We are living longer but dying more slowly

We are living longer but dying more slowly 

The compression and decompression of morbidity

It is important to understand terms. Mortality is death: it is inevitable and the term “saving lives” is strictly incorrect; the term should be “prolonging lives”. The maximum human life-span is slightly in excess of 100 years; if free of disease or major injury, people would live to that age. In reality the average life expectancy in the UK during the late 20th century has been about 70 years for men and 75 years for women. During the past forty years the average life expectancy has risen rapidly by about eight years, and a much higher proportion of the population now live beyond their 100th birthday.

Morbidity is the presence of disease, or the after-effects of disease or major injury. Morbidity is illness that if it does not cause death will cause disability. It will reduce our functioning within our society or our families. It will take much of the fun out of life, although many people have a remarkable ability to have a full life despite considerable health disadvantage. There is a difference between life expectancy and active life expectancy. The compression of morbidity brings the active life expectancy closer to the life expectancy.

The Compression of Morbidity

I have read very many medical papers during the past fifty years, and I have saved and collected a few thousand of them, most as photocopies but during the past few years as pdfs. It is very important to obtain information from original research. It is also important not to forget it, or at least not to forget where to find it!

One paper that impressed me at the time was “The Compression of Morbidity”, written by James Fries and colleagues of Stanford University, California. It was published in The Lancet in1989.

It indicated a major change in the health profile of the population during the 20th century. In the first half of the 20th century people experienced several years of morbidity, that is functional deterioration, before death, usually at about 70 years of age.

Morbidity illustrated as blue shaded area

However during the second half of the 20th century things became different. People maintained good function, and death occurred after just a short period of ill-health and functional deterioration, which are recognised as being the inevitable part of “old age”. This compression of morbidity into a much shorter time at the end of life was obviously considered to be a good thing.

Morbidity illustrated as blue shaded area

Fries regarded this important change to be the result of good medicine, and especially of good public health. This was in response to McCormick and Skrabanek from Dublin, who felt that modern medicine, while being very important to individuals, was of little benefit to the population at large. The health of the population is determined by engineers and not by doctors. They give as an example seat-belt legislation; drink-driving legislation would be a similar example, and of course water engineering.

McCormick and Skrabanek worked in the public health department in Dublin. Skrabanek sadly died from prostate cancer at a young age. They challenged much accepted but incorrect wisdom, and they wrote much good sense extremely clearly, in a good Dublin tradition. Some of their work is listed at the end of this post, and it is well worth reading.

The Benefits of Modern Medicine

What is there about modern medicine that could have led to freedom from disability in the later years of life? There are several possibilities.

Perhaps the most commonly-used aid to mobility has been the aluminium walking frame, as invented in 1949 by William Cribbes Robb, of Stretford, a suburb of Manchester, England. This and similar mobility aids can be of great benefit, but they are valuable only to those who have morbidity. They do not prevent morbidity; they just help the disabled retain a small form of mobility.

Reversal of visual failure by cataract extraction and lens implantation clearly reduces morbidity. Blindness is a major cause of disability and its cure is extremely valuable. Cataracts are very common in the elderly and a large number of surgical procedures are carried out at present. 

Cataract operations USA

But this has not always been the case and it is only in the 21st century that we have seen widespread cataract surgery, but very little before the publication of Fries’ paper in 1989. This has not been responsible for a significant reduction in the morbidity of the population.

Hip (and later knee) joint replacement surgery has been perhaps the most important medical innovation to reduce morbidity. It was pioneered by a remarkable surgeon, Sir John Charnley (1911-1982), who was working in Manchester in the 1960s when I was a newly-qualified doctor. His surgical centre became Wrightington Hospital in Lancashire, England.

Sir John Charnley

A large number of hip and knee replacement procedures have been performed in recent years in the UK, 14,424 hip replacements in 2003 increasing to 83,125 in 2014, and a similar number of knee replacements. 

Hip and knee joint replacements, UK

Joint replacement surgery has undoubtedly reduced disability, sometimes in a very major way. However we can see that large-scale joint replacement is a very new development and would not have “compressed morbidity” at the time and on the scale described by Fries and colleagues in 1989.

I find it difficult to understand how medical interventions could have reduced  morbidity in the last years of life on the large scale identified by Fries and colleagues. But there is an intervention by Nature that clearly did.

The epidemic of death - coronary heart disease

Reduction of morbidity and disability in later life can be prevented by sudden and premature death at an early age. War with a large number of casualties would do this, and this happened during the first half of the 20th century. The prolonged morbidity of the population during this time, as identified by Fries and colleagues, would have been much greater without the two world wars.

However the 20th century was characterised by one of the greatest epidemics – coronary heart disease (CHD), in the UK and also described in the USA. This undoubted epidemic started in the mid-1920s, reached its peak in about 1970, and is currently very close to its end. 

Epidemic of coronary heart disease

The epidemic of CHD caused about 10 million deaths in the UK alone. It was responsible for 25% of all deaths at the height of the epidemic. Deaths from CHD occur now almost exclusively in the very elderly.

Now that the epidemic of CHD has almost come to an end, the compression of morbidity has also come to an end. This has been happening since its peak, and since 1970 about 10 million people in the UK have not died from CHD, assuming they would have done had the 1970 incidence of deaths from CHD (550 per 100,000 per annum, age standardised) been maintained. They have thus lived longer than they would have done without CHD, and many of them very much longer.

I repeat the illustration of the number of non-CHD deaths:

Numbers not dying from CHD in the UK since the 1970 peak

And also the great and exponential increase in the number who live to reach their 100th birthday:

Centenarians in the UK, projected beyond 2015

The Decompression of Morbidity

So in the pre-1980 years, men would work until the age of 65 years, live a further five or ten years, and then die, usually suddenly. Living to the age or 90–100 is different. People find that it is not possible to work after the age or 70 or 75 years, as physical deterioration then takes place. We therefore find perhaps 20 years of morbidity, from age 80 to age 100. 

We are now experiencing the “Decompression of Morbidity”. On average we are now returning to an increasing level of chronic illness and disability during several years before death after the age of 90 or 100. This is illustrated in Figure.

Morbidity illustrated as blue shaded area

This is already putting tremendous strains on the economy, and the problem is going to be much bigger. Pension funds must support not just 10 years of retirement but perhaps 30 years. This puts a burden on the working population who pay into the pension funds. 

Many of the retired will be unable to survive an independent life, but will require support at home or residential care. For both there is a cost, but more importantly there is a need for labour. Where will it come from? Importing the labour from overseas creates a “Ponzi Scheme” – it just makes the problem far worse in the future when the immigrant care-workers themselves become old.

The crisis has already happened in the UK, and no doubt in other countries. The demand for emergency admission to hospital has increased to beyond the number that can be accommodated. The elderly and frail have a longer recovery time for a given illness, the reason being a lower level of physiological reserve. Discharge from hospital might be delayed because of social factors at home. Length of stay is thus longer, with a requirement for more hospital beds. The hospital expenses exceed income and debt results. 

But again and more importantly, if there is a need for more hospital beds, from where do we obtain a greater number of doctors and nurses? Early warning of the huge increase in the number of the very elderly has effectively been ignored during the past 40 years, but to plan for this future appears to be beyond human ability.

What are the ethical considerations if we import doctors and nurses from other countries whose need for health professionals are greater than our own?

BBC February 29th 2016

The future

The present problem is very serious, and the future can only be regarded as a nightmare. It is unlikely to be possible to provide ideal social and health care when after 2030 the number of centenarians exceeds 100,000, and the number of those between 90 and 100 about three times that. This group of the population will have a level of disability and cannot be expected to be part of the workforce, a significant proportion of which will need to care for them. It is inevitable that people who are viewed as elderly but without serious disability will need to join the caring workforce, perhaps as volunteers rather than as paid staff.

Population control requires war, famine and pestilence. We have none of these at present. It is too late for simply a reduction of the number of births, and this will be necessary now only for the benefit of the 22nd century. 

Further pestilence is very likely and new epidemics will occur. But now we are able to spot epidemics very early, as international epidemiological systems are in place, mainly the World Health Organisation. Modern medicine also has a great ability to intervene very rapidly. 

Large population increases will inevitably come to an end but in rather unpleasant ways. It is difficult to know which to choose. Who wants massive casualties from another world war? Who wants famine on a large scale? Who wants pestilence? 

But coronary heart disease (CHD) was an epidemic, almost certainly the result of a pestilence. 

CHD caused very large numbers of deaths without significant suffering, mainly sudden and unpredicted death. The deaths occurred in middle age, and usually a very short time after productive work had come to an end. It certainly constrained the number of very elderly and compressed very significantly the morbidity of the population. 

In the future we might look back on CHD and view it as an advantage to the population sent by nature. 


References:

Fries JF. Aging, natural death, and the compression of morbidity. N Engl J Med 1980; 303: 130-136.

Fries JF, Green LW, Levine S. Health promotion and the compression of morbidity. Lancet 1989; 333: 481- 483.

McCormick J, Skrabanek P. Coronary heart disease is not preventable by population interventions. Lancet 1988; 332: 839-841.

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.

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.

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

I have provided a more detailed outline of ECG changes in another Post. 

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.

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. 

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.

References:

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.

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