Will new pill to stop a clot save me from a stroke?
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I have recently been prescribed Pradaxa to prevent clots and have been told there is a 3 per cent chance of me having a stroke. Is this a high risk, asks Lionel Jenkins, New Zealand
I have recently been prescribed Pradaxa to prevent clots and have been told there is a 3 per cent chance of me having a stroke. Is this a high risk?
Lionel Jenkins, New Zealand.
The drug that you have been prescribed, Pradaxa (generic name dabigatran), is one of what we call the novel anticoagulants.
These are newly-developed drugs for suppressing the natural tendency for blood to clot, and are usually prescribed to patients with atrial fibrillation — where electrical activity in the heart goes haywire, causing it to beat irregularly.
A complication of atrial fibrillation is a higher risk of clots and, therefore, strokes. This is because blood that should get pumped around the body begins to pool and thicken in the atrium, the blood-collecting chambers of the heart.
If a clot then breaks away and is pumped out of the left ventricle — the heart’s main pumping chamber — it can travel up the narrow blood vessels that feed the brain and can block the supply of oxygen-rich blood.
When that happens, the risk of death is very high — but it depends on the size of the clot and the blood vessel that’s blocked, which, in turn, affects how much of the brain is deprived of blood.
Prior to the arrival of these novel anticoagulants, the most common treatment was warfarin.
For many doctors, it is still the first-line treatment, but it does have a nuisance value, as patients need regular blood tests to monitor the dose and achieve the correct degree of anticoagulation, or blood-thinning.
The novel anticoagulants avoid these difficulties because they inhibit blood clotting at a different point in the process and they all have a simple, regular dosing regimen — usually a pill to take once or twice daily.
Studies have shown that Pradaxa, the drug you have been prescribed, is as effective as warfarin at preventing unwanted clotting. There have been well-publicised concerns about a higher bleeding risk with it. However, a recent study suggests otherwise for most people.
The drug that you have been prescribed, Pradaxa (generic name dabigatran), is one of what we call the novel anticoagulants
In general, anticoagulation has been shown to reduce the risk of stroke in atrial fibrillation by around two-thirds.
Before a prescription is given, a patient is assessed for the risk of stroke using a tool called CHA2DS2-VASc Score.
With this, you’re given a point for each additional risk factor. For example, gender (one point for being female); age (one point for those aged 65 to 74, and two points if you are 75 or over); stroke adds two points; and the incidence of vascular disease (such as previous heart attack), diabetes, high blood pressure, and congestive heart failure all add one point each.
A patient can therefore score between zero and nine points. A score above two merits anticoagulation. Your doctor will have used such an assessment before prescribing Pradaxa.
A score of two has an annual stroke risk of 2.2 per cent — that means in any given year, a stroke will affect between two and three people in every 100.
Your score must have been higher than two, as you say your risk of stroke is 3 per cent.
These are newly-developed drugs for suppressing the natural tendency for blood to clot, and are usually prescribed to patients with atrial fibrillation — where electrical activity in the heart goes haywire, causing it to beat irregularly
Nevertheless, a stroke risk of 3 per cent within the next year is not particularly high.
Bear in mind that this is your current risk of stroke, before taking anticoagulant medication.
Sticking to the regimen that’s been prescribed to you will reduce this risk to 1 per cent or so, which I judge to be a good risk reduction — and worthwhile.
Three years ago, I had a prolapse and was fitted with a pessary ring. I have since suffered a heart attack and had three stents (metal tubes) fitted.
I’d like to have an operation to fix the prolapse once and for all, but my doctor says it is a last resort. I don’t understand why. I am 73.
Ann Mockett, Bedlington, Northumberland.
You’ve raised a subject that’s extremely common, and yet one that many women find difficult to discuss: pelvic organ prolapse, where one or more of the pelvic organs herniates into the vagina as the support tissues weaken as a result of age, obesity and/or childbirth damage. Around 50 per cent of women who’ve given birth naturally have some degree of uterine prolapse, and about 10 to 20 per cent will have symptoms such as incontinence as a result.
Pessaries are devices placed in the vagina that reduce prolapse mechanically, providing ‘scaffolding’ to hold up the uterus. They are a trouble-free alternative to surgery, or an interim arrangement.
Some patients prefer a pessary to surgery, as it has few side-effects and can be used continuously for as long as necessary.
If these don’t work, or as a permanent solution (pessaries must be washed and changed regularly by a GP), surgery often involves a vaginal hysterectomy and then a reconstruction of the pelvic floor.
But some patients who have other illnesses may not be suitable for it.
You have had a heart attack and subsequent stent surgery — so to give you a general anaesthetic may be too dangerous, which may be why your doctor is cautious.
Having said that, fixing the prolapse is not major surgery and can be done under spinal anaesthetic, rather than a general anaesthetic, which could otherwise have complications for the heart.
I know of patients who have successfully undergone surgery despite heart attacks or stents.
You have plenty of years ahead and it is reasonable to request a referral for surgery.
By the way… At last, a clue to the cause of chronic fatigue
I was beginning to despair whether science would ever reveal any breakthrough on the subject of chronic fatigue syndrome, a condition in which I have had a particular interest throughout my career.
But, at last, there is evidence that this is, as long suspected, an inflammatory disease.
One theory has been that this debilitating disorder is due to a dysfunction of the response of the body to infection — but this has never been established.
I was beginning to despair whether science would ever reveal any breakthrough on the subject of chronic fatigue syndrome, a condition in which I have had a particular interest throughout my career
The latest research, published a few weeks ago by Georgetown University in the U.S., uncovered molecular changes in the brain that are specific to chronic fatigue syndrome. In particular, levels of certain microRNA — responsible for regulating protein production (proteins tell our cells what to do) — diminished after exercise in chronic fatigue patients, compared with healthy people, which could provide a basis for better diagnosis.
These findings add to research carried out earlier this year by Stanford University in California.
This showed that patients with chronic fatigue — those with a history of at least six months of unexplained physical and mental fatigue, malaise after exertion, sleep dysfunction, pain, neurological and cognitive symptoms — had raised levels of 17 cytokines, proteins that are the fingerprints of inflammatory processes. And the higher their level of cytokines, the more severe the illness.
This has established a strong immune component of the disease, the evidence that we have long awaited.
There is still a way to go, and this is by no means a complete answer, as, in some medical circles, the very existence of this disease remains controversial.
But I believe this is proof of chemical and inflammatory involvement, which points the way to new avenues of research: light, at last, at the end of a long tunnel, hopefully offering the prospect of future treatment — and prevention.