. My brilliant Neurologist told me that she had treated someone who had a stroke in a yoga class.
I’ve just read the NICE guidance that mentions using Omeprazole if the patient suffers from dyspepsia. However, Omeprazole is also metabolised by CYP2C19.
On the subject of drugs that are metabolised by CYP2C19, I respond quickly and very well to Diazepam, but selective serotonin reuptake inhibitors really wind me up so I can’t take them. What’s the chance that I have an ultra-rapid response? After all, I was one of the 6 in 100,000 whose lungs have a bad reaction to dronedarone and amiodarone.
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It’s interesting talking to academics about studies and trials for stroke procedures. I have twice read protocols where the person who has had a stroke (or the next of kin) is asked to read an explanation of the procedure, then sign a form that you’ve read it and fully understood it! Most of us in a full stroke don’t know what’s happened or who we are, let alone understood what we are given to read. Additionally, 70% of people immediately after a stroke have a visual disability. It’s much like when I had peritonitis: sign the consent form or …
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I had an ischaemic stroke, no atrial fibrillation, , and consultant put me on Clopidogrel, an anti platelet , for life. Surprised you think I should be on an anticoagulant? He was the main Professor at the large teaching hospital I was treated at. Hope he knows his stuff!!
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I’m not surprised that you were prescribed clopidogrel, as you didn’t have atrial fibrillation. In you re-read my second paragraph, an ischaemic stroke related to atrial fibrillation is likely to have long term management with an anticoagulant. It follows that an ischaemic stroke not related to atrial fibrillation will be treated with an antiplatelet.
It’s better if people describe their condition in full. On a separate forum about stroke, someone wrote they had a fall that had caused hemianopia. It transpired that she had fallen off a horse, not had a fall because of a stroke.
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