Could it be that CHD, atheroma pathology has its origins amongst the ‘so young’? No, its an ‘old man’s disease’. Women were largely unaffected until after menopause. So its an ‘old man and woman’s disease’.What has changed? Well the extensive research into the origins and behavior of atheroma, fortunately over the last century, have revealed biological features that many in cardiology have been reluctant to accept as relevant to atheroma, or CHD. But the arterial lesions seen in the fetus, infant and child, endothelial cushions, fatty streak, fibrous plaque, and variations on that theme, are now accepted as primordial lesions for atheroma with time.
The study of these early lesions in this very young cohort commenced in the 1920’s and have continued until recently.Much of the work has been done by cardiac pathologists and there has been a reluctance in the cardiac clinical world to accept the thesis that initially, these lesions were fore-runners of future atheroma, CHD. It makes fascinating reading of research in vivo, of these deceased young, dissecting, coronary, basilar, renal arteries and the Aorta with a range of sophisticated instruments.This data was linked with similar studies of the young in the armed forces who died ‘naturally’ or in combat. A progression of morphology, an evolution of these lesions became apparent, with the later addition of lipid material, sometimes haemhorrage, thrombosis and calcification. This area of research, particularly the WWI,WWII, Korean and Vietnam young male autopsy studies, demonstrated that atheroma disease and CHD, although presenting clinically later in life, had its origins much earlier.Was there a medical, moral or economic case to pursue this ‘silent’ disease much earlier? Yes there was and it involved ‘avoidance’ behaviour, education and co-operation of the individual, the public. In the affluent world it has been a failure as the growing prevalence of CHD indicates.
The very first lesions were described as cushions, thickenings, most frequently found at bifurcations and thought to be pressure buffers in the arterial system, where blood flow was divided. Some of these lesions could near occlude flow in one conduit. They were found in the epicardial coronary arteries, where movement, lengthening and shortening, under systolic and diastolic pressure was thought to contribute. While the cushions arose at the junctions of the epicardial and intra myocardial arteries, they did not venture down the intra-muscular arteries.The cushions were more common proximally. This distribution is what we observe today with obstructing more complex atheroma lesions we demonstrate on angiography and ultra-sound.Its taken near on a century to confirm that the original cushions are the fore-runners of atheroma lesions. BUT, many early atheroma lesions, fatty streaks, fibrous plaques arise elsewhere, in the arterial system too, other than bifurcations. They do not arise in the low pressure venous system.In the 2nd and 3rd decade, all lesion gtypes arise. In the 3rd decade lipopotein(fat-cholesterol) is recognised, for the first time.
The early cushions, thickenings, often seen in the fetus first, are collections of mucopolysaccharides that then fracture the internal elastic lamina, and fibroblast and smooth muscle cells become active and thicken the intima with the endothelial cell, elastic lamina and media.The histology and biochemical changes that arise in lesions that evolve, include lipid phagocyte cells. Cellular and non cellular lipid is noticed first in the late teenage and early 3rd decade lesions. But remember the clinical presentation of this disease by narrowing of the artery or when the lesion leaks material and thrombus(clot) effects the same, is significantly later, although occurring earlier now.
All the early artery lesions inspite of what they looked like(fatty streak), had no evidence of lipid (fat) until much later, and were considered physiological. Did they arise in the progeny of mothers with abnormal lipid profiles?Yes, breast milk has a generous supply of lipids. The lipid protagonists avoided this area of research and were silent on the female gender difference of CHD. Oestrogen was the hormone saviour of the female sex for the worlds leading killer.Key’s 7 Countries Study was amongst males only. Well women confounded that with a change in life practice and nutrition. Some would say, as they became liberated, male identified, they shared our CHD burden. I would say some features of ‘liberation’have changed their CHD burden.
Barker, over three decades ago demonstrated that men and women in the UK who were born prematurely or of low birth weight, died prematurely of cardiovascular disease, CHD, stroke or hypertension. Low birth weight arose more commonly in low socio-economic areas of Britain then. Apart from its medical importance, this data had political and social significance.Has it been acted on?Well medicine needed an explanation and borrowed early data from the animal and botany research fraternity on the area of epigenetics. Medicine should never rely on political, social or economic support of science. We now know that gene expression, behaviour,(not structure) can be influenced by the nature of the gene enviroment, in this case the metabolic, physiologic status of the mother and fetus.Could this play a part in these early lesions and if not, why did low birth weight adults from deprived localities, die prematurely from cardiovascular disease?We know that cytomegalovirus infection is markedly more common, ubiquitous amongst the socially and economically deprived, as we found in the Central Queensland Aboriginal Study. Could this virus play a role in these early lesions?I am unaware of any studies of these lesions, looking for infectious agents.
Risk factor lists are as well known as the ten commandments and just as ineffective, because they are ignored. If the public knew that by the 2nd and 3rd decade, most in the affluent world will have early lesions of atheroma, CHD; knowing they have disease, will hopefully motivate them to survival. Its not really a lottery or bad luck. The aim then is to ensure these lesions do not evolve into obstructive lesions, that can disable and kill.If you do not know or are unsure how you avoid this dangerous evolution, consult your GP. No, magazines, internet, health books, health professionals, nurses, chemists, the Health Dept., will not take responsibility for your situation. Your GP is trained to diagnose, treat and manage your disease and has a professional and legal obligation to do so when you see them. They also have an obligation to advise on the nutrition practices to avoid disease, for the family and the newborn.State sponsored ‘cheaper’ and less knowlegable alternativies should be avoided.
Barkers studies and results, linked like ‘lego’ with growing epigenetic knowledge concerning the factors and enviroment provided maternally, that influenced the fetus in its developement. It became more apparent that the mothers metabolic and physiological homeostasis before and during pregnancy was potentially able to influence future biological factors and diseases.Woman was ‘biologically precious’.