Читать книгу A Statin Nation - Dr Malcolm Kendrick - Страница 11

The heart is supplied with blood by several different coronary arteries, which branch off at regular intervals. Let’s say there are four of them – not quite right, but it will do (some people have coronary arteries that others do not possess). The naming system is complex.

All the coronary arteries supply blood to different sections of the heart. The left anterior descending (LAD) artery, for example, supplies blood to the left ventricle that does the heavy lifting of pumping blood out of the aorta at high pressure. The LAD is, therefore, the most ‘mission critical’ artery in the heart although, obviously, they are all pretty important.

Classically, when you have a heart attack, one of the coronary arteries will suddenly get blocked by a blood clot. This usually happens when a vulnerable plaque ruptures. This, in turn, drastically reduces the blood supply and the area of the heart supplied by that artery can infarct, which is why heart attacks are often called myocardial infarctions (MIs) by the medical profession.

Most textbooks define an infarct as ‘death’ or ‘necrosis’ of heart muscle. However, this is simply wrong. It is true that a certain amount of heart muscle affected will die, and the remnants of dead cells will then be cleared away. But, assuming that you survive the MI, a repair process kicks into action to convert heart muscle cells (myocytes) into scar tissue. To repeat, infarction does not represent heart muscle death. Yes, some cells die, but most of them simply stop contracting in a desperate attempt to save energy. These cells are then converted into scar tissue, which requires very little oxygen to survive.

This is a tightly controlled process, ensuring that the basic structure of the heart remains intact. If this did not happen, an infarcted area of the heart would simply disintegrate, which would be instantly fatal. The infarction process was well described in the paper ‘Infarct scar – a dynamic tissue’:

Following MI, with loss of necrotic cardiac myocytes [dead heart muscle cells], a reparative process is quickly initiated to rebuild infarcted myocardium [rebuilding the area of heart damaged by sudden blood loss] and maintain structural integrity of the ventricle. A series of cellular responses are called into play driven largely by cell-cell signalling that serves to regulate tissue repair. Initially, inflammatory cells are attracted to and invade the site of injury … new blood vessels are formed (angiogenesis), and fibroblast-like cells appear and replicate. This early inflammatory phase of healing with resultant granulation tissue formation is followed by a fibrogenic phase that eventuates in scar tissue – a rebuilding of infarcted myocardium.1

Apologies for the jargon, but I thought it was worthy of full inclusion as I want you to know that we are most certainly not looking at a simple, passive process in MI. The infarcted area does not die. Instead it is reconstructed into scar tissue, but obviously this area of the heart cannot pump afterwards as it will be made of passive scar tissue, rather than healthy, contracting heart muscle cells (myocytes).

Sometimes, after an obstructive blood clot, the heart muscle does not infarct when the blood supply is lost. Instead, the affected area of heart muscle simply stops beating and enters a state known as hibernation. Just like in a hibernating bear, everything is still turning over, but at a very low rate. So, the myocytes are still alive but no longer contracting in order to reduce oxygen demand.

These hibernating areas can spring back to life if the blood supply improves. Alternatively, they can remain in hibernation for years, only to fully infarct at some point in the future, presumably after giving up hope of ever having enough oxygen to function. In some cases, the heart muscle does not infarct or hibernate, it simply struggles on, but will protest loudly if you try to exercise. This painful protest is called angina. Angina can also develop when a coronary artery gradually narrows over time, and is often called ischaemic (from ischaemia, meaning lack of oxygen) heart disease (IHD).

At one time, it was thought that if a coronary artery was fully blocked, this would inevitably lead to death. However, in 1912 an American doctor called Herrick became the first to describe an arterial blockage, without the patient dying. A non-fatal MI.

Since that initial observation, it has been increasingly recognised that many MIs are not fatal. Indeed, in many cases people are completely unaware that they have even had an MI. Whilst the classic heart attack is described as someone clutching at their chest, in agony, with pain going down the left arm and up into the jaw, sweating and pale, this is not always the case.

‘If the patient has no symptoms or atypical symptoms, the MI may be categorised as “silent”. In some (but not all) cases, silent MI may be later identified and referred to as “unrecognised MI”. Unrecognised MI is a common and clinically significant event.’2

How can it be that some MIs result in agonising, crushing pain, whilst other MIs are silent? Frankly, I have no idea, but silent MIs are more common in women, the elderly and people who have other, underlying conditions, e.g. diabetes. That doesn’t explain why they are silent. It is just an observation.

To complicate things even further, you can find people with symptomatic MIs, ECG (heart trace) changes that are indicative of an MI, and raised cardiac enzymes that are all fully diagnostic of an MI, where no blockage of any artery can be found. This is known as myocardial infarction with non-obstructed coronary arteries (MINOCA). This can represent up to 25 per cent of MIs. And in addition to these variants, it is fully possible for a blood clot to form in a completely non-atherosclerotic artery and go on to cause an MI. This is relatively uncommon, but does happen.

Finally, for now, although I could go on far longer if I included all possible forms of heart attack, you can have Takotsubo syndrome. This has almost all the signs of a classic MI: chest pain, breathlessness, collapse, raised cardiac enzymes and ECG changes, etc., and you can even die of it. Yet there is no blood clot, no area of infarction and no true MI at all. This is sometimes called broken heart syndrome and is usually brought on by sudden, emotional stress. The Japanese were the first to recognise this phenomenon, and so named it because the left ventricle (the main pumping chamber of the heart) changes shape and ends up looking like an octopus pot – a takotsubo. You mean you didn’t know what a Japanese octopus pot looks like?

Well, the left ventricle ends up looking like an octopus pot anyway, Which proves something that I have banged on about for years, namely that human emotions have a significant impact on physical health – and, of course, vice versa. More later.

DIAGRAM 4

Whilst there are many different type of heart attack, it remains true that the classic MI is the most common event, and the process is as follows. Over many years, a coronary artery narrows, as the underlying atherosclerotic plaque enlarges. Then the plaque ruptures, leading to the formation of a fully obstructive blood clot. This cuts off blood supply and an infarction will ensue. Around 40 per cent of classic MIs are immediately fatal.

One further complicating factor that I need to mention is that the heart can create new, smaller blood vessels over time known as collateral circulation. If your coronary arteries have been getting more and more blocked, over the years, newly created blood vessels can and will bypass the narrow areas to keep the oxygen supply going. If the collateral circulation is sufficiently well developed, this can fully protect the heart from a blood clot finally blocking a narrowed coronary artery. In some people, all their coronary arteries are completely blocked yet they can still function well. Indeed, they can live quite happily for years, without even knowing they have no open (patent) arteries.

Incidentally, it is not usually the infarction that is deadly with an MI. What kills you is damage to the electrical conduction system within the heart, i.e. the electrical condition fibres that run through the heart muscle. If the damage to this nervous system is widespread, you may end up in ventricular fibrillation (VF).

In VF the conduction system goes haywire, resulting in the main pumping chambers of the heart – the ventricles – failing to beat in a coordinated manner. They just twitch and spasm as electrical impulses fire about all over the place. This reduces blood flow to zero which, in turn, leads quite rapidly to death. If someone goes into VF, it can be possible to shock the heart back into its normal rhythm using a defibrillator. They are now found everywhere, even in remote telephone boxes, gyms and libraries. This is an excellent scheme because, from the onset of VF, you have about four to five minutes to act before the lack of oxygen supply to the brain leads to irreversible damage. So, the sooner you can shock someone back into normal rhythm, the better.

Luckily, modern defibrillators can virtually talk you through the process. You switch them on, stick the pads on the chest, stand back and they know what to do. They will recognise if someone is in VF or not, and shock accordingly. You become a mere bystander. However, if there is no electrical activity at all, giving a flat-line on the ECG, the defibrillator cannot work as there is no activity to restore. In this case cardio pulmonary resuscitation (CPR) is the only way to keep someone alive for long enough to get the person to hospital in time. At which point, other more complicated matters can be attempted. But bear in mind that well-performed CPR can keep people alive for hours – so please don’t stop when you get tired or disheartened.

In the immediate aftermath of an MI, assuming you are not in VF, and assuming you are not already dead, once you reach the hospital many different things can now happen. You could simply be given an aspirin, which slows or stops blood clots from forming. In fact, you probably will already have been given one. You might also be given a clot buster, such as tissue plasminogen activator (tPA). This converts plasminogen, an inactive substance incorporated into all blood clots, into plasmin. Plasmin rapidly slices blood clots apart, through an action called fibrinolysis. Fibrin consists of long, sticky stands of protein that bind blood clots tightly together. Fibrinolysis makes the clots disintegrate. Alternatively, you could have an emergency bypass graft operation. This is where veins are stripped out of your leg and used to bypass the blockage in the artery in your heart.

DIAGRAM 5

However, these activities are now considered somewhat ‘five minutes ago’. Nowadays, the most common treatment is percutaneous coronary intervention (PCI), when a thin probe is inserted into an artery in your arm or leg. It is then cunningly directed into the blocked coronary artery, whereupon a balloon will be inflated to widen the artery. At which point, in most cases, a metal lattice framework that has been wrapped around the balloon is opened out. This provides a rigid structure to keep the artery fixed open after the balloon has been deflated and pulled back out. This is called a stent and the procedure stenting. After this you will be put on a cocktail of different drugs to take for the rest of your life … But that is a different story.

It must be said that the treatment of an MI has improved beyond all recognition. In the bad old days, the only treatment following an MI was pain relief and a stern instruction to lie immobile in bed for six weeks, during which time the heart muscle further deteriorated. In addition, the chances of developing a blood clot in your leg, then dying of the resultant pulmonary embolism (PE) went through the roof. (In PE, the clot in your leg breaks off and travels to the lungs where it gets stuck.)

In hospitals, death from MI has reduced from around 60 to about 9 per cent(ish). My figures here may be disputed, but this is a difficult area to pin down. Whatever the exact figures, things have got much better. And a great deal of this can be put down to earlier mobilisation following an MI, some of it due to drug treatment, some due to better control of electrical activity in the heart, some to PCI/stenting, insertion of pacemakers and the use of implantable defibrillators. I feel that matters are now getting close to optimum in MI management.

What is certainly true is that if I had an MI, I would want to be whisked to the nearest big, shiny hospital where experienced doctors could do a PCI, thank you very much. Of course, I do not intend to have an MI as I am pretty certain that I know how to prevent it from happening, which reminds me of James Fixx, who stated that running would prevent him from having a heart attack. To quote the New York Times: ‘James F. Fixx, who spurred the jogging craze with his best-selling books about running and preached the gospel that active people live longer, died of a heart attack Friday while on a solitary jog in Vermont. He was 52 years old.’3

Make of that, what you will. As a believer that exercise is indeed good for you, I will state that he would have died earlier if he had not taken up running. Other interpretations may be deemed valid.