Dr Richard Bogle PhD FRCP FESC FACC DHMSA
Consultant Cardiologist
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Is there more to PCI than COURAGE?

6/3/2016

1 Comment

 
Currently there is much debate whether angioplasty and stenting (known as PCI) alters prognosis in stable coronary artery disease. The COURAGE trial published nearly 10 years ago indicated that optimal medical therapy was the key to modifying prognosis and that scaffolding narrowed coronary arteries with stents was not very important. Since then there have been growing calls to reign in the exuberant practice of the “Balloonatics” and the “Stentaholics” with criticism of interventional cardiologists’ for performing “Too much angioplasty” guided by the wonderfully named “oculostenotic reflex”.

Despite COURAGE a large body of evidence has also been accumulated showing that coronary ischaemia, whether silent or associated with angina, is associated with a worse outcome for patients and there is data from COURAGE showing that PCI is more effective at relieving ischaemic than optimal medical therapy. Current guidelines are very focused on detection of ischaemia and using that to guide PCI. It is interesting that PCI has been around for almost 40 years, millions of procedures have been performed, and yet there is still a huge debate on whether the treatment is more effective than tablets for the treatment of stable coronary artery disease.

A recent paper provides an interesting perspective and was an analysis of the REACH registry. REACH is a large multinational registry that collected data on 68,000 patients from December 2003 to June 2004. About 30,000 of them had a history of coronary artery disease and the study compared the outcomes of those patients with and without prior coronary revascularization. They found that those patients with a history of PCI had much better outcomes than those with no history of revascularization. These data should reassure patients who have had revascularization, but also lead us to revisit whether optimal medical therapy is as optimal as its proponents would lead us to believe. Of course in a registry study it is not possible to exclude bias completely even with complex statistical approaches and propensity matching. For example, some patients will have undergone angiography and been found to have minor disease, others might have had severe and extensive disease not amenable to any form of revascularization. However the study does provide reassurance that PCI may improve prognosis as well as be effective for the treatment of angina.

So how should we manage patients with angina in 2016. Should we offer optimal medical therapy first and then only offer angiography to those with continuing symptoms? Should we try to demonstrate ischaemia and if we find it proceed to angiography? Should we proceed straight to angiography and then consider the anatomical appearances and make a decision based on the lesion severity or with a pressure wire. If ischaemia is demonstrated should the extent play a role in the decision-making process for both angiography and revascularization? From the simple times of the oculostenotic reflex things have become a lot more complex and uncertain. NICE guidelines for assessment of patients with chest pain reduced the threshold to recommend invasive coronary angiography as the first line test but does early angiography risk decisions being made on the basis of the anatomy alone. Once the information about the coronary anatomy is known it cannot be unknown and may have a significant influence on the decision making process. Take an patient with a single episode of chest pain, who has a borderline exercise ECG and then turns out to have a 90% mid right coronary artery stenosis. Most people knowing this piece of information would be keen for treatment to relieve the stenosis rather than just receive medicines. Psychologically having an effective treatment for your narrowed coronary artery might be expected to have both a physical but also an important psychological benefit, although this has never been investigated. Results from the ISCHEMIA trial may help us to better understand this question but in the meantime patients present to cardiologists and decisions have to be made in an area of uncertainty. Also we can’t also pin all our hopes on the results of the ISCHAEMIA trial. What we can be sure of is the debate between PCI and OMT will continue for a long time to come.


1 Comment
Alan Bailey
17/8/2016 02:59:50 pm

I don’t know if this post is appropriate here. Apologies if it’s not.

I've followed Dr Bogle's blog for some time now (ever since he performed an angioscopy on me at St Anthony's hospital in Cheam). I'm not a doctor, but as someone who has serious furring of the arteries, I am seriously interested in any new developments that may hold the promise of defurring them. No luck so far but I have come across something that may hold promise.

Kate Rheume-Bleue in her book "Vitamin K2 and the Calcium Paradox" makes what seems to me as a laymen a strong case for taking K2 supplements either in tablet form or via a Japanese product called Natto.

Like you I probably get quite a few leaflets come through the letter box with outrageous claims of the health benefits of a particular supplement. I then quickly discard them since they are never based on any good evidence, just some mumbo-jumbo science. So I'm naturally cautious about Kate Rheume-Bleue's claims but she does produce evidence. This is mainly based on early research by Dr Weston A Price (between WW1 and WW2) and "the Rotterdam Study. J Nutr 2004 Nov,134(11):3100-05". Both these studies suggest that Vitamin K2 supplements could be of benefit although there can be no doubt that more evidence is needed.

My understanding of her science is as follows.

Vitamin K1 is produced in new grass. Cows eat the grass and turn Vitamin K1 into Vitamin K2. A major source of our K2 has been from drinking milk and/or eating beef. Unfortunately since WW2 cows are now fed grain supplemented with Vitamins A and D and are kept indoors. Grain contains little, if any, K1. As a consequence only a small amount of K2 is produced by a cow and we have become K2 deficient. Adequate intake of Vitamin K2 is required by us since, unlike Vitamin K1, it is not recycled in the body. The other good source of Vitamin K2 was once eggs.

According to Rheume-Bleu Vitamin K2 has two major effects.

1. It activates osteocalcin which attracts calcium into the bones. (Vitamins A and D together have a synergistic effect of boosting osteocalcin production and so adequate intake of these is also required). Lack of K2 is a major cause of osteoporosis.

2. It activates Matrix GLA Protein (MGP) which removes calcium from soft tissues such as arteries and veins. (Magnesium intake is also important since among other benefits it is essential for the absorption and metabolism of Vitamin D which in turn stimulates MGP production). Lack of K2 is a major factor in the furring up of arteries.

The problem for me is that I have no way of checking the science and would like to know whether what she suggests is reasonable. I must add the caveat that many of the immediate questions you may have are probably answered in her book but having read the book I can try to answer them. Can anyone help?

Alan Bailey

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    The opinions expressed in this blog are strictly those of the author and should not be construed as the opinion or policy of my employers nor recommendations for your care or anyone else's. Always seek professional guidance instead.

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