As I mentioned in Part 26, one of the little nuggets of joy my cardiologist dropped on me was the possibility of a hole in my heart. I initially rubbished the idea, but slowly it’s gained ground as a logical prospect.
As I’ve got older, and my respiratory problems have progressed to COPD, increasingly, the reality of living with this illness has parted company with what spirometry shows – though my own regular monitoring shows a different picture to that at my annual spirometry session, which benefits my GP’s budget more than it ever benefits me.
So actually, a hole in my heart might well explain why walking as little as 12 paces – to the bathroom for a pee, for example – leaves me breathless, and spirometry says it shouldn’t.
It would also explain the consultant cardiologist, in 1995/6 who insisted I don’t have COPD (though emphysema was showing on x-rays by then anyway!), but who offered no other explanation for my condition.
Spirometry, however has never matched my chronically breathless everyday reality – I get breathless typing, FFS! And nobody but me has ever asked why that should be, and answer came there none. Until now – possibly.
Frankly, though, there is no doubt that I have COPD, neither does Arrowe Park Hospital, officially – that, at least, is in my records – it might not actually be as severe as it seems to me (and no, it’s not psychological – I’ve lived with severe respiratory illness my whole life, I know more about it than the average GP), but a hole in my heart would explain the disparity between reality and spirometry – the fact that this has NEVER occurred to anybody previously just illustrates how crap my medical care has been.
One thing I do know, for certain, is that the consultant’s plan to catheterise my left ventricle via the already damaged aortic valve isn’t going to happen – the procedure carries a 22%** risk of an “acute cerebral embolic event” within 48 hours – stroke, by any other name (severity figures are elusive, but I don’t care – any stroke is bad news).
**I’ve said 24% in the past – just a memory glitch.
That’s way too high a risk, and as I have a history of TIAs, totally precludes this investigation as far as I’m concerned, especially as my brain is one of the few parts that still works properly.
The paper from which I got that information is “Should we cross the valve: the risk of retrograde catheterization of the left ventricle in patients with aortic stenosis,”** was published in the American Heart Journal , July 2004.
**That’s me, and the stenosis – narrowing – of the aortic valve is caused, in my case, by calcification of the valve. As far as I have been able to establish, and I’ve been looking at this for six months, since it was diagnosed, the calcium plates the three leaves of the valve, which, to me, suggests that some of it being scraped off by a catheter is a very real risk – and you don’t want flakes of calcium in the rising aorta, heading for the brain, that’s for sure.
As I mentioned in Part 26, one of the little nuggets of joy my cardiologist dropped on me was the possibility of a hole in my heart. I initially rubbished the idea, but slowly it’s gained ground as a logical prospect.
As I’ve got older, and my respiratory problems have progressed to COPD, increasingly, the reality of living with this illness has parted company with what spirometry shows – though my own regular monitoring shows a different picture to that at my annual spirometry session, which benefits my GP’s budget more than it ever benefits me.
So actually, a hole in my heart might well explain why walking as little as 12 paces – to the bathroom for a pee, for example – leaves me breathless, and spirometry says it shouldn’t.
It would also explain the consultant cardiologist, in 1995/6 who insisted I don’t have COPD (though emphysema was showing on x-rays by then anyway!), but who offered no other explanation for my condition.
Spirometry, however has never matched my chronically breathless everyday reality – I get breathless typing, FFS! And nobody but me has ever asked why that should be, and answer came there none. Until now – possibly.
Frankly, though, there is no doubt that I have COPD, neither does Arrowe Park Hospital, officially – that, at least, is in my records – it might not actually be as severe as it seems to me (and no, it’s not psychological – I’ve lived with severe respiratory illness my whole life, I know more about it than the average GP), but a hole in my heart would explain the disparity between reality and spirometry – the fact that this has NEVER occurred to anybody previously just illustrates how crap my medical care has been.
One thing I do know, for certain, is that the consultant’s plan to catheterise my left ventricle via the already damaged aortic valve isn’t going to happen – the procedure carries a 22%** risk of an “acute cerebral embolic event” within 48 hours – stroke, by any other name (severity figures are elusive, but I don’t care – any stroke is bad news).
**I’ve said 24% in the past – just a memory glitch.
That’s way too high a risk, and as I have a history of TIAs, totally precludes this investigation as far as I’m concerned, especially as my brain is one of the few parts that still works properly.
The paper from which I got that information is “Should we cross the valve: the risk of retrograde catheterization of the left ventricle in patients with aortic stenosis,”** was published in the American Heart Journal , July 2004.
**That’s me, and the stenosis – narrowing – of the aortic valve is caused, in my case, by calcification of the valve. As far as I have been able to establish, and I’ve been looking at this for six months, since it was diagnosed, the calcium plates the three leaves of the valve, which, to me, suggests that some of it being scraped off by a catheter is a very real risk – and you don’t want flakes of calcium in the rising aorta, heading for the brain, that’s for sure.