Nutritional Biochemistry | Prof. Dr. Stefan Lorkowski - Arteriosclerosis

Nutritional Biochemistry


Prof. Dr. Stefan Lorkowski








Nutritional Biochemistry  >>  Institute of Nutrition Science  >>  Friedrich Schiller University Jena




















Historic background


Leonardo da Vinci was probably the first to describe the macroscopic appearance of atherosclerotic arteries. When he illustrated the arterial lesions in an elderly man at autopsy, he suggested that the thickening of the vessel wall might be due to “excessive nourishment” from the blood. In general terms, Leonardo da Vinci’s conclusion still holds true, yet another tribute to the great man’s tribute.

The term »arteriosclerosis«, a synonym of the term »atherosclerosis«, was introduced by the German-born French surgeon and pathologist Johann G.C.F.M Lobstein many years later in 1833. Lobstein considered arteriosclerosis as a hardening of the arterial wall caused by the remodeling of the tissue in response to ageing, metabolic dysfunction and hemodynamic stress.

The German physician Felix J. Marchand coined the term »atherosclerosis« (from the Greek words »athere«, gruel and »scleros«, hard) to emphasize the macroscopic features of the disease. In Anglophone regions, the word »atherosclerosis« is often used synonymously with arteriosclerosis. The word »atheromatosis« was coined by the London surgeon Joseph Hodgson in 1815 to describe the fatty degeneration characteristic of atherosclerotic arteries. This term is still used as a synonym of arteriosclerosis or atherosclerosis.

Rudolf Virchow, a German pathologist and statesman, was the first to introduce the idea of atherosclerosis as an inflammatory process; a concept that is still valid today and is at the time of writing a field of very active research.

Frequency and clinical importance


Atherosclerosis is a partly inflammatory, partly degenerative condition affecting the large and medium-sized arteries. Most, perhaps even all, adults develop atherosclerosis to some degree, so that the disease may be regarded as ubiquitous. The important question, therefore, is not its absolute prevalence, but the degree to which it causes clinically significant disease. This in turn is related not so much to the atherosclerotic process per se but to the complications it causes by either reducing the blood flow in the affected artery, a process termed ischemia, or by provoking clotting of the blood in the affected vessel. These clots may remain at the site of their formation and are then called thrombi. Alternatively, they may break off in whole or in part and be carried with the blood flow to cause blockage at some distant location. Such moving blood clots are called emboli (plural of embolus). If a thrombus is not large enough to block the artery completely, it may cause no symptoms and gradually be incorporated into the atherosclerotic plaque. Indeed, many older atherosclerotic lesions show histological evidence of incorporated thrombi, so that this is probably the more likely fate of thrombi. However, a large-enough thrombus may completely block (occlude) the artery in which it forms, cutting off blood flow in the affected vessel. If this is an end-vessel, i.e. the exclusive supply of an area of tissue, then this area of tissue will be completely starved of oxygen and die in a process called infarction.


About 40% of all deaths in developed countries are due to cardiovascular disease, and most of these cardiovascular deaths are due to complications of atherosclerosis (see Table 1 for data from Germany as an example of a Western developed country). In Germany, for example, about 250.000 people suffer a myocardial infarction every year. Despite improvements in intensive care, about half of the people suffering a first myocardial infarction will die within four weeks. A main reason for this is that in up to a half of all cases, a first myocardial infarction occurs “out of the blue” without any warning symptoms. These stark statistics underline the need for measures to prevent myocardial infarction from occurring in the first place. These include refraining from smoking, eating a balanced diet, taking regular exercise and avoiding being overweight. Treatment of other risk factors, in particular high cholesterol levels, high blood pressure or diabetes mellitus are also important in reducing heart attack risk. As the world's population ages, and as many countries improve economically, the impact of atherosclerosis worldwide is set to increase dramatically in the next 30 years. A measure of this is that in 2003, infectious disease was for the first time in the history of mankind supplanted as the number one killer. This dubious distinction now goes to atherosclerosis.

Major clinical features and complications


As noted above, many of the clinical features of atherosclerosis are due to the formation of a thrombus at the site of an atherosclerotic plaque. When this occurs in the heart, the result is a myocardial infarction, which is commonly known in the US as a “coronary” and in Britain and its former colonies as a “heart attack”. If the process occurs in the brain, the result is a stroke. More rarely, blockage of an artery supplying the lower limb, or a kidney, or part of the gut may occur, resulting in the death (necrosis) of these tissues. A feature of atherosclerosis occurring particularly in the arteries of the neck is that many small emboli may be formed over time causing temporary blockage of small brain arteries. This may lead to multiple small strokes (transient ischemic attacks) from which patients recover in a short space of time. Such transient ischemic attacks require urgent attention, as they are often the harbingers of a full-blown stroke. Finally, it has become clear in recent years that many cases of dementia in the elderly are due not to Alzheimer's disease, but to diffuse atherosclerosis of the arteries of the brain, sometimes accompanied by multiple transient ischemic attacks. This is termed vascular dementia.


Previously, it was thought that clotting occurs mainly at the site of advanced disease. However, more recent research has shown that smaller atherosclerotic plaques termed “culprit lesions” are more often associated with thrombotic events. These culprit lesions are metabolically active, and are characterized by a soft lipid core covered by a fibrous cap. In most cases, the event leading to thrombosis appears to be a tear of the fibrous cap in a process called plaque rupture. This exposes the circulating blood to the interior of the atherosclerotic lesion, which triggers the clotting cascade in the blood. In some cases, it appears that thrombosis may occur even without rupture when there is a break in the layer of cells lining the artery at the location of an atherosclerotic plaque. Such a break in this layer of cells is termed superficial erosion.


Other important clinical features of atherosclerosis relate to the ability of some plaques to reduce flow in the affected artery that the oxygen supply of the downstream tissue is imperitted. An oxygen supply that is adequate under resting circumstances may no longer be sufficient when tissue demand rises as, for example, during exercise. This lack of oxygen causes pain in the affected tissue. If this occurs in the heart, the result is angina pectoris, if it occurs in the legs it results in a condition known as intermittent claudication. A further important complication of atherosclerosis concerns the aorta, which is the main artery leading from the heart. Atherosclerosis of the aorta may weaken the wall of this vessel to such an extent that it bulges out. This is called an aortic aneurysm. An aortic aneurysm may bleed into the surrounding tissue, causing pain. Alternatively, and catastrophically, it may burst, leading to massive internal bleeding and sudden death.



Risk factors


Atherosclerosis is a complex disease that does not occur for a single reason. Epidemiological studies have identified factors that influence both the susceptibility to atherosclerosis and its progression and outcome. Disease mediators that influence the clinical outcome of atherosclerosis are termed “risk factors”. Risk factors may be divided into those that can be modified and those that cannot. Non-modifiable risk factors include age, male sex, certain genetic mutations and a positive family history of early-onset atherosclerosis. The modifiable risk factors for atherosclerosis include smoking, overweight and obesity, lack of exercise, psychological stress, low social status, poor diet, high blood pressure, high LDL, low HDL, high triglycerides, high levels of a lipoprotein called Lp(a), and the presence of diabetes mellitus.



Adapted from

Lorkowski & Cullen. Atherosclerosis. Encyclopedia of Life Sciences 2006.









Adaptive thickening




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Stefan Lorkowski | 2008-2010


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