One of two deaths in Europe can be ascribed to cardiovascular disease (CVD), and a third of men and one in four of women who die before age 65, die from CVD. The main background of these clinical manifestations is to be found in the circulatory system, the main task of which is to provide oxygen and energy to bodily organs. The organs are reached through arterial vessels to and venous vessels from the organs. The most common disorders of the vessel wall are due to the pathogenic processes associated with atherosclerosis and with hypertension.

The morphological changes of the artery wall have been examined and described in various kinds of animal and human studies. They have been subject to both experimental and observatory studies. The relevant research fields range from molecular biology to public health. The methodologies and study subjects range from paper and pencil surveys of thousands of men and women, who are examined in large cohorts, to cellular mechanisms, which mediate the atherosclerotic processes in the vessel wall.

CVD is the disease, which is the number one killer in all countries, not only in the Western world but lately also in developing nations of the third world.

In epidemiology and public health, both prevalence and incidence figures are central.

In addition the concept of “risk factors” is crucial.

Risk factors have been shown to be statistical predictors of CVD, thus they have been observed to precede the clinical manifestations of CVD. However, they should not be confused with true causal factors, for that role they would have to be demonstrated as causal in experimental studies.

Atherosclerosis starts early in life. In a postmortem study of young Americans, who died from external causes, relatively advanced atherosclerotic changes were seen in the coronary arteries. These were found in a small proportion of men, already in their teen age years. In the age group 30–34 years such changes were observed in, every fifth man. In women of the same age, 1 out of 12 had coronary artery changes, which were indicative of an atherosclerotic process (McGill et al. 2000).

Although these vessel wall changes were observed in early age, the clinical manifestations usually occur much later in life. Hence the disease has a long symptom-free clinical course. The atherosclerotic process is known to increase with increasing age and to accelerate with and be dependent upon lifestyle as well as upon genetic predisposition (Naghavi et al. 2003a, b).

In order to visualize the atherosclerotic changes, angiographic examinations of the coronary arteries with X-ray opaque dye are frequently conducted. Although these are clinically useful and highly informative diagnostic procedures, they may be difficult to interpret and subject to great variations. A normal coronary angiogram is no guarantee for healthy vessel walls (Naghavi et al. 2003a, b).

Some changes in the vessel wall would not be defined as stenotic changes, because they do not cause a readily detected narrowing of the vessel lumen. Such changes may also have the potential to rupture, and be the cause of a rapidly developed clot that can obstruct the blood flow.

Atherosclerotic processes in turn may lead to a variety of clinical manifestations:

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