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The history of heart attacks

Professor Thomas Lüscher, consultant cardiologist and director of education, research and development



I have a talk entitled, “From Eisenhower’s heart attack to modern cardiology,” which I first gave at Harvard University and then around the world.


Ike, as the Americans called him, had a myocardial infarction – a heart attack – on 23 September 1955. His physician didn’t really realise that he had an infarction at all, and it was 12 hours before he was brought to hospital. I always say today his doctor would be brought to jail for malpractice, but at the time treatment options were so limited it did not matter.


Although they had the electrocardiogram (ECG), there were no cardiac enzyme tests for heart attacks in those days, no coronary angiograms, and cardiac imaging options were very limited compared to today.


They had access to morphine and nitroglycerine, but they used no heparin and there were no defibrillators, so fatal arrhythmias (abnormal heart rhythms) were not treatable. 


There was no aspirin, no thrombolysis, and no stenting to open up blood vessels in the heart. It’s difficult to imagine nowadays.


So they just drank tea and waited and prayed for a good outcome. Eisenhower miraculously recovered with tender loving care only, though he looked a bit pale afterwards.

 

In 1950, half of the patients who suffered a myocardial infarction died in hospital – and that’s only the ones who made it to hospital! 


Nitroglycerine and defibrillation


The first guy who discovered amyl nitrate, a sort of nitro-glycerine, for medical use was a Scotsman, Sir Thomas Lauder Brunton, who worked at University College London and St. Bartholomew's Hospital and was made a Fellow of the Royal Society in 1874. 


Amyl nitrate and nitro-glycerine dilate the arteries and relieve angina (chest pain caused by reduced blood flow to the heart muscles).

 

Alfred Nobel, who actually invented nitro-glycerine for dynamite, also had a heart condition but he refused to take it, because he thought he might explode!

 

Defibrillation was an absolutely huge breakthrough. It was seen as the first time you could survive your own death. If you have ventricular fibrillation, you need an electric shock, otherwise it’s 100 per cent mortality – everybody dies.

 

In 1956, Paul Zoll changed everything when he published ‘Termination of ventricular fibrillation in man by externally applied counter shock’ in the New England Journal of Medicine


If you look at the ECGs of the time, you can see quite clearly: a ventricular tachycardia, boom – the electric shock – and then a normal heart rhythm. It was monumental.


Aspirin and cardiac catheterisation


Then of course came aspirin, through a Londoner this time, Sir John Vane, who discovered that it inhibits platelet function and received the Nobel Prize in 1982. Initially the producer Bayer in Germany said on the aspirin label, ‘not to be used on cardiac patients’ because they felt it was only a fever remedy.


So, in 1950, half of the patients who suffered a myocardial infarction died in hospital. Then they invented defibrillation which reduced mortality substantially.


Next came beta blockers, which open up blood vessels and improve blood flow, invented by another Englishman, Nobel Prize winner Sir James Black. Then resuscitation was invented, followed by coronary angioplasty and implantable defibrillators.


In 1977, Andreas Grüntzig in Zurich was the first to dare to enter the coronary arteries and to use a balloon catheter – that he had built on his kitchen table!


As so often, teams at Royal Brompton were at the forefront, performing the UK's first coronary angioplasty in 1980 and Ulrich Sigwart who implanted the first coronary stent worked at this organisation.


Education for prevention


In Sweden they have had the Swedeheart registry since 2010 – three decades of patients’ mortality data due to cardiac problems, and you can see how it has fallen.


Today, in the UK, mortality is just ten per cent if you make it to hospital. And remember, these days we manage to bring patients in terrible condition into hospital. 


Just look at Harefield: they come by helicopter, or by ambulance, sometimes after having been resuscitated.

These patients are frequently much, much sicker – they wouldn’t even have reached hospital in days gone by.


At Harefield, we have a really good ‘door to balloon’ time for primary angioplasty (one of the fastest treatment times in the country at 27 minutes, against a national average of 42) and an excellent team. They save lives.


So the next question is: why are ten per cent of people still dying? The answer is this: if you come to Harefield, for example, with acute coronary syndrome, which is what we call it today, if you can say ‘hello’ to your medical team, the mortality rate is just a few per cent.


If you can no longer speak, because you have been resuscitated and been intubated so you can breathe, or because you’re in cardiogenic shock and dizzy, the mortality rate rises to 40 per cent. It’s 20 times higher.


So what do we have to do to make it even better? I think the most important thing is we have to educate the public and the families of these patients, about what to do if they encounter a loved one or stranger who dropped dead. 


Everybody should know how to perform cardio-pulmonary resuscitation until an ambulance arrives. Indeed, the brain can survive only a few minutes after a cardiac standstill.


Even then, many people will go on to have a second heart attack in the future. If they have a defibrillator at home and can be treated, they have a very good chance of making it to hospital. Defibrillators are about £3,000 to £5,000, they’re not cheap, but they are genuinely life-saving. 


The importance of cardiopulmonary resuscitation (CPR)


In Switzerland, everyone who passes their driving test has to prove they went to a resuscitation course before they are given a licence. If someone collapses in the street, you know what to do and it does save lives.


The brain, everything that makes you you, this neural network in your head, won’t survive more than seven to nine minutes when the heart stands still. After that, everything that makes you you is gone.


We looked at this in a large cohort of 1,000 patients who had had a heart attack. Of those who die, a third died of brain damage. They don’t wake up after a prolonged cardiac standstill.


Let’s say a biker drops dead anywhere in London. Someone dials 999. Depending on where the ambulance is, it might take them seven to nine minutes to get there. 


Now if there’s someone who is courageous enough to try and resuscitate the biker and administer CPR, they can save a life.


In future, if someone arrives and their heart simply isn’t beating or is too weak to support the circulation, the vision would be to put them on ECMO (extra corporeal membrane oxygenation) to give us enough time to reconstitute their heart with percutaneous coronary intervention and stenting (tube-shaped device that keeps the arteries open) and possibly stem cell therapy or have a completely implantable artificial heart. That’s a vision of the future.


Initial trials of stem cells show they don’t really work as well as we hoped they would. One of the problems is that these cells are as old as the patient is. They’re taken them from the bone marrow – say you are 65 and you have a heart attack – the cells to try and rescue the heart are also 65. 


That’s one reason why stem cell therapy doesn’t work yet, but it’s a big hope for the future and possibly we will one day be able to re-programme these cells genetically to make them work. In mice, it works but it humans we haven’t seen the same effect. 


The problem with cholesterol 


And then of course, I come on to prevention. Let’s say you have an infarction (obstruction of blood supply), you go to hospital, you survive, you’re one of the lucky ones.


Over the next three years, the risk of having another ‘event’ – for example another heart attack or a stroke – is anything between 10 and 20 per cent. One in five patients will come back to the hospital because of heart failure, angina, or for another related procedure. 


The point is: the underlying disease has only been fixed for a while but the basic process, which is atherosclerosis, or cholesterol laden arteries, is progressive in nature.


So we have to stop and reverse that process if we want to be better in future. And there is a lot of hope there – the primary driver is cholesterol, and what’s interesting is our LDL levels – that’s the bad guy, the harmful type of cholesterol – in our arteries.


Compare the levels of LDL in for example mice, monkeys, rabbits and humans. It’s so much lower in other species. They don’t suffer from infarctions.


But we do. Humans are the only species in history to have extremely high LDL levels and the only species that gets atherosclerosis of the blood vessels and dies of myocardial infarction or stroke.


It’s not even dependent on diet: on average, 85 per cent of cholesterol is primarily genetic in nature while just 15 per cent comes from what we eat. Of course, if you fast like hell your LDL levels go down somewhat and, like everything, it depends on the individual.


Many years ago, we did an experiment in the team where we ate six eggs in the morning or nothing – we saw no difference in our LDL levels.


The people who are the biggest absorbers will react to changing their diet a bit better, and 15 per cent is enough to make a difference. 


Of course, it’s tempting to blame modern diets, but when they put Egyptian mummies in a CT scanner – people that died 5,000 years ago – they found they had terrible coronary arteries!


Dealing with LDL


Heart attacks are mainly about cholesterol. Of course, high blood pressure, diabetes, stress and other causes contribute too. Some people just have bad genes – something we don’t understand yet.


When it comes to cholesterol, let’s start with statins: they inhibit the pathway in the liver which produces cholesterol, so they inhibit it being produced in the first place.


Then you have the newer PCSK9 inhibitors, which help regulate cholesterol levels. Using them, we can markedly increase the amount of cholesterol which is absorbed and metabolised by the liver.


In 2003, a French-Canadian team discovered a gene mutation which codes for the protein PCSK9 which regulates cholesterol: African Americans have a ‘missense mutation’ of this protein and, in turn, low LDL cholesterol. In the future, we’ll move beyond drugs towards genetic therapy.


Soon, swallowing a tablet every day, the inconvenience of that, the worry if you forget – think about it, it’s terrible! It’s a pain in the neck, that’s why some people find it hard. 


We could end up, some day, with an injection that silences this protein once a year, maybe eventually even once in a lifetime.


Other factors


Other risk factors like high blood pressure can be treated if patients take drugs – blood pressure targets are getting lower and lower – and there’s a lot of debate about what is a normal blood pressure.


When Franklin D Roosevelt became President, he had a blood pressure of 140 over 60. Then with the pressure of the Presidency, 180 over 100, then came Hitler, and it went up further, but you can actually see it drop on 6 June 1944, D-Day when Eisenhower did a good job. His blood pressure came back to 180. 


It remained high, shot up after Yalta (the second wartime meeting of Churchill, Stalin and Roosevelt) when he died of a cerebral haemorrhage it was 340 over 190. 


Today we can easily treat blood pressure and largely prevent stroke and myocardial infarction in such patients.


Diabetes is still a big problem, and the obesity epidemic is a huge problem. There are only a few drugs that are effective against cardiac death in patients with diabetes. One inhibits the re-uptake of glucose in the kidneys, so you pee out sugar rather than absorb it. That is the first breakthrough in diabetes care.


Science fiction or near future?


Why do we get older? Why do we die? Most of these diseases that we treat are basically age-dependent. People generally do well, until they’re 40 or 50, and then problems start.


We know there are genes that prolong life and others that shorten it. When they put different animals on a low calorie diet, just a bit less than they’d like, they live longer, have less wrinkles, and baboons for example have less grey hair.


We know there are genes responsible for ageing. Take, for example, a mouse. He’s going to live, say, three years maximum, as long as he doesn’t meet a cat. If you knock out their ageing genes, they live to four.


If you think about it, evolution has held the answer all along. Some mayflies live for five minutes, some tortoises for well over 100 years.


And then you have humans. There was a paper in Nature which calculated if everything is optimal, theoretically, for example you have a mutation for PCSK9, you don’t smoke, you exercise, you have lucky genes, and so on, you would live to 115.


Which brings us onto precision medicine. In the next 20 years, we will learn so much about our genes. At the moment, we can measure all the mutations you have within a week or so. 


Eventually we will have so much information about an individual that we can personalise treatment so much better. So we’ll be able to say, ‘this guy needs a PCSK9 inhibitor, this woman needs their blood pressure lowing to 110’ and so on.


None of this is going to be cheap, and the NHS will have some difficult choices to make.


But the good news is that everything that is successful eventually becomes cheaper and cheaper. Look at coronary stents. 


When I was a young consultant, they were so expensive the whole team would talk about a patient and make the decision of whether to use one or not!


Now we do it right away, it’s normal treatment, at a fraction of what it would have cost when it was brand new.


And, while it’s certainly exciting to talk about all these new possibilities and technology, don’t forget stents are 30 years old this year, and still saving lives.

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