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

CHD  in 1967–1970

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.

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.

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.

The 20th century CHD epidemic - report from the USA

Tucson, Arizona

Several of my Posts refer to the epidemic of coronary heart disease (CHD) that occurred in the 20th century, and which is now almost over. I reported this in the medical literature (Quarterly Journal of Medicine) in 2012.

People may question my assertion that there has been an epidemic of CHD, but as I have mentioned previously the evidence is well documented. The national documentation requires a level of organisation which is not always present but it is present in the highly sophisticated civil service of the UK and the documents are readily available. The national registration of deaths has been present since the late 19th century, and the great advantage of the NHS is that vast quantities of data have been created and saved.

I have just come across a publication from a medical team from the University of Arizona School of Medicine, concerning “The 20th century epidemic of CHD”. It was published in 2014 in the American Journal of Medicine. The study is based on exclusive USA data and no reference is made to my earlier work, which used mainly UK data.

It mentions that “heart disease” was only the fourth common cause of death in the USA in the early years of the 20th century, but by the middle of the century it had become the most common cause. It did not identify rheumatic and syphilitic heart disease which were present in the early years, but they were declining as causes of death. The deaths from these causes would have reduced to zero by 1970. Something new was appearing to increase substantially the total number of deaths from heart disease.

Working in Chicago, Dr James Bryan Herrick (1861-1954) was in 1912 the first to diagnose myocardial infarction (MI), the most serious and important manifestation of CHD. This is a sudden episode of severe chest pain with collapse and high risk of early death, loosely called a “heart attack”. The clinical diagnosis was straight-forward but it required pathological corroboration from autopsy evidence to understand the condition. A few years later Herrick was one of the first to use the electrocardiogram (ECG) as an aid to diagnosis of MI. Herrick was also the first to identify Sickle Cell Disease, initially called Herrick’s Disease.

But the diagnosis did not just depend on clinical features and ECG. The condition had a high mortality rate. Pathology was of supreme importance and the autopsy was a vital way to learn.  At the time imaging procedures were effectively unknown, X-ray machines identifying only major damage to bones. 

The correlation between clinical features and findings at autopsy (clinico-pathological correlation) was a major part of medicine until very recently. Whereas in the earlier years of the 20th century the ward round would end in the autopsy room, in later years it would end in the X-ray imaging department. Continuous learning is integral to clinical medicine and looking inside the body is part of this.

And so the pathology of MI, and CHD in general, became well established during early part of the 20th century. The emergence of CHD, the new epidemic, was clear and beyond dispute. There were those who wondered how they could have missed the diagnosis in the years before the First World War, but although they did not fully understand this, the disease was simply not present at that time.

Figure 1. Decline of deaths from CHD in the USA

The emergence of a new disease was certainly a mystery, but during the first half of the 20th century there were more important events in the USA and Europe, such as two world wars and a catastrophic economic depression between them. As Dalen and colleagues point out, it was the subsequent sudden decline in deaths from CHD in the late 1960s, clear from good quality national data, that caused surprise.

Figure 2 The rise and fall of deaths from heart disease in the USA

The data is not entirely clear. Figure 1 shows deaths from CHD per 100,000. I assume that the data are age adjusted but this is not stated. Similar for Figure 2, but this shows all heart deaths and not just CHD. There is no data given for specific CHD deaths before the 1965 peak but the increase in total heart deaths was clearly due to the emergence of the new CHD.

The peak of CHD deaths is identified as 466 per 100,000 per year, slightly lower than 522 in the UK. The peak in the west of Scotland was an astounding 960 deaths per 100,000 men per year. The decline of heart disease deaths in the USA appears to be only to 130 per 100,000 per years, but this is total deaths. Although the overall decline is the result of many fewer CHD deaths, in the UK the CHD deaths had declined to only 40 per 100,000 per year (age adjusted) in 2007.

Dalen and colleagues also report autopsy findings in US soldiers killed in wars. In the young men who died in the Korean war (1951–1953),  pathological evidence of CHD was found in 77%. This had fallen to 45% in those who died in the Vietnam war (1968–1978), and to 8.5% in those who died in the Iraq and Afghanistan wars (2000–2011). There is clearly a major decrease of the pathological basis of CHD, corresponding to the decrease of deaths in the general population.

Figure 3: CHD findings at autopsy in young US soldiers killed in wars

The clinical consequences of CHD were diminishing at the same time, as judged by the decline of admissions to hospital on account of sudden onset of MI.

Figure 4: Admissions to hospital in the USA on account of MI

It is interesting to note that the decline was slightly earlier in the younger age-group (<65). This suggests a cohort effect – exposure to the cause was lower or modulated in those born later.

It is also interesting to note that CHD became a milder disease during the years after about 1970, and this is born out by doctors such as myself who were in clinical practice at that time.

Figure 5: Inpatient death rate following admission for MI, USA

The milder nature of CHD can be seen in the rapid reduction in hospital mortality rate. It is remarkable now to imagine a 37% mortality rate for those admitted on account of MI in the years slightly before and after 1970. This high mortality rate was also recorded in the UK literature at the time, and I remember it well.

And so putting together Figures 3, 4 and 5, we can see that there has been a major reduction of CHD, judging from autopsy and clinical data, a major decline in the incidence of MI, and also a major  decline in the case-fatality rate of those admitted to hospital on account of MI. The result is a major reduction of overall death rate from CHD. These were also the findings of the long-term MONICA project, set up in 1973 to try to find an answer to the mysterious decline in deaths from CHD.

It is very important that in their paper Dalen and colleagues recognise that there was a true epidemic of CHD - that there was a sudden onset, a peak and then a rapid decline. It would be a great contribution to knowledge and research if the epidemic were to be acknowledged generally. There are however many “epidemic deniers”, who assume that CHD has always been present.  This means that they need not consider its emergence, but this is clearly very important if we want to understand its decline. Those who deny the epidemic of CHD are obviously completely ignorant of the very clear data.

There have been reports of arterial disease being found in Egyptian mummies. Although this has given apparent justification to the epidemic deniers, it is not the same thing as CHD and it must not imply that CHD has been continuous during the past 4000 years.. There is no reason to assume that there has been only one epidemic of CHD in recent years and particularly in the distant past.

Figure 6: The 20th century epidemic of CHD in the UK

The observation of an epidemic is clear. The next stage is speculative, to consider possible causes, to produce hypotheses that can be tested by continuing research.

This will best be developed in another post.

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The decline of deaths from Coronary Heart Disease worldwide

The decline of the epidemic of CHD

Many of my Blog Posts refer to the 20th century epidemic of coronary heart disease, CHD. Many people must wonder if I have got it all wrong. Was there really an epidemic? Why do we not read of this "epidemic" elsewhere?  I also fail to understand this - surely other doctors and other observers must have read the original articles in the extensive medical literature. But sadly, perhaps not.

A new and recent publication in the International Journal of Epidemiology (reference at the end) was brought to my attention this week by my friend Dr Luca Mascitelli. The study looks at the decline of CHD deaths since 1980 in the countries of UK, Australia, Sweden, USA, Canada, Spain, France, Japan. 

Precise records of death require sophisticated medical services and also national public health and reporting systems. These are not always present and so it is necessary to obtain data from those countries where they do exist. The countries included in this study provide a large data set, as accurate as it is possible to be. 

It is clear from this study that there has been a major decline of age-related CHD deaths internationally, by up to 80% between 1980 and 2007. The title of the study suggests a follow-on from the Seven Countries Study, that we have seen. Now that epidemiology is much more sophisticated the new study is of much better quality and its findings are much more reliable.

The higher the incidence of age-related CHD deaths in 1980, the greater is the subsequent proportionate fall. This is an international phenomenon. There are of course countries, not in this study, in which CHD deaths do not appear to have presented an important public health problem. This could be a reporting problem but if present, then CHD would have been overshadowed by many other diseases.

The decline of age-related CHD deaths is substantial and universal, in men and in women, as shown in Figures 1 and 2.

Figure 1 CHD change in men, 1980-2007

Figure 2 CHD change in women, 1980-2007

We can also see the absolute decline, expressed as age-adjusted death rate per 100,000. In Figure 3 we see the death rates in men. Each county is represented by a series of vertical columns, each representing a period of time. All show a progressive reduction of death rate.

Figure 3: reductions in CHD death rates for men, 1980-2007

In 1980 the highest death rate from CHD was in the UK, with USA, Sweden, Australia and Canada close behind. Spain and France had lower rates of CHD deaths, and this well-known. In all countries in the study there was a major decline.

Japan is the outlier as usual with a very low number of CHD deaths. This is probably due to a high fish diet and location of most of the population at a low latitude fairly close to the equator, giving good exposure to the sun which also provides good vitamin D levels. The decline of CHD deaths was also seen in Japan, as part of the international trend.

Figure 4 shows the same trends in women. Please note that the numbers on the vertical axis are different. Compared with Figure 3 we can see that the death rate in women has been only about one third that in men. This is also well-known.

Figure 4: reductions in CHD death rates for women, 1980-2007

The decline in CHD deaths has been well and repeatedly documented. Our risk of dying from CHD is  now low, and this is why there are so many people living so long. The new epidemic is that of very old age, the elderly now being those who 40 years ago by good fortune did not not die a premature death from CHD, a fate that at that time was experienced by many. 

I stress that the mortality data are age-adjusted. There is no useful purpose in comparing the mortality rate of 50 year-olds at one time or place with 75 year-olds at another. People still die of CHD today, but they are mainly the very old, age greater than 75. We can see this clearly in Figure 5.

Figure 5: Deaths from CHD in the UK in 2010

It is interesting to note that above the age of 75 the current risk of dying from CHD is equal between men and women. Figure 5 shows the number of actual deaths in 2010 and not death rates. The equal numbers might reflect the fact that there are more women than men in this age-group.

It is clear that people below the age of 75 years, those born in the second half of the 20th century, are at much less risk, and that risk has probably diminished progressively during this time.The high risk of CHD appears to be among those born before, during or shortly after World War 2, a "cohort effect". It is as though there was during that time an environmental agent that has either disappeared or to which we have developed immunity.

The data in the study that we having been viewing started at 1980, but the death rate had been declining in the UK and the USA since 1970. The decline of stroke deaths started slightly earlier in about 1960 (Figure 6).

Figure 6: decline of cardiovascular mortality in the USA, expressed as percentage change each year

In the UK, the age-adjusted mortality rate in men in 1980, as shown in the present study (Figure 3), was 460 per 100,000, whereas in 1970 it was 520, representing 11.5% decline in ten years. 

Two important papers were presented in the UK documenting the decline of CHD between 1990 and 2002, in both men and women, and extrapolating (perhaps without justification) to the end of the epidemic by about 2020. The first was a report by the UK Government Department of Health. It was very much a "snap-shot" looking at just a twelve-year period.

Figure 7: Decline of CHD deaths in the UK, 1990-2002

The second was a paper written by Dr John Appleby, chief economist of the UK King's Fund for the study of health. He reported the decline of CHD death rates  between 1979 and 2007, comparing the UK with France. The latter started at a much lower level and so as the graph lines came together the proportionate fall in France was much less.

Figure 8: Decline of CHD deaths in the UK and France, 199-2007

But there is another aspect to the recent paper in the International Journal of Epidemiology, as appears in the title:

The low number of CHD deaths in Japan, compared to Europe, North America and Australia, was perhaps first brought to attention in the Seven Countries Study. The explanation generally given is that it is the result of a low animal fat and a high fish diet of the Japanese. The average blood cholesterol levels in Japan were also noted to be low, and these findings became an important foundation of the diet-cholesterol-heart hypothesis, which we now know to be seriously flawed and not viable.

In the present study, it was found that whereas in Japan the CHD death rate went down in men by 27% between 1980 and 2007, the average blood cholesterol level rose. This was not expected as the levels had gone down slightly in other countries. We can see the change in Figures 9 and 10. The graphs shows the average total cholesterol levels in the blood for the four age-groups shown for the years 1990 and 2008. 

Figure 9: Average blood cholesterol level by age, Japan, Men

Figure 10: Average blood cholesterol level by age, Japan, Women

This finding could have led to the conclusion that the findings in Japan, and also the worldwide reduction of CHD deaths, were incompatible with the diet-heart-cholesterol hypothesis, which would therefore be invalidated. However I suspect that this was not mentioned in the paper as such a controversial view could not be published.

The reason for the declines are usually stated to be the result of medical, pharmaceutical and public health interventions. There is no question that there has been a substantial reduction in cigarette smoking, and this was recorded in the paper. The reductions ranged between 7.1% in French men and 25.5% in Japanese and Canadian men, whereas in women there was a maximum reduction of 21.3% in Canadian women but an increase of 1.8% in French women. We can see than changes by comparing the rates in 1980 and 2012 in Figure 11.

Figure 11: cigarette smoking in 1980 in 2012, men and women

It is interesting to note the high prevalence of cigarette smoking in Japanese men. Despite this there is a very low incidence of deaths from CHD. We have already seen this in Greece, suggesting a major paradox, and now we see the Japanese extension of the Greek paradox. Where there is plenty of sun, there are few deaths from CHD regardless of cigarette smoking. Cigarette smoking cannot be regarded as the cause of CHD but it accelerates it, causing death about ten years earlier than in non-smokers.

It is also suggested that the decline in CHD deaths is due to the widespread use of statin medications. This is not likely to be the case because statins were only introduced in the 1990s. At present in the UK about 25%of people aged 70 take statins, and about 10% at the age of 50 years. We also know the small effect of statins. Even just after the height of the epidemic of CHD, in the 1980s, the benefit of treatment with a statin for five years benefitted only one in 90 very high risk men in the west of Scotland. With current much lower levels of death rate from CHD, it is likely that fewer than 1 in a 1,000 will benefit. The decline of CHD deaths would appear to have been spontaneous rather than the result of medical intervention.

The epidemic

Although there have been many descriptions of the dramatic decline of CHD deaths, such as those displayed above, these do not in themselves identify an “epidemic”. It is only when the corresponding onset  of the disease is identified that it can be called an epidemic. 

It appears to be only in the UK that good quality data are available on population mortality in the later part of the 19th and the first half of the 20th centuries, and the years leading up to 1970. These have been analysed by Dr Maurice Campbell (1891-1973), a leading cardiologist from Guy’s Hospital, London, and the first editor of the British Heart Journal. He was a highly respected physician. His important and unique work on the emergence of CHD during the 1920s seems have been forgotten - it is as though the study of CHD started only in 1980, or perhaps 1970.

Campbell’s study appeared in two short papers in the British Medical Journal in 1963. He noted the emergence of CHD in about 1924, with a doubling of deaths every few years, that is an exponential increase. He dealt with suggestions that this was just a change in diagnosis. He found evidence in the national records of an increase in total deaths from heart disease, at a time when deaths from syphilitic heart disease and rheumatic heart disease were diminishing considerably (helped by penicillin). 

I will present details of this very important work in a future Post.

We see therefore both the details of a major reduction of deaths from CHD since 1970, and also the emergence of CHD before 1970.

This data is published. Why is it not read, understood and made available to the public?

It is clear that there has been a true epidemic of CHD.

Figure 12: The 20th century epidemic of CHD in the UK

References:

Akira et al. International Journal of Epidemiology, 2015, Vol. 44, No. 5 p1614-24

British Heart Foundation. Coronary Heart Disease Statistics, 2014 edition.

Stamler J. The marked decline in coronary heart disease mortality rates in the United States, 1968-1981; summary of findings and possible explanations. Cardiology 1985; 72: 11-22.

UK Department of Health. The National Service Framework for Coronary Heart Disease: Winning the War on Heart Disease. The Stationary Office: London 2004.

Appleby J.  Does poor health justify NHS reform?  Brit Med J 2011; 342: 310

Campbell M. Death rates from diseases of the heart: 1876 to 1959. Brit Med J. 1963; 2: 1963. 

Campbell M. The main cause of increased death rate from diseases of the heart: 1920-1959. Brit Med J. 1963; 2: 712-717. 

Grimes DS. An epidemic of coronary heart disease. Quart J Med 2012; 105: 509-518.