Wednesday 23 March 2016

The population without pestilence - life after the end of the epidemic of CHD

Life after the end of the epidemic of  coronary heart disease.

Pestilence - William Blake, 1805. Museum of Fine Arts, Boston.

I have described in previous Posts that during the second half of the 20th century we experienced a very serious epidemic, that of coronary heart disease (CHD). It occurred in the UK, in the USA, and in all "western" countries. It became the major cause of death, responsible for the deaths of 25% of the population. It was clearly very serious, but not at the time acknowledged as an epidemic. People, especially men, died prematurely in large numbers before the age of 70 years. The epidemic has now effectively come to an end.

The populations of what we call the western world are now free of major diseases. Not only has the epidemic of CHD come to an end, but the risk of an individual developing a stroke has diminished profoundly, and cancer risk has also declined (the larger population means that there are more people with cancer).

There have been no major wars during the past half-century, and consequently there has been a remarkably low number of deaths from warfare. There is no famine: we are all well-fed, arguably too well-fed. We are healthier and many more of us live longer than at any time in history.

The large number of premature deaths from CHD at the height of the epidemic can be seen in Figure 1, data from 1968.

Figure 1: Profile of age of death, 1968
Men in particular show a bulge of deaths in middle age, and very few lived beyond the age of 85. The death profile for women was much better, with a wider spread of deaths throughout the latter decades of life.

These life expectancy tables were taken for granted at the time. They were natural, and a great improvement on the first half of the 20th century, when there were many deaths from what were  diseases obviously caused by micro-organisms. The fact that life expectancy for men was shorter than that for women was presumed to be the effect of smoking and alcohol, industrial and wartime injuries, and generally a more careless male approach to life.

In 1968–1970 the major cause of death in the population was myocardial infarction (MI), the most important and at that time the usually fatal clinical manifestation of CHD. This was again part of nature, the assumption being that it had always been present, an assumption that we now know was seriously wrong.

I have indicated in previous posts that the rapid decline in deaths from CHD was sudden and completely unforeseen. It was also unexplained, but of course many people assume that it was the result of medical interventions. This was not the case as most of the decline occurred twenty years before effective treatments became available.

Between 1970 and 1990 the CHD death rate in England & Wales dropped from its peak of 550 to about 100 per 100,000 per year (an 85% reduction). This was not appreciated or acknowledged at the time and it would appear that has not incorporated into health service planning.The assumption would have been that an annual; mortality rate from CHD would have continued at 550 per 100,000.

Figure 2 shows the decline.

Figure 2: Decline of deaths from CHD

What it meant was that in 1980 300 per 100,000 people in the UK did not die from CHD, that is who would have done had the 1970 mortality rate been sustained. By 1990 this was 450 per 100,000. These people would thereafter live into an older age and experience the infirmity that is inevitably part of it.

During the years 1970 to 2010 a very large number of people each year did not die, as shown in Figure 3.

Figure 3: Numbers not dying from CHD
The number of people not dying because of the end of the epidemic of CHD was cumulative year on year. In total it was about 16,000 per 100,000 of the population. With the UK population of 60 million, this represents just under ten million, during the 40 years 1970 to 2010. 

Normally with steady state population the number deaths per year equals total population divided by the average age at death. With the UK population of 60 million and with average age at death of 75, we would expect a total of 800,000 deaths per year, which amounts to 32 million deaths in 40 years. This equates to the 1970 level of 25% of deaths being due to CHD.

The increasing number people not dying from CHD represents a fairly rapid population growth, but of people mainly beyond working age and at an age of increasing health and social care requirements.

Of course not all the ten million who have not died from CHD during the past 40 years will still be alive. The population growth will not be so much, but whereas CHD usually resulted in sudden death from MI, the ten million people will experience or will have experienced a much slower process of dying, with much greater health need. 

The profile of ages of deaths in the UK can be seen in Figure 4. 

Figure 4: Profile of ages at death, 2010

The contrast with Figure 1 is remarkable. The late middle age bulge for male deaths has disappeared completely. For women there are many fewer deaths in late middle age and more in the very elderly. Note also many fewer deaths in the first year of life.

A further recent change in the age structure of the population is an increase in centenarians. The number of those living beyond the age of 100 years rose from 1080 in 1970 to 12,640 in 2010. We can see from Figure 5 that the rise is exponential.

Figure 5: Number of centenarians in the UK

Unless another epidemic occurs to control the population of the very elderly, it is estimated that the number of centenarians will be 22,000 in 2020, 90,000 by 2034, and 250,000 by 2050.

The socio-economic effects of this are already noticeable and will be increasingly so in the future.

It would appear that throughout human existence famine, war, and pestilence are necessary to control the size of the population. At the present time we have none of them.

The Four Horsemen of the Apocalypse, Pestilence, War, Famine, Death.

Wednesday 2 March 2016

The epidemic of coronary heart disease – the peak in 1967–70

CHD  in 1967–1970

Other Posts have indicated that during the 20th century we experienced an epidemic of deaths from coronary heart disease (CHD). There was a clear onset in about 1924, well defined from national data. There was a dramatic decline after 1970 in the UK, and after 1960 in the USA. This has also been well-defined from even more accurate data. The decline has occurred during my working lifetime, and I have clear memories of its peak incidence in 1970.

The years 1967-1970 were important years. The music was exciting and fashions were changing. I had just started work as a doctor. The work was demanding with very long hours (we lived in the hospital and effectively worked all the time), but it was all good fun with a wonderful environment of learning and great camaraderie. Friendships lasted a long time, as did what we learned and the vast clinical experience that we generated.

hospital doctors
Resident medical staff of the Manchester Royal Infirmary 1970.
I - the Resident Medical Officer (senior resident) - am seated in the centre on the front row

We saw many patients with rheumatic heart disease – heart failure due disease of the heart valves, in turn the result of rheumatic fever, usually in childhood. New cases were becoming rare, and the existing patients were able to benefit from the very new heart valve replacement surgery. We saw the occasional patient with heart disease resulting from syphilis in earlier life, but this was becoming of historical interest.

Perhaps the most important thing that was happening in these years was something of national and indeed of international importance that we did not understand or even think about at the time. We were oblivious to the fact that the 20th century epidemic of coronary heart disease (CHD) had reached its peak and was about to decline. 

In previous Posts I have presented much of the convincing evidence of the decline of deaths from (CHD) in the UK since the peak in 1967–1970. I have illustrated (in 2013) that in the UK we experienced an epidemic of CHD, and I have also presented details of a similar epidemic in the USA

There are many publications of the data and they all point to the same thing. The decline of CHD deaths has been rapid, spontaneous, international, and unexplained. The assumption that medical and public health interventions have been responsible for the decline cannot be correct if we consider the years 1970–1990, the time of the most dramatic decline of deaths.

Figure 1: The epidemic of CHD in the UK

For those of us working in acute medicine in1970, the scene was both dramatic and tragic. I qualified in medicine in 1966, and in 1970 I was the Resident Medical Officer (RMO) of the Manchester Royal Infirmary, a very busy teaching hospital with a large number of emergency admissions. Every day we would see patients admitted on account of an obvious and severe heart attack, the more precise medical term being myocardial infarction (MI). 

Figure 2: The heart and the coronary arteries

Myocardial infarction means literally death of heart muscle (myocardium) due to interruption of its blood supply. This is in turn is the result of a blockage of one of the branches of the two coronary arteries (right and left) that supply the heart muscle with blood. The name "coronary" is given because they form a coronet (crown) around the upper part of the heart. The underlying disease of the coronary arteries is atherosclerosis causing perhaps an 80% obstruction, with a fresh blood clot giving rise to a complete blockage of the artery and subsequent myocardial infarction.

Not only would we see the patients presenting as emergencies, but we would see the pathological details in the autopsy room, most of the deceased having experienced sudden death before admission to hospital. The epidemic of CHD was dramatic and catastrophic. Suddenly and for the first time, heart disease became by far the most common cause of death. Men and women died in their prime. 

The patients with MI were usually men of working age. They had experienced severe sudden crushing chest pain, and they had usually been in good health previously. They looked very ill, and on immediate examination they were cold and clammy, gasping for breath, and with low blood pressure. The diagnosis was easy but would perform an electrocardiogram (ECG) and this would show dramatic abnormalities, the characteristics of MI.

ECG changes

Figure 3: the normal ECG and its constituent wave-forms

The normal ECG (Figure 3) shows a P wave, representing atrial depolarisation and contraction, a QRS complex, representing venticular depolarisation and contraction (systole), followed by a flat ST segment, and a T wave that represents repolarisation (electrical recovery) of the ventricles.

Figure 4: Obvious ECG changes of Myocardial Infarction, an everyday occurrence in 1970 but seen only rarely today

In the many patients with acute MI who we used to see, the ECG changes were not subtle but were very obvious, with indications of serious and extensive damage. We would see immediate ECG abnormalities as shown in Figure 4, namely  a small Q wave (initial down-stroke) with high ST segment and large T wave. The changes are so clearly different from the normal ECG in Figure 3.

During the few next hours the changes would progress to a deep Q wave, flattening of the ST segment and inversion of the T wave. The loss of the upright R wave and the change to a deep Q wave indicates death of a significant proportion of heart muscle.

Figure 5: ECG showing changes of MI in the recent or distant past

If a patient had a history of a previous MI, then an ECG abnormality such as in Figure 5 would pose the problem as to whether it would be a historic abnormality or an indication of a recent MI. In this situation the ECG would be of limited value. Another test would be necessary - a blood enzyme test. 

When heart muscle cells are damaged or die as the immediate result of an MI, proteins leak out of the cells into the blood and there they can be detected and measured. The first of these to be identified was  the enzyme creatine kinase (CK-MB), and in the clinical context of chest pain, elevation of its blood level would indicate an MI. But CK-MB also appears in the blood after injury to skeletal muscle, even after an intramuscular injection. The next abnormal blood protein indicator to be identified was troponin, which was more specific for heart muscle.

myocardial infarction
Figure 6: enzyme rise following MI

In more recent years

I have described the common problem in 1967–70, a patient with an MI, ECG showing an elevated ST segment, whether or not a Q wave had appeared. This is now called a STEMI, meaning ST Elevation MI.

In 1967-1970 the mortality rate at onset of MI was almost 50%, and in those who survived long enough to attend hospital it was about 35%. There were few overall survivors.

In addition there are patients with chest pain that sounds like an MI, with the patient not being obviously ill, and in whom the ECG would be normal. Such patients have become increasingly common since 1970, during which time severe MI has become more rare, but health awareness more important and hospital attendance more common. 

The diagnosis - "ruling in" and "ruling out"

The ECG is not always of definite diagnostic value: an abnormal ECG can "rule in" an MI if the changes are new and appropriate, but it cannot "rule out" an MI if it is normal. This is a common problem with many medical tests, including X-rays and scans. In this case we find that the ECG has "high specificity" (no false positives – if a positive ECG then a certain diagnosis) but "low sensitivity" (many false negatives – a ECG might be normal in the presence of MI). 

To "rule in" the diagnosis of MI in someone with chest pain and a normal ECG, the enzyme blood test is necessary. If there is a strong clinical suggestion of an MI and the result is elevated, then a diagnosis of MI would be made. This would be a NSTEMI, meaning Non ST Elevation MI, in other words effectively a normal ECG

The troponin test is more specific of MI than is CK (fewer false positives) but it also more sensitive, meaning that more MIs are diagnosed. 

Changing diagnosis of MI

In more recent years the troponin test has been replaced by the high-sensitivity troponin-T  (HsT) test. This is even more sensitive and so even more people with chest pain and a normal ECG are now diagnosed with MI (NSTEMI) than would have been the case in the past. 

Does this matter? In the past a large numbers of people with chest pain, normal ECG and normal CK or troponin would have left hospital with a diagnosis of “Chest pain ? cause”. Research has shown that such people would have an excellent outlook with a low risk of death or MI in the next few years [1]. Some of these people are now likely to receive a diagnosis of MI (NSTEMI).

The definition of MI has clearly changed in the 21st century and so changes in the incidence of MI are far from clear. We should only compare like with like. The  change in diagnostic criteria of MI will  inevitably increase the number of people diagnosed, what is called "disease creep", or "patient mongering". 

What is clear is that the number of deaths from MI and CHD have declined enormously. This is of the greatest importance, as death has been the major effect of MI and CHD, and the definition of death has fortunately not changed !

Death rates

In 1970 sudden death was a major manifestation of MI, perhaps more common than chest pain. Those who survived to be admitted to hospital were still at great risk of death. It is scarcely believable now that patients with MI had a hospital mortality rate of about 35%. The death rate dropped rapidly from the hectic days of 1970, probably due to a combination of new medical interventions but mainly because the disease became much more mild. We can see in Figure 5 the reducing mortality rate, and also the higher mortality rate in the older age-group [2].

Figure 7: In hospital case-fatality rate following MI

There were two reasons for death. One was that such a large part of the heart muscle was irreversibly damaged and so the heart could not function adequately to sustain life. This was left ventricular failure (LVF) or cardiogenic shock. Once common, this is now rare. Unfortunately heart muscle cannot regenerate.

The other is “cardiac arrest”, well known to all. Sometimes the heart has stopped completely (cardiac standstill, or asystole). More common is ventricular fibrillation – the heart is shimmering with no no co-ordinated contraction, no function and no beat. 

Figure 8: ECG of Ventricular Fibrillation

This can however be reversed by electric shock - defibrillation - which co-ordinates the contraction of muscle fibres of the heart. It can but might not always restore the normal rhythm of the heart.

CPR and the CCU

The peak of the epidemic in1970 saw the introduction of cardio-pulmonary resuscitation (CPR). It involved, and it still does involve, external cardiac massage and intermittent inflation of the lungs. 

The defibrillator was invented, by Dr Frank Partridge and Professor John Anderson at the Royal Victoria Hospital, Belfast. The first models were very large, and I remember the first one that I saw and used in Manchester. There was just one for the hospital. It was large and on a trolley. Racing from one ward to another with it was dramatic and time-consuming. 

Figure 9: Defibrillator from Belfast, 1967

The next step was to concentrate the patients with MI on to a newly developed coronary care unit (CCU) so that cardiac monitoring would identify VF or other serious rhythm disturbances hopefully before the patient were to collapse, and then the specialist nurses, the doctors and the defibrillator would be available immediately. This was all new in 1970, the peak of the epidemic.

Community CPR

As defibrillators became miniaturised, more of them could be placed around the hospital, and later outside the hospital in strategic community places, such as squash courts. In the final decades of the 20th century we would still hear of middle-aged men collapsing and dying while playing squash, but that does not seem to happen now. 

Figure 10: modern defibrillator
There is a great awareness of CPR in the community as a whole, and many people have attended CPR courses. I would imagine that the great majority of such defibrillators would not have been used, and they would be very intimidating to potential general pubic users. 

The other task is the identification of ventricular fibrillation. This initially required an ECG recording with immediate interpretation (Figure 8). Further developments of the defibrillator have included an active ECG recording, and later automatic defibrillation as the machine itself will identify VF.

Temporary pacemakers

In the 1970s and into the 1980s, one of the dangers following an MI was “heart block”. The pulse would become very slow and the patient’s condition would deteriorate rapidly. 

What happens is a blockage of transmission of the normal electrical impulse throughout the heart, from the right atrium to the ventricles. This is due to damage to the conduction tissue that is embedded in the heart muscle. The atrial beats (P waves) occur regularly at a normal rate of about 70 per minute, but the ventricular beats (QRS complexes) occur in a detached way, and at a slower rate of about 30 per minute .
Figure 11: ECG of complete heart block

It would be essential to increase the ventricular (pulse) rate back to about 70 per minute. The way to achieve this would be the insertion of a temporary pacemaker. This involves passing a wire through the veins from the ante-cubital fossa on the arm, the front part of the elbow from where blood samples are usually taken. The wire is passed through the veins under X-ray screening until it is positioned in the apex of the right ventricle. The battery-powered pacemaker unit is then attached and a rate set, usually 70 per minute. The stimulus from the pacemaker gives regular ventricular pulsation.

Figure 12: position of a temporary pacemaker wire

Many of these were used in the 1970s and early 80s. Heart block was a major and fairly frequent complication of MI. Usually the heart block recovered after a few days and the pacemaker wire was then removed. Sometimes there was no recovery and so a permanent implanted pacemaker was necessary.

The senior resident staff of the hospitals became very skilled at inserting pacemakers, and would be undertaking about three procedures per week. But suddenly, at the end of the 1980s, the demand fell to about one per month, or then even fewer. This meant that outside the cardiology department no doctor had adequate training or experience. It was further evidence that MI was becoming a much milder disease.

Medical contributions

The numbers of patients with definite or suspected MI was greater than the new CCUs could accommodate. Many were on general medical wards, and as rhythm disturbances of the heart were common and recognised as important, cardiac monitors were frequently to be seen at the bedside. The patterns and bleeps were valuable to the doctors, and in addition they were intriguing to the visitors. 

Much more was necessary on the CCU other than awaiting and then reversing VF. The challenge was to prevent the occurrence of VF.

There were various fashions for medical suppression of VF, using for example intravenous lignocaine. It fell out of use after a trial in 1972 showed that it had no advantage over just intravenous saline.

Also intravenous glucose and insulin were used, given to stabilise heart muscle cells by increasing intracellular potassium. Subsequent research showed no advantage.

Many other medications and interventions were used:
  • pacemakers
  • warfarin (anticoagulant)
  • aspirin, clopidogrel (anti-platelet) 
  • thrombolytic agents (“clot-busting drugs”)
  • clofibrate (cholesterol-lowering)
  • statins (cholesterol lowering, and other more important effects)
  • stents
Details of these treatments will be in a different Post.

The decline of MI and CHD deaths.

A major reduction of the incidence of MI has occurred, but most people seem to be unaware of this. It has however been clear, not just from national statistics (which perhaps few people read) but also from the observations of those in practice during the height of the epidemic. 

The reason for the rapid decline of deaths from CHD is not explained. In fact in 1978 there was a Bethesda Conference in the USA to try to identify the reason for the decline in CHD deaths. As a result the MONICA (Multinational MONItoring of trends and determinants in CArdiovascular disease) project was set up to search for an explanation [3]. Twenty years later the report stated that the decline was the result of a decline in CHD events as well as a reduction in the mortality rate following a CHD event. That is as far as the explanation went [4].

Figure 13: decline in CHD deaths in the USA

A contemporary report from New Zealand recorded a 20% reduction in coronary heart disease mortality in the 13 years following 1968. The data from this study suggested that: "Factors other than the improved care of myocardial infarction patients are responsible for the decline in coronary heart disease mortality rates in New Zealand." [5]

Professor John Hampton of the University of Nottingham, UK, reported in 1982 on the 25% reduction of mortality from CHD in the previous decade. He suggested that the reduced mortality rate was apparent before there were any substantial alterations to what were generally thought to be the causative factors, and certainly before the introduction of effective medical interventions [6].

The reduction of death rate following MI at its peak in about 1970 was clearly remarkable. MI became not only a less common, but also a much milder disease. What newly qualified doctors see in the hospitals today is just a shadow of what I saw in 1970.

We can see this below. Figure 14 shows the present mortality pattern of the population of England and Wales. It comes as no surprise that the older we get the more likely we are to die.

Figure 14: Mortality pattern of the population in 2010
However things were very different in 1968, at the time described in this post and when I was first working as a young doctor. We can see in Figure 15 the huge bulge of male deaths between the ages of 40 and 80 years, and a less pronounced bulge in the death profile for women. 

The effect of the epidemic of coronary heart disease
Figure 15: Mortality pattern of the population in 1968

The disappearance of the bulge of deaths in adulthood is due to the disappearance of CHD as a major cause of death in this age-group. Most CHD deaths are now above the age of 85.

Why did CHD become milder? Why did it decline? Why is it now so uncommon below the age of 80 years? Where did it come from?

There is no acknowledged conclusion but I will present the possible explanations in a future Post.


1. Wilcox RG, Roland JM, Hampton JR. Prognosis of patients with "chest pain ?cause". Brit Med J 1981: 282; 431-433.

2. Dalen JE, Alpert JS, Goldberg RJ, Weinstein RS. The epidemic of the 20th century: coronary heart disease. Amer J Med 2014: 127; 807-812.

3. National Institutes of Health. National Conference on Health Research Principles, 3 and 4 October, 1978: conference report. Bethesda, Department of Health, Education, and Welfare. Public Health Service, National Institutes of Health, 1978.

4. Tunstall-Pedoe H, Kuulasmaa K, Amouyel P, Arveiler D, Rajakanyas AM, Pajak A. Myocardial infarction and coronary deaths in the World Health Organisation MONICA project. Circulation 1994; 90:582-612.

5. Stewart AW, Beaglehole R, Fraser GE, Sharpe DN. Trends in survival after myocardial infarction in New Zealand, 1974 – 81. Lancet 1984; 324:444-446.

6. Hampton JR. Falling mortality in coronary heart disease (editorial). Brit Med J 1982; 284:1505-1506.

A simple view of the ECG

A simple view of the electrocardiogram (ECG)

This Post should be taken together with the Post entitled:
"The epidemic of coronary heart disease – the peak in 1967–70”.

We have all heard of the ECG, and today everyone will have seen
the ECG in use in health centres, in hospitals, or on television programmes. We are accustomed to seeing paper traces, and on the television programmes flashing lights and electrical traces.

There is no necessity to go into details and I will indicate only the basic features. The reason for doing this is that many of my Posts have been on the subject of coronary heart disease (CHD), the major clinical consequence of which is myocardial infarction (MI), loosely called a heart attack. The ECG is a major defining feature of the MI. A Post on this subject will appear shortly and so I have written this Post on the ECG in anticipation. To include clinical MI details and details of the ECG in a single Post would be cumbersome.

The normal ECG

The standard ECG has 12 simultaneous recordings taken from nine leads, each looking at the heart from a different direction and therefore able to detect abnormalities in different parts of the heart. I will not go into any detail, about these 12 recordings.

The normal ECG shows three components:

  • the “P” wave results from contraction (electrical depolarisation) of the atriums (atria);
  • the “QRS” complex results from contraction (electrical depolarisation) of the ventricles;
  • the “T wave” results from recovery (electrical repolarisation) of the ventricles.

The QRS complex has three components, Q,R and S. 

  • Q is an initial downward (negative) deflection of the recording. This does not occur in the normal ECG, except certain leads that need not concern us. It appearance usually indicates serious damage.
  • R is an upward (positive) deflection. it is usually the initial part of what is effectively an RS complex. It can however follow an initial Q wave.
  • S is a downward (negative) deflection that follows an R wave. It is not always present.

It might be asked as to why the nomenclature of the waves is in the form of the letters “P….T”. The answer lies in the history of the electrical recording of the heart. 

The Heart

There is no necessity to go into the structure of the heart in detail, just a reminder of the circulation sequence of right atrium, right ventricle, pulmonary artery and circulation through the lungs, then left atrium, left ventricle and aorta leading into systemic circulation.

The relaxation phase of the ventricles (diastole) sucks blood into the right and left sides of the heart, and then the early contraction of the atriums (the P wave) completes the filling of the ventricles with a final “push”. The contraction of the ventricles follows (systole) with ejection of blood into the pulmonary and systemic circulations.

The heart has a natural pacemaker to control its rate to to stimulate an orderly contraction. It is called the sino-atrial (SA) node and it is situated in the right atrium, at the point of entry of the major veins, the superior and inferior vena cava.

Electrical conducting tissue of the heart

Spread of electrical impulse within the heart

The electrical impulse that stimulates contraction of the heart muscle starts in the upper part of the right atrium and spreads across both atriums. It is picked by a secondary pacemaker, the atrioventricular (AV) node, which is situated it the junction of the atriums and the ventricles. This passes the signal though two bundles of conductive tissue, one in the wall of each ventricle. These stimulate an orderly contraction of the ventricles.

How the heart works

During the 1780s Luigi Galvani (1737–1798) at the University of Bologna, followed by Alessandro Volta (1745–1827) discovered that muscles contract (twitch) in response to electrical stimulation, the “frog legs experiments”. The interaction between electricity and muscles was far from clear, but during the following century it gradually became more clear.

Luigi Galvani

Alessandro Volta

In the 1880s it was realised that the heart muscle, like skeletal muscle, worked by electro-chemical processes. Chemical reactions created an electric potential (like in a battery) and sudden release of that electric potential (depolarisation) enabled immediate muscle activity, that is contraction as that is what muscle do. Following this muscle action the chemical process would re-charge the electric potential within the cells of the heart muscle, the process of repolarisation).

We can see this in the ECG: the first thing that happens is the P wave. This is a recording of the electrical depolarisation of the atriums (preferred international English, otherwise atria). The muscle bulk of the atriums is low and so the P wave is of very small amplitude. There is no visible wave produced by the repolaristion of the atriums  as  it coincides with the QRS complex that represents the depolarisation of the ventricles.

The QRS complex is followed after a brief delay (technically the Q-T interval) by the T wave, representing the repolarisation of the ventricles. There is then a rest until the next heart beat, the next P wave.

The depolarisation of the ventricles leads their immediate contraction and thus the blood within the ventricles is ejected into circulation, from the right ventricle into the pulmonary artery and thus through the lungs, and from the left ventricle into the aorta. The muscle of the left ventricle is of much greater thickness than the right (the blood must be propelled a much greater distance and against a much greater pressure) and its depolarisation makes the dominant contribution to the QRS complex.

The history of the ECG

The slow advances during the 19th century of the understanding of the physiology, the functioning, of the heart led to some practical albeit rudimentary developments. The British physiologist Augustus Waller (1856–1922) was a lecturer at St Mary’s Hospital, London. In 1870 he invented a device for recording the electric activity of the heart. He used “A,B,C….” to identify the recorded phases of the heart beat. He used a capillary tube filled with mercury to identify the electrical impulse of the heart, a change in height of the mercury column allowing a pattern to be observed.

Augustus Waller
Willem Einthoven

In 1902, the Dutch physiologist Willem Einthoven constructed a different type of machine, a string galvanometer, which was very cumbersome and required five men to operate it. When it came to a side-by-side assessment of the two machines, the wave-forms on Einthoven’s ECG were given the symbols “P,Q,R,S,T”. Despite being of no practical value in respect of patient care (remember that Einthoven was a physiologist and not a clinical cardiologist) it proved to be a superior method of recording heart  activity and its nomenclature has persisted. It was about 15 years later that the ECG came into clinical use, and the machines have become much smaller over years.

Einthoven's ECG machine, 1902

The use of the ECG

Early concerns were of the functioning of the heart, and they were purely academic studies. Coronary heart disease (CHD) and myocardial infarction (MI) were almost completely unknown at the time of Waller and Einthoven. 

Earlier, before his fame and knighthood, Sir James Mackenzie (1853–1925), the father of English cardiology, was working in Burnley, Lancashire, and at its hospital (where I worked). He invented a mechanical “polygraph”, a device that recorded the rhythm of the heart. 

Sir James Mackenzie

The subsequent electrical recordings were superior but it was only the rhythm of the heart that was of clinical importance. 

Abnormalities of heart rhythm

The most well-recognised abnormality of rhythm is atrial fibrillation AF). The characteristic of this is a complete irregularity of the pulse, which might become very fast. If this is the case then the pulse will also be low in volume. The output from the heart (cardiac output) is low because the filling phase of the heart (diastole) is too short to allow the ventricles to fill adequately with blood. Also the final push of filling, atrial contraction, is absent.

Atrial fibrillation is a failure of the atriums to contract properly because they are “fibrillating”, that is very rapid unco-ordinated contraction of individual muscle fibres (cells). There are no P waves. The spread of the electrical impulse from the SA node into the atriums is impaired. The response of the ventricles via the AV node is haphazard, and so the ECG shows an irregularity of the QRS complexes.

ECG: atrial fibrillation

It was for the treatment of atrial fibrillation that Digitalis was introduced by the Birmingham-based botanist and physician William Withering (1741–1799). This treatment was an extract of the plant Digitalis purpurea (common foxglove) and was based on a folk medicine for the treatment of “dropsy”, this being oedema or swelling of the legs due to heart failure, atrial fibrillation often being associated.

William Withering

Also common are ventricular ectopic beats, that all people might experience as a “missed beat”. They are only very rarely of importance. A ventricular ectopic beat occurs spontaneously, not triggered by or following an atrial beat. The ECG will show a QRS complex, out of sequence with the others and not preceded by a P wave. The QRS complex is likely to be a different appearance depending on the part of the ventricle from which it originated.

ECG: 2 ventricular ectopic beats

The atrial beats and ventricular beats can become disconnected, and this is called “heart block”. The P waves will be present and also the QRS complexes, but the sequence of them is random. The AV node is not picking up or transmitting the stimulus from the atriums. The ventricles will develop their own rhythm, but the rate becomes very slow. This causes problems such as blackouts, and an implanted artificial pacemaker is necessary to speed up the heart.

ECG: complete heart block, dissociation of P waves and QRS complexes

Finally for our purposes there is ventricular fibrillation (VF). The ventricles just fibrillate like jelly wobbling. There is no actual contraction of the heart and this is what happens in a “cardiac arrest”.

ECG: ventricular fibrillation

The ECG in CHD and MI

It was only in the 1920s that the ECG was used in the diagnosis of MI as it was only in that decade that the disease appeared. 

The ECG recorded from an individual tells us of events that have happened in the past - ten seconds ago or ten years ago. There is no prediction of the future.

Similarly there is no feature of CHD as such. CHD is a disease (atherosclerosis) that takes place in the arteries on the surface of the heart. The ECG tells us about damage to the heart muscle and the conducting tissue within the muscle.

Only when something is happening either now or in the past does the ECG become abnormal. Someone can have a normal ECG today but develop an MI tomorrow. We cannot predict future health from an ECG. There is no reassurance value from a “routine” ECG performed at a time of good health.

The detection of MI is the main use of the ECG, after identification of rhythm disturbances. It is quite simple and there are two specific changes.

A Q wave might appear, and this indicates major damage to the heart muscle. It is a permanent abnormality and remains as a historical marker of an MI in the past. When a Q wave is seen it cannot be concluded that an MI has just occurred. This would only be the case if it was not present on a previous ECG, or after other tests have been performed. A Q wave resulting from MI is often followed in the long term by an inverted T wave.

ECG: Q wave followed by inverted T wave

ST segment elevation after an MI is a temporary abnormality at the time of the event. If the ECG is delayed after the development of chest pain, the ST elevation might be missed, having resolved rapidly.

ECG: ST segment elevation, also small Q waves

When the Q wave is associated with ST segment elevation the diagnosis of an acute MI is clear. This is a "STEMI", ST Elevation MI.

ECG: small Q wave with high ST segment elevation

The ECG in angina

Angina used to be a disabling but not fatal result of CHD. It is recurrent chest pain occurring on exercise, due to a narrowing of a coronary artery. The ECG at rest is normal, but on exercise ST segment elevation might occur (the exercise ECG). There can rarely be transient elevation of the ST segment at the time of a severe attack of angina.


I hope that this brief review of the ECG is informative but not incomprehensible.