The main underlying theme of this book is heart disease – what causes it and what doesn’t. But the term ‘heart disease’ is virtually meaningless. A pedant would say that heart disease is a ‘disease of the heart’, but there are hundreds of them, most with complex names – myocarditis, pericarditis, ventricular hypertrophy, Woff-Parkinson-White Syndrome, to name but four.
Fig. 1 Blockage in right coronal artery
However, the big daddy, the one that kills most people, is not truly a disease of the heart at all. It is a disease of the arteries that supply blood to the heart, and is usually called atherosclerosis. ‘Athero’, or ‘atheroma’, describes the build up of grey-white/fatty gunk in the artery walls. These thickenings are sometimes called atheromatous plaques, or just plaques. ‘Sclerosis’ means general thickening and hardening. One of the other confusing elements when reading about heart disease is the amount of jargon. AKA medical terminology.
Atheromatous plaques come in many different varieties. The American Heart Association even has a grading system from one to five, and then further subsections into type 5(i) and 5(ii) … and probably type 4(B), subsection (ii) paragraph 6. You get the picture.
Plaques are generally thought to progress from an initial ‘fatty streak’, as found in the arteries of most ten-year-olds, which gradually becomes bigger and thicker. Eventually, the plaques can reach the point where they actually calcify, turning arteries into stiff, almost bonelike tubes. The process of turning from a fatty streak into a calcified plaque is supposed to take years and years, although no one knows for sure how long things take because no one has ever hung around to watch an individual plaque going through its lifecycle (not in a human being, at least). The general assumption seems to be that it all takes decades.
Having said this, it is not the mature, stiff, calcified plaque that is the problem; it is an intermediate stage, the so-called ‘unstable’ plaque. At some point during their (allegedly) slow development, plaques turn into something that looks like a cyst lurking within the artery wall; a thin capsule surrounding a semi-liquid centre full of goo. This goo is made of all sorts of stuff. Fats, dead white cells, broken down bits of blood clot etc.
The great danger with this type of plaque is that the thin wall surrounding the goo bursts, or breaks down. This ‘goo exposure’ sends a hugely powerful message to the blood-clotting system, and results in a blood clot (also called a thrombus) forming over the burst plaque. If the blood clot is big enough then it completely blocks the blood supply to whatever organ that particular artery was supplying:
Fig. 2 Development of a blood clot in an artery
If that organ happens to be the heart, then the heart muscle downstream will become starved of oxygen. It may then ‘infarct’ (‘infarction’ means the localised necrosis – or cell death – that results from obstruction to the blood supply). In medical speak, this is a myocardial (heart muscle) infarction, often shortened to an MI. In layperson speak, this is a heart attack. It is estimated that about 50 per cent of heart attacks are fatal, and people mostly die in the first hour. For those who survive the first hour, though, a myriad of medical interventions have now been developed.
Among the earlier developments were clot-busting drugs, designed to break down the clot that is blocking the artery. These are still widely used, and are pretty effective – assuming you managed to ‘bust’ the clot before the heart muscle became too badly damaged. That said, the humble blood-thinning aspirin can be almost as good, at about one-millionth of the cost.
However, cardiologists now have much better toys to play with, and the latest type of treatment for an acute heart attack employs a long, thin catheter, which is inserted into an artery in the groin. Under X-ray guidance; this is then fed up to the heart, directed into the artery that is blocked and then stuck through the clot. A balloon is then inflated, opening up the artery even further. Nowadays, a small metal framework known as a stent is wrapped round the balloon, and this folds out into a rigid ‘support’ that sits where the clot was, keeping the artery open. The entire procedure is known as angioplasty. It’s all exceedingly clever, and horribly expensive (See Fig. 3).
Fig. 3 Procedure for an angioplasty
For those in whom clot-busters and stents haven’t worked, there is the Coronary Artery Bypass Graft (CABG), or ‘cabbage’ – although doing a cabbage in an acute situation is pretty much the last resort of last resorts. Or, as we used to say in Scotland, TOTS, which stands for Tatties Over The Side (a tatty is a potato) – a reference to the point in a storm when the crew has to ditch the very last bit of cargo to save the ship.
Ergo, a CABG in an acute MI – when clot-busters or angioplasty hasn’t worked – is TOTS time. You see, the jargon is quite simple once you get the hang of it.
Quite how much impact all of this cleverness has had on overall mortality rates from having a heart attack is a moot point. Around fifty per cent of people die before reaching hospital, so they can’t be saved. Another forty per cent, or so, were always going to survive no matter how badly the hospital cocked up. So, at very best, these techniques can improve survival after a heart attack by about ten per cent, and we are nowhere near achieving this yet. Perhaps two or three per cent more people survive a heart attack now than about ten or twenty years ago.
Don’t get me wrong. If I had a heart attack I would want a cardiologist warming up the cath lab, ready to stick a stent right up the old femoral artery. No question about it. Nothing but the best for me, thank you very much. But when it comes to heart attacks, cure is always going to be very much less impressive than prevention. Even if it is much less sexy.
Before we move on, I need to provide a little more information about ‘infarctions’ elsewhere in the body. Because although plaques most often develop in the arteries supplying blood to the heart (coronary arteries), plaques are perfectly capable of developing elsewhere in the body too. Quite often, big plaques form in the arteries in the neck (carotid arteries). As these arteries supply blood to the brain, this is clearly a danger spot. However, the carotid arteries very rarely block completely. What most often happens is that a clot forms over the carotid plaque, then a bit breaks off and travels up into the brain through ever-smaller arteries.
Once the clot reaches an artery that is too narrow for it, it gets stuck, and this dams up blood supply to an area of the brain, leading to a cerebral (brain) infarction. This is the commonest version of a ‘stroke’. The other type of stroke occurs when an artery in the brain bursts, causing a bleed into the brain tissue. This is called a cerebral haemorrhage.
In fact, one of the reasons why it has been so hard to develop an effective treatment for stroke is that, clinically, it is impossible to tell the difference between an infarct/blockage, and a bleed/haemorrhage. You need to do a brain scan to know, for sure, what type of stroke has occurred. You can’t give a clot-busting drug to someone having a stroke, because, if they are having a ‘bleed’, the drugs will make things far, far, worse. In fact, you will almost certainly kill them. And, by the time you have managed to get a brain scan done, it is usually too late to give any drug at all, because the damage will already have been done.
Moving on from that cheery subject. Apart from the heart and the brain, you can have infarctions in the kidneys, the guts, the eyes – almost anywhere, in fact. (At this point, it occurs to me that I should, perhaps, have inscribed the words DON’T PANIC on the cover of the book.)
Perhaps the scariest place to develop big plaques is in the aorta, the major blood vessel that leads out of the heart and down through the chest and abdomen. If the aorta develops big plaques, the wall can lose structural integrity and balloon outwards, creating a great big ‘aneurysm’ (see Fig. 4). This is like having an unexploded bomb in your chest, just waiting to go off. And when an artery this big fails – kaboom! In medical speak, this is known as a ruptured aortic aneurysm. In general, it is something to be avoided. Some people survive – so long as the leak is small, that is.
Fig. 4 Comparison between normal aorta and aorta with aneurysm
• Heart disease is really a disease of the arteries supplying blood to the heart.
• The ‘disease’ is atherosclerosis (or the development of discrete atherosclerotic plaques).
• Plaques can also develop in arteries almost anywhere in the body.
• Plaques are dangerous when they burst, or ‘rupture’, as this stimulates the formation of a blood clot over the ruptured area. This can completely block the artery, causing the tissue downstream to infarct.
POSTSCRIPT
Nothing written in this chapter is contentious. It is all broadly accepted and represents mainstream thinking and research. Although, as with everything scientific, there are bound to be points where some people would say ‘That’s not quite true’ or ‘I disagree with that description.’
However … however. I would hate to give the impression that everything is quite as simple as I have indicated. The reality is that nothing in the area of heart disease is pure black and white. Here are three facts for you to ponder.
Fact one:
A post-mortem study found that a group of Japanese had the same degree of atherosclerosis in their arteries as a group of American men. Yet the rate of death from heart disease in the Japanese example was one-sixth that of America in middle-aged men and women. At least, it was at the time of the study ‘Comparison of aortic atherosclerosis in the United States, Japan and Guatemala’, by Gore I, Hirst AE and Koseki Y (American Journal of Clinical Nutrition, 1959; 7:50–54).
Fact two:
In the majority of cases, the blood clot (thrombus) thought to have triggered the heart attack will have formed days, or even weeks, before the heart attack itself. Does this mean that acute blockage of a coronary artery does not cause a heart attack? (An addendum to fact two is that, in many cases, no blockage in an artery can be found at postmortem.)
Fact three:
Men who dig out coal in very deep mines in Russia often die very young from heart attacks. The average age at death is 41. Yes, 41. On autopsy, most of them show signs of several previous heart attacks, yet few of them have any history of having had a heart attack, or chest pains. Does this mean that most heart attacks do not cause chest pain?
Finally, to emphasise the point that things are far more complicated – and far more interesting – than the current almost mechanical view of heart disease and heart attacks (according to which the arteries are seen as a pipe carrying blood, and the heart as a simple pump), consider the following.
A myocardial infarction is defined as ‘localised necrosis resulting from obstruction to the blood supply.’ Sounds simple, but think again. ‘Necrosis’ means tissue death. Below, I have included a picture of the end result of frostbite. In frostbite, areas of the body – particularly the fingers or toes – freeze, then become blackened and dead, and finally fall off. They are often referred to as ‘necrotic areas’.
Fig. 5 Injuries resulting from frostbite
Imagine, for a moment, what would happen if the bit of heart muscle affected by a lack of blood supply – the area of myocardial infarction – actually did die, as in frostbite. You would end up with a blackened, dead bit of heart muscle that would then, inevitably, fall off. At which point you would have a big hole in the side of your heart. Which, I think I can state with absolute confidence, would be 100 per cent fatal.
But this does not happen – ever. What happens is that the area of infarcted tissue changes from muscle, which requires a lot of oxygen to function, into a form of scar tissue, which can survive on very little oxygen. In short, heart muscle does not actually become necrotic, or die, following a heart attack. Instead, what happens is a process of cell alteration, or adaptation – which means that, at some point, the cells affected by a lack of blood supply are deciding whether or not to ‘infarct’ and change into scar tissue or, instead, to remain as fully functioning heart muscle. How and why do they make this decision? Who knows.
What we do know, however, is that in people with established heart disease you can find regions of the heart where muscle is ‘hibernating’. It hasn’t converted to scar tissue, but it isn’t contracting either. It’s simply sitting and waiting. Waiting for what? For the blood supply to recover, presumably. How long can heart muscle wait like this? Quite a long time. Weeks at least, perhaps months, maybe years.
I hope this example makes it clear that ‘heart attacks’ are far from simple things whereby a pipe (the artery) blocks up, oxygen supply dries up and muscle then dies. It is true that the artery blocks up, but after that a hugely complex process swings into action that may, or may not, result in heart muscle converting into scar tissue.
In addition, the artery itself is fully capable of opening up again – which is why, presumably, the heart muscle sits ‘hibernating’, waiting for blood supply to return. Failing this, the heart may grow new arteries to bypass the blockage. This is known as developing ‘collateral’ circulation.
And the same degree of complexity goes for almost every other aspect of heart disease. Thus, atherosclerosis is not a case of a pipe gradually thickening with cholesterol, like a central-heating system clogging up. This seems a nice simple analogy, but it is hopelessly flawed. Take, for example, this cutting from the Savannah Morning News. Don’t ask me anything about this newspaper – I was sent the cutting by a fellow cholesterol sceptic, as it seemed to him the perfect example of a stupid analogy:
Photos taken inside clogged city sewer pipes look nearly identical to medical photos of the blood vessels of patients who have spent a lifetime gorging on fried chicken, sausage, and bacon. ‘It’s like your arteries,’ said John Parker, environmental compliance inspector with the city’s Water and Sewer Department. ‘Grease builds up in there. It’s gory.’ And just like in the body, clogs can form little by little, the accumulation of lots of neighbors each sending a little grease down the drain.
There are so many ways in which this analogy is wrong, that I just can’t possibly outline them all here. Hopefully, by the time you have finished this book you will understand that anyone making such a statement needs to be taken out and slapped repeatedly with a wet kipper.
