What is a mother vessel
Atherosclerosis arises differently than expected
Professor Axel Haverich is a very well-known cardiac surgeon and director of the Clinic for Cardiac, Thoracic, Transplant and Vascular Surgery at the Hannover Medical School (MHH).
The cardiologist journal "Circulation" has now given him the opportunity to make his personal ideas about the development of atherosclerosis known to a wider public under the heading "On my mind".
Haverich intends nothing less than to give atherosclerosis research a new direction - and in a very concrete sense: While according to current understanding, the process of atheromatous change in the vascular wall runs from the inside to the outside - namely from the lumen-side intima into deeper wall layers , according to Haverich's theory, the direction is exactly the opposite, namely from the outer wall of the arteries to the media and intima.
This development starts with the degeneration of tiny supply vessels in the outer wall layer called adventitia.
Research has spawned many theories
For more than a century, researchers have struggled to decipher the pathogenesis of atherosclerosis. Many theories arose from this. More recently, the "response to injury" hypothesis propagated by the American researcher Russell Ross has met with approval.
Thereafter, tiny injuries to the intima, which consists of an endothelial cell layer, set the atherosclerotic process in motion. These injuries can therefore have many causes such as high blood pressure, damage from bacterial toxins, viruses or antigen-antibody reactions.
The endothelial cell damage then leads to tissue proliferation induced by growth factors and to the migration of smooth muscle cells from the media into the intima and the formation of fat-storing foam cells.
Macrophages are supposed to convert into foam cells by absorbing modified (oxidized) "low-density lipoproteins" (LDL). So-called "fatty streaks" develop as an early form of atheromatous plaques.
With the LDL, the blood lipids came into play as an important component of the pathogenesis. As a result, chronic inflammatory reactions were increasingly discussed as part of the complex pathogenesis.
Haverich does not share the common notion that blood lipids accumulate on the intima and, in the course of an inflammatory and immunological reaction, create stenosing vascular lesions that affect deeper layers.
For him, the events begin elsewhere, namely in Adventitia. In larger arteries there are tiny vessels in this outer wall layer - called vasa vasorum - that supply the vessel wall with oxygen and nutrients.
Atherosclerosis - A Microvascular Disease?
These supply vessels can close. According to Haverich, inflammatory reactions can be the trigger for such closures, which in turn can be caused by viruses, bacteria, fine dust particles or oxidized LDL particles.
As with coronary occlusion with resulting myocardial infarction, occlusions of the vasa vasorum lead to infarctions in the arterial wall. The cells dead as a result of ischemia, including fat deposits, would then be broken down by the immune system in a "repair process".
This would create "cell waste" in the form of plaques, which led to the thickening of the inner wall of the vessel and ultimately to the "closure of the mother vessel".
Atherosclerosis is therefore primarily a microvascular disease of the adventitia and not a disease of the large arteries, which are only affected secondarily as a result of the microvascular disorder, argues Haverich.
Skepticism is based on experience
His skepticism towards the conventional explanatory model of atherogenesis results from daily experiences in the operating room. During bypass operations, it can regularly be observed that certain coronary segments are massively affected by plaque infestation, while others are still in an almost virgin state.
This observation of focal vascular changes can also be made in other arteries, it speaks against atherosclerosis as a generalized disease.
The common feature of the plaque-free segments is that they are "surrounded by muscle on the outside," according to the cardiac surgeon. In addition, smaller arteries that are not supplied by Vasa vasorum are hardly affected by plaques. This enables cardiac surgeons to use chest wall arteries as bypass grafts.
At first there are no practical consequences
The explanatory model offered does not currently have any practical consequences. According to the new hypothesis, preventing degeneration or regenerating Vasa vasorum could be theoretical approaches to prevent atherosclerosis.
It remains to be seen whether future clinical research will ever find practical solutions here or look for them at all. Otherwise, it is to be expected that a sensible lifestyle with a healthy diet, abstinence from nicotine and sufficient physical exercise will also benefit the vasa vasorum - which is why Haverich once again recalls these preventive measures.
He also advocates the prevention of infections, for example through flu vaccinations.
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